Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. β-alanine (β-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic β-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO2peak = 50 ± 6 mL·kg−1·min−1) ingested 3.2 g/day of β-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4–6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of β-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and β-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of β-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.
Andrew J.R. Cochran, Michael E. Percival, Sara Thompson, Jenna B. Gillen, Martin J. MacInnis, Murray A. Potter, Mark A. Tarnopolsky and Martin J. Gibala
Éder Ricardo Petry, Vinicius Fernandes Cruzat, Thiago Gomes Heck, Paulo Ivo Homem de Bittencourt Jr. and Julio Tirapegui
Liver L-glutamine is an important vehicle for the transport of ammonia and intermediary metabolism of amino acids between tissues, particularly under catabolic situations, such as high-intensity exercise. Hence, the aim of this study was to investigate the effects of oral supplementations with L-glutamine in its free or dipeptide forms (with L-alanine) on liver glutamine-glutathione (GSH) axis, and 70 kDa heat shock proteins (HSP70)/heat shock transcription factor 1 (HSF1) expressions. Adult male Wistar rats were 8-week trained (60 min/day, 5 days/week) on a treadmill. During the last 21 days, the animals were daily supplemented with 1 g of L-glutamine/kg body weight per day in either l-alanyl-L-glutamine dipeptide (DIP) form or a solution containing L-glutamine and l-alanine in their free forms (GLN+ALA) or water (controls). Exercise training increased cytosolic and nuclear HSF1 and HSP70 expression, as compared with sedentary animals. However, both DIP and GLN+ALA supplements enhanced HSF1 expression (in both cytosolic and nuclear fractions) in relation to exercised controls. Interestingly, HSF1 rises were not followed by enhanced HSP70 expression. DIP and GLN+ALA supplements increased plasma glutamine concentrations (by 62% and 59%, respectively) and glutamine to glutamate plasma ratio in relation to trained controls. This was in parallel with a decrease in plasma ammonium levels. Supplementations increased liver GSH (by 90%), attenuating the glutathione disulfide (GSSG) to GSH ratio, suggesting a redox state protection. In conclusion, oral administration with DIP and GLN+ALA supplements in endurance-trained rats improve liver glutamine-GSH axis and modulate HSF1 pathway.
Martin J. Turner and Alberto P. Avolio
International guidelines suggest limiting sodium intake to 86–100 mmol/day, but average intake exceeds 150 mmol/day. Participants in physical activities are, however, advised to increase sodium intake before, during and after exercise to ensure euhydration, replace sodium lost in sweat, speed rehydration and maintain performance. A similar range of health benefits is attributable to exercise and to reduction in sodium intake, including reductions in blood pressure (BP) and the increase of BP with age, reduced risk of stroke and other cardiovascular diseases, and reduced risk of osteoporosis and dementia. Sweat typically contains 40–60 mmol/L of sodium, leading to approximately 20–90 mmol of sodium lost in one exercise session with sweat rates of 0.5–1.5 L/h. Reductions in sodium intake of 20–90 mmol/day have been associated with substantial health benefits. Homeostatic systems reduce sweat sodium as low as 3–10 mmol/L to prevent excessive sodium loss. “Salty sweaters” may be individuals with high sodium intake who perpetuate their “salty sweat” condition by continual replacement of sodium excreted in sweat. Studies of prolonged high intensity exercise in hot environments suggest that sodium supplementation is not necessary to prevent hyponatremia during exercise lasting up to 6 hr. We examine the novel hypothesis that sodium excreted in sweat during physical activity offsets a significant fraction of excess dietary sodium, and hence may contribute part of the health benefits of exercise. Replacing sodium lost in sweat during exercise may improve physical performance, but may attenuate the long-term health benefits of exercise.
