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User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 44, Issue 1. Previous Article Next Article. Article Information. Article Navigation. Commentaries December 14 Is Being Physically Active Enough to Be Metabolically Healthy?
The Key Role of Sedentary Behavior Mary O. Whipple ; Mary O. This Site. Google Scholar. Judith G. Regensteiner ; Judith G. Audrey Bergouignan Audrey Bergouignan. Corresponding author: Audrey Bergouignan, audrey. bergouignan iphc. Diabetes Care ;44 1 — Connected Content.
A commentary has been published: Sedentary Time and Metabolic Risk in Extremely Active Older Adults. Get Permissions. toolbar search Search Dropdown Menu. toolbar search search input Search input auto suggest. Figure 1.
View large Download slide. Search ADS. Sedentary Behavior Research Network SBRN — Terminology Consensus Project process and outcome. Association of sedentary behaviour with metabolic syndrome: a meta-analysis. Sedentary time and its association with risk for disease incidence, mortality, and hospitalization in adults a systematic review and meta-analysis.
Sedentary time in adults and the association with diabetes, cardiovascular disease and death: systematic review and meta-analysis. Does physical activity attenuate, or even eliminate, the detrimental association of sitting time with mortality?
A harmonised meta-analysis of data from more than 1 million men and women. Accelerometer-measured sedentary and physical activity time and their correlates in European older adults: the SITLESS study.
Screen-based entertainment time, all-cause mortality, and cardiovascular events: population-based study with ongoing mortality and hospital events follow-up.
Improving self-reports of active and sedentary behaviors in large epidemiologic studies. Combined effects of time spent in physical activity, sedentary behaviors and sleep on obesity and cardio-metabolic health markers: a novel compositional data analysis approach.
Identifying the critical gaps in research on sex differences in metabolism across the life span. van Hoye. Validation of the SenseWear Pro3 armband using an incremental exercise test. Whitaker KM , Gabriel KP , Buman MP , et al.
J Am Heart Assoc. Accessed October 8, Ekelund U , Tarp J , Steene-Johannessen J , et al. Dose-response associations between accelerometry measured physical activity and sedentary time and all cause mortality: systematic review and harmonised meta-analysis.
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Sedentary Behavior, Physical Inactivity, and Metabolic Syndrome: Pilot Findings From the Rapid Assessment Disuse Index Study. in Journal of Physical Activity and Health. Kerem Shuval Kerem Shuval Search for other papers by Kerem Shuval in Current site Google Scholar PubMed Close.
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Article Sections Methods Study Design Measures RADI Scores Metabolic Syndrome Covariates Statistical Analysis Results Discussion. Export References. ris ProCite. bib BibTeX. enw EndNote.
x Crossref PubMed Gardiner PA , Healy GN , Eakin EG , et al. x false. Crossref PubMed Whitaker KM , Gabriel KP , Buman MP , et al. l Crossref PubMed Ekelund U , Tarp J , Steene-Johannessen J , et al. Importantly, the amount of nonexercise activity or sitting patterns is not addressed in any detail by the recommendation, and we believe this will be a critical issue for further research.
However, the clarifications do help in separating how the public can distinguish between exercise and the distinctive sedentary and nonexercise activity behaviors illustrated in Fig. A major reason for our knowing less about inactivity and nonexercise activity than about structured exercise has been the practical hurdle of quantifying sitting time and patterns of spontaneous nonexercise movements.
This is being overcome in part with better use of accelerometers and inclinometers. When people are standing up, there are generally movements, or at least light fidgeting-like movements 15 , Critical for any confusion about dose-response issues is the fact that there is great variability within Fig.
Biological determinants contribute to this 15 , Supporting the mass of the body in combination with spontaneous movement or very slow ambulation 1 mph raises whole-body energy expenditure 2.
Nonexercise movements decrease significantly as people age and become more sedentary Thus, given the small differences in daily energy balance necessary to explain weight gain over many years 52 , it is plausible that postural allocation plays a role in human obesity.
A major question raised by the inactivity physiology paradigm is whether the typical person who already does not perform structured exercise regularly will have increased risks of diseases in the coming years as a result of too much sitting.
If so, then a secondary question relates to the minimal and optimal patterns of nonexercise physical activity necessary to prevent specific metabolic concerns for specific cohorts, such as controlling glucose metabolism in people with diabetes or controlling triglycerides and HDL cholesterol in people with dyslipidemia.
