Initiating Treadmill Training In Late Middle Aged Rats Exacerbates Skeletal Muscle Protein Carbonyl Accumulation In Senescence

Abstract

Age-related loss of muscle mass and function exhibits a marked acceleration from late middle age to senescence and may in part be due to an increase in oxidative damage. Exercise training is one method that may slow this process. PURPOSE: This study was carried out to test the hypothesis that long term exercise training initiated at late middle age would attenuate the age related increase in oxidative damage in senescence via an increase in endogenous antioxidant enzyme activity. METHODS: 29 mo old male F344BN rats were treadmill trained 5 d/wk for 2 mo and then 4 d/wk for the last 3-5 mo for 1 h each day (35T), while another group remained cage bound (35C). A young sedentary cage bound group (7C) was also included. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) activities were measured spectrophotometrically in the mixed vastus lateralis muscle. Cross sections from the gastrocnemius muscle were fluorescently labelled for slow myosin heavy chain, dystrophin and carbonyls. RESULTS: SOD, CAT, and GPX activities all increased with age. SOD activity had a further ∼25% increase with training. Fiber area was smaller in 35C and 35T compared to 7C across all fiber types. Type IIa fiber area was lower in 35T compared to 35C (825±102 μm2 vs 1579±175 μm2) as were type IIb/x fibers (35T: 1468±266 μm2 vs 35C: 2488±348 μm2). Type I fiber area was similar between 35T and 35C (35T: 1528±179 μm2, 35C: 1619±191 μm2). 35T had a greater percentage of small fibers (CSA≤1000 μm2) than 35C and small fibers were virtually non existent in 7C. Carbonyl intensity was 50% greater in 35C than 7C, and 150% and 25% greater in 35T than 7C and 35C, respectively. Carbonyl intensity was higher in smaller muscle fibers across all muscle phenotypes. CONCLUSION: Although exercise training initiated at late middle age was able to increase antioxidant defences, contrary to our hypothesis there was a greater accumulation of oxidative damage in response to exercise training in senescence. Supported by NSERC, CIHR, AHFMR