Exercise can induce short-term increases in the sensitivity and responsiveness of skeletal muscle glucose transport to insulin. The purpose of this study was to determine the effect of carbohydrate deprivation on the persistence of increased insulin sensitivity and responsiveness after a bout of exercise. Three hours after a bout of exercise, epitrochlearis muscles from carbohydrate-deprived (fat fed) rats showed a 25% greater increase in 3-O-methylglucose (3-MG) transport in response to a maximal insulin stimulus compared with muscles of nonexercised rats; this increase in insulin responsiveness had reversed 18 h postexercise. Muscles of rats fed carbohydrate showed no increase in insulin responsiveness 3 h after exercise. The effect of 60 microU/ml of insulin on 3-MG transport was approximately twofold greater in muscles studied 3 h after exercise than in nonexercised controls regardless of dietary carbohydrate intake. This increase in insulin sensitivity was lost within 18 h in carbohydrate-fed rats but persisted for at least 48 h in carbohydrate-deprived rats. Muscle glycogen increased approximately 41 mumol/g in the rats fed carbohydrate for 18 h, and only approximately 14.5 mumol/g in the rats fed fat for 48 h, after exercise. The persistent increase in insulin sensitivity after exercise in carbohydrate-deprived rats was unrelated to caloric intake, as muscles of fasted and fat-fed rats behaved similarly.
Exercise is associated with an increase in permeability of muscle to glucose that reverses slowly (h) in fasting rats during recovery. Previous studies showed that carbohydrate feeding speeds and carbohydrate restriction slows reversal of the exercise-induced increase in glucose uptake. This study was designed to evaluate the roles of glucose transport, glycogen synthesis, and protein synthesis in the reversal process in rat epitrochlearis muscle. In contrast to recovery in vivo, when muscles were incubated without insulin in vitro, the exercise-induced increase in muscle permeability to sugar reversed rapidly regardless of whether glucose transport or glycogen synthesis occurred. Inhibition of protein synthesis did not prevent the reversal. Addition of 33% rat serum or a low concentration of insulin to the incubation medium markedly slowed reversal in vitro. We conclude that 1) prolonged persistence of the increased permeability of mammalian muscle to glucose after exercise requires a low concentration of insulin, and 2) reversal of the increase in permeability does not require glucose transport, glycogen synthesis, or protein synthesis.
Glucose transport can be stimulated via two separate pathways in muscle. One is activated by insulin, the other by contractile activity and hypoxia. Polymyxin B, a cationic antibiotic that displaces Ca2+ from anionic phospholipids, is reported to selectively inhibit the stimulation of glucose transport by insulin in muscle. A purpose of the present study was to determine whether the inhibition by polymyxin B is actually restricted to insulin. We found that polymyxin B (250 micrograms/ml) significantly inhibited the stimulation of glucose transport in rat skeletal muscles not only by insulin and vanadate but also by hypoxia, electrical stimulation, and K+. Polymyxin B also decreased the tension developed in response to electrical stimulation or K+. Although polymyxin B inhibited the increase in sugar transport activity induced by insulin and hypoxia, it had no inhibitory effect on sugar transport after it had been stimulated by these agents. These results show that the inhibitory effect of polymyxin B on the stimulation of glucose transport is not specific for insulin action. They suggest that polymyxin B inhibits a step that is common to the two pathways for stimulating glucose transport in skeletal muscle.
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