Energy deficit after exercise augments lipid mobilization but does not contribute to the exercise-induced increase in insulin sensitivity.
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.
Newsom
Sean A
SA
School of Kinesiology, University of Michigan, 401 Washtenaw Ave., Ann Arbor, MI 48109-2214, USA.
Schenk
Simon
S
Thomas
Kristin M
KM
Harber
Matthew P
MP
Knuth
Nicolas D
ND
Goldenberg
Naila
N
Horowitz
Jeffrey F
JF
D000222:Adaptation, Physiological; D000328:Adult; D001706:Biopsy; D001786:Blood Glucose / Q000378:metabolism; D050528:Diet, Carbohydrate-Restricted; D002149:Energy Intake; D004734:Energy Metabolism; D015444:Exercise; D005951:Glucose Tolerance Test; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D007700:Kinetics; D050356:Lipid Metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000503:physiopathology; D010084:Oxidation-Reduction; D019308:Palmitic Acid / Q000097:blood; D014280:Triglycerides / Q000097:blood
D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D019308:Palmitic Acid; D006003:Glycogen