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OBJECTIVE-Obesity and diabetes are characterized by the incapacity to use fat as fuel. We hypothesized that this reduced fat oxidation is secondary to a sedentary lifestyle.
RESEARCH DESIGN AND METHODS-We investigated the effect of a 2-month bed rest on the dietary oleate and palmitate trafficking in lean women (control group, n = 8) and the effect of concomitant resistance/aerobic exercise training as a countermeasure (exercise group, n = 8). Trafficking of stable isotope-labeled dietary fats was combined with muscle gene expression and magnetic resonance imaging-derived muscle fat content analyses.
RESULTS-In the control group, bed rest increased the cumulative [1-^sup 13^C] oleate and [d^sub 31^]palmitate appearance in triglycerides (37%, P = 0.009, and 34%, P = 0.016, respectively) and nonesterified fatty acids (NEFAs) (37%, P = 0.038, and 38%, P = 0.002) and decreased muscle lipoprotein lipase (P = 0.043) and fatty acid translocase CD36 (P = 0.043) mRNA expressions. Plasma NEFA-to-triglyceride ratios for [1-^sup 13^C]oleate and [d^sub 31^]palmitate remained unchanged, suggesting that the same proportion of tracers enters the peripheral tissues after bed rest. Bed rest did not affect [1-^sup 13^C]oleate oxidation but decreased [d^sub 31^]palmitate oxidation by -8.2 ± 4.9% (P < 0.0001). Despite a decreased spontaneous energy intake and a reduction of 1.9 ± 0.3 kg (P = 0.001) in fat mass, exercise training did not mitigate these alterations but partially maintained fat-free mass, insulin sensitivity, and total lipid oxidation in fasting and fed states. In both groups, muscle fat content increased by 2.7% after bed rest and negatively correlated with the reduction in [d^sub 31^]palmitate oxidation (r^sup 2^ = 0.48, P = 0.003).
CONCLUSIONS-While saturated and monounsaturated fats have similar plasma trafficking and clearance, physical inactivity affects the partitioning of saturated fats toward storage, likely leading to an accumulation of palmitate in muscle fat. Diabetes 58:367-376, 2009
In our search of the environmental factors that fuelled the pandemic of obesity, we face a paradox. Although sedentary lifestyle has been highlighted for decades as one of the main factors triggering weight gain, the physiology of physical inactivity has received little attention (1). Clearly, the causal relationships between sedentary behaviors and obesity are essentially based on epidemiological studies or on the indirect beneficial effects of exercise training (2). None of these studies provide...