MARCH 26, 2019 BY ERIC TREXLER

The Metabolic Adaptation Manual:

Problems, Solutions, and Life After
Weight Loss
Why does dieting suck so much? This article is your comprehensive guide to metabolic
adaptation and life after weight loss

Table of Contents [hide]

o
 Elevate your training and nutrition with an expert coach
 Part 1. The Problem: Metabolic Adaptation To Weight Loss
o Mitochondrial Efficiency
o The Role of Hormones
o Effects on Energy Expenditure
o Conclusion
 Part 2. The Solutions to Metabolic Adaptation
o Dealing With Reductions in Energy Expenditure
o Balancing Macros To Maintain Muscle and Performance
o Managing Cardio For Successful Weight Loss
o Other factors to consider
 Sleep and stress
 Supplements
o Conclusion
 Part 3: Life After Weight Loss
o Body Fat Overshooting
o Reverse Dieting Versus Recovery Dieting
o How Long Does Recovery Take?
o Psychological Aspects After Weight Loss
o Conclusion
 Summary
o
 Elevate your training and nutrition with an expert coach
o Spread the love
o Related
I n 2013, I showed up for a graduate school interview with a great

deal of enthusiasm and a diverse array of potential research topics in

my head. Later that year, I showed up to actually begin graduate
school. I was about 40 pounds lighter, too depleted to display anything
resembling enthusiasm, and my most pressing research question was
now crystal clear: Why does dieting suck so much?

As you might have inferred, I did a bodybuilding competition that

year. This is a unique case of weight loss, in which the changes occur
fairly rapidly, and the end goal is an exceptionally low body fat level.
However, the rigors and challenges of weight loss are not entirely
reserved for physique athletes, and the robust physiological defenses
against weight loss apply to a wide variety of dieters. I began my
graduate school career by writing a review paper about the
physiological hurdles we face in the weight loss process, which guided
me toward a series of small studies on the matter. This three-part
article discusses the problems we observed, the solutions I propose,
and some suggestions to promote a smooth transition to life after
weight loss.

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Part 1. The Problem: Metabolic

Adaptation To Weight Loss
The great irony of weight loss is that our modern problems were our
ancient saviors. Think back to a much simpler time, before humanity
was encumbered by desk jobs and student loan debt. Our evolutionary
ancestors woke up each day for the purposes of obtaining
nourishment, avoiding harm, and keeping the species viable, and that
was enough for them. But this was also a time when food availability
was highly uncertain. In terms of survival and reproductive success,
fortune favored the individuals most able to store up energy when
food was widely available, so they could rely on it when food was hard
to come by. This is the general premise of the Thrifty Gene Hypothesis;
while the hypothesis is an oversimplification that fails to fullydescribe
the modern epidemics of obesity and cardiometabolic disease, it
remains a basic but useful conceptualization of the modern plight of
dieters. Our ability to effectively store fat allowed our ancestors to
stay alive during times of famine, but it also predisposed us to store a
whole bunch of unwanted energy (fat) in an era of unprecedented food
availability. Metabolic adaptation is an intentionally broad term that
describes the collection of responses our body has to fight back
against weight loss attempts and can be viewed as the “other side” of
the Thrifty Gene Hypothesis. While much attention has been dedicated
to our ability to store fat during times of feast, metabolic adaptation
addresses our body’s ability to use energy more economically in times
of famine. With complementary systems to promote fat acquisition
and oppose fat loss, we have been endowed with the gift (or curse)
that made us perfectly suited to survive ancient famine and struggle
with modern weight loss.

Since we’re talking about survival mechanisms, this article is written to

address the challenges that come with somewhat intense weight loss
attempts. A male that diets from 23% body fat to 18% body fat over a
reasonable time frame is not coming face to face with his impending
starvation, so the magnitude of adaptation is typically mild. When
weight loss attempts become more extreme – either by losing huge
amounts of weight, losing weight very rapidly, or pushing body fat
storage close to the minimum amount required for survival – the
adaptations become much more pronounced. While many equate
metabolic adaptation (Figure 1) with an adaptive drop in energy
expenditure, also known as adaptive thermogenesis, the full breadth of
metabolic adaptation also involves alterations in a wide range of
hormones, neuroendocrine control of appetite, and even reproductive
function. The specific sites of adaptation range from the most
powerful control centers of the brain to the microscopic mitochondria
within our cells.
 Figure
1. A basic theoretical model of metabolic adaptation. A/A/T
hormones = Anabolic, Anorexigenic, and Thermogenic hormones; O/C
hormones = Orexigenic and Catabolic hormones. Dotted lines represent
inhibition. Source: https://jissn.biomedcentral.com/articles/10.1186/1550-
2783-11-7© Trexler et al; licensee BioMed Central Ltd. 2014
Mitochondrial Efficiency

If you remember high school biology class, you might know

mitochondria as the powerhouses of the cell, and adenosine
triphosphate (ATP) as the energy currency of the cell. These two
metaphors provide the basic foundation from which we understand
macronutrient metabolism. When you want to use energy to make a
biological “purchase,” such as protein synthesis, muscular movement,
nerve transmission, or virtually anything else, you’re going to need to
come up with the form of energy currency that is accepted. You take in
dietary energy in the form of carbohydrate, fat, protein, and alcohol;
this is like accepting payments in euros, Japanese yen, and Swiss
francs, but living in a place where you can only use US dollars to make
purchases. Macronutrient metabolism is the process by which these
various currencies are converted to the currency you need (ATP), and
mitochondria play a huge role in the process.

A comprehensive review of macronutrient metabolism is well beyond

the scope of this article, but a very simplified explanation will suffice.
When we need some ATP, we ultimately funnel the majority of our
stored or eaten energy toward two primary pathways: aerobic
glycolysis and the tricarboxylic acid (TCA) cycle (also known as the
Krebs cycle). Both processes directly produce a little bit of ATP, but
they also produce nicotinamide adenine dinucleotide (NADH) and/or
flavin adenine dinucleotide (FADH2). These make their way to the
inner membrane of mitochondria, where the majority of total ATP
production takes place in a process known as oxidative
phosphorylation. Electrons are passed from NADH and FADH2 down
the electron transport chain; this process causes protons to be pumped
from inside the inner membrane to the space that exists between the
inner and outer membranes of mitochondria. This establishes an
electrochemical gradient, and the protons “want” to get back across
the inner mitochondrial membrane.

If oxidative phosphorylation was 100% efficient, all of the protons

would form an orderly line in front of the ATP synthase enzyme, use
this transporter to cross back over the inner mitochondrial membrane,
and ATP would be created in the process. But energy conversion isn’t
100% efficient. Consider the combustion engine in your car; the
chemical energy of gasoline is converted to the mechanical energy of
movement, but not with perfect efficiency. The inefficiency of this
conversion results in heat production, to the extent that the engine
requires a cooling system to help dissipate this excess heat. The
human body is no different, and heat is the byproduct of our
metabolic inefficiency. Under normal conditions, oxidative
phosphorylation is about 40% efficient, give or take. This means that
roughly 40% of the available energy actually gets used for ATP
production, with the remaining ~60% dissipated as heat. However, this
efficiency can be altered.

When some of the protons in the intermembrane space circumvent

ATP synthase and “leak” back across the inner membrane, ATP
is not produced in the process. In this case, the body completes the
preliminary steps of metabolizing the macronutrient, releasing heat
energy in the process, but doesn’t actually produce the ATP that
makes the whole process worth it. This leakage is comprised of basal
proton leak, which is largely dictated by a transport protein called
adenine nucleotide translocase (ANT) and the fatty acyl composition of
the inner mitochondrial membrane, and inducible proton leak, which is
actively regulated by uncoupling proteins (UCPs). These proteins get
their name from the term uncoupled respiration, which describes the
process in which energy substrates are metabolized but result in heat
production rather than ATP synthesis. The infamous weight loss drug
2,4-dinitrophenol (DNP) works by uncoupling respiration; the result is
a potentially disastrous and sometimes fatal increase in metabolic rate
and heat production. That is, of course, an extreme example that
doesn’t occur with normal physiological processes.
In mammals, uncoupled respiration due to proton leak is a non-
negligible contributor to energy expenditure, accounting for about 20-
30% of resting metabolic rate in rats under normal circumstances.
Proton leak is higher in warm-blooded animals than cold-blooded
animals, and proton leak in mammals is inversely related to body mass
due to differences in body temperature regulation. So, proton leak
probably accounts for a smaller percentage of metabolic rate in
humans compared to rats. Nonetheless, its impact is large enough to
have meaningful effects, as demonstrated by the observation that
proton leak correlates with weight loss success and that diet-resistant
individuals with below-average weight loss outcomes tend to
experience less proton leak. Aside from these apparently innate
differences in proton leak between individuals, there is evidence to
suggest that the magnitude of proton leak adapts in response to
energy restriction and weight loss.

Much of the research pertaining to weight loss and proton leak is done
in rodents; while this requires a small leap of faith in assuming that
the results are relevant to human beings, it allows for an otherwise
impossible level of experimental control. In rodents, studies
using short-term (two weeks to two months), medium-term (six
months), and long-term (12 to 18 months) calorie restriction have
reported decreased proton leak, which is indicative of an adaptive
increase in mitochondrial efficiency. Conceptually, it appears that
mitochondria sense the relative lack of energy availability and adapt in
a manner that reduces wasteful proton leak. This increases the ability
of mitochondria to meet their ATP-production “quota” while burning
fewer calories in the process. Exactly how they go about doing this is a
bit less straightforward. In these rodent studies, an unexpected but
consistent observation was that UCP-3 protein content increased,
which is counterintuitive; while proton leak decreased, this protein
that facilitates proton leakage actually increased. Human studies,
however, indicate the opposite.

One study evaluated UCP-2 and UCP-3 mRNA levels in lean, obese, and
weight-reduced humans. They found that muscle levels of UCP-3 were
reduced in people who had lost weight and stabilized at their reduced
weight, which is intuitively consistent with reduced proton leakage.
Another study by a different research group reported similar findings,
with lower UCP-3 mRNA expression observed in individuals who had
undergone prolonged energy restriction to induce weight loss. Perhaps
the strongest evidence supporting the importance of proton leak and
UCP-3 comes from a 2002 study in which “diet-responsive” and “diet-
resistant” individuals were classified based on weight loss results, then
compared on a variety of parameters. Results showed that diet-
responsive individuals lost 43% more weight, and this difference was
accompanied by significantly higher rates of proton leak and UCP-3
mRNA levels. Taken together, it seems likely that rodents and humans
share a common strategy in which mitochondrial proton leakage is
reduced in response to energy restriction, as a fairly straightforward
means of conserving scarce energy stores. While differing changes in
UCP-3 expression between rodents and humans are less
straightforward, it is possible that subtle distinctions exist with regard
to the mechanisms by which they restrict proton leakage.

The Role of Hormones

Uncoupled respiration and proton leak are heavily mediated by

hormonal controls. One of the most notable hormones affecting
energy expenditure is thyroid hormone (TH; particularly the more
biologically active form, triiodothyronine [T3]). Low TH levels are
consistently associated with low metabolic rates, and high TH levels
are consistently associated with high metabolic rates. Part of this
effect is related to the fact that TH stimulates ATP-consuming
processes and muscle ATP consumption, which increases the body’s
overall demand for ATP. When ATP demand is increased, production
increases to match, which requires us to burn more of the calories we
consume and/or tap into our fat storage for energy. A substantial
portion of TH’s effect on metabolic rate, however, is related to proton
leak. Thyroid hormone increases basal leak, with protons simply
traversing the inner membrane itself or being transported via ANT,
and also increases inducible leakage by stimulating UCP-3 expression
and activation. In a large number of weight loss studies, including
both case studies and observational studies in physique athletes, an
unfortunate reality of weight loss is a reduction in TH levels, which
likely contributes to a reduction in proton leak.

Thyroid hormone also stimulates the metabolic activity of brown

adipose tissue (BAT), a type of fat tissue that specializes in uncoupled
respiration. The primary purpose of BAT is to generate heat. Its
mitochondria are loaded with uncoupling proteins; when BAT is
activated, it burns calories like crazy, but yields a bunch of heat rather
than ATP due to this uncoupling. While BAT makes substantial
contributions to energy expenditure in small mammals and human
babies, especially in cold conditions, it was long thought that humans
do not have BAT in adulthood. Advances in research techniques have
increasingly enabled researchers to identify the presence of brown
adipose tissue (and a similar thermogenic fat known as beige adipose
tissue) in adults in amounts that could make small, but non-negligible,
contributions to energy expenditure. While BAT is likely to play a very
small role in the overall picture of energy expenditure during weight
loss, reduced activation of this tissue via TH reductions may
contribute to weight loss-induced reductions in uncoupled respiration.

When it comes to metabolic adaptation, TH is definitely not the

hormone assuming most of the blame. In fact, the observed drop in TH
is influenced, at least in part, by a more influential hormone called
leptin. Leptin is primarily produced by fat cells, but production is only
high when they are full and happy. When we lose weight, our fat cells
store less energy than they used to, and they begin producing less
leptin as they shrink in size. Even before we lose a meaningful amount
of weight, leptin drops substantiallyjust from a few days of energy
restriction, which is most closely related to the reduction of dietary
carbohydrate (rather than fat or protein). The hypothalamus is a brain
structure that serves as a key regulator of appetite and metabolism,
and leptin receptors in the hypothalamus allow fat cells to
communicate their fullness directly to the brain. As we’ll see
throughout this article, leptin is a high-profile mediator of countless
aspects of metabolic adaptation (Figure 2), eliciting effects on TH,
reproductive hormones, hunger hormones, cortisol, and multiple
components of energy expenditure. Metabolic adaptation entails a lot
more than just reduced energy expenditure, and the widespread
effects of leptin are a major reason for that. Staying on the topic of
uncoupled respiration and BAT, high leptin levels stimulate the
sympathetic nervous system via the hypothalamus, which results in
activation of BAT and a resulting increase in energy expenditure.
Leptin also stimulates thermogenesis (i.e., energy
expenditure) directly in skeletal muscle, independently of BAT. Weight
loss studies consistently show reduced leptin levels, with a
corresponding reduction in energy expenditure. In addition, human
BAT is indirectly activated by insulin as well. This insulin-mediated
effect is most markedly promoted by high-carbohydrate meals, which,
unfortunately, tend to be pretty hard to come by in the later stages of
a weight loss diet.

