by Monica Mollica
Part 1 of 3 on the deleterious effects of too much sitting
Are you struggling to lose that extra flab and all those nasty calories that seem to be glued to your waistline? Do you ever wonder why, despite your hard training and dieting, you still have those annoying love handles? Then maybe you should try to implement the NEAT way to fat loss…
NEAT – the ignored component of physical activity, metabolic regulation and total daily caloric expenditure
When it comes to fat loss, a key is to increase your energy expenditure. Therefore, the traditional prescription for fat loss has focused on exercise as a means of revving up your energy expenditure to burn off excess fat. While exercise (both cardio and weight lifting) is essential for fat loss, there is one other less known, albeit important, component of total daily energy expenditure that could be the missing link in your fat loss endeavor. Enter NEAT…
NEAT stands for non-exercise activity thermogenesis (or non-exercise activity energy expenditure). NEAT is the energy expenditure induced by non-exercise bodily movements in daily life, i.e. lifestyle embedded physical activity [1].
The term “physical activity” represents the full continuum of movement, with “exercise” being a subcategory representing the higher end of this continuum [2]. The remainder that falls below the exercise threshold is “non-exercise physical activity”, and is illustrated in the graphic below [3].
Sedentary behaviors (typically in the contexts of television viewing, computer use, workplace sitting, and time spent commuting) are a new focus for research in the physical activity and health field [4-8]. As will be outlined below, emerging evidence is showing that there is a physiological distinction between too little exercise vs. too much sitting, i.e. exercise deficiency and sitting excess are each unique states with difference health consequences.
Sedentary behaviors include sitting during commuting, in the workplace and domestic environment, and during leisure time. Actually, the word “sedentary” comes from the Latin “sedere”, which means “to sit’. Sedentary behaviors, a.k.a inactivity, are defined by both posture (sitting or reclining) and low energy expenditure; they don’t elevate energy expenditure substantially above the resting level [4, 7-10]. In other words, sedentary “activities” incur an energy expenditure at the level close to 1 – 1.5 metabolic equivalent unit (METs) [11-13]. This can be compared to moderate/vigorous physical activity, or “exercise” such as brisk walking or running, which elevates energy expenditure 3-10 times resting metabolic rate, i.e. 3–10 METs [12, 13].
One MET is the energy cost of resting quietly, often defined as 1 cal/kg/hour (or 1 cal per 2.2 lb per hour) [11, 13]. To find out your “resting hourly burn rate”, i.e. how many calories you burn resting per hour, just divide your weight in lb by 2.2. For ex. a person weighing 150 lb will burn 68 cal (150 lb / 2.2), another person weighing 220 lb will burn 100 cal (220 lb / 2.2). It’s a rough estimate (actually an over-estimate by some 20% [11]), but you get the idea.
Different activities elevate caloric expenditure over resting level as follows: [5]
Sitting still 3.7 %
Sitting while fidgeting 54 %
Standing still 13 %
Standing while fidgeting 94 %
Slow strolling 154 %
Fast strolling 202 %
Even though standing still doesn’t markedly elevate caloric expenditure over sitting still, it is not considered to be a sedentary activity because muscle activity in the legs during standing is 2.5 times higher than during sitting [14]. During standing, postural muscles (predominantly in the legs) are continually contracting to keep the body upright and maintain balance. This muscle activity during standing in turn stimulates an enzyme called muscle lipoprotein lipase (LPL) [10]. LPL is the rate-limiting enzyme for the breakdown of fats circulating in the blood stream, and uptake of free fatty acids into muscle for use as energy (that is, fat burning) [10, 15-18]. LPL has been studied heavily because this enzyme has a central role in several aspects of fat metabolism [17, 18]. LPL also has a major influence on the partitioning of fatty acids between different tissues, plasma cholesterol metabolism and the subsequent downstream intracellular effects related to fat availability [17, 18]. Thus, the differences between standing and sitting aren’t trivial. More on muscle LPL below.
NEAT vs. Sitting Time
Inactivity and non-exercise activity have gained growing attention because the proportion of time spent doing purposeful exercises usually make up only a fraction of the day, leaving much time for sedentary activities [10]. Assuming 8 hours of sleep, we have 16 hours per day at our disposal. Studies that objectively measured physical activity show that people in the US on average spend about 8 hours daily, i.e. half of their waking time, being sedentary [19]. Those employed in sedentary occupations are sedentary for approximately 11 hours per day [20]. The graphic below illustrates the major contexts for sedentary behavior and their distribution over a typical adult’s waking hours [3].
Therefore, it is no wonder that individual differences in light physical activity outside of intense exercise have greater influence on inactivity time than the time we spend exercising [14]. This was confirmed in another study where some individuals participated in substantial amounts of intense exercise but otherwise had a relatively low overall daily physical activity energy expenditure [21]. Thus, even when adhering to the exercise guidelines recommending at least 30 min/day of moderate-to-vigorous intensity activity at least 5 days per week [22], this does not automatically mean that people will not engage in excessive “baseline” sitting over the rest of the day. Because of this large amount of time we have at our disposal outside of formal exercise time, whether you spend most of your non-exercising time sitting, reclining, or standing and moving around, is a significant issue. this is underscored by the finding that 1 hour of daily physical exercise cannot compensate the negative effects of inactivity on insulin level and blood lipids if the rest of the day is spent sitting [23]. And as outlined below, too much inactive sitting can be what’s missing in your fat loss equation…
NEAT – small things add up fast in favor of fat gain or fat loss
This is true for both credit cards and energy expenditure. Energy expended during the day, outside of typical exercise (standing, fidgeting like movements while seated and while standing, ambulation) can vary by up to 2000 calories per day between individuals [21, 24, 25], and thus may substantially contribute to the daily energy expenditure [5, 21, 26]. This can be explained by the very large variability between people in total inactivity times, ranging from 40 to 91% [14].
It have been estimated that energy demands have dropped by over 400-500 cal/day due to occupational and domestic computerized environments, mechanization, and TV/media [27]. Therefore, even one hour of daily exercise might not be enough to achieve fat loss or fat gain prevention [28, 29].
What does research say about NEAT as a tool to keep body fat under control?
Caloric expenditure
To examine NEAT’s role in obesity, a study recruited 10 lean and 10 mildly obese sedentary people and measured their body postures and movements every half-second for 10 days [30]. The measurements were made using micro-sensors that subjects wore under their clothes and allowed body postures and movements to be accurately measured. It was found that obese individuals were seated 2.7 hours more per day than lean individuals. It was concluded that if obese individuals adopted the NEAT-enhanced behaviors of their lean peers, they might expend an additional 350 calories per day [30], as illustrated in the following diagram [31].
This finding was confirmed in a later study which compared activity energy expenditure and daily activity patterns (using accelerometers) in lean and obese people [32]. It was found that obese women sat 2.6 h more each day (12.7 h vs. 10.1), stood 2 h less (2.7 h vs. 4.7 h) and spent half as much time in moving around activity than lean women (2.6 h vs. 5.4 h) [32]. After controlling for differences in fat-free mass, the lean subjects expended 400 calories more per day than the less active and more sedentary obese subjects [32].
It is interesting to note that this difference in magnitude of caloric expenditure between NEATers and non-NEATers is about the same as the formal exercise prescription dose that obese people are urged to adopt in order to induce a negative energy balance and fat loss (2500 cal/wk or 360 cal/day, corresponding to 75 min of brisk walking/d) [33, 34]. Thus, NEATing like standing/ambulating/fidgeting is of substantial importance for controlling body fat.
Interesting Statistics
Another study found that time spent watching TV is associated with risk of obesity and type 2 diabetes [35]. After adjusting for age, smoking, exercise levels and dietary factors, the following risk percentages were documented:
Each 2 hours/d increment in TV watching is associated with:
– 23% increase in obesity and a 14% increase in risk of diabetes.
Each 2 hours/d increment in sitting at work is associated with:
– 5% increase in obesity and a 7% increase in diabetes.
In contrast, standing or walking around at home (2 hr/d) is associated with:
– 9% reduced risk for obesity and a 12% reduced risk for diabetes.
Each 1 hour per day of brisk walking is associated with:
24% reduced risk for obesity and a 34% reduced risk for diabetes.
In this study population, it was estimated that 30% of new cases of obesity and 43% (95% CI, 32%-52%) of new cases of diabetes during a 6 year follow up could be prevented by adopting a relatively active lifestyle (less than 10 hr/wk of TV watching and at least 30 min/day of brisk walking) [35]. Many other studies support the association between sitting time and body fat gain [29, 36-43].
