High-intensity exercise leads to reductions in muscle substrates (ATP, PCr, and glycogen) and a subsequent accumulation of metabolites (ADP, Pi, H+, and Mg2+) with a possible increase in free radical production. These factors independently and collectively have deleterious effects on muscle, with significant repercussions on high-intensity performance or training sessions. The effect of carnosine on overcoming muscle fatigue appears to be related to its ability to buffer the increased H+ concentration following high-intensity work. Carnosine, however, has other roles such as an antioxidant, a metal chelator, a Ca2+ and enzyme regulator, an inhibitor of protein glycosylation and protein-protein cross-linking. To date, only 1 study has investigated the effects of carnosine supplementation (not in pure form) on exercise performance in human subjects and found no improvement in repetitive high-intensity work. Much data has come from in vitro work on animal skeletal muscle fibers or other components of muscle contractile mechanisms. Thus further research needs to be carried out on humans to provide additional understanding on the effects of carnosine in vivo.
Gulshanara Begum, Adam Cunliffe and Michael Leveritt
Stephanie Whisnant Cash, Shirley A.A. Beresford, Thomas L. Vaughan, Patrick J. Heagerty, Leslie Bernstein, Emily White and Marian L. Neuhouser
Limited evidence suggests that very high-intensity exercise is positively associated with DNA damage but moderate exercise may be associated with DNA repair.
Participants were 220 healthy, Washington State 50- to 76-year-olds in the validity/biomarker substudy of the VITamins And Lifestyle (VITAL) cohort, who provided blood samples and completed questionnaires assessing recent physical activity and demographic and health factors. Measures included nested activity subsets: total activity, moderate- plus high-intensity activity, and high-intensity activity. DNA damage (n = 122) and repair (n = 99) were measured using the comet assay. Multivariate linear regression was used to estimate regression coefficients and associated 95% confidence intervals (CIs) for relationships between MET-hours per week of activity and each DNA outcome (damage, and 15- and 60-minute repair capacities).
DNA damage was not associated with any measure of activity. However, 60-minute DNA repair was positively associated with both total activity (β = 0.21, 95% CI: 0.0057–0.412; P = .044) and high-intensity activity (β = 0.31, 95% CI: 0.20–0.60; P = .036), adjusting for age, sex, BMI, and current multivitamin use.
This study is the first to assess broad ranges of activity intensity levels related to DNA damage and repair. Physical activity was unrelated to DNA damage but was associated with increased repair.
Roy C.M. Mulder, Dionne A. Noordhof, Katherine R. Malterer, Carl Foster and Jos J. de Koning
Previous research showed that gross efficiency (GE) declines during exercise and therefore influences the expenditure of anaerobic and aerobic resources.
To calculate the anaerobic work produced during cycling time trials of different length, with and without a GE correction.
Anaerobic work was calculated in 18 trained competitive cyclists during 4 time trials (500, 1000, 2000, and 4000-m). Two additional time trials (1000 and 4000 m) that were stopped at 50% of the corresponding “full” time trial were performed to study the rate of the decline in GE.
Correcting for a declining GE during time-trial exercise resulted in a significant (P < .001) increase in anaerobically attributable work of 30%, with a 95% confidence interval of [25%, 36%]. A significant interaction effect between calculation method (constant GE, declining GE) and distance (500, 1000, 2000, 4000 m) was found (P < .001). Further analysis revealed that the constant-GE calculation method was different from the declining method for all distances and that anaerobic work calculated assuming a constant GE did not result in equal values for anaerobic work calculated over different time-trial distances (P < .001). However, correcting for a declining GE resulted in a constant value for anaerobically attributable work (P = .18).
Anaerobic work calculated during short time trials (<4000 m) with a correction for a declining GE is increased by 30% [25%, 36%] and may represent anaerobic energy contributions during high-intensity exercise better than calculating anaerobic work assuming a constant GE.
