A B S T R A C T Male rats at 5 wk of age were subjected to 13 wk of intensive treadmill running to study the effect of exercise on adipose tissue cellularity and lipolysis.
This experiment was designed to determine if the adaptive increase in adipose tissue epinephrine-stimulated lipolysis (ESL) observed in exercise trained rats is related to decreased adipocyte size or a direct response to exercise. Two levels of treadmill exercise and three levels of food restriction were imposed on male rats over a 12 week experimental period to create a distribution of adipose tissue cell sizes. Epinephrine-stimulated lipolysis was subsequently measured in the isolated adipocytes from rats trained at two different exercise levels and in untrained rats fed either ad libitum or 16%, 27%, or 35% dietary restriction. Energy restriction was effective in reducing body weight and to some extent epididymal fat pad weight; however, adipocyte size and number were not significantly affected. Exercise in both groups of trained rats was effective in reducing adipocyte size; however, cell size did not differ between training groups. The group receiving the greatest amount of daily exercise had significantly greater ESL indicating that the adaptive increase in lipolytic potential seen in adipose tissue of exercise trained rats is a true metabolic adaptation not secondary to reduced cell size.
In brief: Preventing hypothermia is crucial to those who work or spend recreation time in cold environments. Adequate energy from the correct proportion of carbohydrates, fats, and proteins can help. Vitamins and minerals are also necessary to prevent nutrition deficiencies and impaired function, but there is no evidence to suggest an increased requirement for them is attributable to cold exposure alone. High protein diets appear to be the worst choice for cold weather work; compared with diets high in carbohydrates or fats, high protein diets increase metabolic water requirements and reduce cold tolerance.
Rats trained by 12 weeks of treadmill running were divided into two groups and fed a control diet or an identical diet supplemented with 0.5% L-carnitine. Adipose tissue fatty acid turnover was subsequently estimated by an odd-carbon fatty acid enrichment method utilizing undecanoate as a marker representative of adipose tissue fatty acids. Compared to sedentary untrained control rats, exercise training increased perirenal adipose tissue turnover rate approximately 70%. Trained rats fed the carnitine supplemented diet did not exhibit any further increase in turnover rate. Neither [1-14C]palmitate oxidation by skeletal muscle homogenates nor palmitycarnitine acyl-transferase activity in skeletal muscle mitochondria was affected by carnitine feeding. The results of this study indicate that exercise training increases the turnover rate of adipose tissue fatty acids, but supplemental dietary carnitine does not. Under the conditions of this study, endogenous skeletal muscle carnitine levels in trained rats appear to be adequate to support the rate of fatty acids oxidation incurred by daily treadmill running.
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