Exercise and skeletal muscle ageing: cellular and molecular mechanisms.
As we age, our skeletal muscle becomes smaller and weaker. In addition, the remaining muscle is more susceptible to damage, particularly following exercise, recovery from damage is severely impaired and muscle is unable to adapt rapidly following sequential periods of exercise. The mechanisms by which skeletal muscle damage occurs are poorly understood and the role that an increased production of free radical species plays in this damage is controversial. However, evidence is emerging which suggests that an increased production of free radicals may act as an activator of the adaptive response in skeletal muscle, resulting in the increased production of antioxidant enzymes and heat shock proteins (HSPs). The increased content of these proteins facilitates rapid remodelling of muscle and provides considerable protection against subsequent periods of damaging exercise. There is considerable evidence that the production of free radicals is modified during the ageing process. The aim of this review is to examine the possible effects of this modification on the ability of muscle cells to respond to stress and the functional effect that this may have on our muscles as we age.
McArdle
Anne
A
Department of Medicine, University of Liverpool, Liverpool L69 3GA, UK. mdcr02@liv.ac.uk
Vasilaki
Aphrodite
A
Jackson
Malcolm
M
D000222:Adaptation, Physiological; D000368:Aged; D000375:Aging / Q000502:physiology*; D000818:Animals; D015444:Exercise / Q000502:physiology*; D005609:Free Radicals / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D018482:Muscle, Skeletal / Q000166:cytology / Q000293:injuries / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology
D005609:Free Radicals; D006360:Heat-Shock Proteins