Figure 2.
Leptin is reduced by fat loss and the presence of an energy deficit, and the
activity of leptin is inhibited by high cortisol levels. As a result of reduced leptin
activity, widespread changes include increased hunger and reductions in
thyroid hormone, sex hormones, non-exercise activity thermogenesis (NEAT),
total daily energy expenditure (TDEE), sympathetic nervous system (SNS)
tone, and brown adipose tissue (BAT) activation.
There are also hormonal effects of energy restriction that extend
beyond mitochondrial efficiency or adaptive thermogenesis. Several
case studies have been carried out in physique athletes, and
alterations in anabolic and catabolic hormones are pronounced and
consistent. One such case studydocumented reductions in testosterone
while cortisol increased; our group did a similar case study and found
similar changes in testosterone and cortisol. Recently, there has been a
lot of discussion about whether or not post-exercise changes in
testosterone play an important role in muscle growth, and
the common consensus is that they do not. But it’s critically important
to distinguish normal, resting testosterone levels from short-term,
post-exercise elevations. Resting testosterone levels do appear to have
an impact on the growth and maintenance of lean mass (otherwise,
professional athletes probably wouldn’t have consistently risked their
careers to elevate it for the last several decades). Aside from its impact
on BAT activation, insulin is also known to have anabolic properties.
While there is some debate over how significant this effect is within
normal physiological ranges of insulin, a study in
bodybuilders documented a reduction in fasting insulin levels during
contest preparation, and insulin changes were significantly correlated
with changes in lean mass. This means that people who had larger
insulin reductions tended to lose the most lean mass. However, it’s
important to note that they also tended to lose more fat mass, so this
could potentially just be demonstrating that some individuals
preserved some additional lean mass by failing to get super lean.

Increased cortisol also contributes to the threat of lean mass loss

while dieting. Multiple case studies have reported elevated cortisol late
in contest preparation, which likely relates to the combination of
energy restriction, training load, and the general stress that
accompanies competition. Manipulating cortisol within normal
physiological ranges has the capacity to alter the maintenance of body
proteins, with higher levels inducing protein breakdown. As we might
expect, there are a couple of case studies showing pretty substantial
loss of lean mass (more than 10 pounds of it) throughout contest
preparation in male bodybuilders. Taken together, these collective
hormonal disruptions during intensive weight loss threaten the ability
to maintain lean mass throughout the diet. This is problematic for
multiple reasons: the loss of lean mass directly opposes the goals of
just about any athlete attempting to lose weight, lean mass is
the primary determinant of resting metabolic rate, and such a loss of
lean mass is also linked to excessive hunger until that lean mass is
restored.

To make matters worse, loss of lean mass is not the only thing driving
excessive hunger. Hunger is probably the most undesirable side effect
of dieting for fat loss, and there are multiple hormonal responses that
play a direct role in the urge to eat. Ghrelin is mainly produced in the
stomach and is primarily known as a messenger to keep the brain
informed about short-term energy availability. After a meal, the
stomach produces less ghrelin, and the brain is aware that additional
energy is not acutely necessary. During times of fasting, its production
increases, and levels ultimately get high enough to induce hunger.
However, there is also evidence that ghrelin plays a role in sensing
long-term energy availability, and diet-induced weight loss increases
24-hour ghrelin levels. Unsurprisingly, two separate case studieshave
documented increased ghrelin levels from the beginning to the end of
contest prep in male bodybuilders.

We previously discussed leptin as a stimulator of BAT activity and

muscle thermogenesis, but its hypothalamic duties do not end there.
When leptin binds with its receptor in the hypothalamus, it initiates a
domino-effect of signaling events that result in decreased
neuropeptide Y (NPY) and agouti-related peptide (AgRP), with
increased pro-opiomelanocortin (POMC) and cocaine-and-
amphetamine-regulated transcript (CART). The result is that leptin
stimulates energy expenditure while also reducing hunger. A weight
loss-induced drop in leptin therefore has the unpleasant bonus of
reducing the number of calories you burn, while increasing your desire
to consume more of them. We know insulin as a potentially anabolic
hormone associated with lean mass retention, but it has appetite-
related roles as well. Insulin receptors are present throughout multiple
brain structures, including the hypothalamus, and insulin reduces
appetite upon binding to these receptors. Cortisol comes into play
here as well, as glucocorticoids (such as cortisol) oppose the effects of
leptin. It’s problematic enough that leptin is reduced during energy
restriction and weight loss, but increases in cortisol also impair the
biological function of the leptin that is still around, thereby amplifying
the negative effects of low leptin levels. Cortisol also promotes fluid
retention, at least in part by binding to mineralocorticoid receptors,
and is linked with appetite stimulation and increased cravings for
palatable foods. Collectively, chronic elevation of cortisol can promote
loss of lean tissue, make weight loss appear to stall by increasing
water retention, exacerbate the effects of low leptin levels, and
potentially increase urges to overeat. As weight loss causes increases
in ghrelin and cortisol with reductions in leptin and insulin, this four-
pronged attack on your hunger regulation yields a very unhappy
dieter.

Hormonal adaptations to weight loss also have the capacity to

interfere with reproductive function, thereby amplifying the
unhappiness. Intuitively, this makes a great deal of sense from an
evolutionary perspective. Low energy availability is perceived as a sign
of insufficient resources in the environment, which is only exacerbated
by the energy cost of gestation and further division of resources to
accommodate a population increase via reproduction. During contest
preparation, male testosterone levels don’t just drop, they plummet.
Aside from the obvious threat to muscle mass retention, lack of libido
is a very common complaint of male physique athletes late in the
contest preparation process. Similarly, female athletes typically
experience a drop in estradiol in response to contest prep, along with
menstrual cycle disruption. The severity of this disruption may
depend upon a variety of factors, including acute energy availability,
magnitude of overall weight loss, body fat percentage, and genetic
predisposition. In less severe cases, menstruation may simply become
more irregular; in more severe cases, menstruation may cease
altogether. A case study of a female figure competitor revealed that
menstruation became disrupted early in the contest preparation
process, had ceased by the end of prep, and did not return until a full
71 weeks after competition. These reproductive side effects are not to
be taken lightly; in addition to being generally unpleasant, there are
long-term consequences to maintaining a prolonged state of sex
hormone suppression, such as impaired bone health and fertility. The
primary hormonal adaptations to weight loss are summarized in
Figure 3.
 Figure 3.
Changes in key hormones that occur during weight loss.
As the previous sections would suggest, I prefer not to think of
metabolic adaptation as just a drop in metabolic rate. Rather, I prefer
to conceptualize it as a multifaceted set of adaptations that involves
regulation of energy expenditure, appetite, reproductive function, and
the balance between anabolism and catabolism. In recent years, the
International Olympic Committee has used the term “relative energy
deficiency in sport,” or “RED-S,” to summarize a similar physiological
state. The biological goal is to constrain energy use during times of
underfeeding, but the effects are widespread, and to discuss them in
isolation from one another is a bit short-sighted. Despite this wide
variety of adaptations to weight loss and energy deficiency, the drop in
energy expenditure, also known as adaptive thermogenesis, is the one
that garners much of the attention in the fitness world. Up to this
point, we’ve mentioned energy expenditure in a couple of esoteric
contexts that have yet to be linked together in a cohesive manner. We
have talked about proton leak, brown adipose tissue activation, and
hormones related to ATP consumption and thermogenesis. But
physique athletes and other dieters rarely utter a single one of those
words in day-to-day conversation about dieting. So, it’s time to put
some of these concepts together to discuss the aspect of metabolic
adaptation that everyone cares about: energy expenditure.

Effects on Energy Expenditure

The effects of metabolic adaptation on energy expenditure are the

ones everyone cares about, because they’re the ones we actually tend
to act on by manipulating our diet and exercise protocols. It becomes
apparent that our energy expenditure is lower when our weight loss
slows down, so we have to either reduce food intake or increase
cardio, and we’d much prefer to do neither. But before getting into
specific aspects of metabolic rate adaptations, we need a quick primer
on energy expenditure in general.

Every day we consume energy and we burn energy; the net balance of
this equation determines whether we gain or lose weight. As indicated
in Figure 4, total daily energy expenditure (TDEE) describes the total
number of calories we burn in a given day, and TDEE is made up of
four components:
  Basal Metabolic Rate (~70% of TDEE in general population)
 This describes the energy required to simply keep our body
“on,” at rest, assuming we lay in bed all day without moving
or eating.
 Thermic effect of feeding (~10% of TDEE in general population)
 This describes the energy used in the process of eating,
digesting, metabolizing, and storing food.
 Exercise Activity Thermogenesis (~5% of TDEE, depending on how
much you exercise)
 This describes the energy used during structured, intentional
exercise.
 Non-Exercise Activity Thermogenesis (~15% of TDEE, depending
on your activity level)
 This describes the energy used for any movement that isn’t
purposeful exercise. This would include walking around your
school or office, doing yard work, taking out the trash, and
even fidgeting in your chair

Figure
4. The approximate relative contributions of basal metabolic rate (BMR),
thermic effect of feeding (TEF), exercise activity thermogenesis (EAT), and
non-exercise activity thermogenesis (NEAT) to total daily energy expenditure
in the general population.
To tie up some loose ends, let’s consider a few terms we have
mentioned haven’t yet fully contextualized. We know that brown
adipose tissue increases thermogenesis, particularly in response to
cold exposure, thyroid hormone, leptin, and insulin; BAT
thermogenesis would therefore primarily affect basal metabolic rate
and the thermic effect of feeding. We noted that thyroid hormone and
leptin increase mitochondrial uncoupling and muscle thermogenesis;
these broad effects would have the potential to affect essentially all
components of energy expenditure. So, all of the mitochondrial and
thermogenesis-related concepts previously discussed
fit somewhere within our four components of energy expenditure, and
sometimes span multiple components. Unfortunately, when we
embark on a weight loss diet, all four components are influenced to
some extent.

Thermic Effect of Feeding

In weight loss diets, the thermic effect of feeding will be reduced for a
very straightforward reason, with no need for any biologically adaptive
explanation: If you eat less food, you won’t burn as many calories in
the process of eating, digesting, metabolizing, and storing it. It
remains unclear whether or not we have an adaptive shift in the
thermic effect of feeding (that is, a disproportionate increase in the
efficiency with which we handle the energy cost of feeding). While
there are some isolated studies suggesting that a small adaptation
favoring a relatively lower thermic effect of feeding does occur, the
collective evidence would suggest that any such adaptation is
negligible in magnitude. For example, Miles et al found that feeding
caused subjects to burn 13% of the calories consumed in an
experimental meal before weight loss. After losing ~7.3 kg over a 12-
14 week period, participants burned 12.5% of the calories consumed in
the very same meal; this amounts to a difference of 3 Calories. Leibel
et al carried out an ambitious study in which some subjects were over-
fed to induce weight gain, and others were under-fed to induce weight
loss. Their results showed that weight gain from intentional
overfeeding did reduce the energy efficiency of feeding, leading to a
relatively greater thermic effect of feeding. In contrast, weight loss
from intentional under-feeding did not increase this efficiency, and the
thermic effect of feeding was not significantly different when
comparing baseline values to the values obtained after weight loss.
Overall, the body of evidence suggests that the thermic effect of
feeding is lower during weight loss dieting, but this is caused by lower
overall food intake and less sympathetic nervous system activation in
response to caloric intake. If there is any adaptation that makes us
more efficient with regard to this thermic effect, it is very small in
magnitude.

Basal Metabolic Rate

A true “basal” metabolic rate is difficult to measure. It requires an

overnight laboratory visit to allow for metabolic rate assessment
directly upon waking, in the absence of food intake or substantial
movement. As a result, labs that are not equipped to house overnight
guests often use resting metabolic rate as a surrogate measurement.
They still require subjects to fast overnight, but they let the subject
come to the lab in the morning. To account for the movement
associated with transportation to the lab, they have the subjects lay
down and rest for a while before the actual measurement occurs.
Under these conditions, resting metabolic rate can be used as a pretty
solid representation of basal metabolic rate, and the terms are often
used fairly interchangeably in the literature.
Weight loss typically involves the loss of both fat mass and fat-free
mass; fat mass is a metabolically active tissue, and fat-free mass is
the primary determinant of energy expenditure at rest. As a result, we
fully expect resting metabolic rate to drop as we lose weight. In many
cases, the drop in resting energy expenditure is greater than we would
expect based purely on the loss of tissue, which suggests that an
energy-conserving adaptation has taken place. The study by Leibel et
al that evaluated the thermic effect of feeding also evaluated resting
energy expenditure; their results indicated that resting metabolic rate
was reduced following weight loss, even when accounting for the
amount of fat-free mass lost. While there are some studies showing no
effect of weight loss on resting metabolic rate, a meta-analysis on the
topic supports the findings of Leibel et al and suggests that resting
metabolic rate is indeed slightly lower in weight-reduced individuals
compared to controls. These data match up quite favorably with data
obtained from competitive physique athletes. For example, case
studies have reported drops in resting metabolic rate that far exceed a
magnitude attributable to lean mass loss and have shown resting
metabolic rates to be consistently lower than
predicted, even after accounting for the amount of lean mass. These
low values in physique athletes are almost certainly related to the
acute effects of energy restriction at the time of measurement, but the
loss of fat mass is most likely a contributing factor. Collectively, the
evidence would suggest that weight loss typically induces a small (but
not negligible) adaptive effect that reduces resting energy expenditure,
and that this is observed in both non-athletic populations and
competitive physique athletes.

Exercise Activity Thermogenesis

Exercise activity thermogenesis is a tough one, because we directly
control it. You decide how much weight training and cardio to do, so
you have the capacity to influence it substantially. For the sake of this
article, we’ll just consider the relative energy efficiency of exercise,
which describes how much energy you burn for a fixed amount of
exercise.

