Search Results

Caffeine ingestion (3-9 mg/kg body weight) prior to exercise increases performance during prolonged endurance exercise and short-term intense exercise lasting ~5 min in the laboratory. These results are generally reported in well-trained elite or recreational subjects. However, there is a lack of well-controlled field studies to determine the applicability of laboratory results to the athletic world. Caffeine does not appear to enhance performance during incremental exercise tests lasting 8-20 min and during sprinting lasting less than 90 s, although research examining sprinting is rare. In addition, the mechanisms responsible for any improvement in endurance and short-term exercise have not been clearly established. The ergogenic effects of caffeine are present with urinary caffeine levels that are below the limit of 12 µg/ml allowed by the International Olympic Committee, which raises serious ethical issues regarding the use of caffeine to improve athletic performance. One solution would be to add caffeine to the list of banned substances, thereby requiring athletes to abstain from caffeine ingestion 48-72 hr prior to competition.

Background: Rest between training sessions can be short for athletes. In these situations, consuming carbohydrate (CHO) postexercise replenishes glycogen stores, which is important for recovery and subsequent performance. Purpose: This study tested whether CHO intake during a 2-hour rest between exercise bouts improved performance in the subsequent bout. Methods: In a randomized, single-blinded, crossover design, 10 recreationally active participants (23 [4] y, 70.8 [6.6] kg, 47.0 [5.4] mL·O₂·min⁻¹·kg·body·mass⁻¹) arrived at the lab postprandial and completed 2 exercise bouts separated by a 2-hour rest. Bouts included 5 × 4-minute intervals at ∼80% peak oxygen consumption separated by 2 minutes at ∼40% peak oxygen consumption and ended with an endurance trial to voluntary exhaustion at ∼90% peak oxygen consumption. During intervals 1 and 4 in each bout, expired gases were collected and O₂ deficit was estimated. Immediately following bout 1, either a CHO (1.2 g CHO·kg·body·mass⁻¹) or placebo solution was consumed. Results: Endurance trial duration decreased in bout 2 versus 1 in both conditions (P < .01) but was ∼35% longer in bout 2 with CHO versus placebo (interaction, P = .03; post hoc, P = .03). Oxygen uptake increased during interval 4 versus 1 in both bouts (P < .01) but was unaffected by CHO (P ≥ .58). O₂ deficit was unaffected by CHO (P = .93), bout, or interval (P ≥ .15). Perceived exertion was higher in bout 2 versus 1 (P < .001) and reduced in intervals 2 and 4 in CHO (P ≤ .01). Conclusions: When rest between training sessions is 2 hours, athletes may improve subsequent performance by consuming CHO during recovery.

Purpose: The purpose of this study was to quantify the internal load of male varsity ice hockey players, using both sessional rating of perceived exertion (sRPE) and the heart rate–derived physiological measure of training impulse (TRIMP), during training sessions and competitions throughout an entire season. Methods: Twenty-seven male varsity ice hockey players (22.1 [1.1] y, 85.9 [5.4] kg, 181.3 [5.1] cm) were included in this longitudinal prospective cohort study. Results: The internal load was significantly higher (P < .001) for games (sRPE: 403 [184] arbitrary units [AU], TRIMP: 98 [59] AU) compared with training sessions (sRPE: 281 [130] AU, TRIMP: 71 [35] AU). The regular season had the highest internal load compared with the preseason and postseason. There was evidence of microcycle periodization with training sessions several days prior to game days having the highest internal load (both sRPE and TRIMP) and tapering down as the subsequent training sessions approached game day. For positional comparisons, the goalies had higher sRPE (346 [151] AU, P < .001) and TRIMP (99 [64] AU, P < .001) compared with defense (sRPE: 295 [130] AU, TRIMP: 65 [29] AU) and forwards (sRPE: 264 [123] AU, TRIMP: 70 [30] AU) for training sessions, but no significant differences were present for competitions. Finally, there was an overall moderate and statistically significant relationship between the sRPE and TRIMP internal load measures (r = .434, P < .001). Conclusions: Internal load was greater during competitions versus training sessions in male varsity ice hockey players, and the microcycle assessment demonstrated that training sessions were tailored to game day. Mesocycle assessment revealed the highest internal loads during the regular season due to dense game scheduling and a short season.

