In the time of coronavirus an awful lot of people are not just working from home they’re also working out at home. That’s a good thing; exercise is a great way to boost the immune system, stay healthy and deal with stress. But for people used to more structured workouts at the gym it can come with a downside. Trying new routines at home that look easy on YouTube, but are harder in practice could potentially increase the risk of injury.
A new study from Japan looks at what happens when you damage a muscle. It won’t help it heal faster, but it will at least let you understand what is happening inside your body as you sit there with ice on your arm and ibuprofen in your hand.
The researchers found that when you damage a muscle, for example by trying to lift too much weight or doing too many repetitions of one exercise, the damaged muscle fibers leak substances that activate nearby “satellite” stem cells. These satellite cells then flock to the site of the injury and help repair the muscle.
The team, from Kumamoto University and Nagasaki University in Japan, named the leaking substances “Damaged myofiber-derived factors” (DMDFs) – personally I think “Substances Leaked by Injured Muscles (SLIM) would be a much cooler acronym, but that’s just me. Gaining a deeper understanding of how DMDFs work might help lead to therapies for older people who have fewer satellite muscle cells, and also for conditions like muscular dystrophy and age-related muscular fragility (sarcopenia), where the number and function of satellite cells decreases.
In an article in Science Daily, Professor Yusuke Ono, the leader of the study, says it’s possible that DMDFs play an even greater role in the body:
“In this study, we proposed a new muscle injury-regeneration model. However, the detailed molecular mechanism of how DMDFs activate satellite cells remains an unclear issue for future research. In addition to satellite cell activation, DMDF moonlighting functions are expected to be diverse. Recent studies have shown that skeletal muscle secretes various factors that affect other organs and tissues, such as the brain and fat, into the bloodstream, so it may be possible that DMDFs are involved in the linkage between injured muscle and other organs via blood circulation. We believe that further elucidation of the functions of DMDFs could clarify the pathologies of some muscle diseases and help in the development of new drugs.”
The study appears in the journal Stem Cell Reports.
3 thoughts on “Repairing damaged muscles”
Has there been any progress made with stem cells for FSH Muscular Dystrophy?
Dear Ray, I’m sorry to say I haven’t been able to find any clinical trials for FSH Muscular Dystrophy. There is a lot of research underway but nothing that is yet ready to be tested in people in a clinical trial. I’m sorry I don’t have better news for you but wish you all the best.
Recent observation showed that muscle damage released components to activate satellite muscle stem cells. That was followed by proliferation and differentiation to accelerate muscle injury regeneration. Previous clinical investigation reported that repeated im. injection of PDGF-BB into patients with muscular dystrophy (DMD) resulted regenerating and necrotic muscle fibers in muscle. The biopsy samples from DMD patients expressed PDGF-BB. However, in vitro revealed that PDGF-BB attracted myoblasts and activated their proliferation. The clinical finding concluded that PDGF-BB may play a protective role in DMD by enhancing muscle regeneration through activation of satellite cell proliferation and migration. PDGF-BB is a family of growth factors that plays important biological function to regulate proliferation, migration and differentiation. In multicellular organisms, each specific cell types including stem cells expresses a variety of growth factor receptors suggests that cell development and behavior in vivo are determined by combinations of interacting stimuli. During the recruitment of cell into the cell cycle, the mitogenic response of cell can be resolved into a two-step process, whereby quiecent(G0) cells are advanced into preliminary (G1) phase of the cell cycle by “competent” or “early response ” factors ( such as PDGF), and subsequently committed to DNA synthesis by the separate action of ” progression factors” (such as EGF and IGF). Neither EGF nor IGF alone constitute a mitogenic signal, but a combination of the two does, suggesting that two factors stimulate complementary components of the signal transduction network, both of which are required to trip an essential switch. Furthermore, PDGF receptor is physically associated with cytoplasmic proteins that can trigger some of the secondary events and that receptor activation is accompanied by autophosphorylation at site capable of influencing receptor-substrate interaction. Among these PDGF receptor -associated proteins are GAP, phospholipase C-g, raf-1 and other. Further research need to be conducted to see the activation of PDGFR associated with GAPDH activity which might contribute to regeneration of muscle.