Waistline
Sitting time is also deleteriously associated with a number of cardiovascular risk factors, including waist circumference, blood glucose, and blood fats [44-46]. Each 10% increase in sitting time has been associated with a 1.2 inch (3.1cm) larger waist circumference [44]. The association between sedentary time and waist circumference is largely independent of exercise participation [46].waist-measuring-man
Not just total sitting time, but also breaks in sitting time are important. Compared to those who during the day have fewest breaks per hour of sitting, those with the breaks per hour of sitting have been found to have1.6 – 2.34 inches (4.1 – 5.95 cm) smaller waist circumferences [45, 47]. Of importance to note is that a break could be as short as 1 min and doesn’t have to be intense type “exercise”, suggesting that regular breaks from sitting time can be easily implemented both during the working day and at home. A walk to the kitchen to take a sip of water, or walking around while drinking your coffee/tee, might be enough.Thus, patterns of sedentary time accumulation are important in addition to total amount of sedentary time.
NEAT – your weapon against vacation and holiday fat gain
We all know about those lucky folks who magically appear to resist fat gain with overeating. These subjective observations have been confirmed in studies that documented a several-fold inter-individual variation in fat accumulation with overeating [48-50]. But what is it that makes those people resistant to fat gain?
To answer this question, a study was designed to find out if there is a component of energy expenditure that shows enough variability to account for the variability in resistance to fat gain during overfeeding [51]. Non-obese volunteers were fed 1000 calories per day in excess of weight-maintenance requirements for 8 weeks. It was found that fat gain varied over 10-fold, ranging from a gain of only 0.8 lb (0.36 kg) to a gain of 9.3 lb (4.23 kg), and that it was changes in NEAT that accounted for this enormous difference. The maximum increase in NEAT was close to 700 kcal/day, and could be accounted for by an increase in strolling-equivalent activity by about 15 min/hour during waking hours.
It could be argued that it is the obese state that causes declines in NEAT. In order to find out whether differences in NEAT are a cause or consequence of obesity, the same obese subjects were put on a diet for 2 months which caused a weight loss of 17.6 lb (8 kg) [51]. However, despite the weight loss, the original NEAT activities were maintained. This indicates that NEAT can be an inherent trait that causes some people to be more spontaneously active than others, and that a low NEAT that contributes to obesity.
The fact that NEAT is a mediator of the resistance to fat gain with overfeeding underscores its power. When people overeat, activation of NEAT dissipates a large part of the excess energy to preserve leanness, while failure to activate NEAT results in fat gain. Those who with overfeeding increase their NEAT the most, gain the least fat. Those who with overfeeding do not increase their NEAT gain the most fat and are predisposed to become obese.
Because the human genetic code has not changed during the past 50 years while obesity has become epidemic, obesity may in part be a consequence of enhanced responsiveness to environmental cues to be seated. But just because you don’t have an innate NEAT drive doesn’t mean you’re lost. Knowing the importance of NEAT as an anti-fat gain weapon, you can cognitively override your gravitation to the chair and consciously decide to simply move around more in your daily life.
Sitting – not just simply the opposite of exercising
Intuitively, sitting might be interpreted as the opposite of exercise, or lack of exercise. However, these two different behaviors each have unique effects, and therefore have to be treated separately. One molecular reason to maintain daily low-intensity ambulating activity is its importance for LDL regulation [15], as mentioned above. Muscle LPL activity is especially important since it is a prerequisite for the uptake and subsequent burning of fat that has been released from body fat stores.
What is intriguing is that sitting, low intensity ambulatory physical activity and high intensity exercise all have difference effects on muscle LPL activity [10]. For example, the reduction in muscle LPL activity in response to sitting is largely restricted to oxidative muscle fibers, while increases in LPL activity in response to exercise is mainly occurring in glycolytic muscle fibers. Further, the relative decreases in LPL activity seen in oxidative fibers following sitting are more than 4-fold greater than the increases observed in glycolytic fibers following vigorous exercise [10, 15, 52].
It is notable that almost all of the LPL activity normally present in the capillaries (small blood vessels) of muscles is dependent upon low-intensity ambulatory activity [15]. Muscle LPL activity decreases during inactivity and is very sensitive to non-fatiguing low intensity contractions, which rapidly reverse the sitting induced reduction in LPL activity [15]. Thus, it is a misconception to think that ordinary spontaneous low-grade movements and weight-bearing activities in daily life are insufficient to elicit specific and notable physiological effects. This is underscored by the finding that those who do not exercise but have a high NEAT have a larger reduction in mortality risk thank those who partake in exercise but have low NEAT [53].
This means that an “active couch potato” might actually be healthier than a “lazy exerciser”. Further support for the independence of sitting and exercise habits in daily life is that the correlation between the two is very weak [44], meaning that one doesn’t necessarily follow the other in the same direction. In other words, going to the gym is no excuse for spending the rest of your day on the couch.
Even if you exercise, sitting can be what’s halting your fat loss…
The fact that the mechanism linking LPL activity to sitting is distinct from that linking LPL activity to exercise, underscores the importance of viewing exercise and sitting as two separate factors influencing fat loss efforts and health outcomes. Too much sitting is not the same as too little exercise.lazy-exerciser
This is supported by evidence showing that sitting time increases the risk for expanded waistlines, obesity, insulin resistance, cardio-metabolic disturbances, cardiovascular disease and all-cause mortality independent of participation in exercise [3, 7, 28, 29, 35, 42, 44, 47, 54-68].
For example, even among the most active people (those exercising at moderate-vigorous intensity for 60 min/day), spending 2- 4 hours per day in sedentary time (television viewing and screen-based entertainment) more than doubles the risk for obesity compared to spending less than 2 hours/day in sedentary pursuits [69]. Compared with people who watch television or videos or use a computer less than 1 h/d outside of work, the risk for the metabolic syndrome (which is a constellation of risk factors, including an expanded waistline) increases by 37 %, 70 % and 210 % for 2, 3 and 4 or more hours/day respectively, regardless of physical activity level [61].
Because the time spent in sedentary behaviors has been shown to be independent of exercise in population research, a recent study sought to examine within an individual whether exercise alters the time of muscular inactivity within his/her usual daily life [70]. Quadriceps and hamstring muscle activities (EMG recordings) and heart rate were measured during 6 days of normal daily living of ordinary people. Reported exercises varied from Nordic walking (aka. pole walking, a high intensity type of walking) to strength training and ball games lasting 30-150 min. It was found that muscular inactivity, defined individually below that measured during standing, comprised 72% of the day without exercise, and 68% of the day with exercise. This difference was not statistically significant (which means it could have occurred by chance). Also, duration of exercise was not correlated with inactivity time. The conclusion from this study is that exercise for fitness, regardless of its duration, does not decrease the inactivity time during normal daily life [70]. Bearing in mind the importance of muscle contractions for LPL activity, this is a very important finding.
Bottom Line
While diet composition has an important impact on nutrient partitioning and the relative amount of body fat that is gained or lost during overfeeding or dieting, the total energy expenditure in relation to you caloric intake is a determining factor in your fat loss efforts. However, sitting time is important not just because it robs you of energy expenditure opportunities. It also has unique molecular level effects that are separate from exercise. The finding that that exercising for fitness does not decrease the inactivity time during normal daily life [70] underscores the importance of increasing daily non-exercise activities.
Evidence is rapidly mounting to suggest that long periods of sitting time have adverse metabolic and health consequences that are not necessarily compensated for by typical exercise. Therefore, if you are serious about losing fat, reducing sitting time, both at work and at home, is as important as is your exercise. Struggles with fat loss are not just about “too little exercise”. Mounting studies are showing the importance of “too much sitting”, and prominent researchers have stated that attacking physical inactivity and excessive sitting could help the battle against obesity [68]. So don’t be surprised when you see public health media campaigns urging us to get our lazy butts off the chairs. Just remember where you read about it first!
Backed up by new scientific research, the new activity prescription for fat loss is “don’t just sit there – stand up and move, move around, more, more often”. Start turning circles in your typical fat loss routine and you might soon see those calories falling off your waistline. Injecting NEAT into your daily life outside the gym can really have a huge impact on your end-of-day caloric burn bottom line, your metabolism, resistance to fat gain, and ultimately on your fat loss success.
In part 2 of this series I will cover the detrimental effects of too much sitting on metabolic outcomes, cardiovascular disease risk factors, diabetes, cancer and mortality. In part 3 you will get lots of practical advice and tactics on how to inject non-exercise physical activity into your daily life and turn yourself into a fat burning NEAT-o-type machine. Stay tuned!
