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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.

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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.

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Deborah K. Fletcher and Nicolette C. Bishop

This study investigated the effect of a high and low dose of caffeine on antigen-stimulated natural killer (NK) cell (CD3CD56+) activation after prolonged, strenuous cycling, as assessed by the early-activation molecule CD69. In a randomized crossover design, 12 healthy male endurance-trained cyclists cycled for 90 min at 70% VO2peak 60 min after ingesting either 0 (PLA), 2 (2CAF), or 6 (6CAF) mg/kg body mass of caffeine. Whole blood was stimulated with Pediacel (5 in 1) vaccine. A high dose of caffeine (6CAF) increased the number of CD3CD56+ cells in the circulation immediately postexercise compared with PLA (p < .05). For both 2CAF and 6CAF, the geometric mean fluorescence intensity (GMFI) of CD69+ expression on unstimulated CD3CD56+ cells was significantly higher than with PLA (both p < .05). When cells were stimulated with antigen, the GMFI of CD69 expression remained significantly higher with 2CAF than with PLA 1 hr postexercise (p < .05). Although not achieving statistical significance, 6CAF also followed a similar trend when stimulated (p = .09). There were no differences in GMFI of CD69 expression between 2CAF and 6CAF. These results suggest that a high (6 mg/kg) dose of caffeine was associated with the recruitment of NK cells into the circulation and that both a high and low (2 mg/kg) dose of caffeine increased unstimulated and antigen-stimulated NK-cell activation 1 hr after high-intensity exercise. Furthermore, there does not appear to be a dose-dependent effect of caffeine on NK-cell activation 1 hr after prolonged intensive cycling.

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Marcus J. Callahan, Evelyn B. Parr, John A. Hawley and Louise M. Burke

When ingested alone, beetroot juice and sodium bicarbonate are ergogenic for high-intensity exercise performance. This study sought to determine the independent and combined effects of these supplements. Eight endurance trained (VO2max 65 mL·kg·min-1) male cyclists completed four × 4-km time trials (TT) in a doubleblind Latin square design supplementing with beetroot crystals (BC) for 3 days (15 g·day-1 + 15 g 1 h before TT, containing 300 mg nitrate per 15 g), bicarbonate (Bi 0.3 g·kg-1 body mass [BM] in 5 doses every 15 min from 2.5 h before TT); BC+Bi or placebo (PLA). Subjects completed TTs on a Velotron cycle ergometer under standardized laboratory conditions. Plasma nitrite concentrations were significantly elevated only in the BC+Bi trial before the TT (1520 ± 786 nmol·L-1) compared with baseline (665 ± 535 nmol·L-1, p = .02) and the Bi and PLA conditions (Bi: 593 ± 203 nmol·L-1, p < .01; PLA: 543 ± 369 nmol·L-1, p < .01). Plasma nitrite concentrations were not elevated in the BC trial before the TT (1102 ± 218 nmol·L-1) compared with baseline (975 ± 607 nmol·L-1, p > .05). Blood bicarbonate concentrations were increased in the BC+Bi and Bi trials before the TT (BC+Bi: 30.9 ± 2.8 mmol·L-1; Bi: 31.7 ± 1.1 mmol·L-1). There were no differences in mean power output (386–394 W) or the time taken to complete the TT (335.8–338.1 s) between any conditions. Under the conditions of this study, supplementation was not ergogenic for 4-km TT performance.

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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.

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Simon P. Roberts, Keith A. Stokes, Lee Weston and Grant Trewartha

Purpose:

This study presents an exercise protocol utilizing movement patterns specific to rugby union forward and assesses the reproducibility of scores from this test.

Methods:

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.

Results:

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).

Conclusion:

Results suggest that measures of rugby union-specifc high-intensity exercise performed during the BURST were reproducible over two trials in habituated participants.

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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.

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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.

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Dajo Sanders, Mathieu Heijboer, Ibrahim Akubat, Kenneth Meijer and Matthijs K. Hesselink

Purpose:

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.

Methods:

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.

Results:

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.

Conclusions:

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.

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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.