This study examined whether acute taurine (T) ingestion before prolonged cycling would improve time-trial (TT) performance and alter whole-body fuel utilization compared with a control (CON) trial and a placebo (PL) trial in which participants were told they received taurine but did not. Eleven endurance-trained male cyclists (27.2 ± 1.5 yr, 74.3 ± 2.3 kg, 59.9 ± 2.3 ml · kg⁻¹ · min⁻¹; M ± SEM) completed 3 trials in a randomized, crossover, blinded design in which they consumed a noncaloric sweetened beverage with either 1.66 g of T or nothing added (CON, PL) 1 hr before exercise. Participants then cycled at 66.5% ± 1.9% VO_2max for 90 min followed immediately by a TT (doing 5 kJ of work/kg body mass as fast as possible). Data on fluid administration, expired gas, heart rate, and ratings of perceived exertion were collected at 15-min intervals during the 90-min cycling ride, but there were no differences recorded between trials. There was no difference in TT performance between any of the 3 trials (1,500 ± 87 s). Average carbohydrate (T 2.73 ± 0.21, CON 2.88 ± 0.19, PL 2.89 ± 0.20 g/min) and fat (T 0.45 ± 0.05, CON 0.39 ± 0.04, PL 0.39 ± 0.05 g/min) oxidation rates were unaffected by T supplementation. T ingestion resulted in a 16% increase (5 g, ~84 kJ; p < .05) in total fat oxidation over the 90-min exercise period compared with CON and PL. The acute ingestion of 1.66 g of T before exercise did not enhance TT performance but did result in a small but significant increase in fat oxidation during submaximal cycling in endurance-trained cyclists.

This study investigated whether the supplement Microhydrin^® (MH) contains silica hydride bonds (Si-H) and if Microhydrin supplementation increased performance or altered metabolism compared to placebo (PL) during prolonged endurance cycling. Seven endurance-trained male cyclists consumed 9.6 g of MH or PL over 48 h in a randomized, double-blind, crossover design. Subjects cycled at ~ 70% of their VO_2peak, coupled with five 2-min bursts at 85% VO_2peak to simulate hill climbs over 2 h. Subjects then completed a time trial, which required them to complete 7 kJ/kg body mass as quickly as possible. Infrared spectrometry analysis showed a complete absence of Si-H bonds in MH. There was no difference in time trial performance between the 2 trials (PL: 2257 ± 120 s vs. MH: 2345 ± 152 s). Measured oxygen uptake, respiratory exchange ratio, carbohydrate (MH: 2.99 ± 0.13 g/min; PL: 2.83 ± 0.17 g/min avg. over 2 h) and fat (MH: 0.341 ± 0.06 g/min; PL: 0.361 ± 0.07 g/min) oxidation rates and all blood parameters (lactate, glucose, and free fatty acids) were all unaffected by MH supplementation. The volume of expired CO₂ and ventilation were significantly greater with MH supplementation (P ≤ 0.05). The results indicate that oral Microhydrin supplementation does not enhance cycling time trial performance or alter metabolism during prolonged submaximal exercise in endurance-trained cyclists.

This study investigated the effects of progressive mild dehydration during cycling on whole-body substrate oxidation and skeletal-muscle metabolism in recreationally active men. Subjects (N = 9) cycled for 120 min at ~65% peak oxygen uptake (VO_2peak 22.7 °C, 32% relative humidity) with water to replace sweat losses (HYD) or without fluid (DEH). Blood samples were taken at rest and every 20 min, and muscle biopsies were taken at rest and at 40, 80, and 120 min of exercise. Subjects lost 0.8%, 1.8%, and 2.7% body mass (BM) after 40, 80, and 120 min of cycling in the DEH trial while sweat loss was not significantly different between trials. Heart rate was greater in the DEH trial from 60 to 120 min, and core temperature was greater from 75 to 120 min. Rating of perceived exertion was higher in the DEH trial from 30 to 120 min. There were no differences in VO_2, respiratory-exchange ratio, total carbohydrate (CHO) oxidation (HYD 312 ± 9 vs. DEH 307 ± 10 g), or sweat rate between trials. Blood lactate was significantly greater in the DEH trial from 20 to 120 min with no difference in plasma free fatty acids or epinephrine. Glycogenolysis was significantly greater (24%) over the entire DEH vs. HYD trial (433 ± 44 vs. 349 ± 27 mmol · kg⁻¹ · dm⁻¹). In conclusion, dehydration of <2% BM elevated physiological parameters and perceived exertion, as well as muscle glycogenolysis, during exercise without affecting whole-body CHO oxidation.

This study determined whether mild dehydration influenced skeletal muscle glycogen use, core temperature or performance during high-intensity, intermittent cycle-based exercise in ice hockey players vs. staying hydrated with water. Eight males (21.6 ± 0.4 yr, 183.5 ± 1.6 cm, 83.9 ± 3.7 kg, 50.2 ± 1.9 ml·kg^-1·min^-1) performed two trials separated by 7 days. The protocol consisted of 3 periods (P) containing 10 × 45-s cycling bouts at ~133% VO_2max, followed by 135 s of passive rest. Subjects drank no fluid and dehydrated during the protocol (NF), or maintained body mass by drinking WATER. Muscle biopsies were taken at rest, immediately before and after P3. Subjects were mildly dehydrated (-1.8% BM) at the end of P3 in the NF trial. There were no differences between the NF and WATER trials for glycogen use (P1+P2; 350.1 ± 31.9 vs. 413.2 ± 33.2, P3; 103.5 ± 16.2 vs. 131.5 ± 18.9 mmol·kg dm^-1), core temperature (P1; 37.8 ± 0.1 vs. 37.7 ± 0.1, P2; 38.2 ± 0.1 vs. 38.1 ± 0.1, P3; 38.3 ± 0.1 vs. 38.2 ± 0.1 °C) or performance (P1; 156.3 ± 7.8 vs. 154.4 ± 8.2, P2; 150.5 ± 7.8 vs. 152.4 ± 8.3, P3; 144.1 ± 8.7 vs. 148.4 ± 8.7 kJ). This study demonstrated that typical dehydration experienced by ice hockey players (~1.8% BM loss), did not affect glycogen use, core temperature, or voluntary performance vs. staying hydrated by ingesting water during a cycle-based simulation of ice hockey exercise in a laboratory environment.