Understandably, there is no public campaign to limit sitting because inactivity physiology is still an emerging area of research and because insufficient evidence may exist to justify sounding the alarm at this point.
A cornerstone paradigm from years of exercise research has been the specificity principle; namely, that the magnitude and qualitative type of adaptive responses depend on the type of exercise training.
It is axiomatic that the low resistances associated with aerobic endurance training will not produce the same responses as high-resistance weight training. Thus, people who desire to maximize strength will lift heavy weights and those who want to maximize endurance performance will run or bicycle long distances with a much lower resistance and greater duration.
The stimulus to skeletal muscles, cardiovascular system, and other organs is vastly different when comparing different exercises. Thus, the corollary is that the underlying cellular regulatory mechanisms responsible for causing the adaptation must also be different. Although the cumulative weekly energy expenditure in people who exercise regularly is a small slice of the pie for total energy expenditure Fig.
Except for maybe weight control, most exercise physiologists would probably agree that there is something special about an exercise deficiency that may not necessarily be substituted for by any factor raising total body energy expenditure. If one accepts this specificity principle for exercise deficiency, the logical corollary would be that a deficiency in the larger slice of the pie because of too little nonexercise physical activity Fig.
Exercise of relatively shorter duration and greater intensity may or may not be able to substitute for a NEAT deficiency since nonexercise activity takes place over a far greater time span every day and continually interrupts sedentary time. This hypothesis is still largely untested, and further research is much needed.
In summary, both exercise and nonexercise physical activity patterns may be healthy, but if one accepts the specificity principle, then one should not assume that people can simply replace nonexercise physical activity deficiency with a bolus of exercise a few times per week.
The cumulative number of the thousands of daily muscular contractions during nonexercise activity requires a greater energy demand than a bolus of continuous exercise Fig.
There is a wide range in the energy demand of NEAT Fig. Efforts are beginning to appear in the medical literature for practical strategies to encourage NEAT-enhancing behaviors 4.
It is easy to forget when studying behaviors e. If sitting really does cause disease, then specific cells within the muscles or other parts of the body must somehow sense and respond to stimuli triggered by prolonged sitting.
Inactivity physiology research is only beginning to identify the molecules responsible for the aforementioned metabolic risk factors for coronary artery disease, such as the control of plasma lipoprotein metabolism 2. Deep venous thrombosis DVT is an example for how too much sitting, not just too little structured exercise, can induce medical problems.
DVT is a serious and potentially life-threatening condition where blood clots develop in the veins deep within idle leg muscles The problem has long been known to be caused by prolonged sitting, as in the air raid shelters in London during World War II 55 , in the s when people began taking extended automobile journeys and flying on airplanes 56 , and even during excessive TV viewing 57 or computer and video game use 58 — Global transcriptional analysis in combination with biochemical information may reveal specific molecular responses within the legs explaining the risk for DVT during physical inactivity T.
Thus, DVT is a clear example for why limiting sitting time is a reasonable prescription for some medical conditions Table 1. DVT prevention is also an example where light, intermittent, and frequent local muscle contractions in the legs might be an optimal physical activity recommendation for preventing this disorder unique to inactivity physiology.
Current practice often attempts to limit bed rest following surgeries or injuries when medically possible. Three weeks of bed rest in otherwise healthy men 61 had a more profound impact on physical work capacity than did three decades of aging in the same men Interestingly, the mechanism responsible for the decrease in maximal oxygen consumption during bed rest was due to stroke volume and cardiac output 61 , whereas during aging the decrease was due to maximal oxygen extraction It may be tempting to infer from this that bed rest studies also offer insights about sitting too much because when people sit they are also immobile and have reduced NEAT.
However, great caution is warranted because bed rest studies typically investigate the effects of lying down for several or more days 63 , While we are unaware of evidence that 1 day of lying down would cause secondary physiological effects impinging upon metabolic events, several days of lying down uninterrupted may have widespread consequences.
Others have reviewed the many physiological responses of bed rest, including a host of neural-humoral changes, orthostatic intolerance, skeletal muscle atrophy, disturbances in fluid balance, etc.