There are a couple “non-metabolic” reasons why you could use less
energy for the same amount of cardio as your weight loss diet
progresses forward. For any kind of locomotive cardio, such as
walking, running, or cycling, the task itself involves generating enough
force to transport the mass of your body. As you lose weight, the mass
is reduced, and you naturally require less energy to transport your
body a given distance. Even for some non-locomotive tasks like
stationary cycling, weight of the limbs is reduced, so slightly less
energy is required to perform the same amount of cycling work.
Another factor that is rarely discussed relates to the fact that a lot of
people, myself included, do absolutely no cardio unless required to.
Many forms of cardio are trainable skills that we become substantially
more proficient at as we do them more frequently throughout a weight
loss attempt. Using running as an example, there are about 22
factors (give or take) that relate to running economy. Many of them are
trainable, meaning that a novice runner can probably make substantial
improvements to their running economy over the course of a few
months. While this improvement in running economy is great for your
joints, it also means you’re probably covering the same distance with
greater efficiency, and therefore burning fewer calories in the process.
Aside from these predictable reductions in exercise activity
thermogenesis in response to a weight loss attempt, there are also
metabolic adaptations that increase energy efficiency and reduce
energy expenditure during exercise.

Researchers at Columbia did a study in which participants completed a

cycling test at their normal body weight, then repeated the test after
either gaining or losing 10% of their body weight. As the researchers
hypothesized, muscle work efficiency at lower exercise workloads was
increased following weight loss and decreased following weight gain.
This means that weight gain caused the participants to use more
energy to produce the same amount of physical work, whereas weight
loss caused the participants to use less energy to produce the same
amount of work. Several years later, the same lab
group replicated their finding, observing that muscle work efficiency
was increased by weight loss and decreased by weight gain. One
concern might be that the participants’ legs weighed less after weight
loss, which may affect the energy expenditure of cycling. Fortunately,
the researchers used little weights in one of these studies to replace
the leg weight that was lost; while the magnitude of the effect was
smaller after weight replacement, a significant effect remained. So, it’s
likely that exercise activity thermogenesis does indeed decrease
(relatively speaking) throughout the course of a contest prep, and this
effect is not exclusively the result of a lighter body or technique-
related improvements in exercise economy. This relative decrease can
certainly be offset by increasing the absolute amount of exercise.
However, as we’ll see in Part 2, such a decision is not without
drawbacks.

Non-Exercise Activity Thermogenesis

Non-exercise activity thermogenesis (NEAT) is the final component to
discuss, and it is unequivocally the most influential when it comes to
adaptive thermogenesis. Part of its impact relates to its capacity to be
so incredibly variable. If I know your body size and composition, I can
give a pretty good estimate of your resting metabolic rate. If I know
your macronutrient intakes, I can give a pretty good estimate of your
thermic effect of feeding. But two individuals of similar body size can
have a daily difference of up to 2,000 Calories when it comes to NEAT.
This variability is huge but not surprising when you consider the wide
range of factors that can affect NEAT. The hypothalamus plays a
primary role in regulating NEAT, in conjunction with components of
the hindbrain and mesolimbic system. The degree of NEAT is likely to
vary based on occupation, sex, age, and season, and the exact cues that
feed into these regulatory centers include temperature, activity level,
food intake, body composition, and a large number of neuroendocrine
inputs.

To mathematically quantify the importance of NEAT in adaptive

thermogenesis, let’s use the approximate numbers presented in a
review by Rosenbaum and Leibel, who are absolute legends in this
area: When a person loses 10% or more of their body weight, their total
daily energy expenditure drops by around 20-25%. Some of this drop
relates to the loss of body mass, but there is also an adaptive
component, as total daily energy expenditure ends up about 10-15%
below what we would expect based on body mass alone. Of that
adaptive component, up to 85-90% can be explained by alterations in
non-resting energy expenditure, and NEAT is by far the biggest
contributor. For an experimental example, Weigle et al studied the
effects of a 23% weight loss on energy expenditure. The results
indicated that total energy expenditure was about 24% lower than
could be explained by the loss of fat-free mass, but resting metabolic
rate was only 2-3% lower than predicted. Taken together, these
observations would suggest that weight loss induced a fairly
substantial reduction of energy expenditure, and this reduction was
largely attributable to reductions in NEAT.

The problem with NEAT is that it can be a bit difficult to measure in an

accurate and affordable manner. For example, Weigle et al made use of
controlled feeding protocols, daily weight changes, and linear
regression to make inferences about NEAT. One of the
classic studies regarding weight loss and NEAT was not actually
intended to study either topic and can be objectively categorized as a
very fortuitous mistake. A small group of people were placed in a 3-
acre dome, which was intended to be a completely closed, self-
contained world with a variety of biomes, much like a dome we could
theoretically set up on a moon or a different planet. This is more or
less the exact plot of a 1996 Pauly Shore movie that received an
implausibly low 4% rating on Rotten Tomatoes. You could argue that
the study fared a bit better than the film, but it was not without some
stumbling blocks. Most notably, the Biosphere inhabitants were
supposed to grow all of their own food, but they were unable to
successfully grow enough calories to support their energy needs. As a
result, the study became an unintentional weight loss study that lasted
a full two years.

Within the first six months, subjects lost 14% of their body weight,
which was maintained until leaving the dome. A week after leaving the
dome, energy expenditure was assessed via a 23-hour confinement in a
respiratory chamber and compared to control subjects. Total energy
expenditure was suppressed in the Biosphere residents compared to
controls, and this difference persisted after adjusting for relevant
characteristics (age, sex, fat mass, and fat-free mass). When in the
respiratory chamber, control subjects had nearly twice as much
spontaneous physical activity (fairly synonymous with NEAT) than the
Biosphere residents. When total energy expenditure was adjusted
for this factor, the difference between Biosphere subjects and control
subjects was no longer significant, which further highlights the huge
impact that NEAT has on energy expenditure during weight loss.
Lending further support to these findings, Leibel et al found a
significant reduction in energy expenditure that was not attributable
to resting metabolic rate, the thermic effect of feeding, or the loss of
lean mass following 10-20% body weight reduction. A
separate study had participants either gain or lose 10% of their body
weight, then maintain it. Weight loss resulted in an absolute non-
resting energy expenditure reduction of 37.5%, whereas weight gain
increased non-resting energy expenditure by 60.2%. Linear regression
showed that the change in non-resting energy expenditure explained
78% of the observed change in total energy expenditure among both
groups. As summarized in Figure 5, it is very clear that weight loss
causes a disproportionate drop in total energy expenditure, and it is
clear that NEAT is the primary component driving this effect.
 Figure
5. The effects of weight loss on various components of energy expenditure,
including total energy expenditure (TDEE), thermic effect of feeding (TEF),
basal metabolic rate (BMR), exercise activity thermogenesis (EAT), and non-
exercise activity thermogenesis (NEAT). Absolute effects pertain to raw,
unadjusted values. Absolute EAT “depends” because one can choose to
complete ever-increasing amounts of exercise, or restrict it altogether.
Relative effects refer to values that are scaled relative to lean body mass
(TDEE, BMR, NEAT), total mechanical work (EAT), or total caloric intake
(TEF). Loosely based on Figure 5 from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174765/
Conclusion

The original question posed was, “Why does dieting suck so much?” It
turns out, the research literature offers us a variety of answers to that
question. Weight loss attempts are met with changes in mitochondrial
function, hormone levels, and energy expenditure. These changes
produce some unpleasant side effects, threaten our ability to gain (or
even keep) muscle mass and strength, manipulate biological cues
pertaining to the regulation of appetite and activity level, and require
us to eat even fewer calories or incorporate even more cardio into our
training program. When metabolic adaptation first became a big
conversation in the fitness scene, it was treated as a controversial
topic. However, the content discussed in Part 1 of this article is
objectively noncontroversial. The scientific literature has rigorously
and repeatedly shown downregulation of energy expenditure, and the
long list of physiological changes that accompany it, in response to
weight loss. The controversy comes from how some of this
information has been discussed, such as implausible anecdotes of fat
gain despite remarkably low caloric intake, or the use of less rigorous
terms like starvation mode. Rest assured, there is not a single member
of our species that can elude the inescapable grasp of starvation; our
caloric needs for weight loss may fluctuate from person to person, but
we all have a number. Furthermore, nobody is failing to lose fat
because they are eating too few calories. Metabolic adaptation places
speed bumps in our path to fat loss, no more and no less. But this
raises the next important question: Can we do anything to circumvent
these speed bumps?

Part 2. The Solutions to Metabolic

Adaptation
As discussed in Part 1, one of the more pressing concerns we face
during weight loss is a reduction in energy expenditure. Part of this is
a result of reducing our body size, but part is also a disproportionately
large reduction in total energy expenditure that is mediated by a
variety of mechanisms involving the mitochondria, hormone levels,
and the brain. We don’t really observe a relative drop in the thermic
effect of feeding during weight loss, and the drop in resting metabolic
rate is fairly modest in magnitude. But the more notable changes are
related to non-resting energy expenditure and skeletal muscle work
efficiency.

Leptin is one of many factors contributing to reductions in energy

expenditure, but it is a key one. This hormone is reliably reduced
during and following weight loss, and it directly communicates the
fullness of adipocytes to the hypothalamus, a brain structure with
huge impacts on energy expenditure, hormone levels, and hunger.
Intuitively, this has led researchers to wonder if leptin replacement
injections would help resolve many of the unwanted changes
associated with low leptin levels. The good news is that experiments
have shown this to be an effective strategy, with leptin replacement
injections reversing the drops observed for total energy expenditure,
non-resting energy expenditure, skeletal muscle work efficiency,
thyroid hormone, and gonadotropic hormones that link leptin levels
with sex hormones and reproductive function. As an added bonus,
leptin administration reverses the hyperphagia, or extreme hunger,
observed with weight loss. The bad news is that you can’t just walk
down the street and buy some pharmaceutical-grade leptin, and even if
you could, it’d be really expensive. So, for our purposes, leptin
replacement is off the table, and we shift our focus toward more
practical strategies.

Dealing With Reductions in Energy Expenditure

While we know that the reduction of non-exercise activity
thermogenesis (NEAT) is a huge contributor to the reduction of energy
expenditure observed with weight loss, there isn’t much we can
consciously do about that in terms of physical activity. Of course, we
could try to be mindful of non-exercise activity during weight loss in a
qualitative sense. Consider a basic example: My mailbox is about 100
feet away from my front door. I get to the front door and realize I
haven’t checked the mail in a couple of days. If I’m not in contest prep,
I am almost certainly walking over and checking; when I’m in contest
prep, it’s far less likely. When I’m not prepping, I tend to pace around
the room when I do my heavy thinking. During prep, this doesn’t
happen. These small, subconscious decisions accumulate throughout
the day, in addition to the stuff that is virtually imperceptible, such as
the energy spent maintaining posture or fidgeting in your chair. For
most people, I encourage them to simply let this stuff go. Nobody
wants to feel like a hamster on a wheel, constantly forcing themselves
to continue some type of pointless motion. For a lot of people, the
psychological burden of trying to consistently increase NEAT costs
way more than the value it returns. Some people try to maintain a
particular step count during a weight loss diet using a pedometer, or
plan short walks throughout the day to stay active; this is a reasonable
middle ground, as long as it doesn’t drive you crazy. Nonetheless, the
more practical and broadly advisable strategies for fighting metabolic
adaptation involve manipulating the overall rate of weight loss and
using nonlinear diet strategies such as refeeds or diet breaks.

Rate of Weight Loss

If the goal is to maintain lean mass and attenuate metabolic
adaptation, it is advisable to avoid excessively rapid weight loss. There
are two main drivers pushing metabolic adaptation: short-term energy
availability, and long-term depletion of energy stores. When actively
dieting to become very lean, both stimuli are
encountered; some degree of energy restriction is unavoidable for
active weight loss, and depletion of fat stores is the entire goal of the
process. While the endpoint of our diet (very low body fat) is going to
bring its fair share of unavoidable adaptations, we can certainly
exacerbate some of the short-term stimuli for metabolic adaptation by
imposing an excessively large deficit to yield more rapid results. For
example, Mero et alstudied the effects of two rates of weight loss in
recreationally trained women; while losing 1kg per week successfully
yielded more weight loss than 0.5kg per week, this came with a
significant reduction in total and free testosterone levels. Garthe et
al studied weight loss in a group of elite athletes, with one group
losing 1.4% of their body mass per week and the other losing 0.7% per
week. In order to prevent total weight loss from skewing the results,
the slow weight loss group dieted for about 60% longer (5.3 weeks
versus 8.5 weeks). Both groups lost the same amount of total weight,
but the fast weight loss group lost a small amount of lean mass,
whereas the slow weight loss group experienced a significant gain of
lean mass. The slow weight loss group also had more favorable
increases in maximal bench press, bench pull, squat, and
countermovement jump performance. Results of this study are in line
with a 2014 review of bodybuilding contest preparation
recommendations, in which weight loss rates of 0.5 to 1.0% of body
mass per week are recommended. While these studies provide
evidence that slower rates of weight loss are generally advisable, they
assume linear calorie reduction. A different, and especially intriguing,
way to alter the timeline of weight loss is to implement nonlinear
approaches that transiently increase or decrease caloric intake for
hours, days, or even weeks at a time.

Intermittent or Non-Linear Caloric Restriction

It has long been understood that weight loss is induced by an energy

deficit, but an energy deficit doesn’t necessarily need to be applied in a
linear fashion. For example, let’s say we intend to induce a daily caloric
deficit of 300 Calories per day. Over a 30-day month, we intend to eat
9,000 fewer Calories than we burn. But we have to decide exactly how
to allocate those calories within each day, within each week, and within
the month. There are some aspects of metabolic adaptation that are
driven by getting really damn lean, or reducing the relative degree of
energy stored in our body. There probably isn’t much we can do about
those stimuli, especially for a physique athlete attempting to approach
semi-starvation levels of leanness. But dietary strategies have emerged
that absolutely alter acute fluctuations in energy availability; these
strategies have assumed a variety of time scales, managing the way
calories are distributed on an hour-to-hour, day-to-day, or week-to-
week basis. But do any of these strategies manipulate acute
fluctuations in energy availability in a manner that meaningfully
attenuates aspects of metabolic adaptation?

