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Results for “sprinting”

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At least 19 recordsLinked to original sources

PubMed2001

Long-term metabolic and skeletal muscle adaptations to short-sprint training: implications for sprint training and tapering.

The adaptations of muscle to sprint training can be separated into metabolic and morphological changes. Enzyme adaptations represent a major metabolic adaptation to sprint training, with the enzymes of all three energy systems showing signs of adaptation to training and some evidence of a return to baseline levels with detraining. Myokinase and creatine phosphokinase have shown small increases as a result of short-sprint training in some studies and elite sprinters appear better able to rapidly breakdown phosphocreatine (PCr) than the sub-elite. No changes in these enzyme levels have been reported as a result of detraining. Similarly, glycolytic enzyme activity (notably lactate dehydrogenase, phosphofructokinase and glycogen phosphorylase) has been shown to increase after training consisting of either long (>10-second) or short (<10-second) sprints. Evidence suggests that these enzymes return to pre-training levels after somewhere between 7 weeks and 6 months of detraining. Mitochondrial enzyme activity also increases after sprint training, particularly when long sprints or short recovery between short sprints are used as the training stimulus. Morphological adaptations to sprint training include changes in muscle fibre type, sarcoplasmic reticulum, and fibre cross-sectional area. An appropriate sprint training programme could be expected to induce a shift toward type IIa muscle, increase muscle cross-sectional area and increase the sarcoplasmic reticulum volume to aid release of Ca(2+). Training volume and/or frequency of sprint training in excess of what is optimal for an individual, however, will induce a shift toward slower muscle contractile characteristics. In contrast, detraining appears to shift the contractile characteristics towards type IIb, although muscle atrophy is also likely to occur. Muscle conduction velocity appears to be a potential non-invasive method of monitoring contractile changes in response to sprint training and detraining. In summary, adaptation to sprint training is clearly dependent on the duration of sprinting, recovery between repetitions, total volume and frequency of training bouts. These variables have profound effects on the metabolic, structural and performance adaptations from a sprint-training programme and these changes take a considerable period of time to return to baseline after a period of detraining. However, the complexity of the interaction between the aforementioned variables and training adaptation combined with individual differences is clearly disruptive to the transfer of knowledge and advice from laboratory to coach to athlete.

Adaptation, Physiological↗

PubMed2004

Muscle metabolism during sprint exercise in man: influence of sprint training.

In order to examine the influence of sprint training on metabolism and exercise performance during sprint exercise, 16 recreationally-active, untrained, men (VO2peak= 3.8+/-0.1 l.min(-1)) were randomly assigned to either a training (n= 8) or control group (n= 8). Each subject performed a 30-sec cycle sprint and a test to measure VO2peak before and after eight weeks of sprint training. The training group completed a series of sprints three times per week which progressed from three 30-sec cycle sprints in weeks 1 and 2, to six 30-sec sprints in weeks 7 and 8. Three mins of passive recovery separated each sprint throughout the training period. Muscle samples were obtained at rest and immediately following the pre- and post-training sprints and analysed for high energy phosphagens, glycogen and lactate; the activities of both phosphofructokinase (PFK) and citrate synthase (CS) were also measured and muscle fibre types were quantified. Training resulted in a 7.1% increase in mean power output (p<0.05), an 8% increase in VO2peak (p< 0.001), a 42% increase (p< 0.01) in CS activity and a 17% increase (p< 0.05) in resting intramuscular glycogen content. In contrast, neither PFK activity nor fibre type distribution changed with training. An increase (p< 0.05) in mean power output and attenuated (p< 0.01) ATP degradation were observed during sprint exercise following training. Glycogen degradation during sprint exercise was unaffected by sprint training. These data demonstrate that sprint training may have enhanced muscle oxidative but not glycolytic capacity.

Adaptation, Physiological↗

PubMed2006

Determinants of repeated-sprint ability in females matched for single-sprint performance.