Ischemic preconditioning (IPC) was initially developed to protect the myocardium from ischemia through altered cardiocyte metabolism. Because of the observed effects on metabolism and oxygen kinetics, IPC gained interest as a potential ergogenic aid in sports. Limited research evaluating the effects of IPC on maximal short-duration activities has been performed, and of the existing literature, mixed outcomes resulting from intrasubject variation may have clouded the efficacy of this technique for enhancing sprint performance. Therefore, the current study employed a randomized repeated-measures crossover design with IPC, placebo (SHAM), and control conditions while using sprint-trained athletes (N = 18) to determine the effect of IPC (3 × 5-min occlusions, with 5-min reperfusion), concluding 15 min prior to maximal 10-s and 20-m sprinting. A visual analog scale was used in conjunction with the sprint trials to evaluate any possible placebo effect on performance. Despite a “significantly beneficial” perception of the IPC treatment compared with the SHAM trials (P < .001), no changes in sprint performance were observed after either the IPC or SHAM condition over 10 m (IPC Δ  < 0.01 [0.02] s, SHAM Δ  < 0.01 [0.02] s) or 20 m (IPC Δ = −0.01 [0.03] s, SHAM Δ < 0.01 [0.03] s) compared with control. Thus, an IPC protocol does not improve 10- or 20-m sprint performance in sprint-trained athletes.

Several previous studies have reported performance decrements in team sport athletes who dehydrated approximately 1.5–2% of their body mass (BM) through sweating. This study measured on-ice sweat loss, fluid intake, sodium balance, and carbohydrate (CHO) intake of 77 major junior (JR; 19 ± 1 years), 60 American Hockey League (AHL; 24 ± 4 years), and 77 National Hockey League (NHL; 27 ± 5 years) players. Sweat loss was calculated from pre- to post-exercise BM plus fluid intake minus urine loss. AHL (2.03 ± 0.62 L/hr) and NHL (2.02 ± 0.74 L/hr) players had higher sweat rates (p < .05) than JR players (1.63 ± 0.58 L/hr). AHL (1.23 ± 0.69%; p = .006) and NHL (1.29% ± 0.63%; p < .001) players had ∼30% greater BM losses than JR players (0.89% ± 0.57%). There was no difference in fluid intake between groups (p > .05). Sodium deficits (sodium loss − intake) were greater (p < .05) in AHL (1.68 ± 0.74 g/hr) and NHL (1.56 ± 0.84 g/hr) players compared with JR players (1.01 ± 0.50 g/hr). CHO intake was similar between groups (14–20 g CHO/hr), with 29%, 32%, and 40% of JR, AHL, and NHL players consuming no CHO, respectively. In summary, sweat rates were high in all players, but the majority of players (74/77, 54/60, and 68/77 of JR, AHL, and NHL, respectively) avoided mild dehydration (>2% BM) during 60 min of practice. However, ∼15%, 41%, and 48% of the JR, AHL, and NHL players, respectively, may have reached mild dehydration and increased risk of performance decrements in a 90-min practice.

Purpose: To determine the effects of low-dose caffeine supplementation (3 mg/kg body mass) consumed 1 h before the experiment on rating of perceived exertion (RPE), skills performance (SP), and physicality in male college ice hockey players. Methods: Using a double-blind, placebo-controlled, randomized crossover experimental design, 15 college ice hockey players participated in SP trials and 14 participated in scrimmage (SC) trials on a total of 4 d, with prescribed ice hockey tasks occurring after a 1-h high-intensity practice. In the SP trials, time to complete and error rate for each drill of the validated Western Hockey League Combines Testing Standard were recorded. Peak head accelerations, trunk contacts, and offensive performance were quantified during the SC trials using accelerometery and video analysis. RPE was assessed in both the SP and SC trials. Results: RPE was significantly greater in the caffeine (11.3 [2.0]) than placebo (9.9 [1.9]) condition postpractice (P = .002), with a trend toward greater RPE in caffeine (16.9 [1.8]) than placebo (15.7 [2.8]) post-SC (P = .05). There was a greater number of peak head accelerations in the caffeine (4.35 [0.24]) than placebo (4.14 [0.24]) condition (P = .028). Performance times, error rate, and RPE were not different between intervention conditions during the SP trials (P > .05). Conclusions: A low dose of caffeine has limited impact on sport-specific skill performance and RPE but may enhance physicality during ice hockey SCs.