al., 2008 ). In the only previous exercise study with HMS, Roberts et al. ( 2011 ) reported that vs. maltodextrin, HMS ingestion (1 g·kg BM −1 ) consumed 30 min before exercise blunted serum glucose and insulin response (eightfold lower) and increased fat oxidation during 150 min of cycling without any
Manuel D. Quinones and Peter W.R. Lemon
Julia H. Goedecke, Virginia R. Clark, Timothy D. Noakes and Estelle V. Lambert
The aims of the study were to determine if medium-chain triacylglycerol (MCT), ingested in combination with carbohydrate (CHO), would alter substrate metabolism and improve simulated competitive ultra-endurance cycling performance. Eight endurance-trained cyclists took part in this randomized, single-blind crossover study. On two separate occasions, subjects cycled for 270 min at 50% of peak power output, interspersed with four 75 kJ sprints at 60 min intervals, followed immediately by a 200 kJ time-trial. One hour prior to the exercise trials, subjects ingested either 75 g of CHO or 32 g of MCT, and then ingested 200 mL of a 10% CHO (wt/vol) solution or a 4.3% MCT + 10% CHO (wt/vol) solution every 20 min during the CHO and MCT trials, respectively. During the constant-load phases of the 270 min exercise trial, VO2, RER, and heart rate were measured at 30 min intervals and gastrointestinal (GI) symptoms were recorded. There was no difference in VO2 or RER between the MCT and CHO trials (P = 0.40). Hourly sprint (P = 0.03 for trial x time interaction) and time-trial times (14:30 ± 0.58 vs. 12:36 ± 1:6, respectively, P < 0.001) were slower in the MCT than the CHO trial. Half the subjects experienced GI symptoms with MCT ingestion. In conclusion, MCTs ingested prior to exercise and co-ingested with CHO during exercise did not alter substrate metabolism and significantly compromised sprint performance during prolonged ultra-endurance cycling exercise.
Elizabeth M. Broad, Ronald J. Maughan and Stuart D.R Galloway
Twenty nonvegetarian active males were pair-matched and randomly assigned to receive 2 g of L-carnitine L-tartrate (LC) or placebo per day for 2 wk. Participants exercised for 90 min at 70% VO2max after 2 days of a prescribed diet (M ±SD: 13.6 ± 1.6 MJ, 57% carbohydrate, 15% protein, 26% fat, 2% alcohol) before and after supplementation. Results indicated no change in carbohydrate oxidation, nitrogen excretion, branched-chain amino acid oxidation, or plasma urea during exercise between the beginning and end of supplementation in either group. After 2 wk of LC supplementation the plasma ammonia response to exercise tended to be suppressed (0 vs. 2 wk at 60 min exercise, 97 ± 26 vs. 80 ± 9, and 90 min exercise, 116 ± 47 vs. 87 ± 25 μmol/L), with no change in the placebo group. The data indicate that 2 wk of LC supplementation does not affect fat, carbohydrate, and protein contribution to metabolism during prolonged moderate-intensity cycling exercise. The tendency toward suppressed ammonia accumulation, however, indicates that oral LC supplementation might have the potential to reduce the metabolic stress of exercise or alter ammonia production or removal, which warrants further investigation.
Christopher C. Webster, Jeroen Swart, Timothy D. Noakes and James A. Smith
Low-carbohydrate high-fat (LCHF) diets have gained in popularity among some ultraendurance athletes because they increase rates of fat oxidation during exercise and “spare” muscle glycogen. 1 However, prevailing opinion holds that carbohydrate restriction would compromise exercise performance at
Steven K. Malin, Brooke R. Stephens, Carrie G. Sharoff, Todd A. Hagobian, Stuart R. Chipkin and Barry Braun
Exercise and metformin may prevent or delay Type 2 diabetes by, in part, raising the capacity for fat oxidation. Whether the addition of metformin has additive effects on fat oxidation during and after exercise is unknown. Therefore, the purpose of this study was to evaluate the effect of metformin on substrate oxidation during and after exercise. Using a double-blind, counter-balanced crossover design, substrate oxidation was assessed by indirect calorimetry in 15 individuals taking metformin (2,000 mg/d) and placebo for 8–10 d. Measurements were made during cycle exercise at 5 submaximal cycle workloads, starting at 30% peak work (Wpeak) and increasing by 10% every 8 min to 70% Wpeak. Substrate oxidation was also measured for 50 min postexercise. Differences between conditions were assessed using analysis of variance with repeated measures, and values are reported as M ± SE. During exercise, fat oxidation (0.19 ± 0.03 vs. 0.15 ± 0.01 g/min, p < .01) and percentage of energy from fat (32% ± 3% vs. 28% ± 3%, p < .01) were higher with metformin than with placebo. Postexercise, metformin slightly lowered fat oxidation (0.12 ± 0.02 to 0.10 ± 0.02 g/min, p < .01) compared with placebo. There was an inverse relationship between postexercise fat oxidation and the rate of fat oxidation during exercise (r = –.68, p < .05). In healthy individuals, metformin has opposing actions on fat oxidation during and after exercise. Whether the same effects are evident in insulin-resistant individuals remains to be determined.
