An investigation of the effects of regular exercise in older males on oxidative stress, skeletal muscle apoptosis, and atrophy-related gene expression in response to muscle insult.
Access RightsWorldwide access
Buford, Thomas Wayne.
MetadataShow full item record
The purposes of the present study were to examine the role of physical activity in males between 55-75 years of age on skeletal muscle strength and biochemical pathways indicative of muscle atrophy before and after eccentric treadmill exercise. Twenty-seven apparently-healthy, non-smoking men (62.22±6.16 yr, 175.26±5.31 cm, 88.74±12.53 kg) participated in the study and were grouped at either physically-active (N=14, at least 15 hours of exercise per month) or sedentary (N=13, no regular exercise). Following a familiarization session, participants completed skeletal muscle performance testing as well as an eccentric treadmill protocol (-17.5% grade) consisting of three 15 minute sets at 75% of VO₂max. Participants donated venous blood prior to, immediately following, and 24h following exercise and a muscle biopsy sample prior to, 3h following, and 24h following exercise. Muscle performance was determined using a Biodex Isokinetic Dynamometer. Venous blood was analyzed for CK, LDH, cortisol, TNFα, IL1β, protein carbonyls, 8-isoprostane, and total antioxidant activity. Skeletal muscle tissue samples were analyzed for mRNA expression of atrophy-related genes (Atrogin1, MURF1, FOXO1, FOXO3, IKKB, Ubiquitin, Ubiqutin E2, HSP27, HSP72, Id1, Id2, Id3, Myostatin, 20S C2, 20S C3, Calpain1, and Calpain2), protein content of pIKBα, Caspase3, Bax, and Bcl2, and DNA binding activity of p53, NFkB p50, NFkB p65, and GC receptor. At baseline, significant differences existed between groups for body weight (p=0.047), VO₂max (p<0.001), % body fat (p<0.001), SBP (p=0.032), mRNA expression of FOXO1 (p=0.043), protein content of Bax (p = 0.015), and several muscular performance variables. Following exercise, significant group x time interactions were observed for cortisol (p=0.048), FOXO1 (p=0.001), IKKB (p=0.013), and ID1 (p=0.049), while a number of group differences were observed for individual time points that indicate improved muscular aging in the physically-active group. The results of the present study indicate that regular physical activity in advanced age attenuates eccentric exercise-induced muscle force decrements. Meanwhile, sedentary individuals appear to exhibit altered muscular signaling in an apparently unsuccessful attempt to preserve muscle mass and force production.