At least in rats, intermittent reloading was able to successfully prevent skeletal muscle atrophy 1 and adverse changes in both myocardial contractility 66 and the cerebral vasculature Lipoprotein lipase LPL regulation has served as the prototype both for understanding how skeletal muscle metabolism contributes directly to lipoprotein risk factors and for insights about how exercise and physical inactivity may impact disease outcomes, though for different cellular reasons.
As far as we know, LPL is the first protein directly interacting with and regulating lipoproteins to be studied at the cellular level during physical inactivity 1 — 3 , 68 , 69 , raising the possibility for other metabolic processes to be impaired during inactivity as well.
Many studies have evaluated the metabolic consequences of altered LPL function. Low LPL has been associated with blunted plasma triglyceride uptake 1 , 70 , 71 and reduced plasma HDL levels 1 , LPL may also have some effects on hypertension 72 , diabetes-induced dyslipidemia 73 , metabolic problems in aging 68 , human metabolic syndrome 74 , 75 , and coronary artery disease severity and incidence in many human studies 76 , Positive effects of LPL on preventing diet-induced adiposity 78 , 79 and insulin resistance 78 , 80 have been reported but not in all models 81 , Experimental elevations in LPL have been reported to reduce diabetic dyslipidemia and limit diet-induced atherosclerosis in transgenic rabbits Increased skeletal muscle LPL has been frequently reported following short-term exercise training 84 , LPL activity was measured in six muscles after intensive training for 2 weeks.
Exercise increased LPL activity 2- to 2. The most oxidative postural leg muscles that already had high LPL due to nonexercise activity did not display any further increase in LPL after training. LPL mRNA gene expression and LPL protein levels were increased in tandem with the same patterns as for LPL activity.
Furthermore, intense continuous electrical stimulation of the motor nerve to a predominantly FTW muscle for 1 month also increased LPL mRNA expression, protein, and activity approximately threefold.
In both rats 85 and humans 84 , the transient temporal pattern for LPL expression after stopping exercise is consistent with a role for pretranslational regulation. Studies that have prevented standing and ambulatory activity of one or both of the hindlimbs of rats 1 , 3 have been reviewed in more detail elsewhere 2.
The physical activity for the referent control group in these studies was limited to the normal spontaneous patterns of standing and intermittent light ambling of rats in the cage no running wheels. The acute 1—18 h and chronic 11 days responses to inactivity were studied 1.
Atrophy of skeletal muscle mass and alterations in food intake or body mass caused by complete loss of mobility were avoided because the chronic inactivity was intermittent for only one-half of each day 1.
Remarkably, most of the LPL activity associated with microvasculature of the most oxidative muscles was lost within 1 day of inactivity Fig. The finding of a rapid loss of functional LPL activity was consistent in both male and female rats and also in mice. The and 6-h data are shown for hindlimb muscles in Figs.
Consistent with LPL function, the clearance of plasma triglyceride by skeletal muscle was decreased significantly Fig. The cellular mechanism for the loss of LPL is being studied in detail 1 — 3 , and some of those findings are summarized here to illustrate the contrast between cellular reasons for an increase in LPL that can occur during exercise and the decrease in LPL during contractile inactivity.
First, notice the type of muscle cells associated with changes in LPL in Fig. With inactivity, there was a profound decrease in LPL in the more oxidative types of muscle.
During normal physical activity, when rats stood on the hindlimbs, LPL activity was significantly greater in the oxidative red muscle regions than in the FTW muscle regions.
The lower levels of LPL in FTW muscle of control animals and the less impressive decrease during inactivity could be explained by the normally low level of recruitment 29 in this type of muscle.
LPL also was not affected by changes in physical activity in continuously working skeletal muscle diaphragm and cardiac muscle. Thus, differential regulation of lipoproteins by LPL during experimentally induced inactivity and normal nonexercise physical activity is linked to local contractile activity and not a generalized response to the systemic energy demands.
Studies with the transcriptional inhibitor actinomycin D 1 indicate that the process decreasing LPL during inactivity may be due to upregulation of a gene other than LPL that quickly switches off the functional LPL activity found on the capillary endothelium Fig.
LPL was rapidly restored to normal within 4 h of intermittent standing and slow walking Fig. This rapid increase in LPL activity was not limited by blockade of gene transcription. In seeking to begin to identify signaling events Fig.
