Lees Simon J, Booth Frank W
Dept. of Biomedical Sciences, Univ. of Missouri-Columbia, Columbia, MO, USA.
Can J Appl Physiol. 2004 Aug;29(4):447-60; discussion 444-6. doi: 10.1139/h04-029.
Sedentary death syndrome (SeDS) is a major public health burden due to its causing multiple chronic diseases and millions of premature deaths each year. Despite the impact of physical inactivity, very little is known about the actual causes of physical inactivity-induced chronic diseases. It is important to study the mechanisms underlying molecular changes related to physical inactivity in order to better understand the scientific basis of individualized exercise prescription and therapies for chronic diseases, and to support improved public health efforts by providing molecular proof that physical inactivity is an actual cause of chronic diseases. Physical activity has a genetic basis. A subpopulation of genes, which have functioned to support physical activity for survival through most of humankind's existence, require daily exercise to maintain long-term health and vitality. Type 2 diabetes (T2D) is an example of a SeDS condition, as it is almost entirely preventable with physical activity. To determine the true role of physical inactivity in the development and progression of T2D, information is presented which indicates that comparisons should be made to physically active controls, rather than sedentary controls, as this population is the healthiest. Use of sedentary subjects as the control group has led to potentially misleading interpretations. If physically active individuals were designated as the control group, a different interpretation would have been drawn. It is thought that there is no difference in GLUT4 concentration between T2D and sedentary groups. However, GLUT4 expression is higher in active controls than in sedentary and T2D groups. Therefore, to obtain causal mechanisms for SeDS in order to allow for scientifically based prevention and therapy strategies, physically active subjects must serve as the control group.
久坐死亡综合征（SeDS）是一项重大的公共卫生负担，因为它每年会引发多种慢性疾病并导致数百万例过早死亡。尽管身体缺乏活动会产生影响，但对于缺乏身体活动所引发的慢性疾病的实际成因却知之甚少。研究与身体缺乏活动相关的分子变化背后的机制，对于更好地理解个性化运动处方和慢性病治疗方法的科学依据，并通过提供分子证据证明身体缺乏活动是慢性病的实际成因来支持改善公共卫生工作而言至关重要。身体活动具有遗传基础。在人类大部分生存历程中发挥作用以支持身体活动来维持生存的一部分基因，需要日常锻炼来保持长期健康和活力。2型糖尿病（T2D）就是SeDS病症的一个例子，因为通过身体活动几乎完全可以预防该病。为了确定身体缺乏活动在T2D发生和发展过程中的真正作用，现提供的信息表明，应该与身体活跃的对照组进行比较，而不是久坐不动的对照组，因为这个群体是最健康的。将久坐不动的受试者用作对照组导致了可能产生误导性的解释。如果将身体活跃的个体指定为对照组，就会得出不同的解释。据认为，T2D组和久坐不动组之间的葡萄糖转运蛋白4（GLUT4）浓度没有差异。然而，活跃对照组中的GLUT4表达高于久坐不动组和T2D组。因此，为了获得SeDS的因果机制以便制定基于科学的预防和治疗策略，必须将身体活跃的受试者用作对照组。
