The article by Jane Kent-Braun, Ph.D., FACSM, (6) combines a muscular component of aging with a neural component to hypothesize a silver lining - as people age, their muscles get weaker, but also less fatigable. The muscular component combines consistent evidence of a shift in fiber-type distribution with age and her own data showing reduced accumulation of H+ and Pi in aged compared with younger subjects' muscles during successive maximum voluntary contractions to make a compelling case for increased metabolic economy of aged muscle. To support the neural component, she reviews a small but consistent literature reporting reduced maximal motor unit discharge rates in aged subjects and hypothesizes a consequent reduced metabolic demand. Together, these mechanisms are hypothesized to increase metabolic economy and decrease accumulation of metabolic products, an adaptation that decreases fatigability in aged muscle.
The literature reviewed in (6) comparing fatigability of younger with that of older people's muscles, shows mixed results attributed in this article to dynamic versus static fatiguing protocols. It is known that fatigue can be caused by many different mechanisms. Kent-Braun's technique identifies fatigue that is associated with less acidosis and lower accumulation of Pi and H2PO4-. Cairns et al. (2) pointed out that various protocols might selectively stress different mechanisms among the manifold possible causes of fatigue, the protocol effectively selecting the mechanism of fatigue. In this context, it is important to ask whether protocols that select for fatigue caused by accumulation of metabolites are the most appropriate to study fatigue mechanisms relevant to problems associated with aging.
We also suggest that the reduction in maximal motor unit discharge frequency among aged subjects may not be a neural adaptation to aging, but rather a corollary to the selective cell death of larger motor neurons that occurs with aging. Motor neurons serving Type I muscle units have lower discharge rates, increased metabolic economy because of both less calcium pumping and lower myosin ATPase rates (1,8), less production of metabolic products, less sensitivity to metabolic products (4), and lower susceptibility to deficits in excitation-contraction coupling (7).
We therefore suggest an alternative hypothesis: a larger proportion of Type I motor unit cross-sectional area confers resistance to some important types of fatigue. Our hypothesis is consistent with that of Kent-Braun (6), but may make the age advantage also a gender advantage, and a general advantage to all of us with slower fiber-type distributions - likely a large population, as the variance in fiber-type distribution in human populations is very large (5).
Type I fibers have long been recognized as less fatigable than Type II under a restricted definition of fatigue. Future studies might relax this restriction. There are emerging experimental approaches that focus on identifying mechanisms of fatigue that are task specific (3). Selected comparisons of tasks, groups of individuals, and interventions with a task-failure approach have potential to delve into the mechanisms that limit performance of many different activities of daily living, providing a translational approach.
Steven L. Lehman
Department of Integrative Biology
University of California-Berkeley
Ladora V. Thompson
Department of Physical Medicine and Rehabilitations
University of Minnesota
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