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以激效作用觀點探討運動之抗老化機轉

Exploring the Anti-aging Mechanism of Exercise from the Viewpoint of Hormesis

摘要


激效作用(hormesis)觀念近來愈見被重視用於解釋遺傳及環境因子抗老化益處的機轉。本文特以激效作用闡明運動抗老化的可能機轉。因運動所產生的活性氧物質(reactive oxygen species, ROS)與開展蛋白(unfolded protein)為刺激抗氧化系統、伴護蛋白、受損分子移除及修復系統、神經滋養因子、抗衰老因子等基因或功能表現的上游分子,在適量時才能發揮良性刺激促成上述現象。活性氧物質的累積與許多神經退化性疾病有密切關係,預防的方式除了規律運動外,還包括控制活性氧物質在人體體內含量,例如限制能量攝取(energy restriction)與認知刺激(cognitive stimulation)等因素。能達到激效作用的活性氧物質劑量為,降低總產生量並微增至足以有效清除的劑量,這也是目前對活性氧物質含量與生理反應看似模糊關係較合理的解釋。未來研究應進一步證實引起活性氧物質的產生是否只是運動與過量能量攝取的共同機轉,而運動對神經細胞的刺激尚能與其他調控神經保護因子的上游訊息傳遞路徑尚有複雜的交互作用。

關鍵字

激效作用 運動 抗老化

並列摘要


The concept of hormesis has been increasingly recognized as a mechanism underlying the beneficial anti-aging effect of certain genetic and environmental factors. This review article elucidates possible mechanisms of anti-aging effect of exercise through hormesis hypothesis. The reactive oxygen species (ROS) and unfolded proteins produced by exercise, which play an important role on the expression of anti-oxidative system, protein chaperon, removing system and repair system of damaged molecules, exert a beneficial stimulation only when the dose is adequate. The accumulation of ROS correlates closely with degenerative neuron diseases. Besides regular exercise, other ways to prevent detrimental effect of ROS including energy restriction and cognitive stimulation. The optimal ROS dose which can achieve hormesis is decreased total ROS generation and intermittently increased to scavenge ROS efficiently. So far, this has been the reasonable explanation to argue the obscure relationship between the ROS dose and physiological response. The future challenge is to clarify if ROS generation is the common pathway between exercise and excess energy uptake and complicated cross-talk exists between oxidative stimuli from exercise and upstream regulators of neuroprotective facto.rs

並列關鍵字

hormesis exercise anti-aging

參考文獻


Andrade, F. H.,Reid, M. B.,Westerblad, H.(2001).Contractile response of skeletal muscle to low peroxide concentrations: myofibrillar calcium sensitivity as a likely target for redox-modulation.The FASEB Journal.15(2),309-311.
Arumugam, T. V.,Gleichmann, M.,Tang, S. C.,Mattson, M. P.(2006).Hormesis/preconditioning mechanisms, the nervous system and aging.Ageing Research Review.5(2),165-178.
Barger, J. L.,Walford, R. L.,Weindruch, R.(2003).The retardation of aging by caloric restriction: its significance in the transgenic era.Experimental Gerontology.38(11-12),1343-1351.
Calabrese, E. J.,Baldwin, L. A.(2002).Defining hormesis.Human & Experimental Toxicology.21(2),91-97.

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