Exercise-trained Animals Research Articles

Adaptation of fat cells to exercise: response of glucose uptake and oxidation to insulin.

The purpose of this study was to determine whether exercise training alters the sensitivity and responsiveness to insulin of glucose uptake and oxidation in fat cells. Female rats were exercised by swimming 6 h/day, 5 days/wk for 12 wk. The swimmers' fat cells were smaller than those of sedentary controls of the same age and similar body weight. A larger amount of insulin was specifically bound by fat cells of the trained rats because of an increase in the number of insulin receptors. The rates of 2-deoxyglucose uptake and of glucose oxidation were higher in fat cells of trained compared with sedentary rats at all insulin concentrations. A maximal insulin stimulus resulted in rates of sugar uptake and oxidation that were about sixfold higher in trained than in sedentary rats' fat cells. This greater responsiveness to insulin could not be explained by the increase in insulin binding but appears to be mediated by adaptation/s) at a step(s) beyond the binding of insulin to its receptors. Our findings suggest that fat cells of exercise-trained animals are adapted for rapid replenishment of energy stores.

Mechanism of enhanced lipolysis in adipose tissue of exercise-trained rats.

The effects of exercise training and food restriction on the regulation of lipolysis were studied comparatively in adipocytes isolated from male and female rats. Exercise training inhibited cell proliferation in parametrial, but not in epididymal adipose tissue, whereas it significantly reduced adipocyte size in both fat depots. Adipocyte capacity for responding lipolytically to epinephrine (10 microns) or to ACTH (1 micron) was markedly increased by exercise training. Enhanced lipolysis was also observed when cells isolated from exercise-trained animals were stimulated by bypassing with dibutyryl cyclic AMP (5 mM) or theophylline (5 mM) the early metabolic steps associated with hormonal activation of the adenylate cyclase complex. Significantly, binding of (-)-[3H]dihydroalprenolol to cellular receptor sites was not affected by exercise training. It is therefore concluded that exercise training increases adipocyte responsiveness to lipolytic hormones at a metabolic step distal to stimulus recognition by adrenoreceptors, possibly at the level of protein kinases or lipases. Food restriction markedly reduced adipocyte size and partially mimicked the effects of exercise training on adipocyte proliferation and lipolysis.

Fiber orientation in hypertrophied canine left ventricle

Myocardial fiber orientation was examined in transmural specimens obtained at the maximum diameter of the left ventricle from five dogs with pressure-overload hypertrophy produced by aortic stenosis, six dogs with volume-overload hypertrophy due to an arteriovenous fistula, and six exercise-hypertrophied greyhounds trained for racing. Hearts arrested in diastole were fixed in situ while the operating end-diastolic pressure was maintained. Fiber orientation changed smoothly from about +60 degrees (with respect to the equator) at the endocardium to about -69 degrees at the epicardium. The majority of fibers near the midwall were oriented circumferentially. These findings are quite similar to those previously reported for normal dogs. In comparison to normals, the left ventricles from dogs with pressure-overload had an increase in longitudinally oriented fibers, i.e. fiber angles between -67.5 degrees and -90 degrees and between +67.5 degrees and +90 degrees; these fibers comprised 10.4 +/- 1.8% of the total fibers in dogs with aortic stenosis vs. 2.9 +/- 1.8% of total fibers in normal dogs (P less than 0.001). Neither the dogs with volume-overload hypertrophy nor exercise-trained animals were significantly different from normals.

Exercise-Induced Increase in the Capacity of Rat Skeletal Muscle to Oxidize Ketones

During and after strenuous prolonged exercise, sedentary individuals develop high blood levels of acetoacetate and beta-hydroxybutyrate whereas exercise-trained animals and human subjects do not. We have investigated the possibility that exercise training can increase the capacity of skeletal muscle to oxidize ketones. In this study we measured rates of D-beta[3-14-C]-hydroxybutyrate and [3-14-C]acetoacetate oxidation, and the levels of activity of the enzymes involved in the oxidation of ketones in homogenates of gastrocnemius muscles of exercise-trained and of untrained male rats. The trained animals had markedly lower blood ketone levels immediately and 60 min after a 90 min long bout of exercise than did the sedentary animals. The rates of D-beta-[13-14C]hydroxybutryate and [3-14-C]acetoacetate oxidation were twice as high in homogenates of muscles from the trained as compared to the sedentary rats. The increases in levels of activity in gastrocnemius muscle in response to the exercise program were: beta-hydroxybutyrate dehydrogenase threefold; 3-ketoacid CoA-transferase twofold; and acetoacetyl-CoA thiolase 55%. This exercise-induced increase in the capacity of skeletal muscle to oxidize ketones could play a role in preventing development of ketosis in the physically trained animal during and following prolonged strenuous exercise.

SERUM ENZYMES AND LACTIC DEHYDROGENASE ISOENZYMES AFTER EXERCISE AND TRAINING IN RATS.

After 16 hr exercise, untrained rats, in contrast to exercise-trained rats, show a marked rise in serum lactic dehydrogenase, aldolase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase, and urea nitrogen. Electrophoretic studies reveal abnormal serum isoenzyme patterns indicating that excess lactic dehydrogenase is derived not only from muscle, but also from heart and probably other organs. Histopathologic studies and serum transaminase ratios support this conclusion. These findings are correlated with necrosis in muscle fibers and fatty changes in muscle, heart, and other organs of untrained rats after prolonged exercise and the absence of such changes in similarly exercise-trained animals. Alterations in cellular permeability best explain the rise in serum enzymes. However, exercise training does not prevent pathologic and serum enzyme and isoenzyme changes induced by epinephrine in oil. Moreover, the adrenergic blocking agent, Dibenamine, which ameliorates such changes induced by epinephrine or hypoxia, does not mitigate the effects of prolonged exercise in untrained rats. These findings suggest that the permeability changes induced by prolonged exercise are not due merely to the effects of hypoxia or of catecholamines released from the adrenal medulla, but are different and perhaps specific.