Sarcopenia is the umbrella name for the progressive loss of muscle mass and strength with age - which may turn out to cover a range of separate mechanisms. The progression of sarcopenia appears to be reduced by the practice of calorie restriction, and might also be slowed by a range of possible therapies such as exercise and dietary leucine supplementation or targeting the myostatin gene and its protein product. Levels of inflammation also show up as a possible contributing factor - more chronic inflammation is a bad thing across the board.

Here is an open access paper that touches on much of what the mainstream research community is investigating when it comes to sarcopenia.

Sarcopenia, the age-related loss of skeletal muscle, is characterized by a deterioration of muscle quantity and quality leading to a gradual slowing of movement, a decline in strength and power, and an increased risk of fall-related injuries. Since sarcopenia is largely attributed to various molecular mediators affecting fiber size, mitochondrial homeostasis, and apoptosis, numerous targets exist for drug discovery. In this paper, we summarize the current understanding of the endocrine contribution to sarcopenia and provide an update on hormonal intervention to try to improve endocrine defects. Myostatin inhibition seems to be the most interesting strategy for attenuating sarcopenia other than resistance training with amino acid supplementation.

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Several researchers have investigated the effect of inhibiting myostatin to counteract sarcopenia using animals. Lebrasseur et al. found that treatment with a mouse chimera of antihuman myostatin antibody (24?mg/Kg, 4 weeks), a drug for inhibiting myostatin, elicited a significant increase in muscle mass and in running performance ... More recently, Murphy et al. showed, by way of once weekly injections, that a lower dose of this anti-human myostatin antibody (10?mg/Kg) significantly increased the fiber cross-sectional area (by 12%) and in situ muscle force (by 35%) of aged mice (21?mo old). These findings highlight the therapeutic potential of antibody-directed myostatin inhibition for sarcopenia by inhibiting protein degradation.

Work on myostatin therapies is one of the topics worthy of greater attention here, as this seems like it would be a generally beneficial gene therapy for everyone - something that, given a good safety profile, most people would want to undergo earlier in life. The first step towards widespread availability for this sort of human enhancement is to develop the necessary medical technology in in the first place, of course, and these days that's only going to happen in the service of treating a specific medical condition.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm