Abstract
The investigation of catecholamine (CA) metabolism in animals subjected to various types of stress (different pain syndromes; cranial trauma; immobilization; cooling) and physical exercise shows considerable similarity among species in the sequence of changes, leading from the activation to the depletion of the sympathoadrenal system. The changes caused by physical exercise tend to be more pronounced in individuals with a genetic predisposition to greater stress responses. Stress adaption, induced by special training or by long-duration exposure to hypoxia, can substantially prevent the changes caused by physical exercise. Trained rats at rest show accelerated CA turnover, and after exercise, adaptive hypometabolic changes. Physical exercise causes both unspecific changes in CA metabolism, similar to those seen after other types of stress, and more specific ones,i. e., suppression of tissue CA synthesis and nonresponsiveness to exogenous L-tyrosine or L-DOPA. Adrenal CA synthesis could be restored in such animals by treatment with glucocorticoids and cyclic-AMP (c-AMP). The depression of CA synthesis after hard physical activity may be a mechanism for protecting the body from the injurious effect of the excessive CA release that would occur under stress.