How about developing muscle strength without exercise? Sounds too lazy? đ
"... For the new study, researchers at the Universities of Melbourne and Copenhagen investigated the molecular signaling responses in muscles before, during and after different types of exercise. ...
performed an analysis of human skeletal muscle from a cross-over intervention of endurance, sprint and resistance exercise ...
From this, they identified a previously uncharacterized gene called C18ORF25, which was among those activated most often. ...
When the team engineered mice to lack this gene, the animals developed smaller skeletal muscle fibers ... Inversely, when they ramped up the gene activity, the animals’ muscles became stronger. ..."
performed an analysis of human skeletal muscle from a cross-over intervention of endurance, sprint and resistance exercise ...
From this, they identified a previously uncharacterized gene called C18ORF25, which was among those activated most often. ...
When the team engineered mice to lack this gene, the animals developed smaller skeletal muscle fibers ... Inversely, when they ramped up the gene activity, the animals’ muscles became stronger. ..."
From the abstract:
"... we performed a phosphoproteomic analysis of human skeletal muscle from a cross-over intervention of endurance, sprint, and resistance exercise. This identified 5,486 phosphosites regulated during or after at least one type of exercise modality and only 420 core phosphosites common to all exercise. One of these core phosphosites was S67 on the uncharacterized protein C18ORF25, which we validated as an AMPK substrate. Mice lacking C18ORF25 have reduced skeletal muscle fiber size, exercise capacity, and muscle contractile function, and this was associated with reduced phosphorylation of contractile and Ca2+ handling proteins. Expression of C18ORF25 S66/67D phospho-mimetic reversed the decreased muscle force production. This work defines the divergent and canonical exercise phosphoproteome across different modalities and identifies C18ORF25 as a regulator of exercise signaling and muscle function."
Phosphoproteomics of three exercise modalities identifies canonical signaling and C18ORF25 as an AMPK substrate regulating skeletal muscle function (no public access)
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