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.

Optimization of different intensities of exercise preconditioning in protecting exhausted exercise induced heart injury in rats

This study was to optimize the exercise preconditioning(EP)intensity in protecting from exhaustive exercise-induced cardiac injury(EECI).A total of 98 male Sprague-Dawley rats were divided into 7 groups(n=14):the control group(C),the exhaustive exercise group(EE)and the EP+EE groups,which include the V10(53.0%VO_(2max)),V15(58.4%VO_(2max)),V20(67.0%VO_(2max)),V26(74.0%VO_(2max))and V30(80.0%VO_(2max))groups.Except the C group,the other groups were subjected to treadmill running.The serum contents of N terminal pro B type natriuretic peptide(NT-proBNP)and cardiac troponin I(cTn-I)were detected by the enzyme-linked immunosorbent assay method,ECG was recorded,heart function was detected by pressure volume catheter and the activities of mitochondrial electron transfer pathway(ET pathway)complexesⅠ,ⅡandⅣwere measured by high-resolution respiration instrument.Compared to the EE group,the EP groups have shown decrease of NT-proBNP and cTn-I,improvement of mitochondrial respiratory function and car-diac function.Compared to other EP groups,the V26 group has shown significant decrease of myocardial enzymes and improvement of mitochondrial function.The correlation analysis showed the EP effect was proportional to EP intensity in the range of 53.0%VO_(2max)-74.0%VO_(2max).High intensity and long duration of exhaustive exercise caused cardiac injury and EP could decrease serum level of NT-proBNP and cTn-I,improve electrical derangement and the left ventricular function,and raise the activities of ET pathway complexesⅠ,ⅡandⅣ.The protection of EP on EECI was improved as the EP intensity was increased from 53.0%VO_(2max)to 74.0%VO_(2max)and when EP intensity was 74.0%VO_(2max),the effect was the most obvious among all the setting EP groups.