The argument about the physiological relevance of oxidative stress and mitochondrial aging rages on. From Figueiredo et al. comes a general mitochondrial oxidative stress review, with a focus on muscle:
There is strong evidence pointing out an age-related increase in the levels of oxidative stress and oxidative damage continuously imposed on mitochondrial biomolecules, which becomes progressively more apparent with advancing age. Since the cellular capacity for repair is not completely efficient, this increased damage might lead to accumulation of dysfunctional proteins, impaired membrane integrity and increased levels of mutant mtDNA, which will proliferate in an irreversible way by means of mitochondrial and cellular division. Consequently, the number of redundant components of intact mitochondria will be reduced, compromising the maximal mitochondrial function and consequently the maximal energetic capacity of skeletal muscle fibers.
The authors propose that, while mitochondria that accumulate some damage often retain sufficient function to operate at basal levels, operation under conditions of stress might tax the aged system beyond the functional capacity to 1) produce energy sufficient for demands and/or 2) efficiently cope with the increased oxidative stress burden of acute stress.
Ouroboros 