期刊文献+

运动如何使人长寿 被引量:1

How Exercise Helps You Live Longer
原文传递
导出
摘要 以往研究一致表明,经常运动的人未来的死亡风险(relative risk in mortality)明显下降,规律运动确实可延长人类寿命,并且这个长寿效果与运动挑战的量成正比。很有趣的是,运动造成能量储存减少,肌肉损伤与氧化伤害指数提高,且与运动强度和伤害指数成正比。为何造成短暂伤害可使人长寿?主要的原因是运动使得人体对细胞除旧布新(cell renewal)。这个结果使组织年轻化,强化身体承受挑战的能力。从另外的角度来看,人体是多细胞生物,能有效联合众多细胞分工合作,应付外在挑战后迅速恢复,仰赖细胞彼此间有效的讯息沟通。老化使细胞间的沟通灵敏度下降,各组织资源分配不均(例如肥胖、癌症、肌少症),为降低人体众多细胞合作共生的负面因素,使人体生存能力下降。运动使肌肉组织持续获得合理的养分分配。缺乏运动者,除了肌肉细胞汰旧换新速度慢外,资源分配给肌肉的量减少,转向脂肪组织与肝脏储存的比例增加,肥胖的脂肪细胞进一步透过内分泌讯息(adipokines)降低肌肉细胞对胰岛素的敏感度,抑制肌肉细胞对葡萄糖的吸收储存能力。肌肉是全身最主要的醣类储存库,养分储存能力退化,除了造成体能下降外,未被吸收的葡萄糖滞留在血液中逐渐形成高血糖而使全身各处蛋白质被糖化增加(protein glycation),被糖化的蛋白因结构改变将遭受免疫细胞辨识为不正常的蛋白,进而释放出大量自由基攻击消灭。因此,高血糖将造成持续性氧化伤害,使全身蛋白进一步氧化,全身蛋白结构进一步改变,造成恶性循环,低度的慢性发炎(Low grade chronic inflammation)或自体免疫攻击(Autoimmune attack),最后发展成糖尿病、高血压、心脏病、中风、癌症等发炎相关疾病。流行病学研究发现生命期血糖上升速度愈快的人,寿命愈短。因此,通过运动使身体年轻化,提高肌肉细胞对胰岛素的敏感度来维持正常的葡萄糖的吸收能力,进而避免高血糖的发生。如此,既可保持好身材、避免肥胖、保持好体能,又可延长寿命。 Previous longitudinal studies have consistently reported that exercise significantly decreases the relative risk of human mortality,indicating its positive effect on extending longevity.In addition,this effect appears to be dose-dependent.Intriguingly,exercise acutely depletes energy storage of cells,causes muscle damage,and increases oxidative stress.The magnitude of the negative effects is also increased in proportion to the exercise amount.How can such a destructive event turning into a life-prolonging consequence for humans? One of the most likely answers is that exercise can enhance cell renewal after destruction.An acute increase in cell turnover is one way to make the tissue a younger population of cells.As a multicellular organism,a massive number of human cells must work cooperatively in precision against the unexpected changing environment that increases entropy.The conversation among partner cells will rely heavily on effective intercellular communications.Cell aging causes a reduced sensitivity of the communication among cells,leading to inaccurate resource(fuel) distribution(such as adiposity,tumorigenesis,sarcopenia).This uneven resource distribution can be detrimental for such a highly cooperative multicellular system,contributing premature death and reduced survival.In a contrary,physical inactivity slows down cell renewal process,decreases fuel distribution towards skeletal muscle leaving more fuel source for adipose tissue and liver.Hypertrophied adipocyte releases signals(adipokines) to circulation and that decreases sensitivity of skeletal muscle to insulin,resulting in decreased glucose uptake from blood.Skeletal muscle is the main tissue for insulin responsive glucose uptake from circulation.Thus,decreases in muscle insulin sensitivity will causes hyperglycemia and reduce physical fitness.Persistent hyperglycemia can cause protein glycation via a non-enzymatic Maillard reaction.This protein conformation change will attract immune attack leading to an increased oxidative stress and protein oxidation(LDL oxidation).Endless protein deformation causing low grade chronic inflammation or autoimmune attack has now been recognized as the pathogenic origin of type 2 diabetes,hypertension,coronary heart disease,stroke,and cancer.Epidemiological evidence indicates that progression of hyperglycemia is a predictor for human mortality.Therefore,rejuvenating skeletal muscle by vigorous exercise is an effective way to maintain high insulin sensitivity for glucose uptake and prevent hyperglycemia,which thus preserves good body shape,prevents obesity,maintains good physical fitness,and prolongs lifespan.
出处 《中国食品学报》 EI CAS CSCD 北大核心 2012年第8期1-10,共10页 Journal of Chinese Institute Of Food Science and Technology
关键词 运动 肌肉 肥胖 发炎 胰岛素 exercise muscle obesity inflammation insulin
  • 相关文献

参考文献25

  • 1Yashin AI,Ukraintseva SV, Arbeev KG, et al. Maintaining physiological state for exceptional survival: What is the normal level of blood glucose and does it change with age?[J]. Mech Ageing Dev, 2009, 130: 611-618.
  • 2Ling PR,Mueller C,Smith RJ,et al. Hyperglycemia induced by glucose infusion causes hepatic oxidative stress and systemic inflammation, but not STAT3 or MAP kinase activation in liver in rats[J]. Metabolism : Clinical and Experimental ,2003,52(7): 868-874.
  • 3Yan SF, Ramasamy R,Schmidt AM. Mechanisms of Disease : advanced glycation end-products and their receptor in inflammation and diabetes complicationsfj]. Nat Rev Endocrinol, 2008, 4(5) : 285-293.
  • 4Prasad S, Sung B, Aggarwal BB. Age-associated chronic diseases require age-old medicine : Role of chronic in-flammation[J]. Preventive Medicine, 2012, (54S) : S29-37.
  • 5Mayer-Davis EJ, D^Agostino R, Karter AJ, et al. Intensity and amount of physical activity in relation to insulin sensitivity[J]. JAMA, 1998,279(9):669-674.
  • 6Pedersen BK. Muscles and their myokines[J]. Journal of Experimental Biology, 2012, 214(2) : 337-346.
  • 7Pedersen BK, kerstrm TCA, Nielsen AR,et al. Role of myokines in exercise and metabolism[J]. Journal of Applied Physiology, 2007, 103(3): 1093-1098.
  • 8He C., Bassik MC., Moresi V.,et al. Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis[J]. Nature,2012, 481 (7382); 511-515.
  • 9Cauza E, Hanusch -Enserer U, Strasser B, et al. The relative benefits of endurance and strength training on the metabolic factors and muscle function of people with type 2 diabetes mellitus[J]. Archives of Physical Medicine andRehabilitation, 2005,86(8): 1527-1533
  • 10Hubert HB. The Importance of obesity in the development of coronary risk factors and disease ; The epidemiologic evidence[J]. Annual Review of Public Health, 1986,7(1): 493-502.

同被引文献4

引证文献1

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部