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Aerobic Exercise Overcomes the Age-Related Insulin Resistance of Muscle Protein Metabolism by Improving Endothelial Function Uand Akt/mTOR signaling

¹Department of Internal Medicine, University of Texas Medical Branch, Galveston
²Department of Physical Therapy, University of Texas Medical Branch, Galveston
³Department of Medicine, University of Southern California, Los Angeles
⁴Department of Kinesiology and Biological Sciences, University of Southern California, Los Angeles

Correspondence: evolpi{at}utmb.edu

Muscle protein metabolism is resistant to insulin's anabolic effect in healthy elders. This is associated with reduced insulin vasodilation. We hypothesized that aerobic exercise restores muscle protein anabolism in response to insulin by improving vasodilation in elders. We measured blood flow (BF), endothelin-1 (ET1), UAkt/mTOR signalingU, and muscle protein kinetics in response to physiological local hyperinsulinemia in 2 groups of older subjects following a bout of aerobic exercise (EX: 70±2yrs; 45min treadmill walk, 70% heart rate max) or rest (CTRL: 68±1yrs). Baseline ET1 was lower and BF tended to be higher in EX, but protein kinetics was not different between groups. Insulin decreased ET1 (P<0.05) in both groups, but ET1 remained higher in CTRL (P<0.05) and BF increased only in EX (EX: 3.8±0.7 to 5.3±0.8; CTRL: 2.5±0.2 to 2.6±0.2, ml/min/100ml leg). Insulin improved UAkt phosphorylation in EX, and increased mTOR/S6K1 phosphorylation and muscle protein synthesis (EX: 49±11 to 89±23; CTRL: 58±8 to 57±12; nmol/min/100ml leg) in EX only (P<0.05). Since breakdown did not change, net muscle protein balance became positive only in EX (P<0.05). In conclusion, a bout of aerobic exercise restores the anabolic response of muscle proteins to insulin by improving endothelial function and Akt/mTOR signaling in elders.

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