One of the theories relating to causes of sarcopenia, the characteristic loss of muscle mass and strength with age, is that it relates to dysfunction in the processing of amino acids such as leucine. There is evidence for leucine supplementation to help slow the progression of sarcopenia, for example. The research here adds more along these lines, though it seems the authors will have to run a redesigned study to see whether or not the cellular differences observed actually produce meaningful results over a longer period of time:
The loss of skeletal muscle mass and quality is common with aging. This loss highlights the development of sarcopenia, where diminished muscle mass and strength are major contributors engendering loss of independence and quality of life for older adults. Current research suggests that reductions in the ability to stimulate muscle protein synthesis and promote proliferation and differentiation of muscle satellite cells may be important contributors to the development of sarcopenia.
It is well known that exercise and the ingestion of essential amino acids (EAA), in particular the amino acid leucine, are important stimulators of muscle protein synthesis through activation of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway. While an anabolic resistance to the independent effects of exercise and EAA or protein is prevalent with aging, combining the two stimuli shows promise in combating sarcopenia via the ability for this combination to maximally stimulate mTORC1 and upregulate the translation initiation machinery. Indeed, we have recently demonstrated that provision of leucine-enriched EAA mixture following a bout of high-intensity resistance exercise (RE) stimulates mTORC1 and prolongs myofibrillar protein synthesis for up to 24 hours post-RE in the very same cohort of older men we examined in this study whereas, in the absence of EAA this mTORC1 response is blunted in older adults.
A host of evidence has suggested increased satellite cell (SC) activation and content following RE in human skeletal muscle, yet we and others have demonstrated a blunting of or a delayed ability to activate and increase the SC pool in older men compared with a younger cohort. EAA and leucine provision has been shown to upregulate SC activity via mTORC1. Therefore, we hypothesized that EAA ingestion, which we have previously shown to potently activate mTORC1 following an acute bout of leg resistance exercise, would enhance skeletal muscle satellite cell proliferative capacity and content in older men. We demonstrate that older men do not appear to increase skeletal muscle satellite cell content at 24 hours following heavy, high volume resistance exercise in the absence of EAA ingestion. However, when 10g of EAA is ingested one hour postexercise we found that MHC I myofiber satellite cell content displays obvious trends to be greater than when older men are not given postexercise EAA. Although this pattern is visually evident in MHC II myofibers and when all myofibers are pooled, the current data set did not reach statistical significance.