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Post-Competition Perils: Hyperphagia, Adipose Overshoot, and Dysphoria
It is common for bodybuilders and physique competitors to engage in a period of
dysregulated behavior characterized by repetitive, uncontrollable hyperphagia
and Bingeing in the days immediately subsequent to competition or to their
lowest achieved adipostatic level. While the eating behavior is by and large the
central component of this post-competition syndrome, it is part of a larger
phenotype which includes both bodyfat overshoot (Dulloo et al., 1997) and a
general dysphoria characterized by a multiplex of feeling/behavioral states
including emotional and/or mental discomfort, restlessness, malaise, depression,
and sleep fractionation.
Extending my work on dynamical systems (and more generally adaptation at lowered
adipostatic states), this article makes a specific contribution to discussing
post-competition issues. It highlights a subtle paradox, in that the worst
symptoms of severely reduced adipostatic states are not necessarily present
during such a time, but rather on the slippery slope out of such a state.
It can be argued that most of the bodybuilding community, whilst aware of the
symptoms noted above during repeated competition cycles, are unaware that they
are in fact physiologically rooted adaptive processes (from a purely
physiological standpoint). In addition, the claim is advanced here that training
and supplementation post-competition may be even more important than training
pre-competition, since it is during this post-competition period that
significant declines in physique and mental resilience occur beyond levels
established before pre-competition preparation was fully set in motion.
Originally noted by Keys et al. (1950) in the infamous Minnesota Starvation
experiment and subsequently corroborated by the Dulloo lab in a number of papers
that re-analyzed the original Minnesota data; there was a marked tendency for
individuals who underwent the starvation period (or a protracted period of
hypoenergetic caloric intake) to engage in voracious hyperphagia and demonstrate
significant body fat gain following release from the starvation requirements.
Indeed, because the body-fat gain following starvation exceeded the absolute
adipostatic levels prior to the deficit (starvation) period, Key's et al. (1950)
termed the phenomenon post-starvation obesity, while the Dulloo group (Dulloo,
et al., 1997) termed the phenomenon post-starvation hyperphagia and body-fat
overshoot.
If we consider the bodybuilder or fitness enthusiast's pre-contest dieting
akin to that of the starvation period of Key's et al. (albeit with some
notable dissimilarities including resistance training and extensive
supplementation use), we can begin to understand the post-contest period, and
the normative metabolic and behavioral-psychological reactions that often cause
great distress for the passionate bodybuilder (natural or not) or fitness
enthusiast.
An account retold from one of Keys original participants in the Minnesota
experiment reflect what has been related to me time and again in numerous
private messages; and as I have also observed in various individuals who I have
trained with (both male and female), and echo reports of post-competition
Binges:
Although they were warned to be careful not to overeat on d 1 [following the
experiment], they were free to eat as they wished. H.S. remembered being taken
to the hospital to have his stomach pumped because he, just simply over did (Kalm
& Semba, 1997, p.1351).
As a group, the Minnesota subjects as well as others who have undergone
significant body weight reductions during extended periods of energetic deficit
(cf. St. Pierre et al., 1996), show persistence in both appetite and hyperphagia
long after refeeding commences. This combination of both increased appetite and
subsequent hyperphagia was termed integrated hyperphagia by Dulloo et al.
(1997). Once again, persistence in Binge behavior and the associated mental
dysphoria with losing the contest physique is a common phenotype of bodybuilders
and fitness (figure) competitors. One such person indicated to me they put on
substantial fat (past pre-competition prep) following competition but also
suffered from notable socioemotional disturbances, including, but not limited
to, depression and social anxiety; which ultimately lead to the inability to
maintain a romantic relationship.
Taken together, the elegant work of Keys, Dulloo and colleagues, should serve
the training community in the sense that following bouts of contest dieting,
counterregulatory processes will soon ensue, leading to behavior which can
seriously threaten maintenance of even pre-competition dieting conditioning
levels. As such, the post-competition period becomes a very critical time when,
as I argue, training and supplementation usage must be dialed in. Before I offer
a few brief, flexible recommendations, there are a few extremely important
details that must be noted with regard to the re-analysis of the Minnesota
starvation data by the Dulloo group.
In re-analyzing the Minnesota starvation data, Dulloo's group found at least two
important variables in the characterization of post-starvation integrated
hyperphagia. The first being that even in spite of increased dietary induced
thermogenesis (DIT) - due to the sympathomimetic actions of excessive
carbohydrate loading (i.e., Bingeing) - there remains a specific metabolic
component favoring fat storage (1990). Thus, even in the presence of increased
DIT (due to metabolic normalization as weight is gained), adipose tissue can be
laid down simultaneously. Dulloo and Girardier (1990) noted that the metabolic
component represented a net 15% reduction in energy expenditure during refeeding.