This study investigated the relationship between VO2max and repeated-sprint ability (RSA), while controlling for the effects of initial sprint performance on sprint decrement. This was achieved via two methods: (1) matching females of low and moderate aerobic fitness (VO2max: 36.4 +/- 4.7 vs 49.6 +/- 5.5 ml kg(-1) min(-1) ; p < 0.05) for initial sprint performance and then comparing RSA, and (2) semi-partial correlations to adjust for the influence of initial sprint performance on RSA. Tests consisted of a RSA cycle test (5 x 6-s max sprints every 30 s) and a VO2max test. Muscle biopsies were taken before and after the RSA test. There was no significant difference between groups for work (W1, 3.44 +/- 0.57 vs 3.58 +/- 0.49 kJ; p = 0.59) or power (P1, 788.1 +/- 99.2 vs 835.2 +/- 127.2 W; p = 0.66) on the first sprint, or for total work (W(tot), 15.2 +/- 2.2 vs 16.6 +/- 2.2 kJ; p = 0.25). However, the moderate VO2max group recorded a smaller work decrement across the five sprints (W(dec), 11.1 +/- 2.5 vs 7.6 +/- 3.4%; p = 0.045). There were no significant differences between the two groups for muscle buffer capacity, muscle lactate or pH at any time point. When a semi-partial correlation was performed, to control for the contribution of W1 to W(dec), the correlation between VO2max and W(dec) increased from r = -0.41 (p > 0.05) to r = -0.50 (p < 0.05). These results indicate that VO2max does contribute to performance during repeated-sprint efforts. However, the small variance in W(dec) explained by VO2max suggests that other factors also play a role.

Adult↗

PubMed2004

Relationships between isokinetic knee strength, single-sprint performance, and repeated-sprint ability in football players.

Previous research has demonstrated that muscular strength of the knee extensors is related to the speed an athlete can produce during a single-sprint performance. Football players, as well as many other athletes on the field and the court, execute multiple sprints during the course of a match. The purpose of this study was to examine the relationships between leg strength, single-sprint speed, and repeated-sprint ability. Thirty-eight football players from 3 codes (soccer, rugby league, rugby union) completed a 12- x 20-m repeated-sprint protocol and were evaluated for peak isokinetic knee extension and flexion torque at 60 degrees .s(-1), 150 degrees .s(-1), and 240 degrees .s(-1). Although single-sprint performance correlated with peak extensor and flexor torque at all velocities, the strongest correlation was observed between relative knee extensor torque at 240 degrees .s(-1) and the initial acceleration phase (0-10 m) of the single-sprint performance (r = -0.714, p < 0.01). However, the data suggest that factors other than strength contribute to repeated-sprint ability. This finding provides new evidence in elucidating the relationship between strength and repeated-sprint performance.

Adult↗

PubMed2004

Effect of 6 weeks of sprint training on growth hormone responses to sprinting.

This study examined the effect of 6 weeks of prescribed sprint training on the human growth hormone (hGH) response to cycle ergometer sprinting. Sixteen male subjects were randomly assigned to a training (n=8) or a control (n=8) group. Each subject completed two main trials, consisting of two all-out 30-s cycle-ergometer sprints separated by 60 min of passive recovery, once before, and once after a 6-week training period. The training group completed three supervised sprint-training sessions per week in addition to their normal activity, whilst control subjects continued with their normal activity. In the training group, peak and mean power increased post-training by 6% (P<0.05) and 5% (P<0.05), respectively. Post-exercise blood pH did not change following training, but the highest post-exercise blood lactate concentrations were greater [highest measured value: 13.3 (1.0) vs 15.0 (1.1) mmol l(-1)], with lower blood lactate concentrations for the remainder of the recovery period (P<0.05). Post-exercise plasma ammonia concentrations were lower after training [mean highest measured value: 184.1 (9.8) vs 139.0 (11.7) micromol l(-1), P<0.05]. Resting serum hGH concentrations did not change following training, but the peak values measured post-exercise decreased by over 40% in the training group [10.3 (3.1) vs 5.8 (2.5) microg l(-1), P<0.05], and mean integrated serum hGH concentrations were 55% lower after training [567 (158) vs 256 (121) min microg l(-1), P<0.05]. The hGH response to the second sprint was attenuated similarly before and after training. This study showed that 6 weeks of combined speed- and speed-endurance training blunted the human growth hormone response to sprint exercise, despite an improvement in sprint performance.

