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.
Samuel T. Howe, Phillip M. Bellinger, Matthew W. Driller, Cecilia M. Shing and James W. Fell
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
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.
Simon P. Roberts, Keith A. Stokes, Lee Weston and Grant Trewartha
This study presents an exercise protocol utilizing movement patterns specific to rugby union forward and assesses the reproducibility of scores from this test.
After habituation, eight participants (mean ± SD: age = 21 ± 3 y, height = 180 ± 4 cm, body mass = 83.9 ± 3.9 kg) performed the Bath University Rugby Shuttle Test (BURST) on two occasions, 1 wk apart. The protocol comprised 16 × 315-s cycles (4 × 21-min blocks) of 20-m shuttles of walking and cruising with 10-m jogs, with simulated scrummaging, rucking, or mauling exercises and standing rests. In the last minute of every 315-s cycle, a timed Performance Test was carried out, involving carrying a tackle bag and an agility sprint with a ball, followed by a 25-s recovery and a 15-m sprint.
Participants traveled 7078 m, spending 79.8 and 20.2% of time in low- and high-intensity activity, respectively. The coefficients of variation (CV) between trials 1 and 2 for mean time on the Performance Test (17.78 ± 0.71 vs 17.58 ± 0.79 s) and 15-m sprint (2.69 ± 0.15 vs 2.69 ± 0.15 s) were 1.3 and 0.9%, respectively. There was a CV of 2.2% between trials 1 and 2 for mean heart rate (160 ± 5 vs 158 ± 5 beats⋅min−1) and 14.4% for blood lactate (4.41 ± 1.22 vs 4.68 ± 1.68 mmol⋅L−1).
Results suggest that measures of rugby union-specifc high-intensity exercise performed during the BURST were reproducible over two trials in habituated participants.
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.
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.
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.
Peter Peeling, Brian Dawson, Carmel Goodman, Grant Landers, Erwin T. Wiegerinck, Dorine W. Swinkels and Debbie Trinder
Urinary hepcidin, inflammation, and iron metabolism were examined during the 24 hr after exercise. Eight moderately trained athletes (6 men, 2 women) completed a 60-min running trial (15-min warm-up at 75–80% HRpeak + 45 min at 85–90% HRpeak) and a 60-min trial of seated rest in a randomized, crossover design. Venous blood and urine samples were collected pretrial, immediately posttrial, and at 3, 6, and 24 hr posttrial. Samples were analyzed for interleukin-6 (IL-6), C-reactive protein (CRP), serum iron, serum ferritin, and urinary hepcidin. The immediate postrun levels of IL-6 and 24-hr postrun levels of CRP were significantly increased from baseline (6.9 and 2.6 times greater, respectively) and when compared with the rest trial (p ≤ .05). Hepcidin levels in the run trial after 3, 6, and 24 hr of recovery were significantly greater (1.7–3.1 times) than the pre- and immediate postrun levels (p ≤ .05). This outcome was consistent in all participants, despite marked variation in the magnitude of rise. In addition, the 3-hr postrun levels of hepcidin were significantly greater than at 3 hr in the rest trial (3.0 times greater, p ≤ .05). Hepcidin levels continued to increase at 6 hr postrun but failed to significantly differ from the rest trial (p = .071), possibly because of diurnal influence. Finally, serum iron levels were significantly increased immediately postrun (1.3 times, p ≤ .05). The authors concluded that high-intensity exercise was responsible for a significant increase in hepcidin levels subsequent to a significant increase in IL-6 and serum iron.
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.
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.
Enda F. Whyte, Nicola Gibbons, Grainne Kerr and Kieran A. Moran
Context: Determination of return to play (RTP) after sport-related concussion (SRC) is critical given the potential consequences of premature RTP. Current RTP guidelines may not identify persistent exercise-induced neurocognitive deficits in asymptomatic athletes after SRC. Therefore, postexercise neurocognitive testing has been recommended to further inform RTP determination. To implement this recommendation, the effect of exercise on neurocognitive function in healthy athletes should be understood. Objective: To examine the acute effects of a high-intensity intermittent-exercise protocol (HIIP) on neurocognitive function assessed by the Symbol Digits Modality Test (SDMT) and Stroop Interference Test. Design: Cohort study. Setting: University laboratory. Participants 40 healthy male athletes (age 21.25 ± 1.29 y, education 16.95 ± 1.37 y). Intervention: Each participant completed the SDMT and Stroop Interference Test at baseline and after random allocation to a condition (HIIP vs control). A mixed between-within-subjects ANOVA assessed time- (pre- vs postcondition) -by-condition interaction effects. Main Outcome Measures: SDMT and Stroop Interference Test scores. Results: There was a significant time-by-condition interaction effect (P < .001, η 2 = .364) for the Stroop Interference Test scores, indicating that the HIIP group scored significantly lower (56.05 ± 9.34) postcondition than the control group (66.39 ± 19.6). There was no significant time-by-condition effect (P = .997, η 2 < .001) for the SDMT, indicating that there was no difference between SDMT scores for the HIIP and control groups (59.95 ± 10.7 vs 58.56 ± 14.02). Conclusions: In healthy athletes, the HIIP results in a reduction in neurocognitive function as assessed by the Stroop Interference Test, with no effect on function as assessed by the SDMT. Testing should also be considered after high-intensity exercise in determining RTP decisions for athletes after SRC in conjunction with the existing recommended RTP protocol. These results may provide an initial reference point for future research investigating the effects of an HIIP on the neurocognitive function of athletes recovering from SRC.