To determine the effect of macronutrient composition of pre-exercise meals on exercise metabolism and performance, 8 trained men exercised for 30 min above lactate threshold (30LT), followed by a 20-km time trial (TT). Approximately 3.5 h before exercise, subjects consumed a carbohydrate meal (C; 3 g carbohydrate/kg), an isoenergetic fat meal (F; 1.3 g fat/kg), or a placebo meal (P; no energy content) on 3 separate occasions in randomized order. Treatments had no effect on carbohydrate oxidation during exercise, but C decreased whole-body fat oxidation during the last 5 min of 30LT and TT, respectively (3.2 ± 1.6 and 4.8 ± 2.1 mmol · kg−1 · min−1, p < .05) when compared to F (13.3 ± 1.6 and 16.5 ± 2.7 mmol · kg−1 · min−1) and P (15.9 ± 2.7 and 17.0 ± 3.2 mmol · kg−1 · min−1). Glucose rate of appearance (Ra) and disappearance (Rd), and muscle glycogen utilization were not significantly different among treatments during exercise. TT performances were similar for C, F, and P (32.7 ± 0.5 vs. 33.1 ± 1.1 and 33.0 ± 0.8 min, p > .05). We conclude that the consumption of a pre-exercise meal has minor effects on fat oxidation during high-intensity exercise, and no effect on carbohydrate oxidation or TT performance.
David Paul, Kevin A. Jacobs, Raymond J. Geor and Kenneth W. Hinchcliff
Kimberly M. White, Roseann M. Lyle, Michael G. Flynn, Dorothy Teegarden and Shawn S. Donkin
The purpose of this study was to test the effect of acute dairy calcium intake on exercise energy metabolism and endurance performance. Trained female runners completed two trials. Each trial consisted of a 90-min glycogen depletion run followed by a self-paced 10K time trial, conducted one hour after consumption of a high dairy (500 mg Ca+2) or low dairy (80 mg Ca+2) meal. During the 90-min run, blood samples and respiratory gases were collected. No treatment main effects of acute dairy intake were found for respiratory exchange ratio (RER), calculated fat oxidation, lactate, glycerol, or 10K time. Following this protocol, acute dairy calcium intake did not alter fat utilization or endurance performance in trained female runners.
Brian J. Martin, Rachel B. Tan, Jenna B. Gillen, Michael E. Percival and Martin J. Gibala
Supplementation with green tea extract (GTE) in animals has been reported to induce numerous metabolic adaptations including increased fat oxidation during exercise and improved performance. However, data regarding the metabolic and physiological effects of GTE during exercise in humans are limited and equivocal.
To examine the effects of short-term GTE treatment on resting energy expenditure (REE), wholebody substrate utilization during exercise and time trial performance.
Fifteen active men (24 ± 3 y; VO2peak = 48 ± 7 ml·kg·min−1; BMI = 26 ± 3 kg·m2(–1)) ingested GTE (3x per day = 1,000 mg/d) or placebo (PLA) for 2 day in a double-blind, crossover design (each separated by a 1 week wash-out period). REE was assessed in the fasted state. Subjects then ingested a standardized breakfast (~5.0 kcal·kg-1) and 90 min later performed a 60 min cycling bout at an intensity corresponding to individual maximal fat oxidation (44 ± 11% VO2peak), followed by a 250 kJ TT.
REE, whole-body oxygen consumption (VO2) and substrate oxidation rates during steady-state exercise were not different between treatments. However, mean heart rate (HR) was lower in GTE vs. PLA (115 ± 16 vs. 118 ± 17 beats·min−1; main effect, p = .049). Mixed venous blood [glycerol] was higher during rest and exercise after GTE vs. PLA (p = .006, main effect for treatment) but glucose, insulin and free-fatty acids were not different. Subsequent time trial performance was not different between treatments (GTE = 25:38 ± 5:32 vs. PLA = 26:08 ± 8:13 min; p = .75).
GTE had minimal effects on whole-body substrate metabolism but significantly increased plasma glycerol and lowered heart rate during steady-state exercise, suggesting a potential increase in lipolysis and a cardiovascular effect that warrants further investigation.
