Metabolic Damage: Can dieting slow down your metabolism?

Across a variety of sports, dieting to compete at lower bodyweights can be advantageous. Specifically, weightlifters, bodybuilders, powerlifters and combat sports (wrestling, mixed martial arts, boxing) require weight loss for their respective competitions. Leaner body compositions can result in a larger strength to weight ratio and improved locomotion. Bodybuilding is a sport where athletes are judged based on the amount of lean body mass and the symmetry of their physiques. To improve their chances of winning, bodybuilders diet to extremely low levels of body fat to increase the definition of their musculature. To achieve the body composition required to be competitive in their sport, bodybuilders spend extended periods of time in a caloric deficit accomplished through reduced calorie consumption and increases in physical activity. The extreme physiological demands of a bodybuilding contest preparation diet can have various behavioral, metabolic, neuroendocrine, and autonomic responses (decreased leptin, thyroid hormone, non-exercise activity thermogenesis) that can hinder dietary adherence and result in rapid weight regain (18, 27, 31, 5, 6, 12). It has been documented that healthy humans undergoing partial starvation and extensive diets incur disproportionate reductions in daily energy expenditure that counter an energy reduced state and drive a return of body fat stores (25). Resulting increases in appetite, decreases in energy expenditure, and increased muscular efficiency could be a consequence of systems favoring weight recidivism after a diet (16, 6, 11, 19, 23). This paper will attempt to explore adaptive thermogenesis (the adaptive properties of metabolism) and the severity of the metabolic, hormonal, and behavioral ramifications of long term dieting and weight loss in bodybuilders.

Effects of Reductions in Bodyweight on Energy Expenditure Partially, decreases in total daily energy expenditure (TDEE) below what would be expected post diet are due to reductions in bodyweight. Components of TDEE include exercise activity thermogenesis (EAT), the thermic effect of food (TEF), non-exercise activity thermogenesis (NEAT), and basal metabolic rate (BMR). Reductions in bodyweight decrease TDEE by directly affecting BMR and NEAT. A loss of metabolically active tissue reduces the energy cost of BMR; the largest constituent of TDEE (8). Decreases in bodyweight also directly impact the amount of energy expended during EAT and NEAT, a considerable difference of energy requirement before, during, and after a contest preparation diet are in large part due to reductions in body mass (31). Decreases in NEAT are a prominent response to rapid weight loss suggesting a possible mechanism for decreasing energy expenditure, the reduced energy cost of physical activity can account for up to 90% of the unexpected drop in energy expenditure when body mass loss is accounted for (9).

Additionally, as a contest prep diet continues calories are decreased to lose fat at a predetermined pace. A decrease in calories consumed will reduce the energy cost of the digestive system. Reductions in daily intake of fiber, protein, and carbohydrates lessen the energy demand of the digestive tract. However, it has been observed that reductions in bodyweight equal to or higher than 10%, are accompanied by decreases in energy expenditure of up to 25%. This 15% discrepancy in TDEE suggests there are other factors influencing a higher decrease in energy expenditure (25). Beyond the decrease observed in TEF, NEAT, EAT, and BMR from losses in body mass, several other endocrine, neuromuscular, and metabolic responses are responsible for reductions in energy expenditure below what would be expected.

Leptin and the Hypocaloric State A variety of hormones are involved in the regulation of bodyweight. Leptin plays a major role in body weight regain and as a metabolic mediator during instances of prolonged dieting through interaction with the central nervous system and a direct peripheral mechanism. In humans and animal models, this adipocyte derived hormone’s absence can cause significant fat gain. When Leptin is released into the bloodstream it influences receptors in the hypothalamus that trigger the expression of specific neuropeptides that regulate energy expenditure and hunger (5). Notably, rodents that had the ventral medial region of the hypothalamus ablated increased food seeking behavior and experienced a reduction in energy expenditure to the point of obesity. Some would consume so voraciously, food became lodged in the trachea and the subject would expire. This response was a result of the inability of leptin to act on the ablated region of the hypothalamus. When these rodents shared circulation with rodents that had their hypothalamus intact, the latter ate so little they became emaciated. From this observation, it can be inferred that leptin’s actions on the hypothalamus have a large impact on behavior, NEAT, and appetite (22, 11).