Adaptation, Physiological↗

PubMed1996

Growth hormone responses to treadmill sprinting in sprint- and endurance-trained athletes.

The purpose of the present study was to examine the growth hormone (GH) response to treadmill sprinting in male (M) and female (F) sprint- and endurance-trained athletes. A group of 11 sprint-trained (ST; 6M, 5F) and 12 endurance-trained (ET; 6M, 6F) athletes performed a maximal 30-s sprint on a nonmotorized treadmill. Peak power and mean power expressed in watts or in watts per kilogram body mass were higher in ST than in ET (P < 0.01) and in the men compared to the women (P < 0.01). Serum GH was greater in ST than in ET athletes, but was not statistically significantly different between the men and the women [mean peak GH: ST 72.4 (SEM 12.5) compared to ET 26.3 (SEM 4.9) mU.1(-1), P < 0.01; men 59.8 (SEM 13.3) compared to the women 35.8 (SEM 7.4) mU.1(-1), n.s.]. Plasma ammonia and blood lactate concentrations were higher and blood pH lower during 1 h of recovery after the sprint in ST compared to ET (all P < 0.01). Multiple log linear regression showed that 82% of the variation in the serum peak GH response was explained by the peak power output and peak blood lactate response to the sprint. As serum GH was still approximately ten times the basal value in ST athletes after 1 h of recovery, it is suggested that the exercise-induced increase in GH could have important physiological effects in this group of athletes, including increased protein synthesis and sparing of protein degradation leading to maintained or increased muscle mass.

Adult↗

PubMed2026

Influence of Repeated-Sprint Bout Duration in Sprint Interval Training Intervention on Physical Performance Adaptations of Young Volleyball Players.

The objective of this study was to examine the effects of repeated-sprint training (RST) with varying bout durations on the physical fitness adaptations of young male volleyball players. Forty athletes were randomly allocated to one of three intervention groups performing RST with varying bout durations and similar repetition volumes, all executed at maximal effort. The 3-sec group (n = 10) completed two sets of 30 bouts, the 6-sec group (n = 10) performed two sets of 15 bouts, and the 9-sec group (n = 10) carried out two sets of 10 bouts, each adhering to a 1:3 work to rest ratio. An active control group (n = 10) engaged solely in regular volleyball training without the RST intervention. Physical fitness measures-including countermovement vertical jump (CMVJ), 10-m and 20-m linear sprints, T-test change-of-direction speed (T-CODS), reactive strength index (RSI), and the Wingate anaerobic power test-were assessed pre- and post-a 6-week training intervention (i.e., 18 sessions). All RST groups showed significant post-intervention improvements in physical fitness (main effect of time, p = 0.001), with greater adaptations compared with the control group and effect sizes ranging from small to very large. The 3-sec bout group demonstrated greater gains in CMVJ, 10-m and 20-m sprint performance, RSI, and peak power output compared with the 9-sec group (all, p < 0.05). Conversely, the 9-sec group exhibited superior adaptations in T-CODS and mean power output relative to the 3-sec group (all, p < 0.05). In conclusion, the 3-sec group experienced greater enhancements in explosive and sprint performances, while the 9-sec group showed superior gains in change of direction and mean power output. These findings indicate that manipulation of sprint-bout duration in RST can be used to optimize distinct performance adaptations in young volleyball players.

Humans↗

PubMed2005

Effects of whole body vibration training on muscle strength and sprint performance in sprint-trained athletes.

