Exercise training is associated with peripheral-cellular and central-cerebral processes, hormonal-neuronal regulation and transmission mechanisms. During the acute training response, peripheral cellular mechanisms are mainly metabolostatic to achieve energy supply and involve associated
cytokine and hormonal reactions.
Glycogen deficiency is associated with increased expression of local
cytokines (interleukin-6, IL-6), decreased expression of
glucose transporters, increased
cortisol and decreased insulin secretion and beta-
adrenergic stimulation. A nutrient-sensing signal of adipose tissue may be represented by
leptin which, as for
insulin,
IL-6 and
insulin-like growth-factor I (
IGF-I), has profound effects on the hypothalamus and is involved in the metabolic hormonal regulation of exercise and training. Muscle damage and repair processes may involve the expression of inflammatory
cytokines (e.g. tumour
necrosis factor-alpha,
TNF-alpha) and of
stress proteins (e.g.
heat shock protein 72). During overreaching and overtraining, a
myopathy-like state is observed in skeletal muscle with depressed turnover of
contractile proteins (e.g. in fast-type glycolytic fibres with a concomitant increase in slow type
myosins). These alterations are influenced by exercise-induced
hypercortisolism, and by decreased somatotropic
hormones (e.g.
IGF-I). The hypothalamus integrates various error signals (metabolic, hormonal, sensory afferents and central stimuli) and therefore pituitary releasing
hormones represent the functional status of an athlete and long-term hypothalamic hormonal and sympathoadrenal downregulation are some of the prominent hormonal signs of prolonged overtraining and performance incompetence syndrome.