Eric T. Trexler and Abbie E. Smith-Ryan
Nutritional supplementation is a common practice among athletes, with creatine and caffeine among the most commonly used ergogenic aids. Hundreds of studies have investigated the ergogenic potential of creatine supplementation, with consistent improvements in strength and power reported for exercise bouts of short duration (≤30 s) and high intensity. Caffeine has been shown to improve endurance exercise performance, but results are mixed in the context of strength and sprint performance. Further, there is conflicting evidence from studies comparing the ergogenic effects of coffee and caffeine anhydrous supplementation. Previous research has identified independent mechanisms by which creatine and caffeine may improve strength and sprint performance, leading to the formulation of multi-ingredient supplements containing both ingredients. Although scarce, research has suggested that caffeine ingestion may blunt the ergogenic effect of creatine. While a pharmacokinetic interaction is unlikely, authors have suggested that this effect may be explained by opposing effects on muscle relaxation time or gastrointestinal side effects from simultaneous consumption. The current review aims to evaluate the ergogenic potential of creatine and caffeine in the context of high-intensity exercise. Research directly comparing coffee and caffeine anhydrous is discussed, along with previous studies evaluating the concurrent supplementation of creatine and caffeine.
Anni Vanhatalo, Andrew M. Jones and Mark Burnley
The critical power (CP) is mathematically defined as the power-asymptote of the hyperbolic relationship between power output and time-to-exhaustion. Physiologically, the CP represents the boundary between the steady-state and nonsteady state exercise intensity domains and therefore may provide a more meaningful index of performance than other well-known landmarks of aerobic fitness such as the lactate threshold and the maximal O2 uptake. Despite the potential importance to sports performance, the CP is often misinterpreted as a purely mathematical construct which lacks physiological meaning and only in recent years has this concept begun to emerge as valid and useful technique for monitoring endurance fitness. This commentary defines the basic principles of the CP concept, outlines its importance to high-intensity exercise performance, and provides an overview of the current methods available for its assessment. Interventions including training, pacing and prior exercise can be used to alter the parameters of the power-time relationship. A future challenge lies in optimizing such interventions in order to positively affect the parameters of the power-time relationship and thereby enhance sports performance in specific events.
Andrew M. Jones and Mark Burnley
The rate at which VO2 adjusts to the new energy demand following the onset of exercise strongly influences the magnitude of the “O2 defcit” incurred and thus the extent to which muscle and systemic homeostasis is perturbed. Moreover, during continuous high-intensity exercise, there is a progressive loss of muscle contractile efficiency, which is reflected in a “slow component” increase in VO2. The factors that dictate the characteristics of these fast and slow phases of the dynamic response of VO2 following a step change in energy turnover remain obscure. However, it is clear that these features of the VO2 kinetics have the potential to influence the rate of muscle fatigue development and, therefore, to affect sports performance. This commentary outlines the present state of knowledge on the characteristics of, and mechanistic bases to, the VO2 response to exercise of different intensities. Several interventions have been reported to speed the early VO2 kinetics and/or reduce the magnitude of the subsequent VO2 slow component, and the possibility that these might enhance exercise performance is discussed.
Mitch D. VanBruggen, Anthony C. Hackney, Robert G. McMurray and Kristin S. Ondrak
The effect of exercise intensity on the tracking of serum and salivary cortisol responses was examined in 12 endurance-trained males (maximal oxygen uptake [VO2max] = 58.2 ± 6.4 mL/kg/min).
Subjects rested for 30 min (control) and exercised on a cycle ergometer for 30 min at 40% (low), 60% (moderate), and 80% (high intensity) of VO2max on separate days. Serum and saliva samples were collected pretrial, immediately posttrial, and 30 min into the recovery period from each trial.
Cortisol responses increased significantly for both serum (40.4%; P = .001) and saliva (170.6%; P = .007) only in response to high-intensity exercise. Peak saliva cortisol occurred at 30 min of recovery, whereas peak serum was at the immediate posttrial sampling time point. The association between serum and saliva cortisol across all trials was examined using concordance correlation (R c) analysis, which accounts for repeated measures. The overall correlation between serum and saliva cortisol levels in all matched samples was significant (R c = 0.728; P = .001). The scatter plot revealed that salivary cortisol responses tracked closely to those of serum at lower concentrations, but not as well at higher concentrations.
Findings suggest salivary measurements of cortisol closely mirror those in the serum and that peak salivary concentrations do not occur until at least 30 min into the recovery from intense exercise.
