Using an integrative approach, this review highlights the benefits of resistance training toward improvements in functional status, health and quality of life among older adults. Sarcopenia (i.e. muscle atrophy) and loss of strength are known to occur with age. While its aetiology is poorly understood, the multifactorial sequelae of sarcopenia are well documented and present a major public health concern to our aging population, as both the quality of life and the likelihood of age-associated declines in health status are influenced. These age-related declines in health include decreased energy expenditure at rest and during exercise, and increased body fat and its accompanying increased dyslipidaemia and reduced insulin sensitivity. Quality of life is affected by reduced strength and endurance and increased difficulty in being physically active. Strength and muscle mass are increased following resistance training in older adults through a poorly understood series of events that appears to involve the recruitment of satellite cells to support hypertrophy of mature myofibres. Muscle quality (strength relative to muscle mass) also increases with resistance training in older adults possibly for a number of reasons, including increased ability to neurally activate motor units and increased high-energy phosphate availability. Resistance training in older adults also increases power, reduces the difficulty of performing daily tasks, enhances energy expenditure and body composition, and promotes participation in spontaneous physical activity. Impairment in strength development may result when aerobic training is added to resistance training but can be avoided with training limited to 3 days/week.

Summary S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) link one-carbon metabolism to methylation status. However it is unknown whether regulation of SAM and SAH by nutrient availability can be directly sensed to alter the kinetics of key histone methylation marks. We provide evidence that the status of methionine metabolism is sufficient to determine levels of histone methylation by modulating SAM and SAH. This dynamic interaction led to rapid changes in H3K4me3, altered gene transcription, provided feedback regulation to one-carbon metabolism and could be fully recovered upon restoration of methionine. Modulation of methionine in diet led to changes in metabolism and histone methylation in liver. In humans, methionine variability in fasting serum was commensurate with concentrations needed for these dynamics and could be partly explained by diet. Together these findings demonstrate that flux through methionine metabolism and the sensing of methionine availability may allow for direct communication to the chromatin state in cells.

Petrella JK, Kim J, Mayhew DL, Cross JM, Bamman MM. Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol 104: 1736-1742, 2008. First published April 24, 2008 doi:10.1152/japplphysiol.01215.2007.-A present debate in muscle biology is whether myonuclear addition is required during skeletal muscle hypertrophy. We utilized K-means cluster analysis to classify 66 humans after 16 wk of knee extensor resistance training as extreme (Xtr, n ϭ 17), modest (Mod, n ϭ 32), or nonresponders (Non, n ϭ 17) based on myofiber hypertrophy, which averaged 58, 28, and 0%, respectively (Bamman MM, Petrella JK, Kim JS, Mayhew DL, Cross JM. J Appl Physiol 102: [2232][2233][2234][2235][2236][2237][2238][2239] 2007). We hypothesized that robust hypertrophy seen in Xtr was driven by superior satellite cell (SC) activation and myonuclear addition. Vastus lateralis biopsies were obtained at baseline and week 16. SCs were identified immunohistochemically by surface expression of neural cell adhesion molecule. At baseline, myofiber size did not differ among clusters; however, the SC population was greater in Xtr (P Ͻ 0.01) than both Mod and Non, suggesting superior basal myogenic potential. SC number increased robustly during training in Xtr only (117%; P Ͻ 0.001). Myonuclear addition occurred in Mod (9%; P Ͻ 0.05) and was most effectively accomplished in Xtr (26%; P Ͻ 0.001). After training, Xtr had more myonuclei per fiber than Non (23%; P Ͻ 0.05) and tended to have more than Mod (19%; P ϭ 0.056). Both Xtr and Mod expanded the myonuclear domain to meet (Mod) or exceed (Xtr) 2,000 m 2 per nucleus, possibly driving demand for myonuclear addition to support myofiber expansion. These findings strongly suggest myonuclear addition via SC recruitment may be required to achieve substantial myofiber hypertrophy in humans. Individuals with a greater basal presence of SCs demonstrated, with training, a remarkable ability to expand the SC pool, incorporate new nuclei, and achieve robust growth. strength training; skeletal muscle; neural cell adhesion molecule; myonucleus; myogenesis EACH MYONUCLEUS WITHIN THE multinucleated skeletal myofiber regulates gene transcription and subsequent protein synthesis over a finite volume of cytoplasm (6,7,23). This volume per nucleus, or myonuclear domain, is not a fixed quantity as evidenced during atrophy due to disuse (3, 24) or aging (25) as loss of cell volume exceeds nuclear shedding. Similarly, our laboratory and others have shown that some initial myofiber hypertrophy can expand the cytoplasmic volume associated with each myonucleus (17,25). This has led some to debate whether the addition of nuclei is required for skeletal myofiber hypertrophy (23). However, a ceiling size on the domain has been suggested (17, 23, 25) based on the concept that sufficient expansion of the myonuclear domain likely puts each nucleus under greater strain to supply the necessary gene products, driving a demand for the a...