Manipulating the energy deficit within a day

Looking at the hour-to-hour time frame, there are a couple of

strategies to consider: manipulation of overall meal frequency, and
time-restricted feeding windows. When it comes to affecting energy
expenditure, high meal frequency is on page one of the bodybuilding
nutrition folklore manual. The premise is that eating causes an acute
increase in energy expenditure (via the thermic effect of feeding), so
frequent meals serve to stoke the metabolic furnace throughout the
day, keeping metabolic rate elevated. I suppose you could also stretch
this to suggest that by providing a more consistent influx of
calories, starvation mode is kept at bay. However, research
has consistently indicated that increased meal frequency has no
meaningful impact on the thermic effect of feeding, resting metabolic
rate, or total daily energy expenditure.

Another popular strategy essentially aims to accomplish the opposite;

rather than eating equally spaced meals throughout the day, time-
restricted feeding encourages dieters to eat all of their meals within a
quite narrow time window each day, often spanning 4-8 hours (Figure
6). This strategy, sometimes called intermittent fasting within the
fitness world, aims to capitalize on the purported benefits of long
fasting periods while still allowing for daily food intake. When it
comes to time-restricted feeding, we still have a lot to learn. Only a
handful of studies have been published to date, and methodological
approaches vary quite a bit. Studies by Tinsley et aland Gill et al opted
not to match caloric intake between the time-restricted feeding and
control groups. Their results generally suggest that time-restricted
feeding windows are a viable method for indirectly reducing caloric
intake; great information, but not what we are looking for.
 Figure 6.
Normal feeding protocols (blue line) typically involve multiple meals, spaced
fairly evenly throughout the day. As such, the cumulative total of calories
consumed increases throughout the entire day, with “pulses” at each meal or
snack. In contrast, time-restricted feeding (red line) requires that all energy
intake for the day occurs within a single, restrictive feeding window lasting 4-8
hours. While the figure shows equal caloric intakes, some people find it
difficult to eat a large number of calories in such a restrictive time window. For
them, this is an effective way to indirectly impose an energy deficit.
Moro et al carried out a study that attempted to match caloric intake
between time-restricted and standard feeding groups during an eight-
week resistance training program, but caloric intakes were set based
on self-reported diet data. To their credit, they had frequent check-ins
with a dietitian to monitor compliance, which is as much as you can do
without actually preparing and feeding the meals to subjects. The
time-restricted group lost about 1kg of weight and the control group
gained about 0.2kg, but dual-energy x-ray absorptiometry results
suggested a preferential fat loss in the time-restricted group (1.6kg vs.
0.3kg). Overall, it’s hard to consider this a clear “win” for time-
restricted feeding. Based on very modest changes in body weight,
reliance on self-reported data for setting diets, a free-living
intervention without controlled meal preparation, and potential
variability in responses to the resistance training program, it’s
probably safest to interpret these results as time-restricted feeding
being as good, with the possibility of being better, than standard
feeding. Stote et al exerted a little more rigorous control over their
crossover trial in which participants completed eight weeks of time-
restricted feeding and eight weeks of standard feeding. They tried to
match caloric intake between conditions by feeding subjects dinner in
the lab and providing packed breakfast and lunch meals, but they ran
into a little issue; while subjects undergoing the time-restricted
feeding protocol reported higher indices of hunger on surveys taken
before their daily meal, they also reported extreme fullness after the
meal and struggled to finish all of the food. The subjects did lose
about 1.4kg of weight over eight weeks of time-restricted feeding, but
also consumed 65 fewer Calories per day compared to their standard
feeding protocol. When considering day-to-day variability of weight,
and this cumulative difference of more than 3600 total Calories
throughout the eight-week trial, a 1.4kg difference seems like a wash.

In terms of control, a recent study conducted by Sutton et al definitely

takes home the grand prize. All meals were prepared by laboratory
staff and consumed in the lab, under direct supervision, utilizing a
crossover design. Caloric intakes were matched over each five-week
feeding period (time-restricted and standard), and the laboratory staff
deliberately set caloric content of meals to prevent weight loss (they
were specifically interested in looking at the effects of altering feeding
windows in the absence of weight loss). They found that weight was
maintained pretty effectively, with only a 0.5kg difference between the
groups. The authors suggest that this difference, which favored an
additional 0.5kg of weight loss in the time-restricted group, may be
attributable to less glycogen storage as a result of longer fasting
durations. In the other studies that attempted to match calorie intake
and observed a slight fat loss benefit from time-restricted feeding, I
have interpreted the favorable results with hesitation. Part of this
hesitation, as previously discussed, is uncertainty over exactly how
well calories were truly matched. However, my hesitation is also
related to the lack of a strong mechanism that would explain any such
benefit. Time-restricted feeding does not significantly affect resting
energy expenditure or total daily energy expenditure, and effects have
been either neutral or slightly unfavorable (from the perspective of
attenuating metabolic adaptation) with regards to leptin, ghrelin,
insulin, thyroid hormone, and testosterone. Stote et al suggest that it
is possible that time-restricted feeding may modestly impact body
composition by increasing the efflux of free fatty acids from fat cells
and increasing gluconeogenesis, but this doesn’t mesh very well with
the most tightly controlled study finding minimal evidence of a change
in total daily energy expenditure. Moro et al propose that the modest
fat mass reduction observed could be linked to increased adiponectin
levels, but Stote et alexerted comparatively more dietary control and
observed modest fat loss with absolutely no change in adiponectin.

In summary, evidence suggests no benefit to increased meal frequency,

at least when it comes to fat loss or energy expenditure. So, there’s no
need to perpetually carry around six Tupperware containers to
continuously stoke the metabolic furnace. While the time-restricted
feeding data is less conclusive, it’s safe to say that time-restricted
feeding has the capacity to help lower caloric intake when calories are
not matched. When they are matched, time-restricted feeding is as
effective as standard feeding for weight loss, with some studies
suggesting a minor benefit. However, the minor benefit seems to
shrink in studies that implement increasingly tighter control of energy
balance, and time-restricted feeding inherently foregoes the benefits of
equally spaced protein feedings on protein turnover in muscle tissue
(Figure 7). To be fair, the previously cited studies that have measured
lean mass do not support the idea that more lean mass is lost during
time-restricted feeding. There are, however, two important caveats to
consider. First, these studies typically measure fat-free mass, not
muscle; as such, broad measurements of fat-free mass may not
directly reflect the protein balance of skeletal muscle. Second, the
likelihood of substantial muscle loss is almost certainly higher in
highly trained individuals attempting to get very lean than in the
samples studied to date. Such a population tends to carry more muscle
tissue, employ a larger caloric deficit, induce more substantial
alterations in anabolic and catabolic hormones, and approach essential
body fat levels to a greater extent than the general population, or even
a recreationally trained population. For less extreme instances of
weight loss, I am of the opinion that time-restricted feeding can be a
valuable strategy for people who prefer to eat fewer, larger meals and
enjoy the psychological benefit of forgetting about food during long
fasting periods. However, early in my bodybuilding career, I
implemented this strategy myself during contest preparation. While it
fit my schedule and eating preferences quite well at the time, I suspect
that a more even meal distribution would have better preserved
muscle tissue.
 Figure
7. Muscle protein synthesis (MPS; green area) transiently increases after
protein feeding; after a while, protein synthesis tapers off and muscle protein
breakdown (MPB; red area) increases. In theory, time-restricted feeding
windows reduce the number of opportunities to spike protein synthesis
throughout the day. For more information, see the following article by Jorn
Trommelen: https://www.strongerbyscience.com/athlete-protein-intake/
Manipulating the energy deficit within a week or a month

Rather that shifting meal times within a day, some studies have
investigated the effects of shifting the days in which calories are
consumed. These protocols often encourage people to have anywhere
from 1-4 “fasting” days per week in which they either consume a mere
25% of their normal energy intake, or skip out on eating altogether. In
the research world, this is known as intermittent fasting or
intermittent energy restriction (note the terminology discrepancy: the
fitness industry often uses “intermittent fasting” to describe time-
restricted feeding, while the research world uses “intermittent fasting”
to describe the implementation of one or more weekly fasting days). In
comparison to time-restricted feeding, many studies have investigated
the weight loss effects of intermittent energy restriction. As displayed
in Figure 8, there are a few types of protocols for intermittent energy
restriction; the most common include alternate day fasting, fasting for
a two-day period, or including two fasts per week on non-consecutive
days. Multiple meta-analyses have investigated the efficacy of these
interventions in comparison to normal, continuous energy restriction,
all with slightly different inclusion criteria and analytical approaches.
All three of these meta-analyses have indicated that intermittent
energy restriction strategies, using a variety of fasting protocols, do
not lead to greater weight loss. However, they also don’t seem to be
substantially worse (at least in untrained subjects). While I maintain
concerns about lean mass retention when using prolonged fasting
periods during fairly extreme dieting, intermittent fasting strategies
that implement short (16-20 hours) or long (24+ hours) fasting
windows can be effectively used by dieters who prefer the way these
protocols fit their daily schedule or satiety preferences.
Figure 8. Popular intermittent energy restriction protocols include alternate-
day fasting, implementation of two consecutive fasting days per week, and
implementation of two weekly fasts on non-consecutive days. Fasting days
often include restricting energy intake to 0-25% of the individual’s daily energy
requirement.
Implementation of “refeeds” offer yet another option for manipulating
energy intake throughout the week. A refeed involves acutely
increasing caloric intake, usually by specifically increasing
carbohydrate intake, and usually for no more than a day or two at a
time. Research has shown that this approach is commonly used by
competitive physique athletes, either through structured refeeds or
unstructured “cheat meals.” The purported benefits of refeeds are
multifaceted; by acutely increasing carbohydrate (and energy) intake,
one could potentially boost leptin and thyroid hormone levels, acutely
increase energy expenditure, enhance muscle and liver glycogen
content, and provide a welcome reprieve from the low-carb food menu
that often accompanies contest preparation, particularly in the later
stages. There is absolutely evidence supporting acute effects of
refeeding on hormones and energy expenditure; one study found that
a three-day carbohydrate refeed, but not a fat refeed, increased leptin
by 28% and total daily energy expenditure by 7%. However, there is a
big problem regarding the applicability of this protocol: it requires
three days of 40% overfeeding, so that 7% increase in energy
expenditure is entirely overshadowed by a huge caloric surplus.
Viewed purely as a weight loss strategy, this is taking one step forward
and several steps backward. Our study on physique athletes observed
a marked increase in resting energy expenditure when comparing
values measured shortly before competition to values obtained shortly
after, which coincided with an increase in food intake. Again, this
marked increase in energy expenditure was nowhere near enough to
compensate for the increase in calorie intake required to induce it.
When it comes to more practical approaches to refeeding, Bill
Campbell’s lab from the University of South Florida has published a
couple of abstractsfrom a seven-week study that provide some useful
data. The study imposed a 25% calorie deficit for a group of resistance-
trained individuals; one group had the same caloric intake every day,
while the other had two consecutive, high-carbohydrate refeed days. In
order to accommodate this two-day increase in energy intake, the
deficit imposed on the other five days of the week was increased to
ensure that both groups had the same overall energy deficit. Results
from the abstracts should be taken with a grain of salt; abstracts are
not reviewed as rigorously as full manuscripts, and the primary
analysis for each abstract found no group by time interactions.
However, some follow-up pairwise comparisons suggested that
refeeding may have conferred slight benefits when it comes to
maintenance of resting metabolic rate and the retention of fat-free
mass.

There is a possibility that longer durations of increased calorie intake

may impart more protective effects, and a few studies shed light on
this possibility. An eight-week study compared standard continuous
energy restriction with an intermittent protocol that had subjects
alternate between one week of energy restriction and one week of
unrestricted eating. The groups lost somewhat similar amounts of
weight over the eight weeks (3.2kg in the continuous group versus
2.0kg in the intermittent group). While the weight loss difference
between groups was almost statistically significant (favoring the
continuous group), the continuous group spent twice as much time in
an energy deficit; as such, the intermittent protocol offered fairly
similar rewards, but at a lower overall cost to the dieter enjoying
breaks every other week. A separate six-week study compared a
standard weight loss diet to a nonlinear approach, in which
participants repeated two-week cycles of a 45% calorie reduction for 11
straight days followed by three days of self-selected eating. In the
standard diet condition, participants simply reduced their caloric
intake by 55% and ate this amount every day. After the six-week weight
loss phase, there was a four-week follow-up period in which subjects
ate around maintenance calories. In this study, the group with three-
day “refeeds” kept their resting energy expenditure a little bit higher
than the other group, and lost a little more weight (expressed as a
percentage of weight lost), despite averaging higher daily caloric intake
throughout the study.

More recently, a study investigated the effects of even longer diet

breaks, with the intermittent group alternating between two weeks of
dieting and two weeks of eating at maintenance. That’s a really
important distinction; the other studies just allowed subjects to self-
select food intake during their “break,” whereas this study carefully
fed them enough to reach, but not exceed, maintenance calories.
Comparatively speaking, this study implemented the highest degree of
control. Calorie intakes were consistently updated based on serial
measurements of metabolic rate, and meals were cooked and provided
by dietitians associated with the study. In order to make a more fair
comparison of the diets, the intermittent group dieted for 30 weeks,
while the continuous group dieted for 16; this way, the breaks were
incorporated, but both groups spent 16 weeks in the same caloric
deficit. Results showed that the intermittent group lost significantly
more fat (12.3kg versus 8.0kg). Reductions in resting energy
expenditure were similar in absolute terms, but the groups clearly had
divergent changes in body composition. After adjusting for fat mass
and fat-free mass, the continuous group experienced a significantly
larger drop in resting energy expenditure than the intermittent group.

Even longer diet breaks have been implemented in the literature. For
example, a 2010 abstract implemented a five-month intervention in
which subjects consumed 1,200 Calories for a week, 1,500 Calories for
three weeks, 2,200 Calories for four weeks, then repeated the cycle. By
the end of month five, participants had lost an average of almost 5kg,
while avoiding significant reductions in resting energy expenditure.
This study did not have a comparator group undergoing continuous
weight loss, but it does offer an extreme example of the dilemma we
face with the concept of refeeds or diet breaks. Refeeds and diet
breaks appear to have the capacity to attenuate metabolic adaptation
to some extent, but they also dramatically extend the timeline of the
diet. As a result, there is a cost-to-benefit ratio that must be
considered when determining the frequency and duration of refeeds or
diet breaks.

