Obesity, diabetes mellitus and physical activity--metabolic responses to physical training in adipose and muscle tissues.
The demand of the untrained skeletal muscle to produce additional mechanical work by utilizing more nutrients is the origin of the structural and metabolic adaptation of the muscle. The expanding capillary surface, in response to a lower vascular resistance during repeated contraction, enables the different fibre types to increase their oxygen extraction, and to adapt their uptake of substrates (glucose, FFA). The muscle fibre types in humans are selectively recruited for differing work intensity but the oxidative potential (SDH) increases in all types with long-term physical training. Details of the mechanism by which insulin promotes glucose uptake are unclear but there is some evidence that the hormonal stimulation involves cellular uptake of the insulin-receptor complex of the membrane. Hypoxia and raised cytoplasmic levels of calcium in muscle cells after work exert an insulin-like action on glucose uptake, which may be ascribed to the intracellular acidity.--The interrelationship between glucose and FFA oxidation is in part regulated by known key enzymes of the contracting muscle, but the exact extramuscular substrate mobilization appears to require both hormonal and supplementary feed-back control in storage organs.--During prolonged muscular exercise, the successive utilization of carbohydrate and fat from endogenous and exogenous stores can, however, in principle be attributed to known hormonal regulation.--Oral intake of glucose solution before and during work evokes a prolonged glucose utilization with relative hyperinsulinemia and hypoglucagonemia, preventing hepatic glycogenolysis. A prerequisite for successful endurance training is the improved capacity to use FFA as substrate. The necessary lipolysis in adipocytes is mainly mediated by an increased cellular exposure and sensitivity to catecholamines, but the delayed adaptation of the fat cells to their hormonal environment, especially insulin, in relation to the progress of the training is likely to modify the lipolytic response.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003920:Diabetes Mellitus / Q000097:blood / Q000503:physiopathology*; D004734:Energy Metabolism; D005934:Glucagon / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D009132:Muscles / Q000378:metabolism*; D009765:Obesity / Q000097:blood / Q000503:physiopathology*; D010806:Physical Education and Training; D005082:Physical Exertion; D051381:Rats
D001786:Blood Glucose; D007328:Insulin; D005934:Glucagon