Today, I’ll point out a few recent papers relevant to the decline of muscle mass and strength that takes place with aging. The research community is somewhere in the midst of the long process of formally defining this process as a disease called sarcopenia. Formally defined or not, sarcopenia is a significant contribution to the frailty of later aging: the weakness, the risk of falling, the loss of vigor. The papers below are one small part of a large body of work that suggests a fair degree of the total burden of sarcopenia is actually self-inflicted: we live in an age of lethargy, within the embrace of comparative wealth and new technologies of ease and transport. As a consequence some aspects of our decline into old age are faster than they might be, even though we benefit greatly from advances in medical technology in all other facets of health in later life. In short, muscle requires maintenance, and most people are far too quick to give up on that work at the first opportunity.
Beyond a lack of exercise, the remaining portion of sarcopenia is not a simple consequence of aging, however. Rather, it is a twining, partially explored mess of interacting mechanisms. Various studies provide compelling evidence for the role of inflammation, stem cell decline, cellular senescence, neurological decline in the links between muscle and nervous system, reduced protein intake in the typical diet of older individuals, an age-related failure to process dietary amino acids, and many more. They are probably all correct, insofar as they each examine only one narrow portion of the progressive disarray of very complex systems. The parable of the blind men and the elephant is frequently invoked in relation to aging research, and with good cause.
I would say that the best approach to the treatment of sarcopenia, as for many portions of the whole of age-related degeneration, is to pursue efforts to repair the known forms of fundamental damage that cause aging. Even if we cannot yet fully trace the consequences of this damage from start to end, the research community should still attempt to reverse it. It is faster to fix the damage and see what happens as a result than it is to map the changing biochemistry of aging at the detail level. If both courses of action proceed in parallel, we can have our cake and eat it, first striking at the root of the problem and then going on to untangle the foliage at our leisure.
This review of the epidemiology of sarcopenia documents evidence of the differential peak and rate of decline for three components linked to the disorder: muscle mass, strength, and physical function. Differences are also apparent in relation to the peak level and subsequent loss rate of these characteristics between men and women; between ethnic groups and over time. The data suggest that the rate of decline in muscle mass is much less rapid than that in muscle strength. This, in turn, is much less pronounced than the rate of decline in physical function. Men have significantly higher levels of muscle mass, strength and function at any given age than women. In contrast, rates of decline seem similar between the genders, for each of the three characteristics.
Environmental risk factors for all three components of sarcopenia include sedentary lifestyles, adiposity, and multi morbidity. The role of cigarette smoking and alcohol consumption are much less apparent than have been observed in studies of osteoporosis or cardiovascular disease. Nutrition has been identified as having an important influence on the development of sarcopenia; in particular, protein intake has the potential to slow the loss of muscle mass, but does not appear to be as influential as in maintaining muscle strength or physical function. Physical activity, in particular resistance training, when performed at higher intensities appears beneficial for muscle strength and functioning. Trials combining protein supplementation and physical activity show promising results in reducing the decline in muscle strength and function with advancing age.
Muscular strength is associated with functional ability in elderly, and older adults are recommended to perform muscle-strengthening exercise. Understanding how improved muscle strength and -mass influence general and specific domains of quality of life is important when planning health promotion efforts targeting older adults. The aims of the present study were to describe changes in health-related quality of life (HRQOL) in older men participating in 12 weeks of systematic strength training, and to investigate whether improvements in muscle strength and muscle mass are associated with enhancements in HRQOL.
We recruited 49 men aged 60-81 years to participate in an intervention study with pre-post assessment. The participants completed a 12-week strength training program consisting of three sessions per week. Tests and measurements aimed at assessing change in HRQOL, and changes in physical performance (maximal strength) and physiological characteristics. Muscle mass was assessed based on changes in lean mass (leg, trunk, arm, and total), and strength was measured as one-repetition maximum in leg extension, leg press, and biceps curl. Two of the eight HRQOL scores, role physical and general health, and the physical component summary scores, increased significantly during the intervention period. Small significant positive correlations were identified between improvements in muscle strength, and better physical and social function. Moreover, a significant increase in total muscle mass was seen during the intervention period.
Skeletal muscle accounts for approximately 40% of total body mass, and it plays an indispensable role in locomotion and metabolism. Skeletal muscle undergoes a gradual loss of fat-free mass, size, and function in the aging process, called sarcopenia. The etiology of sarcopenia is complex and involves the interplay of various factors such as oxidative stress, physical inactivity, imbalanced protein homeostasis, apoptosis, inflammation, malnutrition, and/or mitochondrial dysregulation. Mitochondria play an essential role in the aging-related muscle deterioration because of their importance in the production of energy and reactive oxygen species (ROS), apoptotic signaling, and calcium (Ca2+) handling. Thus, the natural aging process, along with coincident inactivity, progressively impairs mitochondrial integrity which might be a leading factor for sarcopenia.
Mitochondrial quality control in aging skeletal muscle is regulated via mitochondrial biogenesis and mitochondrial turnover; however, the regulation of these processes seems to be less sensitive to the effects of exercise compared to that in young, healthy muscle. Regulation of mitochondrial quality in skeletal muscle can be also accomplished by other cellular systems including ubiquitin proteasomal degradation, lysosomal regulation, and apoptosis. In particular, the lysosomal system has been recently suggested as a key player for regulating autophagy/mitophagy, as well as mitochondrial energy balance. Indeed, a key component of lysosomal biogenesis, the transcription factor TFEB, appears to determine exercise capacity, and we have suggested a coordinated function between TFEB and PGC-1α during both denervation- and CCA-induced skeletal muscle remodeling, suggesting an importance of maintaining a balance between mitochondrial biogenesis and lysosomal system for the muscle quality control. Therefore, it will be interesting for future studies to examine aging-related alterations in the lysosomal system in skeletal muscle, as well as to study how endurance and/or resistance exercise regulates lysosomal capacity in aging muscle. These findings will suggest a possible pharmaceutical target for improving aging-related mitochondrial dysregulation in skeletal muscle.