If you’re keeping your caloric intake within a reasonable range (i.e., not
dramatically overeating), a once-weekly refeed probably isn’t going to
be enough to make a meaningful effect. If you implement four refeeds
per week, you’re mostly not on a diet, from a mathematical
perspective, and it’s hard to make your weekly caloric deficit large
enough to promote substantial weight loss. To keep fat loss
progressing forward and attenuate metabolic adaptation, two refeeds
per week is probably the number most people should aim for. Refeeds
should absolutely emphasize carbohydrate intake, and caloric intake
should be increased to right around maintenance level. Some argue
that these refeeds should be placed on consecutive days, to allow a
longer duration of time to physiologically “adjust” to being out of a
deficit. Others argue that refeeds should be staggered throughout the
week; they contend that metabolic adaptations are exacerbated by
spending several days in a row in an energy deficit. A large portion of
the leptin drop observed with weight loss occurs in the first week. For
example, a study demonstrated that a huge fall in leptin occurs during
the first four days of energy restriction, followed by a much slower
decline over the following 24 days. By providing a refeed every three
or four days, you could potentially provide a timely pulse of energy
balance to keep metabolic adaptation at bay.

At this point, you can’t really say either approach is definitely wrong. I
lean toward consecutive refeeds rather than splitting them up for a
few reasons. From a theoretical perspective, we have operationalized
metabolic adaptation as a coordinated response to prevent starvation.
It’s hard to imagine that a single meal (or a couple meals) would
convince our hypothalamus that, despite our prolonged confrontation
with starvation, our circumstances have completely changed, such that
we would rapidly override one of our most important survival
responses. If we draw inferences from some tangentially relevant data,
alternate-day fasting can be used to assess the effects of short but
frequent refeeds. In rats, alternating between one day of fasting and
one day of eating increased leptin, which had favorable effects on
weight control and food intake compared to control rats. However,
these results are confounded by the fact that one human day equals
about 34 rat days, from a biological perspective. In humans, one
alternate-day fasting study showed that the intervention did cause
weight loss, but reduced leptin by 40%. Another trial compared
alternate-day fasting to a “normal” weight loss group; over the eight-
week intervention, both groups had similar reductions in weight,
leptin, and resting metabolic rate. It’s also important to note that the
rise in leptin after consuming a meal is not immediate; according to
one study, it’s not until about the fifth hour after a meal that leptin
levels appreciably rise, and they continue to rise thereafter. Studies
generally show that leptin reductions from short-term energy
restriction can be restored within about 12-24 hours of refeeding, but
leptin levels also begin fallingagain within hours of the return to
energy restriction. This is coupled with the facts that leptin clearance
is especially rapid in lean people, and that many of the downstream
benefits we hope to obtain from a leptin spike require multiple-step
processes that take some time to play out. With a one-day refeed, I
question exactly how much of an opportunity we would have to
physiologically capitalize from any observed alteration in leptin.
Finally, and most importantly, I’ve actually seen research with two-day
refeeds done in lean, resistance-trained people, and it produced
modest but favorable results. Once one decides to implement refeeds
on consecutive days, the lines between refeeds and diet breaks become
blurred. How much time is sufficient? Two days? A week? Two weeks?

There are a lot of contextual factors that determine how refeeds or

diet breaks are most effectively used, but it’d be intellectually lazy to
leave the answer at, “it depends.” For general weight loss that is
intended to be permanent, a two-week diet break could be very doable,
and the results from the MATADOR study implementing this
technique are quite strong. A bodybuilder that is ahead of schedule, or
willing to dedicate to a more prolonged contest prep period, can
probably commit to a one-week break implemented every 3-4 weeks,
or implemented as needed. If you’re an early-career bodybuilder with
plenty of room to grow before you reach your genetic potential for
muscularity, you’ll have to carefully consider how much of your year
you’d like to spend cutting; while a seasoned pro near their genetic
limit ought to take their time, an amateur with plenty of mass to gain
should probably avoid excessively long preps. If you’re behind
schedule and unable to accommodate weeklong pauses, more frequent
two-day refeeds might be the preferred option. If you’re more
interested in some of the “other” benefits of refeeding (such as a brief
psychological break, flexibility with high-carbohydrate foods, or
glycogen replenishment prior to a particularly important training
bout), a refeed every 3-4 days could make sense for you. Each type of
refeed or diet break is a slightly different tool with slightly different
pros and cons. According to a published protocol, we should have
some more relevant research at some point in the near future. Until
then, we’re left with a few conclusions: refeeds and diet breaks are
viable tools to help attenuate metabolic adaptation, the benefit of
attenuating metabolic adaptation comes with the cost of extending the
total duration of weight loss, and the “ideal” manipulation of deficit
days and maintenance days isn’t fully understood at this time.

Balancing Macros To Maintain Muscle and

Performance

Dropping Protein

Moving beyond strategies to target the root causes of metabolic

adaptation, we have opportunities to alter our dietary intakes to
manage some of the secondary effects resulting from metabolic
adaptation. Calories must be reduced for the diet to promote weight
loss, but there are unique drawbacks associated with lowering intakes
of each individual macronutrient.

When evaluating the success of a weight loss diet, the two primary
outcomes of interest are: 1) how much weight has been lost, and 2)
how much of the weight lost was actually fat mass. In a short-term
study (one week) back in 1988, Walberg et al compared isocaloric diets
with 0.8 g/kg/day or 1.6 g/kg/day of protein. While the study was
almost certainly too short to detect meaningful body composition
differences using underwater weighing, the nitrogen balance analysis
revealed that the lower protein group was is negative nitrogen balance,
with the higher protein group in positive nitrogen balance. These
changes in nitrogen balance are consistent with reduced breakdown of
lean tissues in the high protein group. More recently, Mettler et
al followed up with a slightly longer study, in which 20 resistance-
trained athletes were randomly assigned to a high-protein weight loss
diet (2.3 g/kg/day of protein) or a control weight loss diet (1.0
g/kg/day of protein) for two weeks. At first glance, the control diet
seemed to be favorable, as they lost more weight during the brief
weight loss diet. However, a closer look would reveal that fat loss was
virtually identical between the two groups, and the difference in
weight loss was due to a significantly greater loss of lean mass in the
control group. Eric Helms published a review on the role of protein
intake during energy restriction in resistance trained (and lean)
athletes; in line with the findings of Walberg et al and Mettler et al, the
collective body of evidence suggests that protein intake must be
prioritized for the retention of lean mass under these circumstances.
As noted in a review by Paddon-Jones et al, protein also carries some
additional fringe benefits with it. Compared to carbohydrate and fat,
protein features a substantially larger thermic effect of feeding and
induces greater feelings of satiety on a calorie-for-calorie basis. As
Helms points out in his protein review, there is a high likelihood that
protein needs are not just important, but actually higher than
normal when lean, resistance-trained individuals are engaged in weight
loss. While typical protein intake recommendations are around 1.4-2.0
g/kg/day, this fails to account for hypocaloric conditions, and
inherently assumes a fairly “typical” body fat level. For these reasons,
Helms scales his recommendations to kilograms of fat-free mass and
recommends daily protein intakes of 2.3-3.1 g/kg of fat-free mass
during energy restriction.

Dropping Fat

Changes in sex hormone levels may be a contributing factor to the loss

of lean mass during weight loss. Beyond weight loss, these sex
hormones certainly contribute to the unpleasant reproductive side
effects of extreme weight loss, and it would be fantastic to attenuate
sex hormone reductions if possible. Over the years, several studies
have identified a link between dietary fat intake and sex hormone
levels. For example, reducing dietary fat intake from 40% of calories to
25% for six weeks led to significant reductions in total testosterone
and free testosterone in healthy men. Another studyusing male
subjects instructed them to consume a diet including 100 g/day of fat
for two weeks, followed by a drop to less than 20 g/day for two more
weeks. This drastic drop in fat intake resulted in a combination of
increased sex hormone-binding globulin and reduced free
testosterone, and both changes are associated with a reduction in the
biological activity of testosterone. In male strength athletes, dietary fat
intake has also been correlated with both resting testosterone levels
and the post-exercise testosterone response to heavy resistance
exercise. Further, the link between dietary fat and sex hormones is not
restricted to men. An intensive two-year trial evaluated the effects of
reducing dietary fat to 15% of calories in premenopausal women;
results showed that women assigned to the low-fat diet ended the trial
with significantly lower levels of estradiol and progesterone and 7%
higher (but not significantly different) levels of follicle-stimulating
hormone, which plays a role in the regulation of estradiol production
and the menstrual cycle. Just as low-fat diets appear to have a
suppressive effect on male testosterone, this finding would suggest
that analogous changes occur in women, with suppressed female sex
hormone levels that could potentially interfere with menstrual cycle
regularity and reproductive function.

Unfortunately, dietary fat intake is only one of the factors influencing

sex hormone levels, and it’s almost certainly not the biggest factor.
Long-term caloric restriction itself has been associated with lower sex
hormone levels in males, in a manner that did not appear to be
attributable to age, body fat percentage, or the proportion of calories
from dietary fat. Research in anorexic females has shown that, even
among anorexic patients who generally have low BMI and chronically
restrict energy intake, body fat percentage seems to be an important
independent predictor of developing menstrual cycle dysfunction and
of eventually recovering from menstrual cycle dysfunction after it has
occurred. This is coupled with the observations that low testosterone
is very consistently observed in males with anorexiaand in published
male bodybuilding case studies, despite the wide range of potential
dietary tactics that could be employed to reach such low levels of body
fat. In addition, testosterone recovery in bodybuilding case studies
often takes several months, with recovery coinciding more closely with
the restoration of body fat levels than increases in dietary fat intake.
Taken together, the available evidence suggests that sex hormones are
reduced to some extent by caloric restriction and extreme leanness,
which are inherently unavoidable when the goal is to get really lean.
So, while it is prudent to avoid exacerbating the downregulation of sex
hormones by excessive reduction of dietary fat, your chances of
manipulating fat intake to completely abolish drops in sex hormones
are slim.

Dropping Carbohydrate

There are also some downsides to reducing carbohydrate intake. A few

published observations in bodybuilders lend some evidence for the
role of carbohydrates in supporting bodybuilding success.
An observational study in natural bodybuilders previously noted that
more successful competitors tended to report higher carbohydrate
intakes at the beginning of preparation compared to less successful
competitors. The primary limitation here, aside from the observational
study design, is that carbohydrate intakes were only significantly
different at the start of the diet, but not the end. Theoretically, if the
plan was to identify nutrition strategies that facilitate a successful
contest prep, the dietary differences toward the middle and/or end of
the diet would be more informative than those at the start. Maestu et
al observed that individuals who had the largest insulin reductions
throughout contest prep also tended to lose the most lean mass. Given
the robust insulin release observed in response to carbohydrate intake,
one might infer that a higher carbohydrate intake would help preserve
lean tissue during a weight loss diet. However, it is important to note
that dietary protein can also be quite insulinemic, and insulin
levels also correlated with the loss of fat mass in this study. So, it is
possible that the people who lost less fat mass had higher insulin
levels and retained more lean mass because they simply didn’t get as
lean as the other competitors in the sample.

Looking beyond these cloudy instances of indirect evidence, there are

more controlled studies that show some direct disadvantages of
slashing carbs from the diet. Whether we are resting or sprinting, we
rely on a combination of three energy systems to supply the ATP
required. At rest, the rate of ATP demand is pretty low, so the aerobic
energy system is able to provide ample ATP, primarily by breaking
down fat. As we begin to engage in activities of higher relative
intensity, the contributions of the anaerobic (phosphagen and
glycolytic) energy systems increase. This is important because the
glycolytic energy system makes a very substantial contribution to
fueling resistance exercise, and by definition this energy system relies
on carbohydrate as the substrate for ATP synthesis. As such, it should
be no surprise that studies have shown carbohydrate restriction to
impair resistance exercise performance. One study put participants
through a glycogen-depleting workout, had them restrict carbohydrate
(1.2 g/kg/day) intake for 48 hours, then assessed resistance exercise
performance. For the three-set squat protocol at 80% of the one-rep
maximum load, carbohydrate restriction caused participants to
perform significantly fewer repetitions during sets one and two. In
addition, the previous study by Walberg et al showed that high protein
diets maintained positive protein balance, but protein was kept high
by reducing carbohydrate intake. An unintended consequence was
that, despite favorable effects on protein balance, the high protein/low
carbohydrate group had a reduction in quadriceps muscle endurance
compared to the group with lower protein and higher carbohydrate
intake. These applied performance outcomes are supported by well-
controlled in vitro studies investigating the link between carbohydrate
and muscle force production. The sarcoplasmic reticulum is a calcium-
storing structure found within muscle cells, and the release of calcium
from the sarcoplasmic reticulum is a critical step mediating a muscle
fiber’s ability to produce force. In instances when carbohydrate intake
is insufficient to replace muscle glycogen use, the glycogen stores
adjacent to the sarcoplasmic reticulum become depleted. Several
studies have shown that this results in lower calcium release from the
sarcoplasmic reticulum, leading to more rapid muscle fatigue and
earlier reductions in force production. As such, strategically utilizing
carbohydrate intake to attenuate the magnitude of muscle glycogen
depletion during energy restriction can be viewed as a preferred
dietary strategy to preserve performance in the gym.

Striking a Balance

At this point, we’ve reviewed the evidence suggesting that your weight
loss diet should be high in protein, high in fat, and high in
carbohydrates in order to maintain muscle, attenuate metabolic
adaptation and related side effects, and support performance in the
gym. Good luck trying to make that work while successfully losing
weight.

Once we’ve acknowledged that perfection is out the window, the

discussion shifts to making this puzzle work as best we can. Sufficient
protein intake is simply non-negotiable, and recommendations suggest
this should be set around 2.3-3.1 g/kg of fat-free mass, which is often
up around 2 g/kg of total body mass or higher (depending on how lean
you are). Once protein is set, it’s important to set a “basement value”
for fat, or a level of fat intake you simply are not willing to go below.
This is a bit of a balancing act; we need to remove calories
from somewhere, and fat calories are a viable option for removal.
However, going too low with fat will likely exacerbate reductions in sex
hormones during weight loss, and we need enough fat to obtain
sufficient essential fatty acids, promote the absorption of fat-soluble
vitamins, and keep the diet reasonably palatable. For most individuals,
fat intakes really shouldn’t drop below around 0.6-0.7 g/kg of total
body mass per day. Once these minimums are set for protein and fat,
the rest of your calories are going to come from some mixture of
carbohydrate and fat; in the interest of performance, I prefer for the
majority to come from carbohydrate. These macronutrient boundaries
have little chance of completely attenuating adaptive thermogenesis,
hormone fluctuations, performance decrements, or the loss of lean
mass. They’re just the best we can do with what evolution gave us.