Ben M. Krings, Timothy J. Peterson, Brandon D. Shepherd, Matthew J. McAllister and JohnEric W. Smith
The purpose of this investigation was to examine to the influence of carbohydrate ingestion (CHOI) and carbohydrate mouth rinse (CHOR) on acute repeat maximal sprint performance. Fourteen healthy males (age: 21.7 ± 1.8 years, mass: 82.3 ± 12.3 kg) completed a total of five 15-s maximal repeat sprints on a cycle ergometer against 0.075 kg ・ kg-1 body mass each separated by 4 min of active recovery. Subjects completed four experimental trials and were randomly assigned one of four treatments: (1) CHOI, (2) CHOR, (3) placebo mouth rinse (PLAR), (4) placebo ingestion (PLAI). Subjects rinsed or ingested six 50 mL 10% CHO solutions throughout each trial. Performance variables measured included rating of perceived exertion, peak heart rate, peak and mean power output, fatigue index, and total work. Significant treatment main effects were observed for mean power output (p = 0.026), total work (p = 0.020), fatigue index (p = 0.004), and heart rate (p = 0.013). Overall mean power output and total work were significantly greater with CHOI (659.3 ± 103.0 watts, 9849.8 ± 1598.8 joules) compared with CHOR (645.8 ± 99.7 watts, 9447.5 ± 1684.9 joules, p < .05). CHOI (15.3 ± 8.6 watts/s) significantly attenuated fatigue index compared with CHOR (17.7 ± 10.4 watts/s, p < .05). Based on our findings, CHOI was more likely to provide a beneficial performance effect compared with CHOR, PLAI, and PLAR. Athletes required to complete repeat bouts of high intensity exercise may benefit from CHOI.
Charles S. Urwin, Dan B. Dwyer and Amelia J. Carr
Sodium citrate induces alkalosis and can provide a performance benefit in high-intensity exercise. Previous investigations have been inconsistent in the ingestion protocols used, in particular the dose and timing of ingestion before the onset of exercise. The primary aim of the current study was to quantify blood pH, blood bicarbonate concentration and gastrointestinal symptoms after ingestion of three doses of sodium citrate (500 mg⋅kg-1, 700 mg⋅kg-1 and 900 mg⋅kg-1). Thirteen participants completed four experimental sessions, each consisting of a different dose of sodium citrate or a taste-matched placebo solution. Blood pH and blood bicarbonate concentration were measured at 30-min intervals via analysis of capillary blood samples. Gastrointestinal symptoms were also monitored at 30-min intervals. Statistical significance was accepted at a level of p < .05. Both measures of alkalosis were significantly greater after ingestion of sodium citrate compared with placebo (p < .001). No significant differences in alkalosis were found between the three sodium citrate doses (p > .05). Peak alkalosis following sodium citrate ingestion ranged from 180 to 212 min after ingestion. Gastrointestinal symptoms were significantly higher after sodium citrate ingestion compared with placebo (p < .001), while the 900 mg.kg-1 dose elicited significantly greater gastrointestinal distress than 500 mg⋅kg-1 (p = .004). It is recommended that a dose of 500 mg⋅kg-1 of sodium citrate should be ingested at least 3 hr before exercise, to achieve peak alkalosis and to minimize gastrointestinal symptoms before and during exercise.
Kellie R. Pritchard-Peschek, David G. Jenkins, Mark A. Osborne and Gary J. Slater
The aim of the current study was to investigate the effect of 180 mg of pseudoephedrine (PSE) on cycling time-trial (TT) performance. Six well-trained male cyclists and triathletes (age 33 ± 2 yr, mass 81 ± 8 kg, height 182.0 ± 6.7 cm, VO2max 56.8 ± 6.8 ml ⋅ kg−1 ⋅ min−1; M ± SD) underwent 2 performance trials in which they completed a 25-min variable-intensity (50–90% maximal aerobic power) warm-up, followed by a cycling TT in which they completed a fixed amount of work (7 kJ/kg body mass) in the shortest possible time. Sixty minutes before the start of exercise, they orally ingested 180 mg of PSE or a cornstarch placebo (PLA) in a randomized, crossover, double-blind manner. Venous blood was sampled immediately pre- and postexercise for the analysis of pH plus lactate, glucose, and norepinephrine (NE). PSE improved cycling TT performance by 5.1% (95% CI 0–10%) compared with PLA (28:58.9 ± 4:26.5 and 30:31.7 ± 4:36.7 min, respectively). There was a significant Treatment × Time interaction (p = .04) for NE, with NE increasing during the PSE trial only. Similarly, blood glucose also showed a trend (p = .06) for increased levels postexercise in the PSE trial. The ingestion of 180 mg of PSE 60 min before the onset of high-intensity exercise improved cycling TT performance in well-trained athletes. It is possible that changes in metabolism or an increase in central nervous system stimulation is responsible for the observed ergogenic effect of PSE.