Fight Aging!

With advancing age, muscle mass and muscle strength are both steadily reduced, leading to sarcopenia and dynapenia. Interestingly, a sizable fraction of the observed outcomes of aging on muscle function in wealthier populations are avoidable, a consequence of our modern age of comfort and machineries of transport. We exercise a good deal less than our ancestors did. Humans evolved in a hunter-gatherer environment of daily exertion. Present day hunter-gatherers exhibit a good deal less heart disease and greater maintenance of muscle mass and function than is the case for those of us who drive to work and the grocery store. Use it or lose it, as they say.

Nonetheless, even the athletic succumb to aging eventually. A great deal is known of the various contributions to muscle aging, such as loss of stem cell function, mitochondrial dysfunction, inflammation, detrimental changes in neuromuscular junctions, and so forth. This is a microcosm of aging as a whole, in that: (a) there is little understanding of which of the many contributions are most important, (b) there is little understanding of how these contributions interact with one another, which are primary, which are secondary, and (c) for every mechanism there is essentially an unlimited amount of exploratory research into relevant cellular biochemistry that could be conducted. Mining sometimes finds gold, fundamental research sometimes finds something that can be turned into a therapy.

From molecular to physical function: The aging trajectory

Aging is accompanied by a decline in muscle mass, strength, and physical function, a condition known as sarcopenia. Muscle disuse attributed to decreased physical activity, hospitalization, or illness (e.g. sarcopenia) results in a rapid decline in muscle mass in aging individuals and effectively accelerates sarcopenia. Consuming protein at levels above (at least 50-100% higher) the current recommended intakes of ∼0.8 g protein/kg bodyweight/day, along with participating in both resistance and aerobic exercise, will aid in the preservation of muscle mass.

Physiological muscle adaptations often accompany the observable changes in physical independence an older adult undergoes. Muscle fibre adaptations include a reduction in type 2 fibre size and number, a loss of motor units, reduced sensitivity to calcium, reduced elasticity, and weak cross-bridges. Mitochondrial function and structure are impaired in relation to aging and are worsened with inactivity and disease states but could be overcome by engaging in exercise.

Intramuscular connective tissue adaptations with age are evident in animal models; however, the adaptations in collagenous tissue within human aging are less clear. We know that the satellite muscle cell pool decreases with age, and there is a reduced capacity for muscle repair/regeneration. Finally, a pro-inflammatory state associated with age has detrimental impacts on the muscle. The purpose of this review is to highlight the physiological adaptations driving muscle aging and their potential mitigation with exercise/physical activity and nutrition.