Weronika N. Abramowicz and Stuart D.R. Galloway
Twelve healthy active subjects (6 male, 6 female) performed 60 min of exercise (60% VO2max) on 3 occasions after supplementing with L-Carnitine L-tartrate (LCLT) or placebo. Each subject received a chronic dose, an acute dose, and placebo in a randomized, double-blind crossover design. Dietary intake and exercise were replicated for 2 d prior to each trial. In males there was a significant difference in rate of carbohydrate (CHO) oxidation between placebo and chronic trials (P = 0.02) but not placebo and acute trials (P = 0.70), and total CHO oxidation was greater following chronic supplementation vs. placebo (mean ± standard deviation) of 93.8 (17.3) g/hr and 78.2 (23.3) g/h, respectively). In females, no difference in rate of, or total, CHO oxidation was observed between trials. No effects on fat oxidation or hematological responses were noted in either gender group. Under these experimental conditions, chronic LCLT supplementation increased CHO oxidation in males during exercise but this was not observed in females
Elizabeth M. Broad, Ronald J. Maughan and Stuart D.R. Galloway
The effects of 15 d of supplementation with L-carnitine L-tartrate (LC) on metabolic responses to gradedintensity exercise under conditions of altered substrate availability were examined. Fifteen endurance-trained male athletes undertook exercise trials after a 2-d high-carbohydrate diet (60% CHO, 25% fat) at baseline (D0), on Day 14 (D14), and after a single day of high fat intake (15% CHO, 70% fat) on Day 15 (D15) in a double-blind, placebo-controlled, pair-matched design. Treatment consisted of 3 g LC (2 g L-carnitine/d; n = 8) or placebo (P, n = 7) for 15 d. Exercise trials consisted of 80 min of continuous cycling comprising 20-min periods at each of 20%, 40%, 60%, and 80% VO2peak. There was no significant difference between whole-body rates of CHO and fat oxidation at any workload between D0 and D14 trials for either the P or LC group. Both groups displayed increased fat and reduced carbohydrate oxidation between the D14 and D15 trials (p < .05). During the D15 trial, heart rate (p < .05 for 20%, 40%, and 60% workloads) and blood glucose concentration (p < .05 for 40% and 60% workloads) were lower during exercise in the LC group than in P. These responses suggest that LC may induce subtle changes in substrate handling in metabolically active tissues when fattyacid availability is increased, but it does not affect whole-body substrate utilization during short-duration exercise at the intensities studied.
Elizabeth M. Broad, Ronald J. Maughan and Stuart D.R. Galloway
In a randomized, placebo-controlled, double-blind crossover design, 15 trained males undertook exercise trials during two 4 wk supplementation periods, with either 3 g L-Carnitine L-tartrate (LCLT) or 3 g placebo (P) daily. Total carbohydrate and fat oxidation during 90 min steady state cycling were not different between 0 or 4 wk within LCLT or P trials (mean ± standard deviation: carbohydrate oxidation P0 99 ± 36, P4W 111 ± 27, LCLT0 107 ± 33, LCLT4W 112 ± 32 g, respectively; fat oxidation P0 99 ± 28, P4W 92 ± 21, LCLT0 94 ± 18, LCLT4W 90 ± 22 g, respectively). Subsequent 20 km time trial duration was shorter after P (P0 31:29 ± 3:50, P4W 29:55 ± 2:58 min:s, P < 0.01), with no significant change over LCLT (LCLT0 31:46 ± 4:06, LCLT4W 31.19 ± 4.08 min:s). Four weeks LCLT supplementation had no effect on substrate utilization or endurance performance.
Heidi M. Staudacher, Andrew L. Carey, Nicola K. Cummings, John A. Hawley and Louise M. Burke
We determined the effect of a high-fat diet and carbohydrate (CHO) restoration on substrate oxidation and glucose tolerance in 7 competitive ultra-endurance athletes (peak oxygen uptake [V̇O2peak] 68 ± 1 ml · kg−1 · min−1; mean±SEM). For 6 days, subjects consumed a random order of a high-fat (69% fat; FAT-adapt) or a high-CHO (70% CHO; HCHO) diet, each followed by 1 day of a high-CHO diet. Treatments were separated by an 18-day wash out. Substrate oxidation was determined during submaximal cycling (20 min at 65% V̇O2peak) prior to and following the 6 day dietary interventions. Fat oxidation at baseline was not different between treatments (17.4 ± 2.1 vs. 16.1 ± 1.3 g · 20 min−1 for FAT-adapt and HCHO, respectively) but increased 34% after 6 days of FAT-adapt (to 23.3 ± 0.9 g · 20 min−1, p < .05) and decreased 30% after HCHO (to 11.3±1.4 g · 20 min−1, p < .05). Glucose tolerance, determined by the area under the plasma [glucose] versus time curve during an oral glucose tolerance (OGTT) test, was similar at baseline (545±21 vs. 520±28 mmol · L−1 · 90 min−1), after 5-d of dietary intervention (563 ± 26 vs. 520 ± 18 mmol · L−1 · 90 min−1) and after 1 d of high-CHO (491 ± 28 vs. 489 ± 22 mmol · L−1 · 90min−1 for FAT- adapt and HCHO, respectively). An index of whole-body insulin sensitivity (SI 10000/÷fasting [glucose] × fasting [insulin] × mean [glucose] during OGTT × mean [insulin] during OGTT) was similar at baseline (15 ± 2 vs. 17 ± 5 arbitrary units), after 5-d of dietary intervention (15 ± 2 vs. 15 ± 2) and after 24 h of CHO loading (17 ± 3 vs. 18 ± 2 for FAT- adapt and HCHO, respectively). We conclude that despite marked changes in the pattern of substrate oxidation during submaximal exercise, short-term adaptation to a high-fat diet does not alter whole-body glucose tolerance or an index of insulin sensitivity in highly-trained individuals.
