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首页> 外文期刊>American Journal of Physiology >Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function.
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Exercise training from late middle age until senescence does not attenuate the declines in skeletal muscle aerobic function.

机译:从晚期的运动培训直到衰老直到衰老不会衰减骨骼肌有氧功能下降。

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摘要

We previously showed that 7 wk of treadmill exercise training in late-middle-aged rats can reverse the modest reductions in skeletal muscle aerobic function and enzyme activity relative to values in young adult rats (Exp Physiol 93: 863-871, 2008). The purpose of the present study was to determine whether extending this training program into senescence would attenuate the accelerated decline in the muscle aerobic machinery normally seen at this advanced age. For this purpose, 29-mo-old Fisher 344 Brown-Norway rats underwent 5 or 7 mo of treadmill exercise training. Training resulted in greater exercise capacity during an incremental treadmill exercise test and reduced percent body fat in 34- and 36-mo-old rats and improved survival. Despite these benefits at the whole body level, in situ muscle aerobic capacity and muscle mass were not greater in the trained groups at 34 mo or 36 mo of age. Similarly, the trained groups did not have higher activities of citrate synthase (CS) or Complex IV in homogenates of either the plantaris (fast twitch) or the soleus (slow twitch) muscles at either age. Finally, protein expression of CS (a marker of mitochondrial content) and peroxisome proliferator-activated receptor-gamma coactivator-1 (relating to the drive on mitochondrial biogenesis) were not higher in the trained groups. Therefore, although treadmill training from late middle age into senescence had significant benefits on running capacity, survival, and body fat, it did not prevent the declines in muscle mass, muscle aerobic capacity, or mitochondrial enzyme activities normally seen across this age, revealing a markedly diminished plasticity of the aerobic machinery in response to endurance exercise at advanced age.
机译:我们此前表明,晚年大鼠的7个跑步机运动训练可以逆转骨骼肌有氧功能和酶活性相对于年轻成年大鼠的价值(Exp Physiol 93:863-871,2008)的适度降低。本研究的目的是确定是否将该培训计划扩展到衰老中,将衰减通常在此先进年龄段的肌肉有氧机械的加速下降。为此目的,29-Mo-Old Fisher 344 Brown-Norway大鼠踩踏跑步机运动训练5或7次。培训在增量跑步机运动试验期间产生了更大的运动能力,并在34岁和36岁的大鼠中减少了体脂百分比并提高了生存率。尽管在整个身体水平上有这些益处,但在34 mo或36℃的训练群体中,原位肌肉有氧能力和肌肉质量并不大。类似地,培训的基团没有柠檬酸合酶(Cs)或复合体IV的常规(快速抽搐)或肌肉(缓慢抽搐)肌肉中的均匀素的活性更高的活性。最后,培训的基团中,Cs(线粒体含量标记物)和过氧化物体增殖物激活的受体-γ-1(与线粒体生物发生器上的驱动有关)的蛋白质表达在训练基团中不高。因此,尽管从中年晚期训练成衰老的跑步机培训对运行能力,生存和体脂具有显着的益处,但它并没有阻止肌肉质量,肌肉有氧能力的下降,或通常在此年龄段的线粒体酶活性,揭示了一个有氧机械的可塑性显着减少了高龄耐力运动的耐受性。

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