Managing Cardio For Successful Weight Loss

Weight loss is dictated by creating an energy deficit, and energy intake

is only half of the equation. Weight loss diets are typically paired with
increases in cardiovascular exercise, and the inclusion of cardio is
almost always part of the approach for physique athletes. Many
studies have been conducted to investigate the effects of adding cardio
to a resistance training program. In some instances, the additional
cardio blunts adaptations to resistance exercise, which is known as
the interference effect (i.e., the cardio interferes with adaptations to the
resistance training program). In short, the root of this interference
is attributed to the stimulation of conflicting cell signaling events that
underpin training adaptations to strength and endurance training, and
additional fatigue induced by additive endurance exercise. Under
normal circumstances, the interference effect impacts power
outcomes more than it impacts strength, and impacts strength more
than it impacts hypertrophy. However, a number of contextual factors
dictate the likelihood of observing a substantial interference effect.
Most notably, as one might expect, more cardio seems to equate to
more interference. Studies implementing two or fewer sessions of
cardio per week have generally failed to observe substantial
interference, whereas studies implementing three or more sessions of
cardio per week often observe statistically significant impairment of
resistance training adaptations. However, there is currently insufficient
evidence to determine if it is the frequency or volume of cardio that is
driving these outcomes, as high-frequency cardio programs also tend
to be higher in volume in the studies published to date.

For physique athletes, the combined load of resistance training and

cardio is at the high end of this frequency/volume discussion toward
the end of contest prep. In case studies we have documented, it’s fairly
typical for both male and female competitors to add up to five or six
cardio sessions per week, on top of an independently demanding 5-6
day per week resistance training program. In addition, these athletes
are fighting an uphill battle in terms of hormones. As discussed in Part
1, weight loss attempts in lean individuals are often accompanied by
decreases in testosterone and increases in cortisol. For years, the
testosterone to cortisol (T:C) ratio has been used as an imperfect, but
informative, marker of overtraining and impaired recovery. Even in
normal-weight athletes with unrestricted caloric intake, excessive
training loads often drive the T:C ratio downward to a level that is
associated with an unfavorable “anabolic-catabolic balance.” The
recovery of physique athletes is also threatened by insufficient energy
intake to maintain body weight (which is unavoidable) and commonly
observed issues obtaining quality sleep (which is pretty hard to fix).
Taken together, the circumstances surrounding weight loss,
particularly in more extreme cases like physique athlete contest
preparation, present conditions in which the likelihood of an
interference effect is increased. Moreover, careless implementation of
excessive cardio has great potential to exacerbate some of the
unfavorable effects observed with metabolic adaptation, especially
those linked to fatigue and hormone fluctuations.

To avoid exacerbating some of these issues, cardio should be

thoughtfully and carefully implemented as part of the weight loss
plan. Unfortunately we have to make some very broad observations
and some tenuous conclusions when viewing the concurrent training
literature, because there is an immense variety of factors that can
fluctuate within a single study design. For example, I might want to
make an inference about how the intensity of cardio affects strength in
the next resistance training bout. A study might shed some insight on
this question, but there will inevitably be confounding factors to
consider (such as the modality of cardio, duration of the overall bouts,
frequency, overall training loads of both resistance training and cardio
components within the study, training status of subjects, sex of
subjects, duration of the study, and the time elapsed between cardio
and strength testing, just to name a few). Whenever you change one
factor in this type of study, there tends to be a ripple effect that
requires alteration to some other factor(s). Nonetheless, a review
by Fyfe et al helps to consolidate some of the information currently
available from concurrent training studies, and some general
recommendations can be made for people who wish to be cautious
with their cardio implementation. Certainly the overall load of training
must be managed, and dieters should err on the side of doing as little
cardio as they can get away with while still supporting fat loss (and
general cardiovascular health, if that’s important to you). There are
also temporal considerations; following endurance exercise, force
production of the trained musculature is typically impaired for at least
six hours. The evidence would suggest that the most prudent approach
would be to perform cardio and resistance training on separate days, if
possible. When cardio and resistance training must be performed in
the same session, it would be preferable to prioritize resistance
training first, which seems to be as effective or slightly more effective
for attenuating interference than performing resistance training after
cardio (we’re talking about the actual bout of cardio here, not a quick
warm-up to get moving before lifting). When it comes to intensity,
things are a bit complicated; high-intensity bouts cut down on the
overall duration of cardio, but really intense bouts call for a level of
physiological arousal that can be quite exhausting and may induce
more residual neuromuscular fatigue. Looking at the literature, it also
appears that running is associated with more interference than cycling,
which may relate to less muscle damage, less residual neuromuscular
fatigue, or less robust stimulation of interfering molecular pathways
with cycling exercise.

Finally, it’d be shortsighted to make cardio-related decisions without

first considering the preferences of the dieter. While a physique
athlete should never aim to exclusively run their way to contest shape,
physique athletes can succeed within a wide range of cardio
implementation strategies, and the restrictions on non-physique
athletes are even less restrictive. Some people hate cardio, and that
shouldn’t be ignored. Dieting for weight loss is already unpleasant
enough, even when done well; the cumulative psychological burden of
spending several hours per week doing something you dread should
not be overlooked, as weight loss success is contingent on both
psychology and physiology. While I’m personally pretty neutral about
cardio in terms of enjoyment, it tends to markedly increase my
hunger. While this doesn’t happen to everybody, I’m also not
alone; research suggests that there is a great deal of variability with
respect to hunger and other compensatory responses to cardio.
Conversely, some people quite enjoy cardio (I think — I’ve never met
one, but I’ve been assured they exist). If that is the case, and they
aren’t exacerbating their hunger or aggravating injuries in the process,
then reasonable amounts of cardio should absolutely be used as part
of the plan to promote an energy deficit.

Other factors to consider

When it comes to attenuating the effects of metabolic adaptation, the

most influential factors under our control have been covered in
previous sections (rate of weight loss, refeeds and diet breaks,
macronutrient intakes, and management of cardio). There are a few
other factors that are a little harder to manage or that make a slightly
smaller impact but deserve acknowledgement nonetheless.

Sleep and stress

Sleep is important for anyone with strength- or physique-related
ambitions. Aside from the negative effects of sleep deprivation on
cognition, mood state, and general physical performance, there
is evidence to suggest that three days of partial sleep restriction
impairs bench press, leg press, and deadlift strength. While there is a
surprising lack of sleep research in the area of resistance
training recovery, it’s a safe assumption that sleep is an important
component. As a fairly obvious, surface-level observation, lack of sleep
seems to impair readiness to train and interfere with voluntary effort.
Sleep restriction also has metabolic and hormonal effects that can
exacerbate aspects of metabolic adaptation. Insufficient sleep impairs
glucose tolerance and insulin sensitivity, while increasing cortisol and
ghrelin levels, decreasing leptin, and increasing hunger and appetite.
Sleep restriction also shifts food preferences toward more calorie-
dense, hedonically rewarding options, thereby threatening dietary
adherence. Sleep-induced increases in cortisol have been observed in
conjunction with reductions in testosterone and IGF-1,
prompting researchers to speculate that insufficient sleep may be
linked with muscle loss and impaired muscle recovery. In support of
these mechanistic findings, a small crossover study found that
individuals lost less fat mass and more fat-free mass during caloric
restriction when they slept 5.5 hours per night compared to 8.5 hours
per night.

Unfortunately, sleep is rarely discussed in the bodybuilding literature.

One of our case studies evaluated sleep, both using objective and
subjective assessments. While the accelerometer-based objective
measurement showed no meaningful change, subjective assessments
showed that sleep quality suffered toward the end of contest
preparation. It’s possible that the accelerometer simply wasn’t
equipped to accommodate the fact that bodybuilders in contest prep
constrain their non-exercise movement to a statue-level degree of
stillness. The subjective reduction in perceived sleep quality supports
widely reported anecdotes of sleep issues during the later phases of
contest prep; even as sleep becomes harder to obtain in more extreme
weight loss attempts, an earnest effort should be made to obtain
it. Strategies to help promote sleep quality include limiting blue light
exposure within 1-3 hours of intended sleep onset and limiting the
intake of stimulants with long half-lives (such as caffeine) late in the
afternoon and evening. Research also suggests that diets relatively
high in protein and carbohydrate, with low or moderate fat intake,
support high quality sleep, as does consumption of a carbohydrate-
rich meal in the evening and avoidance of going to sleep while hungry.
Unfortunately, these are luxuries that might not be feasible on a more
intense weight loss diet. More practically speaking, a handful of
supplements (including melatonin, tryptophan, valerian, and
magnesium) are purported to have beneficial effects on sleep.

It’s also prudent to discuss the effect of stress in the context of

metabolic adaptation, as stress, sleep, and metabolism are all inter-
related. Stress can induce sleep loss, sleep deprivation can increase
subjective stress and anxiety, and both subjective stress and sleep
deprivation can influence metabolism. The effects of stress are
primarily dictated by cortisol, with downstream effects on
testosterone, leptin, ghrelin, appetite, and a shift toward more hedonic
and calorically dense food preferences. Excessive stress yields
outcomes quite similar to sleep deprivation, and the two often go
hand-in-hand. Unfortunately, stress can sometimes be hard to avoid
during a fairly intense weight loss phase (or life in general), especially
if the stress of an impending competition is involved. Aside from
general stress management techniques, the most direct approaches to
mitigate excessive stress during weight loss include prioritizing
effective sleep habits, allowing a flexible timeline for your weight loss
goal, and avoiding diet and exercise strategies that cause stress
because you hate doing them so much. Adaptogen supplements, such
as rhodiola rosea and ashwagandha, may also play a role in
attenuating the effects of high stress levels.

Supplements

When it comes to practical strategies for attenuating metabolic

adaptation, I would be remiss to neglect the potential applications of
supplements altogether. However, I broach the subject with great
trepidation, as I’ll explain shortly.

There are indeed some supplements and/or over-the-counter drugs

that promote energy expenditure and fat loss, such as ephedrine, p-
synephrine (bitter orange), yohimbine, caffeine, nicotine, and
capsaicin. Each one comes with drawbacks. Ephedrine is banned in
many countries, including the United States, due to the receipt of
several severe adverse event notifications. P-synephrine is essentially a
less potent version of ephedrine; its side effects are less potent, but so
are its effects on energy expenditure. Until more research on p-
synephrine becomes available, I’m not entirely convinced that its
effects are meaningful enough to support its use. Yohimbine is known
to cause anxiety symptoms in many people, interacts with several
drugs, has some quality control issues with regard to dosing in
products, and ought to be used in conjunction with fasted cardio
(which I rarely recommend) to maximize its benefit. Caffeine’s effect
on metabolic rate is fairly modest, and it’s quite easy to go
“overboard” with caffeine intake as you start becoming habituated to
its effects. It’s not uncommon to hear about dieting individuals that
are taking in pretty hefty caffeine doses daily (sometimes over
1,000mg per day), and unsurprisingly experiencing restlessness,
anxiety, headaches, or insomnia as a result. Nicotine is quite addictive,
and it seems a bit unethical to 1) advocate the off-label use of a drug
for unintended purposes, such as a weight loss aid, and 2) advocate
the use of an addictive substance that, despite having a far more
favorable safety profile than tobacco, may still have independent
adverse health effects of its own. Finally, there is capsaicin, the
extracted component that gives cayenne and chili powder their “kick,”
and capsiate, a less pungent analog of capsaicin. Research does
suggest that these chili pepper components increase metabolic rate,
especially at higher doses (135-150mg capsaicin or 6-9mg
dihydrocapsiate), in a reasonably safe manner. However, the
magnitude of this effect is fairly modest, and by no means a miracle
strategy for keeping metabolic adaptation at bay. There is also
emerging evidence that ephedrine and several dietary
components (including capsaicin, resveratrol, curcumin, green tea,
berberine, fish oil, conjugated linoleic acid, and all-trans retinoic acid)
may activate brown adipose tissue and/or promote the “browning” of
adipose tissue, a process by which white fat cells begin behaving more
like brown fat cells by increasing uncoupled thermogenesis. However,
the evidence for such an effect is quite preliminary and largely derived
from non-human research models. So, aside from a morning or pre-
workout caffeine boost and generous servings of cayenne powder on
some meals, I do not advocate (or implement) any supplement
strategies specifically for the purpose of maintaining energy
expenditure during weight loss.

Many of the supplements suggested to promote energy expenditure

are also purported to attenuate hunger. In addition, some non-
thermogenic supplements are thought to suppress appetite or
promote satiety, such as ginger, 5-HTP, caralluma fimbriata, and alpha-
lipoic acid, among others. For each, high-quality evidence in human
subjects is fairly limited. Aside from the use of supplements, there are
some very practical dietary strategies to promote satiety and mitigate
hunger. Examples include selecting foods with relatively high satiety
index values, eating high-volume foods with low caloric density,
drinking green tea with meals, and consuming conventional foods with
generous amounts of red pepper. While there are some supplements
and strategies that may have minor effects on appetite, I generally
advise against the premise of aggressively “hiding from hunger”
during more extreme weight loss attempts. With small, sustainable
weight loss attempts, you may never actually reach a point of
substantial hunger. If preparing for a physique competition, hunger
will be a reality, and it’s probably best (from a psychological viewpoint)
to just embrace that. When you try to plan your whole day around
avoiding the threat of hunger, it gives hunger way too much power
over your subjective well-being. Hunger is, after all, a natural and
appropriate response to the restrictions you’re imposing, so it is
remarkably difficult to override and there is no reason to fret over it.

