2015年11月5日訊 /生物谷BIOON/ --近日，來(lái)自瑞典卡羅林斯卡醫(yī)學(xué)院的研究人員在國(guó)際學(xué)術(shù)期刊PNAS上發(fā)表了一項(xiàng)最新研究進(jìn)展，他們發(fā)現(xiàn)了短期高強(qiáng)度間隔性鍛煉帶來(lái)益處背后的細(xì)胞學(xué)機(jī)制，這一發(fā)現(xiàn)也為解釋為何抗氧化劑會(huì)破壞耐力訓(xùn)練效果提供了部分線索。
幾分鐘的高強(qiáng)度間隔性鍛煉足以對(duì)機(jī)體產(chǎn)生一定獲益，作用效果至少等同于完成一些傳統(tǒng)的更加花費(fèi)時(shí)間的耐力訓(xùn)練。高強(qiáng)度鍛煉在愛(ài)好運(yùn)動(dòng)的人群中甚至是一些肌肉功能受到損傷的病人中越來(lái)越流行，但幾分鐘的高強(qiáng)度鍛煉為何會(huì)如此有效一直沒(méi)有得到闡釋。
為了研究高強(qiáng)度鍛煉過(guò)程中肌肉細(xì)胞所發(fā)生的變化，研究人員要求男性志愿者做30秒最大運(yùn)動(dòng)量的騎行，隨后休息4分鐘，再以這種循環(huán)方式重復(fù)6次。之后研究人員從志愿者的大腿部位提取了肌肉組織樣本。
Hakan Westerblad教授這樣說(shuō)道：'我們的研究表明三分鐘的高強(qiáng)度鍛煉足以改變肌肉細(xì)胞的鈣離子通道，這會(huì)引起肌肉細(xì)胞在管理鈣離子方面產(chǎn)生持續(xù)性變化，這種變化對(duì)于機(jī)體來(lái)說(shuō)是一種絕佳的適應(yīng)性信號(hào)，比如會(huì)促進(jìn)新線粒體的形成。'
線粒體就像細(xì)胞的能量工廠，刺激形成新的線粒體會(huì)增加肌肉的耐力。研究人員發(fā)現(xiàn)高強(qiáng)度鍛煉會(huì)促進(jìn)肌肉細(xì)胞的鈣離子通道產(chǎn)生變化，而實(shí)驗(yàn)證明這種變化是由自由基增加所引起的。
細(xì)胞內(nèi)存在抗氧化系統(tǒng)幫助捕獲并中和自由基，而類似維生素E和維生素C這樣的抗氧化劑也會(huì)作為常見(jiàn)的飲食補(bǔ)充成分或作為天然成分存在于食物中。在這項(xiàng)研究中，研究人員在高強(qiáng)度間隔鍛煉前后用抗氧化劑對(duì)分離出來(lái)的小鼠肌肉進(jìn)行處理，結(jié)果表明抗氧化劑移除了鍛煉對(duì)鈣離子通道造成的影響，這也部分解釋了為何抗氧化劑會(huì)削弱肌肉對(duì)耐力訓(xùn)練的應(yīng)答。
最后，研究人員還指出，他們對(duì)高水平運(yùn)動(dòng)員進(jìn)行了檢測(cè)，三分鐘高強(qiáng)度間隔鍛煉并不會(huì)影響他們肌肉細(xì)胞的鈣離子通道，他們的機(jī)體已經(jīng)建立了更加有效的抗氧化系統(tǒng)。（生物谷Bioon.com）
Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2 leak after one session of high-intensity interval exercise
Nicolas Placea,1, Niklas Ivarssonb,1, Tomas Venckunasc,1, Daria Neyrouda,d, Marius Brazaitisc, Arthur J. Chengb, Julien Ochalae, Sigitas Kamandulisc, Sebastien Girardd, Gintautas Volungevi?iusc, Henrikas Pau?asf, Abdelhafid Mekidecheg, Bengt Kaysera, Vicente Martinez-Redondob, Jorge L. Ruasb, Joseph Brutonb, Andre Truffertg, Johanna T. Lannerb, Albertas Skurvydasc, and H?kan Westerblad
High-intensity interval training (HIIT) is a time-efficient way of improving physical performance in healthy subjects and in patients with common chronic diseases, but less so in elite endurance athletes. The mechanisms underlying the effectiveness of HIIT are uncertain. Here, recreationally active human subjects performed highly demanding HIIT consisting of 30-s bouts of all-out cycling with 4-min rest in between bouts (≤3 min total exercise time). Skeletal muscle biopsies taken 24 h after the HIIT exercise showed an extensive fragmentation of the sarcoplasmic reticulum (SR) Ca2 release channel, the ryanodine receptor type 1 (RyR1). The HIIT exercise also caused a prolonged force depression and triggered major changes in the expression of genes related to endurance exercise. Subsequent experiments on elite endurance athletes performing the same HIIT exercise showed no RyR1 fragmentation or prolonged changes in the expression of endurance-related genes. Finally, mechanistic experiments performed on isolated mouse muscles exposed to HIIT-mimicking stimulation showed reactive oxygen/nitrogen species (ROS)-dependent RyR1 fragmentation, calpain activation, increased SR Ca2 leak at rest, and depressed force production due to impaired SR Ca2 release upon stimulation. In conclusion, HIIT exercise induces a ROS-dependent RyR1 fragmentation in muscles of recreationally active subjects, and the resulting changes in muscle fiber Ca2 -handling trigger muscular adaptations. However, the same HIIT exercise does not cause RyR1 fragmentation in muscles of elite endurance athletes, which may explain why HIIT is less effective in this group.
