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在中老年晚期开始进行运动训练,可最大限度地保护肌肉收缩功能,并增加衰老大鼠肌细胞的氧化损伤。

Initiating exercise training in late middle age minimally protects muscle contractile function and increases myocyte oxidative damage in senescent rats.

机构信息

Muscle and Aging Laboratory, Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada.

出版信息

Exp Gerontol. 2010 Nov;45(11):856-67. doi: 10.1016/j.exger.2010.07.003. Epub 2010 Jul 17.

Abstract

Age-related loss of muscle mass and function exhibits a marked acceleration from late middle age to senescence and exercise training is one method that has been proposed to slow this process. The purpose of this study was to determine if long-term treadmill exercise training initiated at late middle age could increase endogenous antioxidant enzyme activity and attenuate the loss of skeletal muscle contractile properties in the gastrocnemius/plantaris (GAS/Plan) and soleus (SOL) muscles of senescent rats (34-36 mo) through a decrease in oxidative damage. Male Fisher 344 × Brown Norway F1-hybrid rats underwent 5-7 mo of treadmill training beginning at late middle age (29 mo). A 7 mo sedentary adult group was used to investigate age-related changes. Aging caused an increase in antioxidant enzyme activities; however, only SOD activity was further increased with exercise training. Exercise training did not attenuate the decrease in twitch or tetanic tension of the GAS/Plan or SOL. It did, however, prevent the increase in twitch half relaxation time of the SOL muscle only. Oxidative damage, as reflected in carbonyl content, was increased with age and even further with exercise training in the GAS muscle. Muscle fibre cross sectional area was decreased with age and even further with exercise training. Interestingly, small muscle fibres showed the highest accumulation of carbonyls. Overall, despite an augmentation of select antioxidant enzyme activities, exercise training from late middle age through to senescence had minimal benefits for muscle contractile properties, perhaps in part due to exacerbated oxidation.

摘要

年龄相关的肌肉质量和功能丧失在从中年后期到衰老期表现出明显的加速,而运动训练是被提出的减缓这一过程的一种方法。本研究的目的是确定从中年后期开始的长期跑步机运动训练是否可以通过减少氧化损伤来增加内源性抗氧化酶活性并减弱衰老大鼠(34-36 月龄)比目鱼肌/跖肌(GAS/Plan)和比目鱼肌(SOL)肌肉收缩性能的丧失。雄性 Fisher 344×Brown Norway F1 杂种大鼠在中年后期(29 月龄)开始进行 5-7 个月的跑步机训练。7 个月的久坐成年组用于研究与年龄相关的变化。衰老导致抗氧化酶活性增加;然而,只有 SOD 活性随着运动训练进一步增加。运动训练并没有减轻 GAS/Plan 或 SOL 肌肉的抽搐或强直张力的下降。然而,它确实仅防止了 SOL 肌肉的抽搐半松弛时间的增加。氧化损伤,如羰基含量所反映的,随着年龄的增长而增加,甚至在 GAS 肌肉中随着运动训练而进一步增加。肌肉纤维横截面积随着年龄的增长而减少,甚至在运动训练中进一步减少。有趣的是,小肌肉纤维表现出最高的羰基积累。总的来说,尽管某些抗氧化酶活性增强,但从中年后期到衰老期进行运动训练对肌肉收缩性能几乎没有益处,这可能部分是由于氧化加剧。

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