Insulin-stimulated protein metabolism in chronic azotemia and exercise.
To determine whether training reduces the acute catabolic stress of an exercise bout, control and azotemic rats, either exercise trained or untrained, were subjected to a bout of exercise or allowed to rest. Protein turnover was measured immediately following exercise in isolated muscles. Azotemia (no exercise) increased protein degradation; acute exercise (no azotemia) decreased protein synthesis. Protein catabolism was greatest in acutely exercised azotemic rats. Training reduced azotemia-induced and acute exercise-stimulated increase in protein degradation. To determine whether this improvement in protein metabolism by training was due to increased insulin sensitivity, the dose-response to insulin was determined. Resistance of protein synthesis or degradation to insulin was not observed in azotemic rats. Either acute exercise or training increased sensitivities of protein degradation and synthesis to insulin; training also increased responsiveness of protein degradation to insulin. Thus exercise training reduced the elevated muscle protein catabolism due to azotemia and/or acute exercise and enhanced the action of insulin on muscle.
Davis
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Klahr
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Karl
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D058186:Acute Kidney Injury / Q000378:metabolism; D000818:Animals; D002908:Chronic Disease; D004351:Drug Resistance; D005260:Female; D007328:Insulin / Q000494:pharmacology*; D009132:Muscles / Q000378:metabolism; D009994:Osmolar Concentration; D005082:Physical Exertion; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D014511:Uremia / Q000378:metabolism*
D007328:Insulin; D011506:Proteins