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Am J Physiol Regul Integr Comp Physiol 297: R744-R755, 2009. First published July 1, 2009; doi:10.1152/ajpregu.90959.2008
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ARTICLES

Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function

Andrew C. Betik,1 Melissa M. Thomas,1 Kathryn J. Wright,1 Caitlin D. Riel,1 and Russell T. Hepple1,2

1Muscle and Aging Laboratory, Faculty of Kinesiology and 2Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada

Submitted 24 November 2008 ; accepted in final form 29 June 2009

We previously showed that 7 wk of treadmill exercise training in late-middle-aged rats can reverse the modest reductions in skeletal muscle aerobic function and enzyme activity relative to values in young adult rats (Exp Physiol 93: 863–871, 2008). The purpose of the present study was to determine whether extending this training program into senescence would attenuate the accelerated decline in the muscle aerobic machinery normally seen at this advanced age. For this purpose, 29-mo-old Fisher 344 Brown-Norway rats underwent 5 or 7 mo of treadmill exercise training. Training resulted in greater exercise capacity during an incremental treadmill exercise test and reduced percent body fat in 34- and 36-mo-old rats and improved survival. Despite these benefits at the whole body level, in situ muscle aerobic capacity and muscle mass were not greater in the trained groups at 34 mo or 36 mo of age. Similarly, the trained groups did not have higher activities of citrate synthase (CS) or Complex IV in homogenates of either the plantaris (fast twitch) or the soleus (slow twitch) muscles at either age. Finally, protein expression of CS (a marker of mitochondrial content) and peroxisome proliferator-activated receptor-{gamma} coactivator-1 (relating to the drive on mitochondrial biogenesis) were not higher in the trained groups. Therefore, although treadmill training from late middle age into senescence had significant benefits on running capacity, survival, and body fat, it did not prevent the declines in muscle mass, muscle aerobic capacity, or mitochondrial enzyme activities normally seen across this age, revealing a markedly diminished plasticity of the aerobic machinery in response to endurance exercise at advanced age.

aging; oxygen uptake; sarcopenia; mitochondria; endurance training



Address for reprint requests and other correspondence: R. T. Hepple, Faculty of Kinesiology, 2500 Univ. Dr., Calgary, Alberta, T2N 1N4, Canada (e-mail: hepple{at}ucalgary.ca)







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