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The Role of Low Energy Expenditure and Sitting on Obesity, Metabolic Syndrome, Type 2 Diabetes, and Cardiovascular Disease

¹Department of Biomedical Sciences, University of Missouri-Columbia, Columbia, MO 65211
²Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211

It is not uncommon for people to spend one-half of their waking day sitting, with relatively idle muscles. The other half includes the often large volume of non-exercise physical activity. Given the increasing pace of technological change in their 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 non-exercise 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 Non-Exercise Activity Thermogenesis (NEAT) 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 (a protein important for controlling plasma triglyceride catabolism, HDL-C, and other metabolic risk factors). Experimentally reducing the normal spontaneous standing and ambulatory time had a much greater effect on LPL regulation, compared to adding vigorous exercise training on top of the normal level of non-exercise 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 non-exercising person may become even more metabolically unfit in the coming years if they sit too much -- thereby limiting the normally high volume of intermittent non-exercise 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 non-exercise activity throughout much of the day.

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