Search Results

This study investigated whether combined ingestion and mouth rinsing with a carbohydrate solution could improve maximal sprint cycling performance. Twelve competitive male cyclists ingested 100 ml of one of the following solutions 20 min before exercise in a randomized double-blinded counterbalanced order (a) 10% glucose solution, (b) 0.05% aspartame solution, (c) 9.0% maltodextrin solution, or (d) water as a control. Fifteen min after ingestion, repeated mouth rinsing was carried out with 11 × 15 ml bolus doses of the same solution at 30-s intervals. Each participant then performed a 45-s maximal sprint effort on a cycle ergometer. Peak power output was significantly higher in response to the glucose trial (1188 ± 166 W) compared with the water (1036 ± 177 W), aspartame (1088 ± 128 W) and maltodextrin (1024 ± 202W) trials by 14.7 ± 10.6, 9.2 ± 4.6 and 16.0 ± 6.0% respectively (p < .05). Mean power output during the sprint was significantly higher in the glucose trial compared with maltodextrin (p < .05) and also tended to be higher than the water trial (p = .075). Glucose and maltodextrin resulted in a similar increase in blood glucose, and the responses of blood lactate and pH to sprinting did not differ significantly between treatments (p > .05). These findings suggest that combining the ingestion of glucose with glucose mouth rinsing improves maximal sprint performance. This ergogenic effect is unlikely to be related to changes in blood glucose, sweetness, or energy sensing mechanisms in the gastrointestinal tract.

This study examined gastric emptying, core temperature, and sprint performance during prolonged intermittent shuttle running in 30 °C when ingesting a carbohydrate-electrolyte solution (CES) or favored water (FW). Nine male soccer players performed 60 min of shuttle running, ingesting fluid before exercise and every 15 min during exercise. Gastric emptying was measured using a double-sampling aspiration technique, and intestinal temperature was monitored via ingested capsules. There were no differences between trials in the total fluid volume emptied from the stomach during each exercise period (P = 0.054). The volume emptied every 15 min was 244 ± 67 mL in the CES trial and 273 ± 66 mL in the FW trial. Intestinal temperature was higher during exercise in the CES trial (P = 0.004), and cumulative sprint time was shorter (P = 0.037). Sprint performance was enhanced by the ingestion of a CES, which resulted in elevated core temperatures, and the rate of gastric emptying remained similar between solutions.

Maintenance of repeated-sprint performance is a goal during team-sport competition such as soccer. Quercetin has been shown to be an adenosine-receptor antagonist and may reduce oxidative stress via inhibition of the enzyme xanthine oxidase (XO). The purpose of the study was to determine the effect of quercetin consumption on performance of repeated sprints and, secondarily, the XO and inflammatory-marker response induced by repeated-sprint exercise. Fifteen recreationally active, young adult men completed 2 repeated-sprint tests (RST), 12 × 30-m maximal-effort sprints (S1–S12), each after 1 wk supplementation with a placebo, a 6% carbohydrate commercial sports drink, or that drink with 500 mg of quercetin-3-glucoside, consumed twice a day (1,000 mg/d). Blood samples were collected before supplementation (B0), at baseline before each RST (B1), immediately after RST (B2), and 1 hr after RST (B3). Mean sprint time increased progressively and was significantly higher by S9 for both treatments (5.9%); however, there were no significant differences between treatments. Percent fatigue decrement (%FD) for placebo (3.8% ± 2.3%) was significantly less than with quercetin (5.1% ± 2.7%). Changes in blood XO, IL-6, and uric acid from B1 to B2 were +47%, +77%, and +25%, respectively, with no difference by treatment. In conclusion, repeated-sprint performance was not improved by quercetin supplementation and was worse than with placebo when expressed as %FD. Quercetin did not attenuate indicators of XO activity or IL-6, a marker of the inflammatory response after sprint exercise.

This study investigated the effect of initial muscle glycogen on performance of repeated sprints and some potential mechanisms for an effect of glycogen on fatigue. Eight subjects performed 2 cycling trials (repeated 60-s sprints) following consumption of either a high carbohydrate (HC) or a low carbohydrate (LC) diet. Muscle biopsies and blood samples were collected at baseline, following a 15% (15% fatigue) and a 30% decline in sprint performance (30% fatigue), when exercise was terminated. Baseline muscle glycogen levels [346 ± 19 HC (SEM) vs. 222 ± 19 mmol/kg dw LC] and total exercise time to 30% fatigue were higher following HC than LC (57.5 ± 10.0 vs. 42.0 ± 3.6 min; p < .05). Similar significant (p < .05) decreases over the entire exercise bout were seen in muscle glycogen (43%), creatine phosphate (CP; 35%), and sarcoplasmic reticu-lum (SR) Ca²⁺-uptake in isolated homogenized muscle (56%) for both trials (p > .05 between trials). The percentage decline in SR Ca²⁺-release was less for HC than LC (36% and 53%, respectively), but this was not statistically different. In summary, HC delayed fatigue during repeated sprints. As the reductions in muscle glycogen, CP, and SR function during exercise were not different by dietary treatment, these data do not support a link between whole muscle glyco-gen and SR function or CP reduction during repeated sprint exercise.

Oral supplementation with creatine monohydrate (Cr. ${\text{H}}_2$ 0) has been reported to increase muscle creatine phosphate levels. The aim of the present study was to determine the effect of such supplementation on performance of a single-effort sprint by elite swimmers. Thirty-two elite swimmers (M = 18, F = 14; age = 17-25 years) from the Australian Institute of Sport were tested on two occasions, 1 week apart. Tests performed were 25-m, 50-m, and 100-m maximal effort sprints (electronically timed with dive start, swimmers performing their best stroke), each with approximately 10 min active recovery. A 10-s maximal leg ergometry test was also undertaken. Swimmers were divided into two groups matched for sex, stroke/event, and sprint time over 50 m, and groups were randomly assigned to 5 days of Cr. ${\text{H}}_2$ 0 supplementation (4 · day⁻¹ x 5 g Cr. ${\text{H}}_2$ 0 + 2 g sucrose, n = 16) or placebo (4 · day⁻¹ x 5 g Poly cose + -2 g sucrose, n = 16) prior to the second trial. Results revealed no significant differences between the group means for sprint times or between 10-s maximal leg ergometry power and work. This study does not support the hypothesis that creatine supplementation enhances single-effort sprint ability of elite swimmers.