Gordon I. Smith, Asker E. Jeukendrup and Derek Ball
At rest, administration of the short-chain fatty acid acetate suppresses fat oxidation without affecting carbohydrate utilization. The combined effect of increased acetate availability and exercise on substrate utilization is, however, unclear. With local ethics approval, we studied the effect of ingesting either sodium acetate (NaAc) or sodium bicarbonate (NaHCO3) at a dose of 4 mmol·kg-1 body mass 90 min before completing 120 min of exercise at 50% VO2peak. Six healthy young men completed the trials after an overnight fast and ingested the sodium salts in randomized order. As expected NaAc ingestion decreased resting fat oxidation (mean ± SD; 0.09 ± 0.02 vs. 0.07 ± 0.02 g·min-1 pre- and post-ingestion respectively, p < .05) with no effect upon carbohydrate utilization. In contrast, NaHCO3 ingestion had no effect on substrate utilization at rest. In response to exercise, fat and CHO oxidation increased in both trials, but fat oxidation was lower (0.16 ± 0.10 vs. 0.29 ± 0.11 g·min-1, p < .05) and carbohydrate oxidation higher (1.67 ± 0.35 vs. 1.44 ± 0.22 g·min-1, p < .05) in the NaAc trial compared with the NaHCO3 trial during the first 15 min of exercise. Over the final 75 min of exercise an increase in fat oxidation and decrease in carbohydrate oxidation was observed only in the NaAc trial. These results demonstrate that increasing plasma acetate concentration suppresses fat oxidation both at rest and at the onset of moderate-intensity exercise.
David S. Rowlands and Will G. Hopkins
The effect of pre-exercise meal composition on metabolism and performance in cycling were investigated in a crossover study. Twelve competitive cyclists ingested high-fat, high-carbohydrate, or high-protein meals 90 min before a weekly exercise test. The test consisted of a 1-hour pre-load at 55% peak power, five 10-min incremental loads from 55 to 82% peak power (to measure the peak fat-oxidation rate), and a 50-km time trial that included three 1-km and 4-km sprints. A carbohydrate supplement was ingested throughout the exercise. Relative to the high-protein and high-fat meals, the high-carbohydrate meal halved the peak fat-oxidation rate and reduced the fat oxidation across all workloads by a factor of 0.20 to 0.58 (p = .002–.0001). Reduced fat availability may have accounted for this reduction, as indicated by lower plasma fatty acid, lower glycerol, and higher pre-exercise insulin concentrations relative to the other meals (p = .04–.0001). In contrast, fat oxidation following the high-protein meal was similar to that following the high-fat meal. This similarity was linked to evidence suggesting greater lipolysis and plasma fat availability following high-protein relative to high-carbohydrate meals. Despite these substantial effects on metabolism, meal composition had no clear effect on sprint or 50-km performance.
Kristin L. Osterberg and Christopher L. Melby
This study determined the effect of an intense bout of resistive exercise on postexercise oxygen consumption, resting metabolic rate, and resting fat oxidation in young women (N = 7, ages 22-35). On the morning of Day 1, resting metabolic rate (RMR) was measured by indirect calorimetry. At 13:00 hr, preexercise resting oxygen consumption was measured followed by 100 min of resistive exercise. Postexercise oxygen consumption was then measured for a 3-hr recovery period. On the following morning (Day 2), RMR was once again measured in a fasted state at 07:00. Postexercise oxygen consumption remained elevated during the entire 3-hr postexercise recovery period compared to the pre-exercise baseline. Resting metabolic rate was increased by 4.2% (p < .05) from Day 1 (morning prior to exercise: 1,419 ± 58 kcal/24 hr) compared to Day 2 (16 hr following exercise: 1,479 ± 65 kcal/24 hr). Resting fat oxidation as determined by the respiratory exchange ratio was also significantly elevated on Day 2 compared to Day 1. These results indicate that among young women, acute strenuous resistance exercise of the nature used in this study is capable of producing modest but prolonged elevations of postexercise metabolic rate and possibly fat oxidation.
Melissa J. Benton and Pamela D. Swan
Research suggests that ingesting protein after resistance exercise (RE) increases muscle protein synthesis and results in greater muscle gains. The effect on energy expenditure and substrate utilization, however, is unclear. This study evaluated the effect of RE and post exercise protein on recovery energy expenditure and substrate utilization in 17 women (age 46.5 ± 1.2 y). A whey-protein supplement (120 kcal, 30 g protein) was ingested immediately after 1 bout of RE (PRO) and a non caloric placebo after another (PLA). VO2 and respiratory-exchange ratio (RER) were measured before and for 120 min after each exercise session. RE resulted in a significant increase in VO2 that persisted through 90 min of recovery (P < 0.01) and was not affected by protein supplementation. RE significantly lowered RER, resulting in an increase in fat oxidation for both PLA and PRO (P < 0.01). For PRO, however, RER returned to baseline values earlier than for PLA, resulting in a reduced fat-oxidation response (P = 0.02) and earlier return to pre exercise baseline values than for PLA. Substrate utilization was significantly different between conditions (P = 0.02), with fat contributing 77.76% ± 2.19% for PLA and 72.12% ± 2.17% for PRO, while protein oxidation increased from 17.18% ± 1.33% for PLA to 20.82% ± 1.47% for PRO. Post exercise protein did not affect energy expenditure, but when protein was available as an alternate fuel fat oxidation was diminished. Based on these findings it might be beneficial for middle-aged women to delay protein intake after RE to maximize fat utilization.
Bettina Mittendorfer and Samuel Klein
Endurance exercise increases the use of endogenous fuels to provide energy for working muscles. Elderly subjects oxidize more glucose and less fat during moderate intensity exercise. This shift in substrate use is presumably caused by age-related changes in skeletal muscle, including decreased skeletal muscle respiratory capacity, because adipose tissue lipolysis and plasma fatty acid availability are not rate limiting. Endurance training in elderly subjects increases muscle respiratory capacity, decreases glucose production and oxidation, and increases fat oxidation thereby correcting or compensating for the alterations in substrate oxidation associated with aging.