Exercise-induced pyruvate dehydrogenase activation is not affected by 7 days of bed rest

Kiilerich K, Ringholm S, Bienso RS, Fisher JP, Iversen N, van Hall G, Wojtaszewski JF, Saltin B, Lundby C, Calbet JA, Pilegaard H. Exercise-induced pyruvate dehydrogenase activation is not affected by 7 days of bed rest. J Appl Physiol 111: 751-757, 2011. First published June 16, 2011; doi: 10.1152/japplphysiol.00063.2011.-To test the hypothesis that physical inactivity impairs the exercise-induced modulation of pyruvate dehydrogenase (PDH), six healthy normally physically active male subjects completed 7 days of bed rest. Before and immediately after the bed rest, the subjects completed an oral glucose tolerance test (OGTT) and a one-legged knee extensor exercise bout [45 min at 60% maximal load (W-max)] with muscle biopsies obtained from vastus lateralis before, immediately after exercise, and at 3 h of recovery. Blood samples were taken from the femoral vein and artery before and after 40 min of exercise. Glucose intake elicited a larger (P <= 0.05) insulin response after bed rest than before, indicating glucose intolerance. There were no differences in lactate release/uptake across the exercising muscle before and after bed rest, but glucose uptake after 40 min of exercise was larger (P <= 0.05) before bed rest than after. Muscle glycogen content tended to be higher (0.05 < P <= 0.10) after bed rest than before, but muscle glycogen breakdown in response to exercise was similar before and after bed rest. PDH-E1 alpha protein content did not change in response to bed rest or in response to the exercise intervention. Exercise increased (P <= 0.05) the activity of PDH in the active form (PDHa) and induced (P <= 0.05) dephosphorylation of PDH-E1 alpha on Ser(293), Ser(295) and Ser(300), with no difference before and after bed rest. In conclusion, although 7 days of bed rest induced whole body glucose intolerance, exercise-induced PDH regulation in skeletal muscle was not changed. This suggests that exercise-induced PDH regulation in skeletal muscle is maintained in glucose-intolerant (e.g., insulin resistant) individuals.