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J Appl Physiol 98: 1612-1618, 2005. First published December 17, 2004; doi:10.1152/japplphysiol.00936.2004
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Energy deficit without reducing dietary carbohydrate alters resting carbohydrate oxidation and fatty acid availability

Jeffrey F. Horowitz, Amy E. Kaufman, Amanda K. Fox, and Matthew P. Harber

Division of Kinesiology, The University of Michigan, Ann Arbor, Michigan

Submitted 27 August 2004 ; accepted in final form 14 December 2004

Reduced carbohydrate (CHO) availability after exercise has a potent influence on the regulation of substrate metabolism, but little is known about the impact of fat availability and/or energy deficit on fuel metabolism when dietary CHO availability is not reduced. The purpose of this study was to determine the influence of a postexercise energy deficit, independent of CHO availability, on plasma substrate concentrations and substrate oxidation. Seven moderately trained men (peak oxygen uptake: 56 ± 2 ml·kg–1·min–1) performed exhaustive cycling exercise on two separate occasions. The two trials differed only by the meals ingested after exercise: 1) a high-fat diet designed to maintain energy balance or 2) a low-fat diet designed to elicit energy deficit. The CHO and protein contents of the diets were identical. The next morning, we measured plasma substrate and insulin concentrations and CHO oxidation, and we obtained muscle biopsies from the vastus lateralis for measurement of pyruvate dehydrogenase kinase (PDK)-2 and PDK-4 mRNA expression by using RT-PCR. Despite identical blood glucose (5.0 ± 0.1 and 4.9 ± 0.1 mM) and insulin (7.9 ± 1.1 and 8.4 ± 0.9 µU/ml) concentrations, plasma fatty acid and glycerol concentrations were elevated three- to fourfold during energy deficit compared with energy balance and CHO oxidation was 40% lower (P < 0.01) the morning after energy deficit compared with energy balance (328 ± 69 and 565 ± 89 µmol/min). The lower CHO oxidation was accompanied by a 7.3 ± 2.5-fold increase in PDK-4 mRNA expression after energy deficit (P < 0.05), whereas PDK-2 mRNA was similar between the trials. In conclusion, energy deficit increases fatty acid availability, increases PDK-4 mRNA expression, and suppresses CHO oxidation even when dietary CHO content is not reduced.

caloric restriction; pyruvate dehydrogenase kinase; fatty acid; exercise



Address for reprint requests and other correspondence: J. F. Horowitz, Div. of Kinesiology, The Univ. of Michigan, 401 Washtenaw Ave., Ann Arbor, MI 48109-2214 (E-mail: jeffhoro{at}umich.edu)




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