About the Author:
————————————–
Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.
Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an young teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a BSc and MSc with a major in Nutrition at the University.
During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.
It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to health, fitness, bodybuilding, anti-aging and longevity.
References:
1. Levine, J., et al., Measurement of the components of nonexercise activity thermogenesis. Am J Physiol Endocrinol Metab, 2001. 281(4): p. E670-5.
2. Caspersen, C.J., K.E. Powell, and G.M. Christenson, Physical activity, exercise, and physical fitness: definitions and distinctions for health-related research. Public Health Rep, 1985. 100(2): p. 126-31.
3. Tremblay, M.S., et al., Physiological and health implications of a sedentary lifestyle. Appl Physiol Nutr Metab, 2010. 35(6): p. 725-40.
4. Hamilton, M.T., et al., Too little exercise and too much sitting: Inactivity physiology and the need for new recommendations on sedentary behavior. Curr. Cardiovasc. Risk Rep., 2008. 2(4): p. 292-298.
5. Levine, J.A., S.J. Schleusner, and M.D. Jensen, Energy expenditure of nonexercise activity. Am J Clin Nutr, 2000. 72(6): p. 1451-4.
6. Owen, N., A. Bauman, and W. Brown, Too much sitting: a novel and important predictor of chronic disease risk? Br J Sports Med, 2009. 43(2): p. 81-3.
7. Owen, N., et al., Too much sitting: the population health science of sedentary behavior. Exerc Sport Sci Rev, 2010. 38(3): p. 105-13.
8. Pate, R.R., J.R. O’Neill, and F. Lobelo, The evolving definition of “sedentary”. Exerc Sport Sci Rev, 2008. 36(4): p. 173-8.
9. Hamilton, M.T., D.G. Hamilton, and T.W. Zderic, Exercise physiology versus inactivity physiology: an essential concept for understanding lipoprotein lipase regulation. Exerc Sport Sci Rev, 2004. 32(4): p. 161-6.
10. Hamilton, M.T., D.G. Hamilton, and T.W. Zderic, Role of low energy expenditure and sitting in obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease. Diabetes, 2007. 56(11): p. 2655-67.
11. Byrne, N.M., et al., Metabolic equivalent: one size does not fit all. J Appl Physiol, 2005. 99(3): p. 1112-9.
12. Ainsworth, B.E., et al., 2011 Compendium of Physical Activities: a second update of codes and MET values. Med Sci Sports Exerc, 2011. 43(8): p. 1575-81.
13. Ainsworth, B.E., et al., Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc, 2000. 32(9 Suppl): p. S498-504.
14. Tikkanen, O., et al., Muscle activity and inactivity periods during normal daily life. PLoS One, 2013. 8(1): p. e52228.
15. Bey, L. and M.T. Hamilton, Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity. J Physiol, 2003. 551(Pt 2): p. 673-82.
16. Zderic, T.W. and M.T. Hamilton, Physical inactivity amplifies the sensitivity of skeletal muscle to the lipid-induced downregulation of lipoprotein lipase activity. J Appl Physiol, 2006. 100(1): p. 249-57.
17. Goldberg, I.J. and M. Merkel, Lipoprotein lipase: physiology, biochemistry, and molecular biology. Front Biosci, 2001. 6: p. D388-405.
18. Olivecrona, T., et al., Lipoprotein lipase: regulation and role in lipoprotein metabolism. Proc Nutr Soc, 1997. 56(2): p. 723-9.
19. Matthews, C.E., et al., Amount of time spent in sedentary behaviors in the United States, 2003-2004. Am J Epidemiol, 2008. 167(7): p. 875-81.
20. Tudor-Locke, C., et al., Time spent in physical activity and sedentary behaviors on the working day: the American time use survey. J Occup Environ Med, 2011. 53(12): p. 1382-7.
21. Thompson, D. and A.M. Batterham, Towards integrated physical activity profiling. PLoS One, 2013. 8(2): p. e56427.
22. Services, U.D.o.H.a.H., Physical Activity Guidelines for Americans 2008, 2008: Available at: http://www.health.gov/paguidelines/guidelines/default.aspx [accessed 3.29.13].
23. Duvivier, B.M., et al., Minimal intensity physical activity (standing and walking) of longer duration improves insulin action and plasma lipids more than shorter periods of moderate to vigorous exercise (cycling) in sedentary subjects when energy expenditure is comparable. PLoS One, 2013. 8(2): p. e55542.
