Exercise initiates a coordinated series of physiological responses, including hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system activation, that, in combination, lead to the appropriate selection and utilization of metabolic substrates. Physical activity acts as a powerful stimulus for the hypothalamic-pituitary axis, leading to the liberation of several neuroendocrine hormones. The nature of this stimulation varies according to the kind of exercise (intensity, duration, aerobic, strength) and subject characteristics (gender, previous training), as well as depending on the time of the day and meal ingestion. As a whole, the neuroendocrine responses to exercise represent an accurate regulator of fuels (glucose, free fatty acids) homeostasis in a special situation characterized by a drastic increase of the energy requirements at muscle level. In this article the current knowledge about this topic is reviewed.

The aim of this study was to examine the independent effect of high lean mass on glucose metabolism, as well as its consequences on the classic relationship between BMI and insulin sensitivity (SI) in 3 groups: 1) 8 strength-trained males with BMI >27 kg/m2 (athletes); 2) 10 sedentary males with BMI >27 kg/m2 (obese); and 3) 12 sedentary males with BMI 22-25 kg/m2 (control). Body composition was measured with impedance analysis. Iv glucose tolerance test was performed at 09:00 h after overnight fast. Estimation of insulin sensitivity and glucose effectiveness by Minimal Model Approach. Plasma glucose and insulin determination by glucose-oxidase and RIA respectively. BMI and lean mass (LM) were greater in athletes than in controls, but there were no differences in fat mass (FM), basal glucose (Gb), basal insulin (Ib), glucose tolerance (Kg), SI, glucose effectiveness (Sg), acute insulin response to glucose (AIRG) and leptin. Obese showed greater FM, leptin, lb and AIRG than athletes, while SI was lower; BMI, LM, Gb, Kg and Sg were similar. BMI, FM, LM, Ib, AIRG and leptin were lower in controls than in obese, while SI index was greater; Gb, Sg and Kg were similar. We found that: 1) Resistance exercise does not modify glucose effectiveness, but can improve insulin sensitivity through FM reduction (LM augmentation alone has no effect on glucose metabolism); and 2) High BMI causes insulin resistance only if it depends on adipose tissue hypertrophy.

Student's t and Pearson's test. Athletes showed similar BMI than overweight subjects: 26.98+/-0.49 vs 27.12+/-0.41 but lower fat mass: 12.53+/-0.96 vs 16.16+/-1.01 % (p=0.0064) and lower leptin: 4.66+/-0.51 vs 7.31+/-0.76 microg/l (p=0.014). Athletes showed higher BMI than controls: 26.98+/-0.49 vs 23.08+/-0.30 (p<0.0001) but similar fat mass: 12.53+/-0.96 vs 12.48+/-0.73% and leptin: 4.66+/-0.51 vs 4.79+0.58 microg/l. Overweight subjects showed higher BMI than controls: 27.12+/-0.41 vs 23.08+/-0.30 (p<0.0001), higher fat mass: 16.16+/-1.01 vs 12.48+/-0.73% (p=0.0064) and higher leptin: 7.31+/-0.76 vs 4.79+/-0.589 microg/l (p=0.014). When leptin was calculated by fat mass no differences were observed between the three groups. There was a significant correlation between leptin and fat mass in all groups. Leptin correlated with BMI in overweight subjects (r=0.438, p=0.0463), but this correlation was not observed either in athletes or in controls. In conclusion 1) regardless of the high BMI characteristic of body builders, no correlation was observed with leptin; 2) trained state induced by resistance exercise does not influence leptin production independently of variations in body composition.

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