One of the most devastating but least-discussed aspects of age-related decline is the onset of frailty, i.e., the progressive loss of robustness in multiple tissues and organ systems. Because frailty comes eventually to every aging person (if they’re lucky enough to live that long), it’s lumped into the category of “normal aging”; possibly as a result, relatively little attention is paid to causes and potential treatments.

Fortunately, this is starting to change, as exemplified by this recent paper from Siriett et al.. The authors address the role of myostatin in sarcopenia, the gradual loss of muscle mass and strength that accompanies advanced aging:

… Myostatin, a negative regulator of pre- and postnatal myogenesis, inhibits satellite cell activation and muscle regeneration postnatally. To investigate the role of myostatin during age-related sarcopenia, we examined muscle mass and regeneration in young and old myostatin-null mice. Young myostatin-null muscle fibers were characterized by massive hypertrophy and hyperplasia and an increase in type IIB fibers, resulting in a more glycolytic muscle. With ageing, wild-type muscle became increasingly oxidative and fiber atrophy was prominent. In contrast no fiber type switching was observed and atrophy was minimal in aged myostatin-null muscle. The effect of ageing on satellite cell numbers appeared minimal, however, satellite cell activation declined significantly in both wild-type and myostatin-null muscles. In young mice, lack of myostatin resulted in increased satellite cell number and activation compared to wild-type, suggesting a greater propensity to undergo myogenesis, a difference maintained in the aged mice. … In conclusion, a lack of myostatin appears to reduce age-related sarcopenia and loss of muscle regenerative capacity.

The experimental system was a full knockout (null), and it remains to be seen whether myostatin function can be present in early life (allowing for normal muscle development; the myostatin-null mice are muscle-bound and look a little ridiculous) but diminished late in life to reap the benefits of avoiding sarcopenia. An answer will have to wait the design of a conditional-knockout model, which is likely already in the works.