The Hornberger Lab

New preprint! We show that mTORC1 is critical for myofibrillogenesis and the radial growth of myofibrils in response to mechanical overload. biorxiv.org/content/10.648… We also propose a model that redefines how mTORC1 might actually drive growth. Full breakdown in this thread 👇

Great team involved in this review based on a conference organized at the University of Jyväskylä, Finland. tinyurl.com/27zupuhc @DrMikeRoberts @MarcasBamman @HornbergerLab @AbigailMackey1 Wim Philip @mackinprof @BradSchoenfeld Gustavo Anne Juha H Elina @cleiton_libardi Juha A

Really nice write-up by Katie Cottingham in @UABNews highlighting our lab’s work! @UABDeptMed @UABHeersink

@jploenneke @grok A conservative guess for unique acronyms in the last 10 years might be in the low-to-mid thousands (perhaps 2,000–10,000+).... C'mon Jeremy, you should easily be able to memorize this many 😛

@jploenneke Hey @grok, how many different acronyms have been used in exercise physiology publications during the last 10 years?

Dear Authors, Just because you can use an abbreviation, doesn't mean you should. Sincerely, Someone trying to read what you did

Research Article by H Kalenta et al. (@TheRasmussenLab) #Hyperactivemuscle #mTORC1 attenuates functional #adaptations to #endurancetraining despite alterations in #mitochondrial and #lipid profiles ow.ly/OZMz50YWefb

@vanevery93 Thanks Derrick. I had to delete the post though. The short url link I created was causing problems for people. I posted a new thread with a better link

@HornbergerLab Incredible work as always! Congratulations to you and the lab!

10/ Limitations worth flagging: The plantaris is essentially all fast-twitch, and MOV is a chronic stimulus. Whether the same mTORC1-dependence holds for slow fibers or intermittent loading (e.g., resistance exercise) is still open.

9/ The proposed model: mTORC1 acts as a gatekeeper of protein RETENTION MOV → ↑ synthesis (mTORC1-independent) + MOV → mTORC1 → ↓ degradation → net accumulation of proteins for myofibrillogenesis and radial myofibril growth. No mTORC1, then degradation evens the score.

New preprint! We show that mTORC1 is critical for myofibrillogenesis and the radial growth of myofibrils in response to mechanical overload. biorxiv.org/content/10.648… We also propose a model that redefines how mTORC1 might actually drive growth. Full breakdown in this thread 👇

10/ Limitations worth flagging: The plantaris is essentially all fast-twitch, and MOV is a chronic stimulus. Whether the same mTORC1-dependence holds for slow fibers or intermittent loading (e.g., resistance exercise) is still open.

9/ The proposed model: mTORC1 acts as a gatekeeper of protein RETENTION MOV → ↑ synthesis (mTORC1-independent) + MOV → mTORC1 → ↓ degradation → net accumulation of proteins for myofibrillogenesis and radial myofibril growth. No mTORC1, then degradation evens the score.