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Am J Physiol Endocrinol Metab 286: E354-E362, 2004. First published November 18, 2003; doi:10.1152/ajpendo.00301.2003
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Excess body fat in men decreases plasma fatty acid availability and oxidation during endurance exercise

Bettina Mittendorfer, David A. Fields, and Samuel Klein

Center for Human Nutrition and Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110

Submitted 7 July 2003 ; accepted in final form 11 November 2003

The effect of relative body fat mass on exercise-induced stimulation of lipolysis and fatty acid oxidation was evaluated in 15 untrained men (5 lean, 5 overweight, and 5 obese with body mass indexes of 21 ± 1, 27 ± 1, and 34 ± 1 kg/m2, respectively, and %body fat ranging from 12 to 32%). Palmitate and glycerol kinetics and substrate oxidation were assessed during 90 min of cycling at 50% peak aerobic capacity (O2 peak) by use of stable isotope-labeled tracer infusion and indirect calorimetry. An inverse relationship was found between %body fat and exercise-induced increase in glycerol appearance rate relative to fat mass (r2 = 0.74; P < 0.01). The increase in total fatty acid uptake during exercise [(µmol/kg fat-free mass) x 90 min] was ~50% smaller in obese (181 ± 70; P < 0.05) and ~35% smaller in overweight (230 ± 71; P < 0.05) than in lean (354 ± 34) men. The percentage of total fatty acid oxidation derived from systemic plasma fatty acids decreased with increasing body fat, from 49 ± 3% in lean to 39 ± 4% in obese men (P < 0.05); conversely, the percentage of nonsystemic fatty acids, presumably derived from intramuscular and possibly plasma triglycerides, increased with increasing body fat (P < 0.05). We conclude that the lipolytic response to exercise decreases with increasing adiposity. The blunted increase in lipolytic rate in overweight and obese men compared with lean men limits the availability of plasma fatty acids as a fuel during exercise. However, the rate of total fat oxidation was similar in all groups because of a compensatory increase in the oxidation of nonsystemic fatty acids.

obesity; lipolysis; substrate



Address for reprint requests and other correspondence: S. Klein, Center for Human Nutrition, Dept. of Internal Medicine, Washington Univ. School of Medicine, 660 S. Euclid Ave; Campus Box 8031, St. Louis, MO 63110 (E-mail: sklein{at}im.wustl.edu).




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