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THE JOURNAL OF SPORTS MEDICINE AND PHYSICAL FITNESS

Rivista di Medicina, Traumatologia e Psicologia dello Sport


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The Journal of Sports Medicine and Physical Fitness 2017 April;57(4):483-9

DOI: 10.23736/S0022-4707.16.06065-5

Copyright © 2016 EDIZIONI MINERVA MEDICA

lingua: Inglese

Exhaustive exercise decreases L-type calcium current by activating endoplasmic reticulum stress

Yanzhuo MA, Lingfeng KONG, Shuying QI, Dongmei WANG

Department of Cardiology, Bethune International Peace Hospital, Shijiazhuang, China


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BACKGROUND: This study investigated effects of exhaustive exercise on L-type calcium current (ICa,L) and the putative intracellular cascade responsible for the effects.
METHODS: Rats were randomly divided into three treatment groups: sedentary (without exercise), exercised to exhaustion and salubrinal injection before each exhaustive exercise period. Exercise group rats were forced to swim until exhaustion each time for 9 days with 5% body weight attached to the head. Salubrinal (1 mg/kg) or an equivalent volume of placebo solution (dimethyl sulfoxide) was injected via the intraperitoneal route daily for the first 3 days, followed by subcutaneous injections of salubrinal (0.5 mg/kg) or placebo solution daily for 9 days (starting 30 min before exercise). After a 1-day recovery period, whole-cell patch clamping was used to investigate the L-type Ca2+ current (ICa,L), with sedentary control rats. Additionally, endoplasmic reticulum (ER) chaperone protein levels were analyzed.
RESULTS: Exhaustive exercise triggered ER stress, demonstrated by elevated expression of ER stress markers: phospho-eIF2α, CCAT/enhancer-binding homologous protein (CHOP) and caspase-12. Compared to controls, ICa,L was inhibited by exhaustive exercise, which was blocked by salubrinal, a selective eIF2α dephosphorylation inhibitor used to inhibit ER stress. These results suggest that ER stress participates in regulation of ICa,L. However, exhaustive exercise did not change the voltage dependence of steady-state activation and inactivation of ICaL, and salubrinal infusion caused no difference in voltage dependence of steady-state activation and inactivation of ICa,L.
CONCLUSIONS: Exhaustive exercise activates ER stress, thus inhibiting ICaL, which may change the action potential duration and contribute to proarrhythmia.


KEY WORDS: Exercise - L-type calcium channels - Endoplasmic reticulum stress

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Publication History

Issue published online: February 21, 2017
Article first published online: February 10, 2016
Manuscript accepted: February 4, 2016
Manuscript revised: January 27, 2016
Manuscript received: August 5, 2015

Per citare questo articolo

Ma Y, Kong L, Qi S, Wang D. Exhaustive exercise decreases L-type calcium current by activating endoplasmic reticulum stress. J Sports Med Phys Fitness 2017;57:483-9. DOI: 10.23736/S0022-4707.16.06065-5

Corresponding author e-mail

slwangdm@126.com