Leptin is largely synthesized in fat tissue with the expression of the OB gene, the gene responsible for production of leptin. The OB gene is expressed significantly higher in subcutaneous fat than in visceral fat (7,26). Circulating leptin concentrations are markedly influenced by body mass index and adiposity, thus there is a direct relationship between amount and size of adipose tissue and leptin production. During maintenance of reduced bodyweight, levels of leptin decrease accompanied by a resulting downregulation of energy expenditure (7,17). Following an extended period of dieting, subjects sustaining a 10% reduction in bodyweight being treated with twice daily leptin injections saw increases in energy expenditure and a reversal of T3 and T4 reductions. Additionally, subjects were recorded to have decreased energy expenditure during physical activity with an average decline of 373 kcals/day following a 10% reduction in bodyweight. After administration of exogenous leptin, energy expenditure during physical activity increased by 339 kcals/day during maintenance of a 10% reduction in bodyweight. The increases in energy expenditure and thyroid hormone produced by leptin administration outline the outcome of increasing leptin levels (26).

Not surprisingly there exists a link between insulin, an important regulator of nutrients, and the expression and production of leptin by white adipose tissue. Humans and rats with tumors on their pancreatic B-cells (insulinoma) have increased circulating levels of leptin that decreased during removal of pancreatic tumors. It’s probable that insulin’s positive expression of leptin at the level of the adipocyte is due to increased glucose transport (7). Leptin has a possible role as modulator of carbohydrate intake.

Prolonged periods in a hypocaloric state during a bodybuilding contest preparation can result in lower levels of leptin that decrease energy expenditure and increase food seeking behavior. Circulating levels of leptin would not completely return to baseline solely with an increase in caloric intake during the diet as they are dependent on actual adipose mass (17). Among bodybuilders and physique athletes it has become common to employ periodic 24-hour bouts of overfeeding, with the increase in calories being contributed in increased carbohydrate intake (31). Periods of overfeeding can acutely increase leptin concentration and mitigate some of the losses in energy expenditure. Females subjected to three days of overfeeding increased plasma leptin levels and energy expenditure by 28% and 7% respectively. Additionally, those who were overfed with carbohydrates increased leptin plasma levels and energy expenditure, those overfeeding with fat did not. Even during the early stages of dieting, significant drops in leptin can be observed before substantial losses in body fat, suggesting leptin acts to defend from reductions in carbohydrate intake. Due to the modest increase in energy expenditure in contrast with a substantially larger increase in leptin concentration, it is presumed that the acute increase can be contributed to TEF from a larger carbohydrate intake and an increase in NEAT (7,14, 21). Thus, periodic refeeding during a contest prep should not be geared towards leptin manipulation, but may serve to increase dietary adherence and acutely mitigate losses in energy expenditure via increased NEAT.

Leptin plays a crucial role in regulating energy expenditure, appetite, and food seeking behavior. During times of low carbohydrate intake and reductions in adipocytes, circulating leptin levels decrease. The absence of leptin to act on the hypothalamus can trigger physiological and behavioral responses that favor a recidivism of fat. This can have an increasingly detrimental effect on diet adherence and energy expenditure. The effects of reduced circulating leptin can only be minimally influenced with short bouts of carbohydrate overfeeding.

Muscular Efficiency and the Thyroid Response to Prolonged Dieting

During maintenance of reduced bodyweight, it has been documented that physical tasks require decreased amounts of energy in contrast to physical activity prior to weight loss. A portion of the reduction in energy demand can be attributed to changes in bodyweight that reduce caloric expenditure during physical activity. Changes in muscular efficiency can account for up to a 35% change in the energy expended during physical activity; when accounted for body mass loss, individuals who maintain a reduced bodyweight require less energy than pre-weight loss demands despite wearing external load to counteract the loss from initial weight (32).

Gross mechanical efficiency of skeletal muscle was significantly increased during maintenance of a 10% reduction below initial bodyweight during cycle ergometry of 10 and 25 watts of power, but not 50. The increases in gross mechanical efficiency diminished upon increasing exercise intensity. In six of the seven subjects studied maintaining a reduction in bodyweight, the adenosine triphosphate cost of contractions in the gastrocnemius muscle during electrical stimulation was decreased (9). In a separate study, subjects’ VO2 had decreased by 11% when peddling against no resistance after a 5% reduction in bodyweight over the span of three weeks. In contrast, high workload skeletal muscle efficiency increases were less significant (15, 29).