Tanja Oosthuyse, Matthew Carstens and Aletta M.E. Millen
Certain commercial carbohydrate replacement products include slowly absorbed carbohydrates such as isomaltulose. Few studies have investigated the metabolic effects of ingesting isomaltulose during exercise and none have evaluated exercise performance and gastrointestinal comfort. Nine male cyclists participated postprandially during three trials of 2-h steady-state (S-S) exercise (60% W max) followed by a 16 km time trial (TT) while ingesting 63 g∙h-1 of either, 0.8:1 fructose: maltodextrin (F:M) or isomaltulose (ISO) or placebo-flavored water (PL). Data were analyzed by magnitude-based inferences. During S-S exercise, ISO and PL similarly increased plasma nonesterified fatty acid (NEFA) concentration (mean change ISO versus F:M: 0.18, 90%CI ± 0.21 mmol∙L-1, 88% likelihood) and fat oxidation (10, 90%CI ± 9 g, 89% likelihood) while decreasing carbohydrate oxidation (-36, 90%CI ± 30.2 g, 91% likelihood) compared with F:M, despite equal elevations in blood glucose concentration with ISO and F:M. Rating of stomach cramps and bloating increased progressively with ISO (rating: 0-90 min S-S, weak; 120 min S-S, moderate; TT, strong) compared with F:M and PL (0-120 min S-S and TT, very weak). TT performance was substantially slower with ISO (mean change: 1.5, 90%CI ± 1.4 min, 94% likely harmful) compared with F:M. The metabolic response of ISO ingestion during moderate exercise to increase NEFA availability and fat oxidation despite elevating blood glucose concentration is anomalous for a carbohydrate supplement. However, ingesting isomaltulose at a continuous high frequency to meet the recommended carbohydrate replacement dose, results in severe gastrointestinal symptoms during prolonged or high intensity exercise and negatively affects exercise performance compared with fructose-maltodextrin supplementation.
Hee-Tae Roh, Su-Youn Cho, Hyung-Gi Yoon and Wi-Young So
We investigated the effects of aerobic exercise intensity on oxidative–nitrosative stress, neurotrophic factor expression, and blood–brain barrier (BBB) permeability. Fifteen healthy men performed treadmill running under low-intensity (LI), moderate-intensity (MI), and high-intensity (HI) conditions. Blood samples were collected immediately before exercise (IBE), immediately after exercise (IAE), and 60 min after exercise (60MAE) to examine oxidative–nitrosative stress (reactive oxygen species [ROS]; nitric oxide [NO]), neurotrophic factors (brain-derived neurotrophic factor [BDNF]; nerve growth factor [NGF]), and blood-brain barrier (BBB) permeability (S-100β; neuron-specific enolase). ROS concentration significantly increased IAE and following HI (4.9 ± 1.7 mM) compared with that after LI (2.8 ± 1.4 mM) exercise (p < .05). At 60MAE, ROS concentration was higher following HI (2.5 ± 1.2 mM) than after LI (1.5 ± 0.5 mM) and MI (1.4 ± 0.3 mM) conditions (p < .05). Plasma NO IAE increased significantly after MI and HI exercise (p < .05). Serum BDNF, NGF, and S-100b levels were significantly higher IAE following MI and HI exercise (p < .05). BDNF and S-100b were higher IAE following MI (29.6 ± 3.4 ng/mL and 87.1 ± 22.8 ng/L, respectively) and HI (31.4 ± 3.8 ng/mL and 100.6 ± 21.2 ng/L, respectively) than following LI (26.5 ± 3.0 ng/mL and 64.8 ± 19.2 ng/L, respectively) exercise (p < .05). 60MAE, S-100b was higher following HI (71.1 ± 14.5 ng/L) than LI (56.2 ± 14.7 ng/L) exercise (p < .05). NSE levels were not significantly different among all intensity conditions and time points (p > .05). Moderate- and/or high-intensity exercise may induce higher oxidative-nitrosative stress than may low-intensity exercise, which can increase peripheral neurotrophic factor levels by increasing BBB permeability.
