Recovery from muscle damage: brain is involved

inhibition due to pain stops muscle rehabilitation. PREMIUM CONTENT subscriber access

Summer is here and we are out and about, overdoing it when it comes to exercise. Aches and pains from muscle strains plague us boomers who routinely overestimate our capacity. So let us look at strategies to reclaim our muscles’ youthful vigor.

Past related ‘muscle’ newsletters:

Muscle Miracles? Delayed Onset Muscle Soreness DOMS - are we exercisers doomed to hurt?

“Workouts cause injury. Injury causes inflammation. Inflammatory cells, macrophages, use stuff found in milk [NAD precursors] to nudge stem cells to proliferate and repair. Working out and massage then squeeze those macrophages out of the injury site. Wash, rinse, repeat.”

Hyaluronic Acid: it is more than just a face filler? HA commercial products galore. But can it be too much of a good thing?

HA makes a cozy niche for muscle stem cells.

“Skeletal muscle has a substantial capacity to recover its structure and function after being damaged. This comes from muscle stem cells (MuSCs), which are normally in quiescence. Muscle stem cells (MuSCs) reside in a specialized niche that ensures their regenerative capacity. Injury signals activate MuSC and promote muscle regeneration activity. MuSCs activate the production of the extracellular matrix component hyaluronic acid (HA), which is required to overcome inhibitory inflammation signaling from the injury niche, exit quiescence, and initiate muscle repair.”

After muscle injury, muscle stem cells must coordinate with immune cells in the inflamed tissue to ensure efficient repair. In response to injury, removal of the transcriptionally repressive histone H3K27me3 modification by KDM6B/JMJD3 allows muscle stem cells to produce hyaluronic acid that is then incorporated into the extracellular matrix. This remodeling of the extracellular matrix allows the muscle stem cell to receive signals from the infiltrating immune cells that then can initiate regeneration.

The histone H3 lysine 27 (H3K27) demethylase JMJD3, but not UTX, allowed MuSCs to overcome inhibitory inflammation signaling by removing trimethylated H3K27 (H3K27me3) marks at the Has2 locus to initiate production of hyaluronic acid. This extracellular matrix integrated signals that directed MuSCs to exit quiescence and initiate muscle repair.”

Muscle Mitochondria Misbehaving = Aging? Does it all come down to ... mitophagy?

“The inflammatory process that causes muscle to atrophy is associated with the accumulation of damaged mitochondria in cells. The increase in the levels of BNIP3 [BCL2 interacting protein 3] a protein related to the clearance process of damaged mitochondria, is linked to better muscle aging.”

New Information is presented in this newsletter that addresses:

• components of age related muscle recovery

• role of brain in physical therapy and as a target

• overall best approaches in knee osteoarthritis