Role of low energy expenditure and sitting in obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease
Role of low energy expenditure and sitting in obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease
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DOI：
10.2337/db07-0882
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发表时间：
2007-11-01
期刊：
影响因子：
7.7
通讯作者：
Zderic, Theodore W.
中科院分区：
文献类型：
--
作者：
Hamilton, Marc T.;Hamilton, Deborah G.;Zderic, Theodore W.
人们醒着的时候有一半的时间是坐着的，肌肉相对空闲，这并不罕见。一天的另一半时间通常包括大量的非运动体力活动。考虑到家庭、社区和工作场所环境中技术变革的步伐日益加快，现代人可能还没有达到缺乏体育锻炼的历史巅峰，即使在那些已经不锻炼的人群中也是如此。我们的目的是研究久坐行为，尤其是久坐，对死亡率、心血管疾病、2型糖尿病、代谢综合征风险因素和肥胖的影响。最近的观察性流行病学研究强烈表明，每天坐着的时间或较低的非运动活动水平可能与这些医学问题有重要的直接关系。现在有必要进行研究，将久坐（不活动生理学）和有组织的运动（运动生理学）所引起的反应区别开来，以区分可能独特的分子、生理和临床效应。从理论上讲，这可能部分是因为非运动活动产热通常比运动占总能量消耗的比例要大得多，或者因为全天任何类型的短暂而频繁的肌肉收缩都可能是短路导致代谢疾病的不健康分子信号所必需的。为维持高水平的每日低强度和间歇性活动的分子原因提供翻译证据的第一系列对照实验室研究之一来自骨骼肌脂蛋白脂肪酶（LPL）（一种对控制血浆甘油三酯分解代谢、高密度脂蛋白胆固醇和其他代谢危险因素很重要的蛋白质）的细胞调节的检查。在实验中，减少正常自发站立和活动时间比在正常水平的非运动活动基础上增加剧烈运动训练对LPL调节的影响要大得多。这些研究还发现，不运动启动了独特的细胞过程，与运动反应有质的不同。总之，有一个不活动生理学研究的出现。这些都开始引起一个新的关注，可能具有重大的临床和公共卫生意义：如果不锻炼的人坐得太多，他们在未来几年的新陈代谢可能会变得更加不健康，从而限制了日常生活中通常大量的间歇性非锻炼性身体活动。因此，如果不活动的生理学范式被证明是正确的，那么未来的可怕担忧可能在于，越来越多的人没有意识到久坐的潜在危险，也没有充分利用一天中大部分时间保持非运动活动的好处。
It is not uncommon for people to spend one-half of their waking day sitting, with relatively idle muscles. The other half of the day includes the often large volume of nonexercise physical activity. Given the increasing pace of technological change in domestic, community, and workplace environments, modern humans may still not have reached the historical pinnacle of physical inactivity, even in cohorts where people already do not perform exercise. Our purpose here is to examine the role of sedentary behaviors, especially sitting, on mortality, cardiovascular disease, type 2 diabetes, metabolic syndrome risk factors, and obesity. Recent observational epidemiological studies strongly suggest that daily sitting time or low nonexercise activity levels may have a significant direct relationship with each of these medical concerns. There is now a need for studies to differentiate between the potentially unique molecular, physiologic, and clinical effects of too much sitting (inactivity physiology) separate from the responses caused by structured exercise (exercise physiology). In theory, this may be in part because nonexercise activity thermogenesis is generally a much greater component of total energy expenditure than exercise or because any type of brief, yet frequent, muscular contraction throughout the day may be necessary to short-circuit unhealthy molecular signals causing metabolic diseases. One of the first series of controlled laboratory studies providing translational evidence for a molecular reason to maintain high levels of daily low-intensity and intermittent activity came from examinations of the cellular regulation of skeletal muscle lipoprotein lipase (LPL) (a protein important for controlling plasma triglyceride catabolism, HDL cholesterol, and other metabolic risk factors). Experimentally reducing normal spontaneous standing and ambulatory time had a much greater effect on LPL regulation than adding vigorous exercise training on top of the normal level of nonexercise activity. Those studies also found that inactivity initiated unique cellular processes that were qualitatively different from the exercise responses. In summary, there is an emergence of inactivity physiology studies. These are beginning to raise a new concern with potentially major clinical and public health significance: the average nonexercising person may become even more metabolically unfit in the coming years if they sit too much, thereby limiting the normally high volume of intermittent nonexercise physical activity in everyday life. Thus, if the inactivity physiology paradigm is proven to be true, the dire concern for the future may rest with growing numbers of people unaware of the potential insidious dangers of sitting too much and who are not taking advantage of the benefits of maintaining nonexercise activity throughout much of the day.