This and other findings with high-fat feeding led to the interpretation that there was an increased sensitivity to plasma lipids during physical inactivity, tending to decrease LPL activity in skeletal muscle 3.
This has practical implications for understanding one reason why nicotinic acid has been so effective in lowering plasma triglycerides and raising HDL cholesterol in clinical cardiology for decades, and it supports a rationale for paying closer attention to unique aspects of inactivity physiology.
A central question to this whole issue of inactivity physiology and nonexercise activity deficiency is whether exercise operates by a different set of cellular mechanisms or simply that all effects of changes in physical activity operate along a continuum. Studies are beginning to appear in the literature 1 — 3 that are important for determining whether the regulation of the lipoprotein risk factors most commonly associated with metabolic syndrome and type 2 diabetes plasma triglyceride and HDL cholesterol in exercise physiology studies are not merely the mirror image of effects of the inactivity physiology studies Fig.
Those studies are the first steps of research for the third tenet of the paradigm of inactivity physiology; i.
This concept, proposed earlier 2 , is that some of the specific cellular and molecular processes explaining the responses during inactivity physiology and exercise physiology are qualitatively different from each other and that sometimes the most potency is gained by maintaining daily low-intensity postural and ambulatory activity.
Table 2 lists examples for how the mechanisms driving LPL responses differ between inactivity physiology and exercise physiology. One day of inactivity had a several-fold greater change in LPL activity than the exercise training response.
The effects of inactivity on LPL suppression were greatest in the most oxidative muscle regions. In contrast to inactivity, exercise by running the same type of rats increased LPL gene expression and LPL activity in the most glycolytic skeletal muscles and not in oxidative muscles Fig.
Both in studies of rats 85 and humans 84 , vigorous exercise has consistently been shown to produce parallel increases in LPL mRNA expression and LPL protein. These two studies showed LPL gene expression rising within the hours after exercise and then falling transiently to normal levels by the next day.
This temporal association is consistent with pretranslational regulation of LPL gene expression. In contrast, neither acute Fig.
Furthermore, the rapid restoration of LPL activity during 4 h of intermittent standing and very slow ambulation was not impaired during blockade of gene transcription Fig. These studies support the specificity principle and the third tenet of inactivity physiology because the cellular responses to inactivity and exercise are qualitatively different.
People spend too many hours in a waking day sitting for the scientific community to neglect the existing yet limited evidence that these behaviors may matter for metabolic diseases.
Furthermore, there are too many hours of nonexercise physical activity in most people's lives to neglect the consequences of reducing this time or to not encourage efforts seeking to determine how this large volume of nonexercise physical activity should fit into public health recommendations in the near future.
Sitting time and nonexercise activity have been linked in epidemiological studies to rates of metabolic syndrome, type 2 diabetes, obesity, and CVD.
This obviously raises the pressing need for interventional studies to more conclusively test for specific negative metabolic effects of prolonged sitting or to compare and contrast the potential benefits of daily nonexercise physical activity and structured exercise.
Translational studies are needed at multiple levels, ranging from cellular research determining whether there are plausible mechanisms regulating risk factors to more epidemiological research identifying clinical outcomes in diverse populations.
As one example, the limited existing evidence indicates that inactivity quickly engages signals for specific molecular responses contributing to poor lipid metabolism by suppression of skeletal muscle LPL activity.
Given the ubiquitous and strong support for the specificity principle that various forms of physical activity produce unique cellular signals and physiological responses, it is reasonable to suspect that studies elucidating the qualitative and quantitative biochemical and clinical effects of sitting too much will yield fascinating insights.
A major question raised by the inactivity physiology paradigm is whether the typical person who already does not perform structured exercise regularly will have increased risks of metabolic diseases in the coming years as a result of too much sitting. The red circle shadows the median of 13, middle-aged men and women adapted from ref.
As described in the text, the majority of people in the general population already do not follow the prescription for enough moderate-vigorous exercise. It logically follows that in people who already do not exercise, it is impossible for higher rates of age-adjusted metabolic syndrome, type 2 diabetes, obesity, and CVD over the coming years to be caused by further exercise deficiency.
Inactivity physiology is a discipline concerned with the future of people who may be sitting too much. Middle-aged men who had to sit many more hours per week and obtain less physical activity had greater risk for premature myocardial infarction A and mortality from coronary artery disease C ref.
