After a year, the drug helped muscles recover faster after exercise because it boosted a hormone that makes mitochondria work better.
Scientific Claim
Increased IGF-1 levels are associated with enhanced mitochondrial oxidative capacity, as measured by phosphocreatine recovery kinetics following exercise.
Original Statement
“after 12 months tesamorelin really improved their recovery like significant and those improvements were strongly associated with increases in IGF-1 just insulin like growth factor one. So in other words, there was better mitochondrial efficiency, better energy handling, and better metabolic flexibility.”
Context Details
Domain
pharmacology
Population
human
Subject
Increased IGF-1 levels
Action
are associated with
Target
enhanced mitochondrial oxidative capacity
Intervention Details
Evidence from Studies
Supporting (2)
The effects of tesamorelin on phosphocreatine recovery in obese subjects with reduced GH.
When people took a drug that raised a growth-related hormone called IGF-1, their muscles recovered faster after exercise, which means their energy-producing parts (mitochondria) worked better.
IGF-1 helps make mitochondria — the energy factories in cells — work better and cleaner, which means cells can recover energy faster after exercise, just like the claim says.
Technical explanation
This paper directly shows that IGF-1 signaling enhances mitochondrial function and protective responses under metabolic stress, including increased mitochondrial biogenesis and turnover — key components of oxidative capacity. While it does not explicitly measure phosphocreatine recovery kinetics, it establishes a direct mechanistic link between IGF-1 and improved mitochondrial efficiency, which underlies the assertion.
Contradicting (1)
When IGF-1 is lowered, the body’s energy system doesn’t seem to compensate — suggesting IGF-1 might be needed for good energy recovery after exercise, so if it’s gone and recovery doesn’t get worse, the link might not be as strong as claimed.
Technical explanation
This study shows that pegvisomant (a GH receptor antagonist) causes a rapid and significant drop in IGF-1 levels, and while it doesn't directly measure mitochondrial function, it implies that lowering IGF-1 disrupts normal metabolic signaling. If IGF-1 were truly linked to enhanced mitochondrial oxidative capacity, its reduction should impair recovery kinetics — consistent with the assertion being true, but the paper's context of IGF-1 suppression without observed mitochondrial compensation indirectly contradicts the necessity of IGF-1 for this function.