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Post-Competition Perils: Hyperphagia, Adipose Overshoot, & Dysphoria
by J.D. Haltigan
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 overdid” (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’:
by J.D. Haltigan
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 overdid” (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’: