Inactivity Causes Resistance to Improvements in Metabolism After Exercise

Edward F. Coyle; Heath M. Burton; Remzi Satiroglu


Exerc Sport Sci Rev. 2022;50(2):81-88. 

In This Article

Abstract and Introduction


Prolonged sitting prevents a 1-h bout of running from improving fat oxidation and reducing plasma triglycerides. This "exercise resistance" can be prevented by taking 8500 steps·d−1 or by interrupting 8 h of sitting with hourly cycle sprints. We hypothesize that there is an interplay between background physical activity (e.g., steps·d−1) and the exercise stimuli in regulating some acute and chronic adaptations to exercise.


Physical inactivity is becoming increasingly more prevalent as fewer people walk for transportation or perform manual labor and more people spend most of their waking hours sitting or standing, often behind a computer screen.[1,2] In fact, 77% of American adults and adolescents are considered to be physically "inactive," and they fail to meet the recommendations of the Physical Activity Guidelines of 150–300 min·wk−1 of moderate-intensity aerobic exercise or 75 min·wk−1 of vigorous-intensity exercise and 2 d·wk−1 performing strength training.[2–4] Because inactivity is associated with a significantly greater risk of cardiovascular disease, diabetes, and cancer,[5] it is imperative that we discover various types of exercise and strategies that can ward off the ailments caused by inactivity.[3,4] Physical inactivity is a global pandemic estimated to result in 5 million deaths per year.[6] The health care costs of inactivity are staggering and estimated to be 53.8 billion per year worldwide.[6]

The first issue to appreciate is that inactivity causes unique detrimental physiological effects and, as such, is more than simply the lack of exercise. It is our premise that inactivity before a 1-h bout of exercise produces unique molecular signals that stall metabolism, with one of its most obvious effects being a reduction in fat oxidation when fasted and during the 6-h period after ingesting a high-fat meal (Figure 1). Furthermore, elevated postprandial plasma triglyceride concentration (PPTG) after acute inactivity seems related to reduced triglyceride uptake by muscle (Figure 1) that has been associated with reduced muscle lipoprotein lipase (mLPL) activity.[7–11] As early as 1979, atherosclerosis, a major risk factor for cardiovascular disease, was described as a "postprandial phenomenon" driven by lipid accumulation in arteries because of prolonged elevation of plasma triglycerides after meals.[12] The discipline of "inactivity physiology" has been pioneered by the works of Frank Booth[13] and Marc Hamilton[7] and others.[14] The profound cardiovascular effects and exercise responses to 21 d of bed rest inactivity were first reported in 1968, with a 30-year follow-up study concluding that bed rest inactivity was comparable to three decades of aging.[15]

Figure 1.

Displayed is the experimental model used to detect exercise resistance. Walking more than 8500 steps·d−1 and performing a 1-h run on day 1 stimulates an increase in fat oxidation and a lowering of plasma triglyceride concentration (PPTG) on day 2. This is a "normal" and healthy response. However, if walking less than 5000 steps·d−1 on day 1, a 1-h run fails to stimulate an increase in fat oxidation or the lowering of PPTG on day 2. When inactive (<5000 steps·d−1), it seems that a 1-h run has no beneficial effect on fat metabolism or that the body is "resistant" to the normally beneficial effects of "exercise" (i.e., exercise resistance).