Why do myostatin inhibitors produce larger muscles but not more strength?
Myostatin inhibitors demonstrably produce larger muscles, but in primates this does not translate proportionally into greater strength, because other inhibitory proteins remain active and take over myostatin's role.
Myostatin is a protein that slows muscle growth. Block that protein and muscles do indeed grow. In mice, both muscle mass and grip strength increase. But in primates, and presumably in humans, strength gains are disappointing even as mass continues to rise.
The reason lies in the selectivity of the inhibition. Myostatin is not the only brake on muscle growth. Activin A and a related protein (GDF11) play the same role. If only myostatin is blocked, those other brakes remain active. The muscles become larger, but their composition differs from muscles that grow through training or through broader hormonal stimulation. That mass therefore delivers less force per kilogram than normal muscle tissue.
When the brake is applied more broadly, blocking both myostatin and activin A at the same time, the picture changes. Animal research then shows both greater mass and greater strength, including in primates. An antibody that fully blocks the receptor (ActRIIB) produced more muscle growth in mice and also protected against strength loss caused by certain medications. In marmosets, the same broad blockade produced more muscle mass and higher force output in isolated muscles after 14 weeks.
In diseased muscle, such as in Duchenne muscular dystrophy, pure myostatin inhibition works somewhat better in mouse models: both mass and strength increased. Diseased muscle cells may simply have more room for improvement than healthy ones. But here too, the translation to humans has not yet been demonstrated.
Clinically, the picture remains unclear. Evidence in humans, particularly in older adults with muscle loss, is scarce. The complex signalling network surrounding myostatin means that a single blockade is probably not sufficient to produce functional strength gains as well.
This answer is based on animal research in mice and primates (marmosets and monkeys), supplemented by two review articles. No randomised studies in humans are available, so cause and effect in humans have not been demonstrated. Effects are clearest in mice; in primates the evidence is already thinner. Broad blockade (activin A plus myostatin) consistently shows greater effects in animals than myostatin inhibition alone, but this has not yet been confirmed in humans. For sarcopenia in older adults, the evidence is explicitly insufficient.