Metabolic disruptions induced by reduced ambulatory activity in free-living humans

Abstract

.-Physical inactivity likely plays a role in the development of insulin resistance and obesity; however, direct evidence is minimal and mechanisms of action remain unknown. Studying metabolic outcomes that occur after transitioning from higher to lower levels of physical activity is the best tool to answer these questions. Previous studies have successfully used more extreme models of inactivity, including bed rest, or the cessation of exercise in highly trained endurance athletes, to provide novel findings. However, these models do not accurately reflect the type of inactivity experienced by a large majority of the population. Recent studies have used a more applicable model in which active (ϳ10,000 steps/day), healthy young controls are asked to transition to an inactive lifestyle (ϳ1,500 steps/day) for a 14-day period. The transition to inactivity resulted in reduced insulin sensitivity and increased central adiposity. This review will discuss the outcomes of these studies, their implications for the cause/effect relationship between central adiposity and insulin resistance, and provide rationale for why inactivity induces these factors. In addition, the experimental challenges of directly linking acute responses to inactivity to chronic disease will also be discussed. inactivity; skeletal muscle; insulin sensitivity; obesity TYPE 2 DIABETES AND CENTRAL OBESITYOBESITY and obesity-associated metabolic diseases are increasing at epidemic rates. The World Health Organization's (WHO) latest estimates indicate that ϳ400 million adults were obese (body mass index Ͼ 30 kg/m 2 ) globally in 2006 and predict that these numbers will rise to 700 million by the year 2015. This increase in obesity parallels a dramatic increase in the number of persons diagnosed with Type 2 diabetes (T2D). In 2009, WHO estimated that more than 200 million people worldwide have T2D, and it is estimated that worldwide T2D rates will double between the year 2000 and 2030 (46). Although excess adiposity in all regions can cause metabolic consequences, excess central adiposity (visceral adiposity) is most tightly linked to the development of T2D (1,3,9,12,13). The current dogma implies that central adiposity first develops, leading to inflammation and/or an increased storage of ectopic lipids in skeletal muscle and liver, which induces insulin resistance and ultimately leads to T2D (31), but this order of events has never been proven (33). The causes of both increased central obesity and type 2 diabetes are undoubtedly multifactorial and complex; however, we (5, 43) and others (15, 23) believe that a lack of regular exercise, or physical inactivity, plays a fundamental role. This hypothesis is backed by epidemiological evidence suggesting that physical inactivity plays a causal role in the development of T2D (20, 21) and obesity (10) while regular physical activity significantly lowers risk (2, 23, 24) for both conditions. While these studies strongly associate inactivity to T2D and obesity, historically, there have been a limited number of stu...

Short-term decreased physical activity with increased sedentary behaviour causes metabolic derangements and altered body composition: effects in individuals with and without a first-degree relative with type 2 diabetes

“…These changes are small, but nevertheless large enough to be clinically significant and thus to pose a serious health threat over a longer term [31]. The metabolic sequelae of these changes include whole-body insulin resistance and dyslipidaemia (increased triacylglycerol and LDL-cholesterol).…”

The utility of a protection motivation theory framework for understanding sedentary behavior

“…This can lead to diseases of the heart. This definition is supported by the literature including systematic reviews (Hamburg et al, 2007;Proper, Singh, Van Mechelen, & Chinapaw, 2011;Saunders, Larouche, Colley, & Tremblay, 2012;Thyfault & Krogh-Madsen, 2011), as well as findings from a focus group that was conducted prior to the study to determine the relevancy of the threat to the sample age group. The reading level for this definition (grade 6.6) was suitable for the general population based on guidelines outlined by DeVellis (2012) and the Flesch grade level readability formula (http://readibility-score.com, 2015).…”

Towards the minimal amount of exercise for improving metabolic health: beneficial effects of reduced-exertion high-intensity interval training

“…The metabolic causes of insulin resistance are numerous and complex but there is accumulating evidence that physical inactivity may be the major initiating factor (Thyfault and Krogh-Madsen 2011), whereas regular exercise is associated with improved muscle insulin sensitivity and thus represents an effective strategy to prevent T2D (Hawley and Gibala 2009). …”

“…In fact, it is now recognised that exercise, rather than just being a useful strategy for improving health, is actually essential for good metabolic and cardiovascular function, of which insulin action is a key component (Thyfault and Krogh-Madsen 2011;Booth et al 2002). With this in mind, the finding that ~6 out of 10 men and ~7 out of 10 women in the UK are currently not achieving the (low) minimum recommended levels of physical activity is a major concern (Allender et al 2008).…”