Conclusion

Metabolic adaptation is going to happen, but there are some very

practical strategies to help attenuate its effects. Daily protein should
generally be set at no less than 2 g/kg of total body mass, and up as
high as 2.3-3.1 g/kg of fat-free mass, when in a sizable caloric deficit.
Fat intake typically shouldn’t go below 0.6-0.7g/kg of total body mass
as a bare minimum value, and dieters should make an effort to
prioritize carbohydrate with whatever calories they have left over.
Slower rates of weight loss should be preferred; especially for fairly
lean individuals, the rate of weight loss should rarely exceed 1% of
body weight per week. In the interest of lean mass retention, recovery,
and maintenance of sanity, reasonable volumes and frequencies of
cardio training should be used to promote an energy deficit. Refeeds
and diet breaks may provide additional protections against the effects
of metabolic adaptation. Refeeds should be implemented 2-3 times per
week, and you can make a reasonably strong (but not indisputable)
argument that these should be situated consecutively. When the diet
timeline allows, these refeeds could be taken a step further with the
implementation of periodic diet breaks, lasting one to two weeks in
duration.

That’s a perfectly suitable plan if you aren’t banking on surviving past

the end of your weight loss phase. For whatever reason, that’s about as
far as most people plan. Fortunately, for the overwhelming majority of
dieters, life goes on after you reach your weight loss goal. Much like
puberty, it’s a chaotic time; your body is changing, hormones are
fluctuating wildly, and it can be a bit stressful if you haven’t been
given a warning about what to expect. Part 3 is that warning and offers
some strategies to plan for a less chaotic transition to life after weight
loss.
Part 3: Life After Weight Loss
For short-term dieting, just about everything works. For long-term
dieting, almost nothing works. There are 8-12 week studies showing
successful weight loss with just about every approach in the book,
but studies suggestthat only about 10-20% of individuals are able to
maintain substantial weight loss in the long term. If you are dieting to
a sustainable body weight and you intend to maintain a large
percentage of your weight loss, research generally suggests that
maintaining high levels of physical activity and frequent monitoring of
body weight are important strategies to promote weight loss
maintenance. Even with these strategies, weight loss maintenance
proves to be a very challenging endeavor. If you’re only planning to
hold your weight loss for a short amount of time (such as dieting for a
weight-based athletic event, a photo shoot, or a physique competition),
then weight regain is expected. However, since we know weight regain
is coming, it should be done intentionally, in a well-planned and
thoughtful manner. Understanding the weight regain literature
facilitates the formulation of such a plan.

Underwhelming success rates with long-term weight loss have

prompted researchers to consider the possibility that metabolic
adaptation may persist beyond active weight loss, and into the weight
maintenance (or weight regain) period. One small but tightly
controlled study sought to determine if energy expenditure remained
suppressed during weight loss maintenance. In order to assess this
research question, they measured total, resting, and non-resting
energy expenditure in three types of people: 1) people at their normal
body weight, 2) people who had maintained a 10% body weight
reduction for the previous 5-8 weeks, and 3) people who had
maintained a 10% body weight reduction for the previous 1-6 years.
Even after adjusting for relevant confounding variables, both weight
loss groups appeared to have total, resting, and non-resting energy
expenditure values that were lower than predicted. When compared to
the normal weight group, both weight loss groups had significantly
lower total and non-resting energy expenditure values, with no
significant difference between recent and sustained weight loss
groups.

Another study assessed participants from the Biggest Loser

competition six years after achieving dramatic weight loss. Participants
had originally lost an average of 58.3kg, and had gained back 41.0kg
by the six-year follow-up study. Resting metabolic rate was 704
Calories below baseline, which is 499 Calories lower than predicted. In
this study, the degree of resting metabolic rate suppression was
correlated with the degree of weight loss that had been maintained,
meaning that individuals who maintained more weight loss displayed a
greater degree of adaptive thermogenesis. The propensity for weight
regain after weight loss is not a coincidental trend; as reviewed
by MacLean et al, many of the aspects of metabolic adaptation that
oppose active weight loss also predispose us to weight regain,
especially if we lost a ton of weight or got really, really lean. As these
two studies have shown, some aspects of metabolic adaptation can
even persist for years after active weight loss. In the time period
immediately following weight loss, we have a body with less
metabolically active tissue, emptier adipocytes, more energetically
efficient tissues, less leptin, lower levels of thermogenic, anorexigenic,
and anabolic hormones, and higher levels of orexigenic and catabolic
hormones. It is a body primed for ravenous eating and precipitous fat
gain.

Body Fat Overshooting

This predisposition to rapid fat gain can be a bit problematic if we

allow it to go completely unchecked. Our adipocytes (fat cells) get
smaller when we lose weight, with a negligible change in the number of
total adipocytes. As previously discussed, a huge ramification of
reduced adipocyte size is that the adipocyte produces less leptin,
which drives metabolic adaptation forward. Even beyond leptin, a
thorough review by MacLean et al describes numerous ways in which
the physiology of adipocytes changes in response to weight loss.
Adipocyte gene expression changes, shifting toward a gene expression
profile that downregulates energy expenditure, increases appetite, and
promotes the storage of nutrients. Smaller (i.e., emptier) adipocytes
react to insulin differently; they take up more glucose in response to
insulin stimulation, and are less sensitive to insulin-induced
suppression of lipid breakdown. They also tend to have lower levels of
adipocyte triglyceride lipase (ATGL), hormone sensitive lipase (HSL),
and lipoprotein lipase (LPL), which are critical for lipid breakdown.
Changes in extracellular matrix structure, sympathetic tone, and
circulating thyroid hormone may be underlying many of the changes
in the metabolic characteristics of adipocytes, ultimately yielding a
physiological environment in which fat storage is promoted.

While weight loss doesn’t alter the number of adipocytes, rapid weight
regain might. Ideally, any weight regain would just refill the existing
adipocytes, but the altered metabolic environment following weight
loss may promote the addition of new fat cells, known as
adipocyte hyperplasia (Figure 9). This effect has been observed in
overfed rats; while it still requires additional research to demonstrate
its relevance to humans, it could be but one of many factors
contributing to fat regain after weight loss. As noted in a review
by Peos et al, this would be particularly disadvantageous for athletes
that complete several weight loss cycles across a career. Addition of
new adipocytes increases the overall capacity for fat storage, and
allows fat to be stored while the original adipocytes have yet to be
fully replenished with energy. In the short-term, this could increase the
likelihood that individuals not only regain the fat they lost, but
actually gain more fat than they lost. In the long-term, this could yield
even more adipocytes with the potential to convey their relative
“emptiness” during the next weight loss attempt, potentially
amplifying some of the physiological signals that promote metabolic
adaptation and oppose weight loss.
Figure 9. A depiction of adipocyte hyperplasia during weight regain following
energy restriction (ER), created by Peos et al. (2019).Source:
https://www.mdpi.com/2075-4663/7/1/22/htm© 2019 by the authors (Peos,
Norton, Helms, Galpin, Fournier). Licensee MDPI, Basel, Switzerland.
Mechanistic rodent data are fascinating, but only if they pan out in
humans. While we don’t have much direct evidence of adipocyte
hyperplasia in re-fed humans, we do have some intriguing
observations of loosely related outcomes. An interesting observation
in studies evaluating weight regain is that the early regain phase is
characterized by selective storage of fat, with minimal restoration of
fat-free mass. This effect, known as post-starvation obesity, has been
observed in several previous studies, including the old Biosphere
study from Part 1 of this article. This could be related to adipocyte
hyperplasia to some degree, but the more prominent driver appears to
be the loss of fat-free mass while dieting (Figure 10).
Figure 10. Both short-term energy deficits and fat mass reduction promote
lower-than-predicted energy expenditure, altered hormone levels, and
excessive hunger (hyperphagia). When the dieter returns to maintenance (or
surplus) calories and regains the fat they lost, hormones trend back toward
baseline levels, and energy expenditure trends toward the predicted value.
However, if the amount of lean mass remains substantially below the baseline
level, hyperphagia may persist.
As explained in a paper by Dulloo et al, adaptive suppression of
metabolic rate is most closely linked to the existence of an energy
deficit and the loss of fat mass; in contrast, hyperphagia is linked
most closely to reductions in fat mass and fat-free mass. With weight
regain, the energy deficit is eliminated immediately, and fat mass is
restored fairly promptly. However, the restoration of fat-free mass
takes longer, and it is common for fat mass to be entirely restored to
pre-diet levels before fat-free mass is fully restored (for a visualization
of this effect using arbitrary numbers, see Figure 11). In this scenario,
hyperphagia continues in order to complete the restoration of fat-free
mass, and the dieter actually regains more fat than they initially lost.
This is known as fat overshooting, and may be driving the results
of observational studies reporting that athletes who engaged in
repeated cycles of weight loss and weight regain tend to have higher
BMIs later in life.

Figure 11. Research commonly shows that fat regain occurs more rapidly than
fat-free mass regain after weight loss. As such, fat mass may be fully restored
before fat-free mass is restored, as shown in the figure. In such a case,
hyperphagia may persist until fat-free mass is fully restored, and body fat
overshooting may occur.
Whether or not adipocyte hyperplasia is an important contributing
mechanism in humans, the available human research indicates that the
physiological environment following weight loss favors weight gain, fat
is preferentially regained in the initial phase of weight regain,
restoration of fat-free mass is a comparatively slower process, and it is
not uncommon to regain more fat than was initially lost. For physique
athletes (or strength/power athletes dieting to fairly low body
weights), this has some important implications for managing the post-
diet period. First, it suggests that the old-school idea of being “primed
for muscle growth,” or banking on some rebound effect of rapid
muscle gain after a weight loss diet, is mythical and unsubstantiated.
We ran a study on the topic, and results showed quite clearly that the
initial, immediate post-show weight gain is largely attributable to
increased water weight, and the additional weight gained in the first 4-
6 weeks was almost entirely fat mass.

Taken together, all of this evidence presents a dilemma for planning

the post-diet phase for physique athletes (or other dieters completing
fairly intense weight loss phases). Certainly, reversing the unfavorable
effects of metabolic adaptation is high on the priority list, which both
improves quality of life and sets the stage for progress toward
continued strength and/or hypertrophy goals. That process is going to
require some additional calories. However, it’s safe to assume that
someone who just completed an arduous fat loss phase would prefer
to avoid immediately gaining all of it (or more) back. This is difficult,
because we are physiologically primed for fat gain after this type of
weight loss, and the added calories in the initial post-diet period
appear to be preferentially diverted toward fat cells for storage. In
order to promote recovery while attenuating excessive fat gain, two
primary approaches for controlled refeeding have emerged: reverse
dieting and recovery dieting.

Reverse Dieting Versus Recovery Dieting

I think my co-authors and I were the first researchers to actually
acknowledge the term “reverse dieting” in a peer-reviewed paper, but
we certainly didn’t coin the term. So, let me begin by giving credit
where credit is due. I first heard the term “reverse dieting” attributed
to Layne Norton; he definitely popularized the term, but neither he nor
I know exactly where it was first used. Based on some digging, it
appears that the term “recovery dieting” is attributable to Jeff Alberts
and the 3D Muscle Journey crew. These could be misattributions, and I
apologize if they are, but I tried.

You can’t really search the research literature for an agreed-upon

definition for these terms, so I’m going to present some operational
definitions that reflect my personal conceptualization of each term
(note: these are my interpretations, so I am not putting words in the
mouth of the individuals who coined these terms). The general premise
with reverse dieting is that calories, mainly from carbohydrate and fat,
are incrementally added back to the diet after the weight loss goal has
been achieved. As the calories slowly increase, the dieter transitions
from a deficit to maintenance to a surplus in a controlled and
methodical manner. As calories are increased in a gradual, stepwise
fashion, metabolic adaptations are reversed over the course of this
process. As a result, energy expenditure increases as caloric intake is
increased, which prevents rapid fat accumulation out of the gate.
Theoretically, this would allow the dieter to begin their offseason with
substantially higher caloric intake than during their weight loss phase,
but with a fairly low level of body fat. Recovery dieting is quite similar,
with somewhat minor differences in the implementation. It seems as if
recovery dieting was essentially introduced in response to excessively
slow implementations of reverse dieting; as a result, recovery diets
often include a very deliberate jump to a small caloric surplus
immediately after the weight loss phase ends, and the approach
generally allows a quicker rise in caloric intake and more directly
embraces reasonable levels (and rates) of fat regain early in the
process.

I don’t see much value in pitting these approaches against each other
to determine which is best. Frankly, I struggle to see “reverse diet
versus recovery diet” as anything but a false dichotomy. Both
approaches seek to address the dilemma of promoting recovery while
mitigating excessive fat storage and weight regain. If we were to
construct a Venn diagram, these terms would have a lot more overlap
than exclusivity. There might be subtle differences with regard to how
quickly calories are added, but there are plenty of factors to consider
when determining how much weight should be regained, and how
quickly. I will certainly acknowledge that a really slowreverse diet
could theoretically leave the dieter in a slight caloric deficit for weeks
after the intended end of the weight loss diet; this would serve only to
delay even the most basic and immediate aspects of recovery, and
make their life unnecessarily difficult. Furthermore, an attempt to
stay too lean during the offseason would likely inhibit an individual’s
ability to fully restore normal hormone levels, reverse the hyperphagia
induced from dieting, and make strength and hypertrophy gains in the
offseason. It’s also relevant to note that a very slow, very strict reverse
diet is unequivocally more challenging and psychologically draining
than the most brutal of contest preps. How do you reasonably
convince yourself to exercise that level of dietary restraint when it
defies all of your physiological cues, and you don’t intend to step on
stage for another 24 months?

These theoretical shortcomings exist, so the ideas reinforced by the

emergence of recovery dieting are helpful and valid. Some might say
that, by acknowledging the potential shortcomings of an extremely
slow reverse diet, I have a preference for recovery dieting by default.
However, I don’t believe that the concept of reverse dieting
necessarily requires such an extreme approach, and I’m not sure how
many people are actually willing and able to implement this type of
protocol after achieving stage-ready levels of body fat. Frankly, I think
both approaches serve to reinforce some very important principles for
how to approach the diet after weight loss has occurred. So, rather
than construct extreme examples of each approach and have them
battle it out, I would much prefer to outline some principles for the
post-diet period.

