Acute adaptation in adrenergic control of lipolysis during physical exercise in humans.

During prolonged exercise, the free fatty acids derived from adipocyte lipolysis are the principal fuel utilized by muscles. In humans, the lipid mobilization from adipose tissue is mainly regulated by insulin and catecholamines: the latter hormones have both beta-adrenergic stimulatory and alpha 2-adrenergic inhibitory effects on lipolysis. The aim of this study was to determine whether rapid alterations in the peripheral action of the regulatory hormones occur during physical work and whether they are of importance for the enhanced lipid mobilization. The acute effects of exercise on the regulation of lipolysis were investigated in isolated adipocytes removed from the gluteal region of 14 healthy volunteers before and immediately after the exercise period. Exercise induced a 20-35% significant increase in the lipolytic response to noradrenaline alone and in combination with the selective alpha 2-antagonist yohimbine and to the pure beta-agonist isoproterenol in isolated adipocytes. The antilipolytic effects of both the alpha 2-agonist clonidine and insulin were unaffected by exercise. Exercise did not influence the specific adipocyte receptor binding of 125I-cyanopindolol (beta-adrenergic receptor), [3H]yohimbine (alpha-adrenergic receptor), and mono-125I-[Tyr A14]insulin (insulin receptor). In conclusion, a single period of submaximal exercise increases adipocyte lipolytic responsiveness to catecholamines through an increased beta-adrenoceptor-mediated effect at steps distal to the receptor binding. Thus the increased peripheral action of catecholamines may be of importance for the observed enhanced lipid mobilization during physical work.