Objective: To test a hypothesized association between resting leptin levels (adjusted for body fat percentage) and symptoms of primary exercise addiction.
Design: Cross-sectional design.
Setting: Habitual amateur exercisers participating in running, fitness, weight training, and biking.
Participants: Twenty men with exercise addiction as defined by the Exercise Addiction Inventory (EAI scores 24-30) and 20 men in an exercise control group (EAI scores 6-16) matched on body mass index.
Main Outcome Measures: Plasma leptin and sex hormones were measured in blood samples collected under fasting and resting conditions. Body composition was assessed by dual-energy x-ray absorptiometry. Eating disorder symptoms were identified by the Eating Disorder Inventory 2.
Results: The exercise addiction group had significantly (P < 0.001) lower leptin levels (1.1 [mu]g/L, SD = 1.3) than controls (4.3 [mu]g/L, SD = 2.9). Even when adjusted for body fat percentage, the addiction group had significantly (P < 0.001) lower leptin levels (0.1 [mu]g/L, SD = 0.1) than the controls (0.2 [mu]g/L, SD = 0.1). Body fat-adjusted leptin correlated with free bioavailable testosterone, but it was only significant in nonaddictive exercisers. None of the exercisers seemed to suffer from an eating disorder.
Conclusions: This is the first study showing that excessive training in exercise addiction is associated with low levels of body fat-adjusted leptin levels.
Clinical relevance: Hypoleptinemia could be involved in the pathogenesis of exercise addiction. However, further studies are needed to explore the potential causal relationship.
Alex’s Notes: Leptin is a hormone produced by fat cells that basically regulates the amount of fat on the body. It is involved in many processes of the body, no doubt, but it is most (in?)famous for its ability to mess with appetite, hunger, and energy expenditure. It correlates highly with body-fat levels, and is depressed during prolonged dieting and in those who are extremely lean.This drop causes reversible decreases in thyroid activity, sympathetic tone, and energy expenditure in skeletal muscle, and increases in muscle efficiency and parasympathetic tone, resulting in a lower basal metabolic rate than an individual at the same weight who has never lost weight. It is one of the foundations of the set-point theory of metabolism. Conversely, in the obese it suppresses hunger and increases energy expenditure via blocking all the nasty effects of neuropeptide Y.
Anyway, Leptin is complicated to say the least and there is still much we don’t know. However, it can be said that higher leptin promotes hormone production and energy expenditure, while lower leptin levels do the opposite. This brings me to the study at hand. Exercise addition is characterized by excessive and obsessive exercise patterns, similar to eating disorders (except with exercise and not food). Indeed the two are often found together in such examples as anorexia, but not always. Primary exercise addiction has exercise itself be the goal, with food regulation a secondary means to enhance physical performance. Knowing this and the basic effects of leptin, the researchers wanted to see if there was a correlation independent of body-fat levels.
The participants performed 1-5 sports on a regular basis that ranged from running and weight training to football, swimming, and racket sports. There were two groups: the addicts and the control, with the former exercising an average of 12 hours per week and the latter an average of five hours per week. That is a huge difference, and can be attributed to the significantly higher scores on the eating disorder symptoms questionnaire, specifically the “drive for thinness” and “perfectionism”. Not surprisingly, body-fat and leptin were significantly lower in the exercise addict group as well, with leptin remaining significantly lower after adjusting for body-fat levels.
Interestingly, levels of free bioavailable testosterone were significantly lower in the exercise addiction group and these levels were also significantly associated with fat-adjusted leptin levels. Remember, leptin is crucial in the starvation response. From an evolutionary perspective, increased physical activity is necessary to locate food, and when you are starving, your body doesn’t care about your testosterone and ability to reproduce. It needs you stay alive first. What is unclear is whether low leptin leads to increased physical activity, or vice-versa. We know intense exercise reduces leptin levels, but would it be far-fetched to think that those with a “need” to exercise simply have lower leptin levels to begin with that drive a psychological mission to exercise or be active in an attempt to “get food”?