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Abstract
Compared to lean counterparts, overweight/obese individuals rely less on lipid during fasting. This deficiency has been implicated in the association between overweight/obesity and blunted insulin signaling via elevated intramuscular triglycerides. However, the capacity for overweight/obese individuals to use lipid during exercise is unclear. This review was conducted to formulate a consensus regarding the influence of overweight/obesity on exercise lipid use. PubMed, ProQuest, ISI Web of Science, and Cochrane Library databases were searched. Articles were included if they presented original research on the influence of overweight/obesity on exercise fuel use in generally healthy sedentary adults. Articles were excluded if they assessed older adults, individuals with chronic disease, and/or exercise limitations or physically-active individuals. The search identified 1205 articles with 729 considered for inclusion after duplicate removal. Once titles, abstracts, and/or manuscripts were assessed, 24 articles were included. The preponderance of evidence from these articles indicates that overweight/obese individuals rely on lipid to a similar extent during exercise. However, conflicting findings were found in eight articles due to the outcome measure cited, participant characteristics other than overweight/obesity and characteristics of the exercise bout(s). We also identified factors other than body fatness which can influence exercise lipid oxidation that should be controlled in future research.
Highlights
Obesity [1] and type 2 diabetes (T2D) [2] are prevalent conditions
Thirteen studies provide no evidence of altered exercise lipid oxidation for overweight/obese compared to normal-weight individuals [23,26,41,42,43,45,46,48,50,53,56,57,58]
The contention that there is a lipid-oxidation decrement associated with overweight/obesity comes predominantly from research indicating that obese individuals demonstrate lower rates of lipid oxidation during fasting when lipid use should predominate
Summary
Obesity [1] and type 2 diabetes (T2D) [2] are prevalent conditions. The insulin resistance (IR) that often predates T2D is linked with overweight/obesity; the mechanistic basis(es) underpinning this association is/are unclear with multiple candidate molecules, systems, and pathways potentially involved [3]. One theory implicates dysfunctional lipid metabolism based on the notion that excess accumulation of lipid in skeletal muscle (intramuscular triglyceride; IMTG) becomes ‘lipotoxic’ and perturbs the insulin signal transduction pathway [4]. It has long been known that IMTG levels are inversely related to insulin action [5]; the presence of elevated IMTG in endurance-trained athletes with high insulin sensitivity (the ‘athlete’s paradox’) indicates more than a simple cause-effect relationship [6]. Contrary to their experimental hypothesis, Amati et al showed that exercise-trained muscle does not possess lower levels of
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