PMID- 20044472
OWN - NLM
STAT- MEDLINE
DCOM- 20100604
LR  - 20211020
IS  - 1522-1601 (Electronic)
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 108
IP  - 3
DP  - 2010 Mar
TI  - Energy deficit after exercise augments lipid mobilization but does not contribute 
      to the exercise-induced increase in insulin sensitivity.
PG  - 554-60
LID - 10.1152/japplphysiol.01106.2009 [doi]
AB  - The content of meals consumed after exercise can impact metabolic responses for 
      hours and even days after the exercise session. The purpose of this study was to 
      compare the effect of low dietary carbohydrate (CHO) vs. low energy intake in 
      meals after exercise on insulin sensitivity and lipid metabolism the next day. 
      Nine healthy men participated in four randomized trials. During the control trial 
      (CON) subjects remained sedentary. During the other three trials, subjects 
      exercised [65% peak oxygen consumption (Vo(2 peak)); cycle ergometer and 
      treadmill exercise] until they expended approximately 800 kcal. Dietary intake 
      during CON and one exercise trial (BAL) was designed to provide sufficient energy 
      and carbohydrate to maintain nutrient balance. In contrast, the diets after the 
      other two exercise trials were low in either CHO (LOW-CHO) or energy (LOW-EN). 
      The morning after exercise we obtained a muscle biopsy, assessed insulin 
      sensitivity (S(i); intravenous glucose tolerance test) and measured lipid 
      kinetics (isotope tracers). Although subjects were in energy balance during both 
      LOW-CHO and CON, the lower muscle glycogen concentration during LOW-CHO vs. CON 
      (402 +/- 29 vs. 540 +/- 33 mmol/kg dry wt, P < 0.01) coincided with a significant 
      increase in S(i) [5.2 +/- 0.7 vs. 3.8 +/- 0.7 (mU/l)(-1) x min(-1); P < 0.05]. 
      Conversely, despite ingesting several hundred fewer kilocalories after exercise 
      during LOW-EN compared with BAL, this energy deficit did not affect S(i) the next 
      day [4.9 +/- 0.9, and 5.0 +/- 0.8 (mU/l)(-1) x min(-1)]. Maintaining an energy 
      deficit after exercise had the most potent effect on lipid metabolism, as 
      measured by a higher plasma triacylglycerol concentration, and increased plasma 
      fatty acid mobilization and oxidation compared with when in nutrient balance. 
      Carbohydrate deficit after exercise, but not energy deficit, contributed to the 
      insulin-sensitizing effects of acute aerobic exercise, whereas maintaining an 
      energy deficit after exercise augmented lipid mobilization.
FAU - Newsom, Sean A
AU  - Newsom SA
AD  - School of Kinesiology, University of Michigan, 401 Washtenaw Ave., Ann Arbor, MI 
      48109-2214, USA.
FAU - Schenk, Simon
AU  - Schenk S
FAU - Thomas, Kristin M
AU  - Thomas KM
FAU - Harber, Matthew P
AU  - Harber MP
FAU - Knuth, Nicolas D
AU  - Knuth ND
FAU - Goldenberg, Naila
AU  - Goldenberg N
FAU - Horowitz, Jeffrey F
AU  - Horowitz JF
LA  - eng
GR  - P30 DK089503/DK/NIDDK NIH HHS/United States
GR  - UL1-RR-024986/RR/NCRR NIH HHS/United States
GR  - 5P60DK-20572/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Randomized Controlled Trial
PT  - Research Support, N.I.H., Extramural
DEP - 20091231
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
RN  - 0 (Triglycerides)
RN  - 2V16EO95H1 (Palmitic Acid)
RN  - 9005-79-2 (Glycogen)
SB  - IM
MH  - Adaptation, Physiological
MH  - Adult
MH  - Biopsy
MH  - Blood Glucose/metabolism
MH  - *Diet, Carbohydrate-Restricted
MH  - *Energy Intake
MH  - *Energy Metabolism
MH  - *Exercise
MH  - Glucose Tolerance Test
MH  - Glycogen/metabolism
MH  - Humans
MH  - Insulin/*metabolism
MH  - *Insulin Resistance
MH  - Kinetics
MH  - *Lipid Metabolism
MH  - Male
MH  - Muscle, Skeletal/*metabolism/physiopathology
MH  - Oxidation-Reduction
MH  - Palmitic Acid/blood
MH  - Triglycerides/blood
PMC - PMC2838634
EDAT- 2010/01/02 06:00
MHDA- 2010/06/05 06:00
PMCR- 2011/03/01
CRDT- 2010/01/02 06:00
PHST- 2010/01/02 06:00 [entrez]
PHST- 2010/01/02 06:00 [pubmed]
PHST- 2010/06/05 06:00 [medline]
PHST- 2011/03/01 00:00 [pmc-release]
AID - 01106.2009 [pii]
AID - JAPPL-01106-2009 [pii]
AID - 10.1152/japplphysiol.01106.2009 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2010 Mar;108(3):554-60. doi: 
      10.1152/japplphysiol.01106.2009. Epub 2009 Dec 31.