Prolonged Exercise Training does not Preserve Mitochondrial Enzyme Activity in Senescent Rats

Abstract

Skeletal muscle aerobic function (VO2max) and mitochondrial oxidative capacity decline with aging, particularly in senescence (SEN). Since exercise training improves muscle VO2max and oxidative capacity in young adult skeletal muscle, our objective was to determine if treadmill training from late middle age (LMA) into SEN would minimize the declines in skeletal muscle aerobic function and oxidative capacity seen in SEN. 62 male rats at late middle age (29 mo) were randomly separated into control and exercise groups. Exercise consisted of 60 m/day treadmill running, 5 d/week for 7 weeks and then decreased to 4 d/week for a total of 5 and 7 mo (until 34 and 36 mo of age respectively). Although running capacity was significantly higher in the trained groups (13% at 34 mo and 21% at 36 mo), muscle VO2max at matched muscle O2 delivery was not significantly greater in the trained groups compared to sedentary controls at either age. Similarly, citrate synthase and cytochrome oxidase activity in the plantaris, soleus and the heart muscle were not different in the trained vs the sedentary groups, suggesting no benefit of training for muscle oxidative capacity. The superior exercise capacity suggests a better overall level of function of the senescent rats; however, contrary to our hypothesis and prior observations in LMA rats, treadmill exercise training between LMA and SEN does not benefit muscle aerobic function or mitochondrial oxidative capacity.Supported by CIHR (AB, RT), CIHR Provincial Training Program in Bone and Joint Health (AB), AHFMR (RT) and NSERC (MT).