If your diet is over, get the hell out of a deficit, immediately. Beyond
that point, any time spent in a deficit is wasted recovery time. If that
puts me in the “anti-reverse-dieting” camp, then so be it. Based on this
reasoning, I don’t really see a lot of utility in using nonlinear
approaches like refeeds or diet breaks; every day should be a surplus,
to some degree. If you want some extra special HUGE surplus days to
accommodate your eating preferences, and that’s why you’re using a
nonlinear approach to calorie distribution, go for it, as long as the “low
calorie” days keep you at or above maintenance calories. If you are
planning to increase calories slowly enough to create a super-charged
metabolic rate, don’t bother. The premise of fabricating a new
metabolic rate from scratch is implausible. We only have the capacity
to restore a transiently suppressed level of energy expenditure, and we
have two primary tools to use: more calories, and more time spent in a
surplus. There are certainly instances in which people slowly raise
calories and manage to reach fairly high caloric intakes while staying
lean, but there are explanations for this that do not require wizardry
as an assumption. In the initial stages of slow overfeeding, they are
simply fixing an impairment. Their metabolic rate is lower than it
should be at the start, and they restore it to its normal level (and, for
some people, “normal” is higher than others). After the impairment of
energy expenditure is restored, there is also the potential for the
opposite effect to occur; in response to overfeeding, some people
dramatically increase their non-exercise activity thermogenesis
to prevent weight gain. There is a great deal of variability between
people for this response; as you might imagine, individuals prone to
weight gain typically have a very minor increase in NEAT when they
are overfed, while individuals resistant to weight gain display large
increases. Furthermore, the individuals who are able to slowly work
toward high caloric intakes while maintaining almost-stage-ready body
composition are still fairly miserable and unrecovered, for the most
part. From a very basic viewpoint, recovery can be viewed in three
stages: elimination of the calorie deficit, restoration of reasonably
sufficient fat mass levels, and restoration of lean mass. Someone who
clings to competition-level body fat is unlikely to achieve fully
comprehensive recovery from the multifaceted barrage of metabolic
adaptation, and unlikely to reach a high enough body fat level (or
energy surplus) to support substantial hypertrophy and strength
improvements in the offseason.
Conversely, if you’re planning to rapidly overfeed to capitalize on a
quick rebound of muscle gain, don’t bother. As previously discussed,
the body is effectively primed for fat accretion, but lean mass gains
are hard to come by in this scenario. To optimize the ratio of weight
that is regained as lean mass (within a realistic range), the best bet is
to get the body into a caloric surplus, nudge the body toward recovery
with incremental caloric increases that promote positive energy
balance and fat mass restoration at a conservative pace, while
engaging in a challenging and progressive resistance training program.
Rapid fat gain would probably expedite the recovery process, but
would come at the cost of an elevated ratio of fat gain to lean tissue
gain and an increased likelihood of fat overshooting.

So, the deficit should be eliminated immediately, and caloric intake

should be gradually increased. Exactly how quickly calories should be
increased depends on who you are and where you’re at in your career.
If you have plenty of muscle to gain before you reach your genetic
limit for muscle mass, you should probably consider pushing the pace
(within reason). If you’ve got several years of training under your belt
and believe you’re close to your genetic ceiling for muscle mass, it
probably makes more sense to stay leaner and take it a bit slower
(assuming you want to stay lean and don’t feel terrible at your desired
body fat level). For the vast majority of lifters who have some more
muscle to gain before they max out their muscular potential, fat gain
should not be avoided. In fact, it should be intentionally restored to a
level that allows for recovery of the endocrine system and substantial
hypertrophy to occur in the offseason. This just needs to happen over
a time course that could reasonably be expected to attenuate
adipocyte hyperplasia, prevent fat overshooting, and allow for lean
tissue restoration to occur alongside fat tissue restoration (rather than
rapid and excessive fat gain, followed by slow lean tissue accretion).
You could probably find enough wiggle room in the definitions of
“reverse dieting” and “recovery dieting” to make this approach fit
either, if you felt so inclined. A summary describing some of the
factors pertaining to how quickly or slowly to increase calories is
presented in Figure 12. But how fast is too fast, and how slow is too
slow? That question can’t be answered without considering how long
recovery is expected to take.
Figure 12. A non-exhaustive list of some of the factors to be considered when
deciding how quickly to increase calories or regain weight following weight
loss
How Long Does Recovery Take?
It’s difficult to say how long it takes to recover from a diet. First of all,
we need to determine what “recovery” entails. During the recovery
period, we observe a reversal of adaptations related to energy
expenditure, hormone levels, physical performance, reproductive
function, sleep habits, and appetite, among others. The reality is that
recovery is multifaceted, and different components of recovery appear
to follow distinct time courses. To make things even more difficult,
our behaviors and general approach to recovery make a huge impact
on how quickly recovery occurs. During the recovery period, we deal
with a ton of factors that are free to vary; some are under direct
volitional control (resistance training load, cardio training load, energy
intake, macronutrient distribution, sleep hygiene), while others are not
(life stressors, heritable predispositions, psychological factors, sleep
quality). When asked about the timeline for recovery, it’s tempting to
say “it depends” and move on. But we might as well make some
observations of the literature and do our best with interpretation.

From the case studies, we see a wide range of timelines for weight
recovery; some physique athletes return to their baseline weight
by nine weeks post-competition, while others are still below baseline
weight a full six monthsafter. On that topic, weight overshooting has
been observed by 5-8 months post-competition, with
both male and female competitors ending up a couple of kilograms
heavier than they started. While the subject described by Rossow et
al did not fully return to his initial bodyweight six months post-
competition, he also had not yet restored his fat-free mass to baseline
levels. Generally speaking, hormones more closely associated with
short-term energy availability (such as ghrelin, thyroid hormone,
insulin, and cortisol) start to show pretty substantial recovery in the
first 3-4 months. Leptin and male testosterone levels seem to take
longer; case studies measuring up to 5-6 months after competition
have failed to document full testosterone and leptin recovery in males.
Generally speaking, these 3-6 month hormone recovery timelines seem
to fit pretty well with the most relevant studyfeaturing a reasonably
large sample. In this study of female physique athletes, 27 dieters were
compared to 23 controls throughout approximately 5 months of
dieting and 4 months of recovery, give or take. By the end of recovery,
body composition had almost fully returned to baseline levels, and
most hormones were still a little below normal, but moving in the
direction of full recovery. Performance recovery seems to vary quite a
bit; for example, Rossow et al described complete recovery of deadlift
and squat performance within four months, but bench press remained
below baseline after six months. Pardue et al reported that absolute
Wingate sprint performance, assessed as both peak and average
power, had increased but not fully recovered five months after
competition. Using squat dynamometry, Tinsley et al showed that peak
force production was modestly suppressed nine weeks after
competition, but the rate of force production remained substantially
below baseline.

While menstrual cycle disruption is a very common observation during

preparation for physique competitions, its restoration after
competition appears to be highly variable. In one case study, the
participant returned to normal body weight by nine weeks post-
competition, and menses resumed approximately three months after
competition. In a different case study, energy availability surpassed 35
Calories per kg of fat-free mass at 10 weeks post-competition, and
body weight and fat mass had been restored by week 20; nonetheless,
it took a full 71 weeks of recovery for menses to resume. Regulation of
the menstrual cycle is affected by a wide range of inputs, and
restoration can take quite a while for many women. For example,
a three-month dietary intervention successfully managed to increase
energy intake and energy availability in female athletes with menstrual
irregularity, but the intervention was ineffective at actually restoring
regular menstruation. Other diet and exercise interventions aimed at
restoring normal menstrual function have reported resumption of
menses around 2-3 months and around 6-7 months after the onset of
intervention. Finally, a nine-month intervention was carried out in 21
dancers and 31 athletes with menstrual disorders. After nine months,
regular menses was restored in only 14.3% of the dancers and 22.6% of
the athletes, and the authors speculated that the “average” time
required for restoration might be upwards of a full calendar year for
this sample. In this sample, restoration of menses was less likely in
subjects who began the intervention with lower levels of body fat and
lower energy availability; the authors speculate that increasing fat
mass was a particularly important factor for resumption of regular
menses. Variable recovery times are even observed in more intensive
approaches; one study using exogenous leptin injections found that
menstruation was restored in seven out of ten subjects, with
menstruation appearing 4-32 weeks following the onset of leptin
therapy.

In summary, different aspects of recovery occur over different

timelines. Total energy expenditure can be partially restored in
response to short-term overfeeding, but full restoration of energy
expenditure seems to take longer. As positive energy balance is
maintained and fat mass is restored over the first 3-6 months,
hormones, energy expenditure, and performance outcomes tend to
start reverting back toward baseline levels. There is a great deal of
variability in recovery timelines between individuals, especially when it
comes to restoring menstrual cycle irregularities. Variability is
certainly related, at least in part, to how the post-diet period is
approached. Recovery is likely to be accelerated in the context of a
larger energy surplus, more expeditious restoration of fat mass and
lean mass, more complete restoration of fat mass and lean mass, more
conservative management of training loads, and more effective
management of sleep and life stressors. As such, more rapid increases
in caloric intake after dieting favor more rapid and complete recovery,
but must be weighed against the increased likelihood of body fat
overshooting. A final aspect of recovery, which may take even longer
than the physiological aspects, involves psychological recovery.

Psychological Aspects After Weight Loss

Just as psychology plays an important role in weight loss, it also plays

an important role in the period immediately following weight loss. The
transition from dieting to maintenance or weight regain can involve
shifts in motivation, perspective, habits, and body image. For this
topic, I will focus on people who are dieting to unsustainable levels of
leanness, such as preparation for a physique competition or photo
shoot. If you’re in this position, we can make two reasonably safe
assumptions: 1) you will experience noticeable fat gain in the weeks
and months following weight loss, and 2) your physique is at
least somewhat important to you. These types of fat loss endeavors
often predispose the dieter to some rituals that probably have more
negative psychological ramifications than we’d like. For example, a ton
of physique athletes adhere to a morning routine in which they wake
up, check their body weight for the day, and take a look in the mirror.
A favorable weigh-in and a subjective improvement in the mirror can
really set the tone for a positive morning during contest prep, and
results from the morning weigh-in are often internalized
dichotomously as “good” or “bad” progress. Luckily, an effective
contest prep virtually assures incremental improvements over time, so
it’s a trend over several months that has a lot more good than bad. But
what happens when weigh-ins are consistently higher each day, and
the mirror assessment reveals incrementally more fat? If the mind is
entrained to perceive a lower weight and a leaner appearance as a
“good” morning check-in, this sets the dieter up for several months of
“bad” mornings. Coupled with the usual weight gain stressors (such as
ever-tightening belts and clothing, a newfound accumulation of
abdominal fat that becomes apparent when you sit down, or noticing
that your glutes are actually covered with adipose tissue when you sit
on a hard chair or bench), this can set the dieter up for a rough time.

The early weight regain phase can be associated with body image
issues, a variety of disordered or problematic eating habits, reduced
motivation, and the general negative affect that physique athletes call
the post-competition blues. Having a plan for the period after weight
loss also involves a psychological component. I’m no psychologist, so
take this with a grain of salt, but it intuitively seems remarkably ill-
advised to leave this component entirely unaddressed. The perspective
for what constitutes a “good” check-in and a “bad” check-in should be
either drastically revised, or thrown out altogether. Positive post-
competition progress for a super-lean physique athlete doesn’t
just allow for some fat regain, it requires it. There is tremendous
benefit to embracing the positive aspects of weight regain: it’s
promoting recovery of your endocrine system, it’s making you feel
better on a day-to-day basis, it’s restoring your energy level, it’s giving
you more dietary flexibility, it’s fueling substantially better training in
the gym, and it is an instance of successfully implementing the post-
competition plan. This shift in perspective has to be intentional and
approached in a proactive manner, primarily to ensure that post-diet
weight gain doesn’t psychologically and emotionally hit you like a ton
of bricks. When psychological recovery is not proactively planned for,
it can sometimes take up to 12-18 months to truly feel “normal” after
a rigorous weight loss diet. When the challenges and stressors that
accompany the period after weight loss are anticipated and planned
for, this timeline can be dramatically shortened.

Conclusion

When you finish a weight loss diet, many of the unfavorable effects of
metabolic adaptation are in full swing, and your body is primed for fat
regain. If you’ve dieted to a reasonably sustainable body fat
percentage, maintenance is certainly achievable. If you’ve dieted to a
physique competition-level body fat percentage, weight regain is an
important part of recovering from the unfavorable metabolic and
hormonal effects of metabolic adaptation. However, if there’s no plan
in place for transitioning from weight loss to either maintenance or a
controlled weight regain process, the likelihood of excessive fat regain
and body fat overshooting is increased. When the weight loss phase
ends, calories should promptly be raised to maintenance levels, at
minimum. Prolonging the energy deficit serves only to inhibit recovery,
but the “ideal” rate at which caloric intake should increase depends on
the goals and circumstances of the individual. For individuals who are
comfortable returning to their initial body weight, metabolic,
hormonal, and performance-related adaptations should be largely
reversed within 4-6 months. Other aspects of recovery, such as
restored menstrual regularity and psychological recovery, are much
more variable between individuals. More conservative approaches to
the post-diet recovery process that seek to delay or minimize fat
regain have the potential to substantially prolong the recovery
timeline.

Summary
 Weight loss attempts are met with changes in mitochondrial
function, hormone levels, and energy expenditure.
 These changes produce some unpleasant side effects, threaten our
ability to gain (or even keep) muscle mass and strength,
manipulate biological cues pertaining to the regulation of appetite
and activity level, and require us to eat even fewer calories and/or
incorporate even more cardio into our training program.
 To mitigate the effects of metabolic adaptation, dieters should
avoid rapid weight loss (>1% of body mass per week), eat
sufficient protein (2.3-3.1 g/kg of fat-free mass), and avoid
excessive cardio volumes and frequencies.
 Refeeds (twice weekly) and diet breaks (1-2 weeks at a time) may
also help to attenuate the effects of metabolic adaptation.
 To avoid body fat overshooting and promote recovery, it’s
important to have a transition plan in place for when the weight
loss diet ends.
 The caloric deficit should not extend beyond the period of
intended weight loss; the rate at which calories should be
increased depends on the goals and circumstances of the
individual.
 For competitors that return to (or near) their initial body weight,
most physiological parameters tend to recover within 4-6 months,
while menstrual cycle regularity and psychological factors are far
more variable and often take longer.
 Conservative approaches that raise calories more slowly may
minimize fat regain, but may also extend the timeline for full
recovery.