PMID- 15608091
OWN - NLM
STAT- MEDLINE
DCOM- 20050818
LR  - 20130926
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 98
IP  - 5
DP  - 2005 May
TI  - Energy deficit without reducing dietary carbohydrate alters resting carbohydrate 
      oxidation and fatty acid availability.
PG  - 1612-8
AB  - 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 
      microU/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 micromol/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.
FAU - Horowitz, Jeffrey F
AU  - Horowitz JF
AD  - Division. of Kinesiology, The University of Michigan, 401 Washtenaw Ave., Ann 
      Arbor, MI 48109-2214, USA. jeffhoro@umich.edu
FAU - Kaufman, Amy E
AU  - Kaufman AE
FAU - Fox, Amanda K
AU  - Fox AK
FAU - Harber, Matthew P
AU  - Harber MP
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20041217
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Dietary Carbohydrates)
RN  - 0 (Fatty Acids)
SB  - IM
MH  - Adult
MH  - Dietary Carbohydrates/*metabolism
MH  - Energy Metabolism/*physiology
MH  - Fatty Acids/*metabolism
MH  - Humans
MH  - Male
MH  - Oxidation-Reduction
MH  - Physical Exertion/*physiology
EDAT- 2004/12/21 09:00
MHDA- 2005/08/19 09:00
CRDT- 2004/12/21 09:00
PHST- 2004/12/21 09:00 [pubmed]
PHST- 2005/08/19 09:00 [medline]
PHST- 2004/12/21 09:00 [entrez]
AID - 00936.2004 [pii]
AID - 10.1152/japplphysiol.00936.2004 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2005 May;98(5):1612-8. doi: 
      10.1152/japplphysiol.00936.2004. Epub 2004 Dec 17.