scholarly journals Effect of pre-exercise carbohydrate availability on fat oxidation and energy expenditure after a high-intensity exercise

Author(s):  
G.A. Ferreira ◽  
L.C. Felippe ◽  
R.L.S. Silva ◽  
R. Bertuzzi ◽  
F.R. De Oliveira ◽  
...  
2018 ◽  
Vol 315 (5) ◽  
pp. E1034-E1045 ◽  
Author(s):  
Kristoffer Svensson ◽  
Jessica R. Dent ◽  
Shahriar Tahvilian ◽  
Vitor F. Martins ◽  
Abha Sathe ◽  
...  

The pyruvate dehydrogenase complex (PDC) converts pyruvate to acetyl-CoA and is an important control point for carbohydrate (CHO) oxidation. However, the importance of the PDC and CHO oxidation to muscle metabolism and exercise performance, particularly during prolonged or high-intensity exercise, has not been fully defined especially in mature skeletal muscle. To this end, we determined whether skeletal muscle-specific loss of pyruvate dehydrogenase alpha 1 ( Pdha1), which is a critical subunit of the PDC, impacts resting energy metabolism, exercise performance, or metabolic adaptation to high-fat diet (HFD) feeding. For this, we generated a tamoxifen (TMX)-inducible Pdha1 knockout (PDHmKO) mouse, in which PDC activity is temporally and specifically ablated in adult skeletal muscle. We assessed energy expenditure, ex vivo muscle contractile performance, and endurance exercise capacity in PDHmKO mice and wild-type (WT) littermates. Additionally, we studied glucose homeostasis and insulin sensitivity in muscle after 12 wk of HFD feeding. TMX administration largely ablated PDHα in skeletal muscle of adult PDHmKO mice but did not impact energy expenditure, muscle contractile function, or low-intensity exercise performance. Additionally, there were no differences in muscle insulin sensitivity or body composition in PDHmKO mice fed a control or HFD, as compared with WT mice. However, exercise capacity during high-intensity exercise was severely impaired in PDHmKO mice, in parallel with a large increase in plasma lactate concentration. In conclusion, although skeletal muscle PDC is not a major contributor to resting energy expenditure or long-duration, low-intensity exercise performance, it is necessary for optimal performance during high-intensity exercise.


2013 ◽  
Vol 9 (2) ◽  
pp. 103-108
Author(s):  
R.J. Bloomer ◽  
T.M. Farney

Intensity of exercise can influence substrate utilization, with increasing intensity resulting in lower rates of fat oxidation and the reliance on carbohydrate as the preferred fuel. Fat oxidation (or more specifically, mobilization) can be assessed via the measurement of circulating glycerol, with most prior research focusing on aerobic exercise and measurements obtained during the actual exercise bout. The present study determined the degree of fat oxidation/mobilization by measuring plasma glyctierol concentrations during the one hour post-exercise recovery period following three difference exercise bouts. On four different days, exercise trained men (n=12; 23.7±1.1 years) either rested quietly or performed aerobic cycle exercise (60 min at 70% heart rate reserve), 60 s cycle sprints at 100% max wattage obtained during graded exercise testing (GXT) - a total of five, or 15 s cycle sprints at 200% max wattage obtained during GXT - a total of 10. Blood was collected before and at 1, 30 and 60 min post-exercise. Haematocrit and haemoglobin were measured to correct for changes in plasma volume. Glycerol was analysed in plasma and the area under the curve was calculated. Glycerol increased across time (P<0.0001) from pre-exercise (8.4±0.3 μg/dl) to 1 min (13.1±0.7 μg/dl), 30 min (11.3±0.6 μg/dl) and 60 min (9.1±0.5 μg/dl) post-exercise, with 1 min and 30 min post-exercise greater than pre-exercise and 60 min post-exercise (P<0.05). Area under the curve was greater (P=0.0004) for aerobic exercise (24.7±2.0 μg/dl/h), 60 second sprints (23.4±1.9 μg/dl/h) and 15 sec sprints (24.4±1.5 μg/dl/h), as compared to rest (15.3±0.8 μg/dl/h), with no differences noted between exercise bouts (P≯0.05). All exercise bouts increase circulating glycerol, with no differences noted between bouts. Although previous data indicate that low intensity aerobic exercise results in greater fat oxidation than high intensity exercise (when assessed during the actual exercise session), our findings suggest that high intensity exercise may result in similar fat oxidation/mobilization as compared to aerobic exercise during the acute post-exercise period.


2001 ◽  
Vol 25 (3) ◽  
pp. 332-339 ◽  
Author(s):  
M Yoshioka ◽  
E Doucet ◽  
S St-Pierre ◽  
N Alméras ◽  
D Richard ◽  
...  

2017 ◽  
Vol 42 (9) ◽  
pp. 986-993 ◽  
Author(s):  
Laurel A. Littlefield ◽  
Zacharias Papadakis ◽  
Katie M. Rogers ◽  
José Moncada-Jiménez ◽  
J. Kyle Taylor ◽  
...  

