In mice with suppressed myostatin, resistance training boosted the production of new mitochondrial proteins, but extra amino acids did not—suggesting that physical stress, not nutrients, drives mitochondrial renewal in this context.
Evidence from Studies
No evidence studies found yet.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
Whether resistance training consistently increases mitochondrial protein synthesis while EAAs do not, across animal models under myostatin inhibition.
A systematic review and meta-analysis of all studies measuring mitochondrial protein synthesis (via 2H2O or 15N) in mice or rats under myostatin inhibition with or without RT or EAA supplementation.
Whether resistance training causally increases mitochondrial protein synthesis more than EAAs under myostatin inhibition in mice.
A double-blind RCT in 80 male C57BL/6J mice treated with sActRIIB-Fc, randomized to RT, EAA, RT+EAA, or control, measuring mitochondrial protein synthesis via 2H2O labeling and COX IV content at 4 weeks.
Whether the frequency of resistance activity correlates with mitochondrial protein synthesis rates in mice treated with myostatin inhibitors.
A prospective cohort study of 120 mice treated with sActRIIB-Fc, stratified by daily ladder climbs (low, medium, high), measuring mitochondrial protein synthesis weekly over 4 weeks.
Whether mice with the highest mitochondrial protein synthesis rates under myostatin inhibition are more likely to have undergone resistance training.
A case-control study comparing 30 mice with >30% mitochondrial synthesis increase (cases) to 30 with <5% increase (controls) among sActRIIB-Fc-treated mice, retrospectively analyzing RT exposure.
Whether there is a correlation between resistance activity and mitochondrial protein synthesis in mice treated with myostatin inhibitors at a single time point.
A cross-sectional analysis of 100 mice treated with sActRIIB-Fc for 4 weeks, measuring daily RT exposure and mitochondrial protein synthesis at endpoint without experimental manipulation.