To determine the effect of macronutrient composition of pre-exercise meals on exercise metabolism and performance, 8 trained men exercised for 30 min above lactate threshold (30LT), followed by a 20-km time trial (TT). Approximately 3.5 h before exercise, subjects consumed a carbohydrate meal (C; 3 g carbohydrate/kg), an isoenergetic fat meal (F; 1.3 g fat/kg), or a placebo meal (P; no energy content) on 3 separate occasions in randomized order. Treatments had no effect on carbohydrate oxidation during exercise, but C decreased whole-body fat oxidation during the last 5 min of 30LT and TT, respectively (3.2 ± 1.6 and 4.8 ± 2.1 mmol · kg−1 · min−1, p < .05) when compared to F (13.3 ± 1.6 and 16.5 ± 2.7 mmol · kg−1 · min−1) and P (15.9 ± 2.7 and 17.0 ± 3.2 mmol · kg−1 · min−1). Glucose rate of appearance (Ra) and disappearance (Rd), and muscle glycogen utilization were not significantly different among treatments during exercise. TT performances were similar for C, F, and P (32.7 ± 0.5 vs. 33.1 ± 1.1 and 33.0 ± 0.8 min, p > .05). We conclude that the consumption of a pre-exercise meal has minor effects on fat oxidation during high-intensity exercise, and no effect on carbohydrate oxidation or TT performance.
David Paul, Kevin A. Jacobs, Raymond J. Geor and Kenneth W. Hinchcliff
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.
Mark D. Haub, Jeffrey A. Potteiger, Dennis J. Jacobsen, Karen L. Nau, Lawrence A. Magee and Matthew J. Comeau
We investigated the effects of carbohydrate ingestion on glycogen replenishment and subsequent short duration, high intensity exercise performance. During Session 1, aerobic power was determined and each subject (N = 6) was familiarized with the 100-kJ cycling test (lOOKJ-Test). During the treatment sessions, the subjects performed a lOOKJ-Test (Ride-1), then consumed 0.7 g ⋅ kg body mass-1 of maltodextrin (CHO) or placebo (PLC), rested 60 min, and then performed a second lOOKJ-Test (Ride-2). Muscle tissue was collected before (Pre-1) and after Ride-1 (Post-1), and before (Pre-2) and after Ride-2 (Post-2), and analyzed for glycogen concentration. Both treatments yielded a significant increase in glycogen levels following the 60-min recovery, but there was no difference between treatments. Time to complete the lOOKJ-Test increased significantly for PLC, but not for CHO. These data indicate that the decrease in performance during Ride-2 in PLC was not the result of a difference in glycogen concentration.
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.
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.
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.
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.
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.
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 (CD3−CD56+) 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 CD3−CD56+ 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 CD3−CD56+ 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.