Does COFFEE Help Build Muscle?

While coffee is associated with a long list of potential health benefits, some of which can be found linked in the Bomb Proof Coffee section of this site, its possible impact on skeletal muscle hypertrophy has not been examined.

This study was done in mice, so it’s actual utility and cross over to humans is unclear, but the mechanisms of action — effects on AMPK, IGF1, mTORC1, and myostatin — do apply to humans. If coffee does impact those pathways in humans as it doses humans actually can consume it, then that would be an interesting finding to be sure. Is this yet another benefit of coffee consumption? More data is clearly needed, but I for one don’t need another reason to drink coffee anyway!

Coffee consumption promotes skeletal muscle hypertrophy and myoblast differentiation.

Food Funct. 2018 Feb 21;9(2):1102–1111.

Abstract

Coffee is a widely consumed beverage worldwide and is believed to help prevent the occurrence of various chronic diseases. However, the effect of coffee on skeletal muscle hypertrophy, differentiation and the mechanisms of action responsible have remained unclear.

To investigate the effect of coffee on skeletal muscle hypertrophy, mice were fed a normal diet or a normal diet supplemented with 0.3% coffee or 1% coffee. Coffee supplementation was observed to increase skeletal muscle hypertrophy, while simultaneously upregulating protein expression of total MHC, MHC2A, and MHC2B in quadricep muscle.

Myostatin expression was also attenuated, and IGF1 was upregulated with subsequent phosphorylation of Akt and mTOR, while AMPK phosphorylation was attenuated.

Coffee also increased the grip strength and PGC-1α protein expression, and decreased the expressions of TGF-β and myostatin in tricep muscle. Coffee activated the MKK3/6-p38 pathway and upregulated PGC-1α, which may play a role in promoting myogenic differentiation and myogenin expression in C2C12 cells. These results suggest that coffee increases skeletal muscle function and hypertrophy by regulating the TGF-β/myostatin — Akt — mTORC1