These general findings were subsequently confirmed in studies in middle-aged women B ref. Distinctive characteristics of patterns of inactivity and nonexercise physical activity M.
A : Skeletal muscle recruitment during nonexercise physical activity by using electromyogram signals of a leg muscle during intermittent standing, brief stepping, sitting, and rising from a chair.
This person took four steps and stood intermittently during this minute while at work and would not have been categorized as exercising. There was a silent signal while sitting, and this was quickly interrupted to stand up again to greet a visitor. B : Quantification of postural allocation with inclinometer technology and ambulation with accelerometry averaged over hourly epochs within the same individual on two different days.
The sensitivity of the accelerometer was arbitrarily set to accurately record stepping time above 1. Comparison of exercise physiology and inactivity physiology in relation to energy expenditure. Components of total energy expenditure A and the energy expended from exercise on top of NEAT B.
Exercise physiology examines responses to exercise and effects of stopping training. Exercise does not typically constitute the majority of activity energy expenditure even in regular exercisers. It thus follows logically that the specificity principle also predicts that some physiological and biochemical responses induced by physical inactivity shown as NEAT deficiency in A are not simply the opposite of the exercise responses.
Activity energy expenditure B is the energy required above basal metabolic rate for exercise or other movement. Energy expenditure was derived from normative values for a reference person weighing 70 kg using a PAL of 1. LPL activity in studies of inactivity A and exercise B physiology is summarized for three skeletal muscles refs.
Acute administration of the transcription blocker actinomycin D was without effect on LPL in rats with a normally higher amount of nonexercise physical activity. Administering the transcription blocker at the initiation of acute inactivity prevented the fall in LPL activity, indicating that a gene is switched on, which is responsible for the lowering of LPL activity A.
Re-initiation of intermittent standing and very slow ambulation 0. Blocking transcription did not impair this process. Lowering of plasma triglyceride and free fatty acid during inactivity with nicotinic acid NA completely prevented the decrease in LPL caused by physical inactivity, while having no effect on LPL activity in muscles with normal spontaneous cage activity C.
Inhibition of several signaling pathways known previously to suppress LPL activity had no effect on the decrease in LPL activity caused by physical inactivity D. The defining characteristics of inactivity physiology and the unique patterns of nonexercise physical activity are listed.
This can be contrasted to exercise physiology guidelines. LPL studies indicate that the underlying cellular events during inactivity NEAT deficiency are distinct from the cellular events after exercise training.
Table is redrawn from refs. org on 7 September DOI: The costs of publication of this article were defrayed in part by the payment of page charges. Section solely to indicate this fact. This study was supported by financial support from the National Institutes of Health Grants HL and HL Sign In or Create an Account.
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Metabolic syndrome is a cluster of conditions that occur Tea detox diets, increasing your lfestyle of Metabolic syndrome sedentary lifestyle disease, stroke and lifestye 2 diabetes. These conditions include Water consumption guide blood pressure, Water consumption guide blood sugar, excess body fat around the synddome, and abnormal cholesterol Cardiovascular health promotion triglyceride levels. People who have synfrome syndrome typically have apple-shaped bodies, meaning they have larger waists and carry a lot of weight around their abdomens. It's thought that having a pear-shaped body that is, carrying more of your weight around your hips and having a narrower waist doesn't increase your risk of diabetes, heart disease and other complications of metabolic syndrome. Having just one of these conditions doesn't mean you have metabolic syndrome. But it does mean you have a greater risk of serious disease. And if you develop more of these conditions, your risk of complications, such as type 2 diabetes and heart disease, rises even higher. Thank Metabolic syndrome sedentary lifestyle seedntary visiting Metabloic. You are using a browser version with limited support Anthocyanins and respiratory health CSS. To obtain Blueberry oatmeal cookies best experience, we Endurance training methods you use sedentarg more up to Blueberry oatmeal cookies lifesstyle or turn Metablic compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Although the Asian population exhibits excessive sedentary behaviour and has a high susceptibility to metabolic syndrome MetSthe nature of these associations remains unclear. This study aimed to investigate the association of sedentary time with cardiometabolic health and examine the association of reallocating sedentary time to light physical activity LPA or moderate-vigorous physical activity MVPA on cardiometabolic health in Japanese adults.
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