Dawn M. Maffucci and Robert G. McMurray
The purpose of this study was to compare the effect a 6-hr versus 3-hr prefeeding regimen on exercise performance. The subjects were 8 active women (21.4 ± 0.9 years, 60.4±2.4 kg, 19.9 ± 1.3% body fat. and 165.6±2.1 cm). All women completed 2 exercise trials (separated by 3—6d) on a treadmill where they ran at moderate intensity for 30 min with 30-s sprints at 5-min intervals, followed directly by increasing incrementally the grade until volitional fatigue was achieved. The exercise trials were performed 3 hr and 6 hr after consuming 40 ± 3 kJ/kg meal. Time to exhaustion was 0.75 min shorter (p = .0001) for the 6-H trials compared to the 3-H trials. There were no significant differences in submaximal or peak oxygen uptake, heart rate, or rating of perceived exertion (p > .05). The 6-H trials compared to the 3-H trials resulted in .05 lower RERs (p = .0002), and a 2 mmol lower blood lactate at exhaustion (p = .012). Blood glucose levels and cortisol responses to exercise were similar between trials (p > .05). However, both resting and post exercise insulin levels were lower during 6-H trials. It was concluded that performance of moderate- to high-intensity exercise lasting 35—40 min is improved by consuming a moderately-high carbohydrate. low fat, low protein meal 3-hr before exercise compared to a similar meal consumed 6 hr prior to exercise. Thus, athletes should not skip meals before competition or training sessions.
Dajo Sanders, Mathieu Heijboer, Ibrahim Akubat, Kenneth Meijer and Matthijs K. Hesselink
To assess if short-duration (5 to ~300 s) high-power performance can accurately be predicted using the anaerobic power reserve (APR) model in professional cyclists.
Data from 4 professional cyclists from a World Tour cycling team were used. Using the maximal aerobic power, sprint peak power output, and an exponential constant describing the decrement in power over time, a power-duration relationship was established for each participant. To test the predictive accuracy of the model, several all-out field trials of different durations were performed by each cyclist. The power output achieved during the all-out trials was compared with the predicted power output by the APR model.
The power output predicted by the model showed very large to nearly perfect correlations to the actual power output obtained during the all-out trials for each cyclist (r = .88 ± .21, .92 ± .17, .95 ± .13, and .97 ± .09). Power output during the all-out trials remained within an average of 6.6% (53 W) of the predicted power output by the model.
This preliminary pilot study presents 4 case studies on the applicability of the APR model in professional cyclists using a field-based approach. The decrement in all-out performance during high-intensity exercise seems to conform to a general relationship with a single exponential-decay model describing the decrement in power vs increasing duration. These results are in line with previous studies using the APR model to predict performance during brief all-out trials. Future research should evaluate the APR model with a larger sample size of elite cyclists.
Samuel T. Howe, Phillip M. Bellinger, Matthew W. Driller, Cecilia M. Shing and James W. Fell
Beta-alanine may benefit short-duration, high-intensity exercise performance. The aim of this randomized double-blind placebo-controlled study was to examine the effects of beta-alanine supplementation on aspects of muscular performance in highly trained cyclists. Sixteen highly trained cyclists (mean ± SD; age = 24 ± 7 yr; mass = 70 ± 7kg; VO2max = 67 ± 4ml·kg−1·min–1) supplemented with either beta-alanine (n = 8, 65 mg·kg−1BM) or a placebo (n = 8; dextrose monohydrate) over 4 weeks. Pre- and postsupplementation cyclists performed a 4-minute maximal cycling test to measure average power and 30 reciprocal maximal isokinetic knee contractions at a fixed angular velocity of 180°·sec−1 to measure average power/repetition, total work done (TWD), and fatigue index (%). Blood pH, lactate (La−) and bicarbonate (HCO3 -) concentrations were measured preand postisokinetic testing at baseline and following the supplementation period. Beta-alanine supplementation was 44% likely to increase average power output during the 4-minute cycling time trial when compared with the placebo, although this was not statistically significant (p = .25). Isokinetic average power/repetition was significantly increased post beta-alanine supplementation compared with placebo (beta-alanine: 6.8 ± 9.9W, placebo: –4.3 ± 9.5 W, p = .04, 85% likely benefit), while fatigue index was significantly reduced (p = .03, 95% likely benefit). TWD was 89% likely to be improved following beta-alanine supplementation; however, this was not statistically significant (p = .09). There were no significant differences in blood pH, lactate, and HCO3 − between groups (p > .05). Four weeks of beta-alanine supplementation resulted in worthwhile changes in time-trial performance and short-duration muscular force production in highly trained cyclists.