Dulloo (1997) further notes that the phenomenon of fat increase occurring more
rapidly than that of active tissues has been noted since the turn of the
century in adults recovering body weight after diseases or famines (p. 30), and
cites both Jamin & Muller (1931) and Kornfeld & Schuller (1931). While a more
comprehensive overview of their models, including that of the P-ratio (Dulloo &
Jacquet, 1999) are outside the scope of this article, the key point of the
foregoing discussion is that fat overshooting is in large part determined by
delayed protein repletion (loss of lean-tissue), which in turn results from a
suppression of thermogenesis favoring the replenishment of adipose reserves (Dulloo,
1997).
The second variable involves the predictive ability of both adipose and lean
tissue loss to promote post-starvation integrated hyperphagia. In an elegant set
of regressions, Dulloo et al., (1997) showed that while adipose loss was the
strongest predictor of integrated hyperphagia, lean tissue loss also added
unique variance (albeit of small magnitude). These correlations were still
present even after controlling for degree of prior energy deficit.
Considering this, it is quite clear that the post-competition phenomenon of
integrated hyperphagia is a relatively ubiquitous phenomenon among those who
have lost substantial body mass. However, the component of mental dysphoria is
an addition this author has contributed independently (as a result of both
personal and vicarious experience), and we can conceptualize both integrated
hyperphagia and mental dysphoria as the post-competition syndrome. I have
written previously on psychoneuroendocrinological contributions to the
post-competition phenotype (cf. Adipose Reduction and bodyfat Setpoint: A Dev.
Reg. Model) and will elaborate on this component of the post-competition
syndrome in future work. Suffice it to say that included in the dysphoric
component are depression, restlessness, fatigue, sleeplessness, and most
importantly, social withdrawal. So, from a training standpoint, how can the
trainee deal with the post-competition syndrome?
It would seem that a simple understanding of the post-competition period, as
presented here, will go a long way to treating this period of training more
appropriately. More specifically there are at least four specific areas where
trainees and competitors can directly address the post-competition syndrome:
1) Psychological: While acute Bingeing post-competition is of the involuntary
subtype, it is argued that subsequent Bingeing (still part of the integrated
hyperphagia matrix) is more voluntary in nature and psychologically triggered.
Psychological triggers are more likely to become effective at triggering Binge
patterns in light of the underlying post-starvation vulnerability (cf. Adipose
Reduction and bodyfat Setpoint: A Dev. Reg. Model). In addition, individual
differences in affect regulation (socioemotional adaptation, attachment) may
also play a key role (for comparative evidence see Hancock, Menard, & Olmstead,
2005). Awareness of psychological cues that trigger Bingeing and insuring that
you take proactive steps to re-engage - in adaptive, positive social situations
(e.g., going out, interacting with others) - may short-circuit the feed-forward
loop of social isolation-Bingeing.
2) training: A least two prominent considerations come to mind. First, and of
obvious import; the more lean mass retained during the dieting period, the more
potential for reductions (albeit subtle) in the experience of integrated
hyperphagia. It would seem that a strong focus on time under tension (TUT)
should be a core component of both the pre and post competition periods. Second,
cardio should be maintained or even increased during the post-competition period
to both compensate for involuntary Bingeing as well as to perhaps inhibit the
metabolic component that appears designed to facilitate fat storage (a more
detailed discussion will be presented in a separate paper). Finally, an
immediate change in training protocol is advised, as this will freshen up the
routine and prevent needless iterations of mental fatigue of having to perform
the same routine - which can lead to an avoidance of the gym (isolation) and
subsequent Bingeing as discussed above.
3) Binge Nutrition: It may be profitable to create a fixed Binge pattern
such that, even during times of involuntary Binges, there are only certain
foodstuffs that you are allowed (provided they enable the quiescence of the
integrated hyperphagia and psychological craving). For example, during times of
integrated hyperphagia, this author has been able to fix his foodstuffs,
allowing fat-free frozen yogurt and specifically (only) butter popped corn cakes
(which contain no HFCS). This may be one factor that has attenuated the
consequence of integrated hyperphagia. Often we hear of Binges on candy,
chocolate, pizza and other calorie dense high-fat, high-carbohydrate foods,
which most certainly will elevate the energy intake.
4) Thermogenic supplementation: A few brief, non-exhaustive comments here.
Thermogenic supplementation, such as the EC(A) stack (and others) should be
continued, possibly increased during this phase (consider 40mg ephedrine/day
rather than 20mg). The reasoning is the same mentioned above in regards to
cardio - the potential to short-circuit the metabolic component favoring fat
storage in spite of increased DIT. Of course, abuse of any Thermogenic during
the dieting phase will reduce any gains one might make by increasing the dosage
during the post-competition phase. That said much of the diet phase can proceed
without the use of Thermogenic aids, simply by maintaining a modest caloric
deficit; restricting intake and increased energy expenditure.