The mechanism for fluctuations in skeletal muscle efficiency that are not contingent on changes in bodyweight are not yet well understood. However, the thyroid hormone axis seems to play a crucial role. Contraction velocity in skeletal muscle has been directly related to distinct isoforms of myosin heavy chains, a major subunit of myosin adenosinetriphosphatase. Both physiological stimuli and hormone activity, specifically thyroid hormones, can cause myosin heavy chain isoform switches (12). Thyroid hormones can affect the relative proportion of fast to slow twitch muscle fiber types. During weight loss, triiodothyronine levels decrease in response to decreased energy intake. This deviation from homeostasis can alter the proportion of carbohydrate metabolism used relative to the amount of carbohydrate stored (24).

Decreasing levels of triiodothyronine and a shift away from carbohydrate metabolism favors the more energy efficient and fat oxidative slow twitch muscle fibers. Hypothyroidism in rats decreases glycolytic capacity and the expression of and less efficient isoforms of myosin heavy chains (15). Lowered triiodothyronine levels because of decreased energy intake in humans could lead to a higher recruitment of fat oxidative slow twitch muscle fibers, thus accounting for the increased skeletal muscle efficiency during low intensity task.

An increase in gross skeletal muscle efficiency can substantiate a lower energy expenditure than expected when bodyweight is accounted for. Prolonged dieting periods in bodybuilders that decrease triiodothyronine levels and increase efficiency during low levels of physical activity can decrease the energy cost of NEAT and contribute to a decreased energy expenditure (9).

Reduced Proton Leak and Increased Mitochondrial Efficiency

Mitochondria regulate vital cellular functions and play a crucial role in ATP production. Uncoupling proteins are inner mitochondrial membrane proteins that cause protons to flow, thus energy substrate oxidation and oxygen consumption occur without the production of ATP. The flow of protons through the inner membrane by way of uncoupling proteins is termed mitochondrial proton leak (13). In brown adipose tissue (BAT) and skeletal muscle, uncoupling protein-1 (UCP-1) and uncoupling protein-3 (UCP-3) transport protons back to the intracellular matrix and produce heat. It has been shown that chronic caloric restriction decreases the amount of proton leak and therefore can lead to decreased energy expenditure (13, 30, 2, 3).

In BAT, caloric restriction inhibits UCP-1 expression and increases energy efficiency by mitigating proton leak. Interestingly, both leptin and thyroid hormone have been shown to regulate proton leak with a correlation between low levels of thyroid hormone and decreased proton leak (31,10,4,30). Such implications should be considered when sustaining a prolonged hypocaloric state during a bodybuilding contest preparation diet, the magnitude and permanence of increased mitochondrial efficiency in humans is still somewhat unclear due to the prevalence of animal models in research. Currently, more research on the topic involving humans is needed to fully understand the scope and limitations of uncoupling proteins and proton leak on energy expenditure.

Limitations

It is pivotal to understand that much of the research using dietary logs and calorie intake recall have limitations due to errors during estimation and underreporting. Dietary underreporting has been seen in both obese and non-obese subjects with higher degrees of underreporting in subjects that have higher cognitive restraint. Bodybuilders undergo high levels of cognitive restraint during contest preparation. This data is especially relevant to any research involving energy intake, expenditure, and adaptive thermogenesis as it introduces a possible error with human subjects. Severe underreporting as defined by an overestimation of 20% or more of energy intake was seen in 37% of individuals in a sample size of 83 subjects (1). Additionally, limited research on adaptive thermogenesis has been conducted on performance athletes and bodybuilders; most research utilizes animal models or an obese population. It is difficult to infer whether the same degree of adaptation would happen in competitive resistance trained bodybuilders.

Implications for the Athlete

Bodybuilding contest preparation diets present a multitude of mental and physiological challenges to athletes that can negatively affect dietary adherence and sport performance. Several biological mechanisms are in place that favor body fat recidivism, these factors are not only relevant to bodybuilders but to a variety of athletes whom compete in weight class driven sports and to many individuals that struggle with obesity and fat loss. Among the constituents of total daily energy expenditure, decreases in NEAT can account for up to 90% of the unexpected drop in energy expenditure when body mass loss is accounted for (9). Leptin and thyroid hormone both act to decrease the caloric cost of physical activity when in an energy depleted state. By researching further into reducing the hormonal impact of weight loss, dietary adherence in a variety of populations could be increased and the psychological and physical ramifications of rapid weight regain can be avoided.

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