24. Black, A.E., et al., Human energy expenditure in affluent societies: an analysis of 574 doubly-labelled water measurements. Eur J Clin Nutr, 1996. 50(2): p. 72-92.
25. Coward, W.A., Contributions of the doubly labeled water method to studies of energy balance in the Third World. Am J Clin Nutr, 1998. 68(4): p. 962S-969S.
26. Levine, J.A., et al., Non-exercise activity thermogenesis: the crouching tiger hidden dragon of societal weight gain. Arterioscler Thromb Vasc Biol, 2006. 26(4): p. 729-36.
27. James, W.P., The fundamental drivers of the obesity epidemic. Obes Rev, 2008. 9 Suppl 1: p. 6-13.
28. Bauman, A., et al., Leisure-time physical activity alone may not be a sufficient public health approach to prevent obesity–a focus on China. Obes Rev, 2008. 9 Suppl 1: p. 119-26.
29. Raynor, D.A., et al., Television viewing and long-term weight maintenance: results from the National Weight Control Registry. Obesity (Silver Spring), 2006. 14(10): p. 1816-24.
30. Levine, J.A., et al., Interindividual variation in posture allocation: possible role in human obesity. Science, 2005. 307(5709): p. 584-6.
31. Ravussin, E., Physiology. A NEAT way to control weight? Science, 2005. 307(5709): p. 530-1.
32. Johannsen, D.L., et al., Differences in daily energy expenditure in lean and obese women: the role of posture allocation. Obesity (Silver Spring), 2008. 16(1): p. 34-9.
33. Schoeller, D.A., But how much physical activity? Am J Clin Nutr, 2003. 78(4): p. 669-70.
34. Jeffery, R.W., et al., Physical activity and weight loss: does prescribing higher physical activity goals improve outcome? Am J Clin Nutr, 2003. 78(4): p. 684-9.
35. Hu, F.B., et al., Television watching and other sedentary behaviors in relation to risk of obesity and type 2 diabetes mellitus in women. JAMA, 2003. 289(14): p. 1785-91.
36. Ching, P.L., et al., Activity level and risk of overweight in male health professionals. Am J Public Health, 1996. 86(1): p. 25-30.
37. Coakley, E.H., et al., Predictors of weight change in men: results from the Health Professionals Follow-up Study. Int J Obes Relat Metab Disord, 1998. 22(2): p. 89-96.
38. Ball, K., W. Brown, and D. Crawford, Who does not gain weight? Prevalence and predictors of weight maintenance in young women. Int J Obes Relat Metab Disord, 2002. 26(12): p. 1570-8.
39. Brown, W.J., et al., Identifying the energy gap: magnitude and determinants of 5-year weight gain in midage women. Obes Res, 2005. 13(8): p. 1431-41.
40. Parsons, T.J., O. Manor, and C. Power, Television viewing and obesity: a prospective study in the 1958 British birth cohort. Eur J Clin Nutr, 2008. 62(12): p. 1355-63.
41. Hancox, R.J., B.J. Milne, and R. Poulton, Association between child and adolescent television viewing and adult health: a longitudinal birth cohort study. Lancet, 2004. 364(9430): p. 257-62.
42. Mummery, W.K., et al., Occupational sitting time and overweight and obesity in Australian workers. Am J Prev Med, 2005. 29(2): p. 91-7.
43. Biddle, S., et al., Sedentary behaviour and obesity: review of the current scientifıc evidence., S.a.F. Department of Health/Department for Children, Editor 2010: London.
44. Healy, G.N., et al., Objectively measured sedentary time, physical activity, and metabolic risk: the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Diabetes Care, 2008. 31(2): p. 369-71.
45. Healy, G.N., et al., Breaks in sedentary time: beneficial associations with metabolic risk. Diabetes Care, 2008. 31(4): p. 661-6.
46. Wijndaele, K., et al., Increased cardiometabolic risk is associated with increased TV viewing time. Med Sci Sports Exerc, 2010. 42(8): p. 1511-8.
47. Healy, G.N., et al., Sedentary time and cardio-metabolic biomarkers in US adults: NHANES 2003-06. Eur Heart J, 2011. 32(5): p. 590-7.