While I am torn on advocating the use of nicotine in this context, I will
indicate that its continued usage through both dieting and post-rebound phases
may exert favorable body composition changes and maintenance. One study (Schwid,
Hirvonen, & Keesey, 1992), albeit in rats, is particularly relevant as it was
framed in a regulatory perspective and it showed that nicotine-reated rats were
able to reduce their setpoint; but also that they showed the same hyperphagic
phenotype as control rats when they were starved beyond this new setpoint.
However, rather than Binge back up to control levels of absolute fat, these rats
overshot their new reduced setpoint briefly, eventually returning to this new
setpoint which was lower than their control (pre-nicotine) values. This
provides comparative evidence for the hyperphagic phenotype in humans as well as
the energy conserving adjustments both during food restriction which spill over
into the refeeding period. I would be remiss not to indicate that one must
obviously reflect on the method of nicotine administration as well as the noted
risks to its usage.
Here I have discussed the normative phenomenon of integrated hyperphagia
observed in individuals who have experienced significant and extended periods of
caloric deficit resulting in a substantial loss of bodyweight. I then applied
this portrait to that of the body-builder or figure competitor following the
competition period. I then offered more specific details regarding variability
in integrated hyperphagia and created a new term, specific to this broad sport,
called the post-competition syndrome. Finally, I have offered some brief
recommendations regarding training, hyperphagic nutrition, and post-competition
Thermogenic supplementation. I have intentionally made an attempt to keep this
contribution less academic in tone while still preserving a highly academic
backdrop (i.e., Keys et al., and Dulloo et al.). For the more scientifically
inclined, specific discussions of the material within will continue both in
future articles as well as in the dynamical thread over at Avant where relevant
mechanisms will be more fully elucidated and theorized.
References
1. Dulloo, A. G. (1997). Human pattern of food intake and fuel-partitioning
during weight recovery after starvation: A theory of autoregulation of body
composition. Proceedings of the Nutrition Society, 56, 25-40.
2. Dulloo, A. G., & Girardier, L. (1990). Adaptive changes in energy expenditure
during refeeding following low-calorie intake: Evidence for a specific metabolic
component favoring fat storage. American Journal of Clinical Nutrition, 52,
415-420.
3. Dulloo, A. G., & Jacquet, J. (2001). An adipose-specific control of
thermogenesis in body weight regulation. International Journal of Obesity, 25,
S22-S29.
4. Dulloo, A. G., & Jacquet, J. (1999). The control of partitioning between
protein and fat during human starvation: Its internal determinants and
biological significance. British Journal of Nutrition, 82, 339-356.
5. Dulloo, A. G., Jacquet, J., & Girardier, L. (1997). Post-starvation
hyperphagia and body fat overshooting in humans: A role for feedback signals
from lean and fat tissues. American Journal of Clinical Nutrition, 65, 717-723.
6. Dulloo, A. G., Jacquet, J., & Girardier, L. (1996). Autoregulation of body
composition during weight recovery in human: The Minnesota experiment revisited.
International Journal of Obesity, 20, 393-405.
7. Hancock, S. D., Menard, J. L., & Olmstead, M. C. (2005). Variations in
maternal care influence vulnerability to stress-induced Binge eating in female
rats. Physiology & Behavior, 85, 430-439.
8. Jamin, F. & Muller, E. (1931). Specific weight of the living man with
clinical applications for recovery of body weight. Munchener Medizinishche
Wochenshrift, 51, 349-362.
9. Kalm, L. M., & Semba, R. D. (2005). They starved so that others could be
better fed: Remembering Ancel Keys and the Minnesota experiment. Journal of
Nutrition, 135, 1347-1352.
10. Keys, A., Brozek, J., Henschel, A, Mickelson, O., & Taylor, H. L. (1950).
The biology of human starvation: 2 volumes. Minneapolis: University of Minnesota
Press.
11. Kornfeld, W. & Schuller, H. (1931). Pattern of lean tissue deposition in
free-living children recovering from tuberculosis. Zeitschrift fur Kinder und
Jugendpsychiatrie, 51, 349-362.
12. Schwid, S. R., Hirvonen, M. D., & Keesey, R. E. (1992). Nicotine effects on
body weight: A regulatory perspective. American Journal of Clinical Nutrition,
55, 878-84.
13. St. Pierre, S., Roy, B., & Tremblay, A. (1996). A case study on energy
balance during an expedition through Greenland. International Journal of
Obesity, 20, 493-495.
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