Effect of a combination of astaxanthin supplementation, heat stress, and intermittent reloading on satellite cells during disuse muscle atrophy

We examined the effect of a combination of astaxanthin （AX） supplementation, repeated heat stress, and intermittent reloading （IR） on satellite cells in unloaded rat soleus muscles. Forty-nine male Wistar rats （8-week-old） were divided into control, hind-limb unweighting （HU）, IR during HU, IR with AX supplementation, IR with repeated heat stress （41.0-41.5 ℃ for 30 min）, and IR with AX supplementation and repeated heat stress groups. After the experimental period, the antigravitational soleus muscle was analyzed using an immunohistochemical technique. Our results revealed that the combination of dietary AX supplementation and heat stress resulted in protection against disuse muscle atrophy in the soteus muscle. This protective effect may be partially due to a higher satellite cell number in the atrophied soleus muscle in the IR/AX/heat stress group compared with the numbers found in the other groups. We concluded that the combination treatment with dietary AX supplementation and repeated heat stress attenuates soleus muscle atrophy, in part by increasing the number of satellite cells.

Alterations in renin-angiotensin receptors are not responsible for exercise preconditioning of skeletal muscle fibers

Endurance exercise training promotes a protective phenotype in skeletal muscle known as exercise pre-conditioning.Exercise preconditioning protects muscle fibers against a variety of threats including inactivity-induced muscle atrophy.The mechanism(s)responsible for exercise preconditioning remain unknown and are explored in these experiments.Specifically,we investigated the impact of endurance exercise training on key components of the renin-angiotensin system(RAS).The RAS was targeted because activation of the classical axis of the RAS pathway via angiotensinⅡtypeⅠreceptors(AT1Rs)promotes muscle atrophy whereas activation of the non-classical RAS axis via Mas receptors(MasRs)inhibits the atrophic signaling of the classical RAS pathway.Guided by prior studies,we hypothesized that an exercise-induced decrease in AT1Rs and/or increases in MasRs in skeletal muscle fibers is a potential mechanism responsible for exercise preconditioning.Following endurance exercise training in rats,we examined the abundance of AT1Rs and MasRs in both locomotor and respiratory muscles.Our results indicate that endurance exercise training does not alter the protein abundance of AT1Rs or MasRs in muscle fibers from the diaphragm,plantaris,and soleus muscles compared to sedentary controls(p>0.05).Furthermore,fluorescent angiotensinⅡ(AngⅡ)binding analyses confirm our results that exercise pre-conditioning does not alter the protein abundance of AT1Rs in the diaphragm,plantaris,and soleus(p>0.05).This study confirms that exercise-induced changes in RAS receptors are not a key mechanism that contributes to the beneficial effects of exercise preconditioning in skeletal muscle fibers.