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作 者:Branden L.Nguyen Toshinori Yoshihara Rafael Deminice Jensen Lawrence Mustafa Ozdemir Hayden Hyatt Scott K.Powers
机构地区:[1]Department of Applied Physiology and Kinesiology,University of Florida,Gainesville,32611,Florida,USA [2]Department of Exercise Physiology,Juntendo University,Tokyo,270-1695,Japan [3]Department of Physical Education,University of Estadual of Londrina,Londrina,10011,Brazil
出 处:《Sports Medicine and Health Science》2021年第3期148-156,共9页运动医学与健康科学(英文)
基 金:the National Institute of Health(R21AR063956 to SKP).
摘 要: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.
关 键 词:Exercise preconditioning Renin-angiotensin system Skeletal muscle disuse atrophy Skeletal muscle
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