Reductions in postprandial lipemia have been observed following aerobic exercise of sufficient energy expenditure. Increased excess postexercise oxygen consumption (EPOC) has been documented when comparing high- versus low-intensity exercise. The contribution of EPOC energy expenditure to alterations in postprandial lipemia has not been determined. The purpose of this study was to evaluate the effects of low- and high-intensity exercise on postprandial lipemia in healthy, sedentary, overweight and obese men (age, 43 ± 10 years; peak oxygen consumption, 31.1 ± 7.5 mL·kg−1·min−1; body mass index, 31.8 ± 4.5 kg/m2) and to determine the contribution of EPOC to reductions in postprandial lipemia. Participants completed 4 conditions: nonexercise control, low-intensity exercise at 40%–50% oxygen uptake reserve (LI), high-intensity exercise at 70%–80% oxygen uptake reserve (HI), and HI plus EPOC re-feeding (HI+EERM), where the difference in EPOC energy expenditure between LI and HI was re-fed in the form of a sports nutrition bar (Premier Nutrition Corp., Emeryville, Calif., USA). Two hours following exercise participants ingested a high-fat (1010 kcals, 99 g sat fat) test meal. Blood samples were obtained before exercise, before the test meal, and at 2, 4, and 6 h postprandially. Triglyceride incremental area under the curve was significantly reduced following LI, HI, and HI+EERM when compared with nonexercise control (p < 0.05) with no differences between the exercise conditions (p > 0.05). In conclusions, prior LI and HI exercise equally attenuated postprandial triglyceride responses to the test meal. The extra energy expended during EPOC does not contribute significantly to exercise energy expenditure or to reductions in postprandial lipemia in overweight men.


2009 ◽  
Vol 108 (2) ◽  
pp. 383-391 ◽  
Author(s):  
Stefano Lazzer ◽  
Claudio Lafortuna ◽  
Carlo Busti ◽  
Raffaela Galli ◽  
Tiziana Tinozzi ◽  
...  

2000 ◽  
Vol 88 (5) ◽  
pp. 1707-1714 ◽  
Author(s):  
J. A. Romijn ◽  
E. F. Coyle ◽  
L. S. Sidossis ◽  
J. Rosenblatt ◽  
R. R. Wolfe

We have studied eight endurance-trained women at rest and during exercise at 25, 65, and 85% of maximal oxygen uptake. The rate of appearance (Ra) of free fatty acids (FFA) was determined by infusion of [2H2]palmitate, and fat oxidation rates were determined by indirect calorimetry. Glucose kinetics were assessed with [6,6-2H2]glucose. Glucose Ra increased in relation to exercise intensity. In contrast, whereas FFA Ra was significantly increased to the same extent in low- and moderate-intensity exercise, during high-intensity exercise, FFA Ra was reduced compared with the other exercise values. Carbohydrate oxidation increased progressively with exercise intensity, whereas the highest rate of fat oxidation was during exercise at 65% of maximal oxygen uptake. After correction for differences in lean body mass, there were no differences between these results and previously reported data in endurance-trained men studied under the same conditions, except for slight differences in glucose metabolism during low-intensity exercise (Romijn JA, Coyle EF, Sidossis LS, Gastaldelli A, Horowitz JF, Endert E, and Wolfe RR. Am J Physiol Endocrinol Metab 265: E380–E391, 1993). We conclude that the patterns of changes in substrate kinetics during moderate- and high-intensity exercise are similar in trained men and women.


2013 ◽  
Vol 114 (6) ◽  
pp. 792-800 ◽  
Author(s):  
Justin R. Trombold ◽  
Kevin M. Christmas ◽  
Daniel R. Machin ◽  
Il-Young Kim ◽  
Edward F. Coyle

Acute exercise has been shown to attenuate postprandial plasma triglyceride elevation (PPTG). However, the direct contribution of exercise intensity is less well understood. The purpose of this study was to examine the effects of exercise intensity on PPTG and postprandial fat oxidation. One of three experimental treatments was performed in healthy young men ( n = 6): nonexercise control (CON), moderate-intensity exercise (MIE; 50% V̇o2peak for 60 min), or isoenergetic high-intensity exercise (HIE; alternating 2 min at 25% and 2 min at 90% V̇o2peak). The morning after the exercise, a standardized meal was provided (16 kcal/kg BM, 1.02 g fat/kg, 1.36 g CHO/kg, 0.31 g PRO/kg), and measurements of plasma concentrations of triglyceride (TG), glucose, insulin, and β-hydroxybutyrate were made in the fasted condition and hourly for 6 h postprandial. Indirect calorimetry was used to determine fat oxidation in the fasted condition and 2, 4, and 6 h postprandial. Compared with CON, both MIE and HIE significantly attenuated PPTG [incremental AUC; 75.2 (15.5%), P = 0.033, and 54.9 (13.5%), P = 0.001], with HIE also significantly lower than MIE ( P = 0.03). Postprandial fat oxidation was significantly higher in MIE [83.3 (10.6%) of total energy expenditure] and HIE [89.1 (9.8) %total] compared with CON [69.0 (16.1) %total, P = 0.039, and P = 0.018, respectively], with HIE significantly greater than MIE ( P = 0.012). We conclude that, despite similar energy expenditure, HIE was more effective than MIE for lowering PPTG and increasing postprandial fat oxidation.


2019 ◽  
Vol 51 (Supplement) ◽  
pp. 327
Author(s):  
Jenna Thompson ◽  
Matthew Wolfe ◽  
Meral Culver ◽  
Kelly E. Johnson ◽  
Justin P. Guilkey

Sign in / Sign up

Export Citation Format

Share Document