48. Bouchard, C. and A. Tremblay, Genetic influences on the response of body fat and fat distribution to positive and negative energy balances in human identical twins. J Nutr, 1997. 127(5 Suppl): p. 943S-947S.
49. Bouchard, C., et al., The response to long-term overfeeding in identical twins. N Engl J Med, 1990. 322(21): p. 1477-82.
50. Bouchard, C., et al., Sensitivity to overfeeding: the Quebec experiment with identical twins. Prog Food Nutr Sci, 1988. 12(1): p. 45-72.
51. Levine, J.A., N.L. Eberhardt, and M.D. Jensen, Role of nonexercise activity thermogenesis in resistance to fat gain in humans. Science, 1999. 283(5399): p. 212-4.
52. Hamilton, M.T., et al., Role of local contractile activity and muscle fiber type on LPL regulation during exercise. Am J Physiol, 1998. 275(6 Pt 1): p. E1016-22.
53. Matthews, C.E., et al., Influence of exercise, walking, cycling, and overall nonexercise physical activity on mortality in Chinese women. Am J Epidemiol, 2007. 165(12): p. 1343-50.
54. Helmerhorst, H.J., et al., Objectively measured sedentary time may predict insulin resistance independent of moderate- and vigorous-intensity physical activity. Diabetes, 2009. 58(8): p. 1776-9.
55. Dunstan, D.W., et al., Associations of TV viewing and physical activity with the metabolic syndrome in Australian adults. Diabetologia, 2005. 48(11): p. 2254-61.
56. Wijndaele, K., et al., Sedentary behaviour, physical activity and a continuous metabolic syndrome risk score in adults. Eur J Clin Nutr, 2009. 63(3): p. 421-9.
57. van der Ploeg, H.P., et al., Sitting time and all-cause mortality risk in 222 497 Australian adults. Arch Intern Med, 2012. 172(6): p. 494-500.
58. Martinez-Gonzalez, M.A., et al., Physical inactivity, sedentary lifestyle and obesity in the European Union. Int J Obes Relat Metab Disord, 1999. 23(11): p. 1192-201.
59. Salmon, J., et al., The association between television viewing and overweight among Australian adults participating in varying levels of leisure-time physical activity. Int J Obes Relat Metab Disord, 2000. 24(5): p. 600-6.
60. Jakes, R.W., et al., Television viewing and low participation in vigorous recreation are independently associated with obesity and markers of cardiovascular disease risk: EPIC-Norfolk population-based study. Eur J Clin Nutr, 2003. 57(9): p. 1089-96.
61. Ford, E.S., et al., Sedentary behavior, physical activity, and the metabolic syndrome among U.S. adults. Obes Res, 2005. 13(3): p. 608-14.
62. Dunstan, D.W., A.A. Thorp, and G.N. Healy, Prolonged sitting: is it a distinct coronary heart disease risk factor? Curr Opin Cardiol, 2011. 26(5): p. 412-9.
63. Dunstan, D.W., et al., Television viewing time and mortality: the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Circulation, 2010. 121(3): p. 384-91.
64. Owen, N., et al., Sedentary behavior: emerging evidence for a new health risk. Mayo Clin Proc, 2010. 85(12): p. 1138-41.
65. Healy, G.N., et al., Objectively measured light-intensity physical activity is independently associated with 2-h plasma glucose. Diabetes Care, 2007. 30(6): p. 1384-9.
66. Patel, A.V., et al., Leisure time spent sitting in relation to total mortality in a prospective cohort of US adults. Am J Epidemiol, 2010. 172(4): p. 419-29.
67. Katzmarzyk, P.T., et al., Sitting time and mortality from all causes, cardiovascular disease, and cancer. Med Sci Sports Exerc, 2009. 41(5): p. 998-1005.
68. Hawley, J.A. and D.W. Dunstan, The battle against obesity-attacking physical inactivity as a primary means of defense. Nat Clin Pract Endocrinol Metab, 2008. 4(10): p. 548-9.
69. Stamatakis, E., V. Hirani, and K. Rennie, Moderate-to-vigorous physical activity and sedentary behaviours in relation to body mass index-defined and waist circumference-defined obesity. Br J Nutr, 2009. 101(5): p. 765-73.
70. Finni, T., et al., Exercise for fitness does not decrease the muscular inactivity time during normal daily life. Scand J Med Sci Sports, 2012.