Petra Stiegler, S. Andrew Sparks and Adam Cunliffe
Maximizing postprandial energy expenditure and fat oxidation could be of clinical relevance for the treatment of obesity. This study investigated the effect of prior exercise on energy expenditure and substrate utilization after meals containing varying amounts of macronutrients. Eight lean (11.6% ± 4.0% body fat, M ± SD) and 12 obese (35.9% ± 5.3% body fat) men were randomly assigned to a protein (43% protein, 30% carbohydrate) or a carbohydrate (10% protein, 63% carbohydrate) meal. The metabolic responses to the meals were investigated during 2 trials, when meals were ingested after a resting period (D) or cycling exercise (Ex+D; 65% of oxygen consumption reserve, 200 kcal). Energy expenditure, substrate utilization, and glucose and insulin responses were measured for 4 hr during the postprandial phase. Although postprandial energy expenditure was not affected by prior exercise, the total amount of fat oxidized was higher during Ex+D than during D (170.8 ± 60.1 g vs. 137.8 ± 50.8 g, p < .05), and, accordingly, the use of carbohydrate as substrate was decreased (136.4 ± 45.2 g vs. 164.0 ± 42.9 g, p < .05). After the protein meal fat-oxidation rates were higher than after carbohydrate intake (p < .05), an effect independent of prior exercise. Plasma insulin tended to be lower during Ex+D (p = .072) and after the protein meal (p = .066). No statistically significant change in postprandial blood glucose was induced by prior exercise. Exercising before meal consumption can result in a marked increase in fat oxidation, which is independent of the type of meal consumed.
Nancy L. Keim, Amy Z. Belko and Teresa F. Barbieri
Energy expenditure (EE) was measured at specific steady-state work rates to determine if body fat percentage or gender was associated with exercise EE, substrate oxidation, or work efficiency. Body fat percentage (leaner vs. fatter men, 9-15% vs. 20-25% fat; leaner vs. fatter women, 16-24% vs. 32-48% fat) was not related to work efficiency or submaximal EE. Fatness affected substrate oxidation in men but not in women. Compared to fatter men, leaner men had higher fat oxidation (6.7 ± 1.6 vs. 1.4 ± 2.0 mg · kg fat-free mass
Jeffrey A. Potteiger, Erik P. Kirk, Dennis J. Jacobsen and Joseph E. Donnelly
To determine whether 16 months of moderate-intensity exercise training changes resting metabolic rate (RMR) and substrate oxidation in overweight young adults.
Participants were randomly assigned to nonexercise control (CON, 18 women, 15 men) or exercise (EX, 25 women, 16 men) groups. EX performed supervised and verified exercise 3–5 d/wk, 20–45 min/session, at 60–75% of heart-rate reserve. Body mass and composition, maximal oxygen consumption (VO2max), RMR, and resting substrate oxidation were assessed at baseline and after 9 and 16 months of training.
EX men had significant decreases from baseline to 9 months in body mass (94.6 ± 12.4 to 89.2 ± 9.5 kg) and percent fat (28.3 ± 4.6 to 24.5 ± 3.9). CON women had significant increases in body mass (80.2 ± 8.1 to 83.2 ± 9.2 kg) from baseline to 16 months. VO2max increased significantly from baseline to 9 months in the EX men (3.67 ± 0.62 to 4.34 ± 0.58 L/min) and EX women (2.53 ± 0.32 to 3.03 ± 0.42 L/min). RMR increased from baseline to 9 months in EX women (1,583 ± 221 to 1,692 ± 230 kcal/d) and EX men (1,995 ± 184 to 2,025 ± 209 kcal/d). There were no significant differences within genders for either EX or CON in fat or carbohydrate oxidation. Fat oxidation was significantly higher for women than for men at 9 months in both CON and EX groups.
Regular moderate-intensity exercise in healthy, previously sedentary overweight and obese adults increases RMR but does not alter resting substrate oxidation. Women tend to have higher RMR and greater fat oxidation, when expressed per kilogram fat-free mass, than men.