Sonya L. Cameron, Rebecca T. McLay-Cooke, Rachel C. Brown, Andrew R. Gray and Kirsty A. Fairbairn
This study investigated the effect of ingesting 0.3 g/kg body weight (BW) of sodium bicarbonate (NaHCO3) on physiological responses, gastrointestinal (GI) tolerability, and sprint performance in elite rugby union players.
Twenty-five male rugby players, age 21.6 (2.6) yr, participated in a randomized, double-blind, placebo-controlled crossover trial. Sixty-five minutes after consuming 0.3 g/kg BW of either NaHCO3 or placebo, participants completed a 25-min warm-up followed by 9 min of high-intensity rugby-specific training followed by a rugby-specific repeated-sprint test (RSRST). Whole-blood samples were collected to determine lactate and bicarbonate concentrations and pH at baseline, after supplement ingestion, and immediately after the RSRST. Acute GI discomfort was assessed by questionnaire throughout the trials, and chronic GI discomfort was assessed during the 24 hr postingestion.
After supplement ingestion and immediately after the RSRST, blood HCO3 − concentration and pH were higher for the NaHCO3 condition than for the placebo condition (p < .001). After the RSRST, blood lactate concentrations were significantly higher for the NaHCO3 than for the placebo condition (p < .001). There was no difference in performance on the RSRST between the 2 conditions. The incidence of belching, stomachache, diarrhea, stomach bloating, and nausea was higher after ingestion of NaHCO3 than with placebo (all p < .050). The severity of stomach cramps, belching, stomachache, bowel urgency, diarrhea, vomiting, stomach bloating, and flatulence was rated worse after ingestion of NaHCO3 than with placebo (p < .050).
NaHCO3 supplementation increased blood HCO3 − concentration and attenuated the decline in blood pH compared with placebo during high-intensity exercise in well-trained rugby players but did not significantly improve exercise performance. The higher incidence and greater severity of GI symptoms after ingestion of NaHCO3 may negatively affect physical performance, and the authors strongly recommend testing this supplement during training before use in competitive situations.
Weiliang Chung, Audrey Baguet, Tine Bex, David J. Bishop and Wim Derave
Muscle carnosine loading through chronic oral beta-alanine supplementation has been shown to be effective for short-duration, high-intensity exercise. This randomized, placebo-controlled study explored whether the ergogenic effect of beta-alanine supplementation is also present for longer duration exercise. Subjects (27 well-trained cyclists/triathletes) were supplemented with either beta-alanine or placebo (6.4 g/day) for 6 weeks. Time to completion and physiological variables for a 1-hr cycling time-trial were compared between preand postsupplementation. Muscle carnosine concentration was also assessed via proton magnetic resonance spectroscopy before and after supplementation. Following beta-alanine supplementation, muscle carnosine concentration was increased by 143 ± 151% (mean ± SD; p < .001) in the gastrocnemius and 161 ± 56% (p < .001) in the soleus. Postsupplementation time trial performance was significantly slower in the placebo group (60.6 ± 4.4–63.0 ± 5.4 min; p < .01) and trended toward a slower performance following beta-alanine supplementation (59.8 ± 2.8–61.7 ± 3.0 min; p = .069). We found an increase in lactate/proton concentration ratio following beta-alanine supplementation during the time-trial (209.0 ± 44.0 (beta-alanine) vs. 161.9 ± 54.4 (placebo); p < .05), indicating that a similar lactate concentration was accompanied by a lower degree of systemic acidosis, even though this acidosis was quite moderate (pH ranging from 7.30 to 7.40). In conclusion, chronic beta-alanine supplementation in well-trained cyclists had a very pronounced effect on muscle carnosine concentration and a moderate attenuating effect on the acidosis associated with lactate accumulation, yet without affecting 1-h time-trial performance under laboratory conditions.