Despite the expanding use of Whole Body Vibration training among athletes, it is not known whether adding Whole Body Vibration training to the conventional training of sprint-trained athletes will improve speed-strength performance. Twenty experienced sprint-trained athletes (13 male symbol, 7 female symbol, 17-30 years old) were randomly assigned to a Whole Body Vibration group (n=10: 6 male symbol and 4 female symbol) or a Control group (n=10: 7 male symbol, 3 female symbol). During a 5-week experimental period all subjects continued their conventional training program, but the subjects of the Whole Body Vibration group additionally performed three times weekly a Whole Body Vibration training prior to their conventional training program. The Whole Body Vibration program consisted of unloaded static and dynamic leg exercises on a vibration platform (35-40 Hz, 1.7-2.5 mm, Power Plate). Pre and post isometric and dynamic (100 degrees/s) knee-extensor and -flexor strength and knee-extension velocity at fixed resistances were measured by means of a motor-driven dynamometer (Rev 9000, Technogym). Vertical jump performance was measured by means of a contact mat. Force-time characteristics of the start action were assessed using a load cell mounted on each starting block. Sprint running velocity was recorded by means of a laser system. Isometric and dynamic knee-extensor and knee-flexor strength were unaffected (p>0.05) in the Whole Body Vibration group and the Control group. As well, knee-extension velocity remained unchanged (p>0.05). The duration of the start action, the resulting start velocity, start acceleration, and sprint running velocity did not change (>0.05) in either group. In conclusion, this specific Whole Body Vibration protocol of 5 weeks had no surplus value upon the conventional training program to improve speed-strength performance in sprint-trained athletes.

Adaptation, Physiological↗

PubMed1984

Plasma LDH and CK activities after 400 m sprinting by well-trained sprint runners.

Blood lactate concentration and the activities of plasma LDH and CK were determined in 13 well-trained middle distance runners after a 400-m sprint. It was found that there is a significant relationship between mean velocity in the 400-m sprint and plasma CK activity (r = -0.56, P less than 0.05), but the mean sprint velocity did not correlate with peak blood lactate concentration (r = -0.09) or plasma LDH activity (r = -0.40). There was a significant negative correlation between mean sprint velocity and H type LDH isozyme activity (r = -0.66, P less than 0.05), and a significant positive correlation with M type LDH isozyme activity (r = 0.66, P less than 0.05). These results suggest that the magnitude of enzyme efflux from tissue into blood may be depressed by training, and that in well-trained sprinters plasma CK and LDH isozyme activities may be better indicators of physical training and/or physical performance than peak blood lactate or plasma LDH activities.

Adolescent↗

PubMed1997

Effect of combined endurance, strength and sprint training on maximal oxygen uptake, isometric strength and sprint performance in female elite handball players during a season.

Eight female handball players from the Norwegian national team were tested for maximal oxygen uptake, maximal isometric strength and maximal running velocity on four occasions during a year. The first test (T1) was made at the beginning of the preparation for a new season, the second (T2) in the middle of the preparation period, the third (T3) at the beginning of the season for the national league, and the fourth (T4) just before the most important tournament for the national team that year. Between T1 and T2 strength training had priority, between T2 and T3 endurance and sprint training had priority, and between T3 and T4 physical training was reduced. Mean maximal oxygen uptake was 51.3 +/- 2.3 ml x kg(-1) x min(-1) at T1 and was at the same level at T2. At T3 and T4 maximal oxygen uptake was increased to 53.8 +/- 2.7 and 53.5 +/- 2.9 ml x kg(-1) x min(-1) (p < 0.05), respectively. Mean maximal isometric strength increased from 154.6 +/- 25.7 at T1 to 168.9 +/- 26.8 N at T3 (p < 0.03). Mean maximal running velocity was 7.85 +/- 0.24 m x s(-1) at T1 and was not significantly changed at T2 and T3, but was increased to 8.02 +/- 0.22 m x s(-1) at T4 (p < 0.03). In conclusion with our training model, where strength training had priority in the first part of the training period, followed by a period where sprint and endurance training had priority, we were able to increase both maximal oxygen uptake and maximal running velocity in female elite handball players in the period with the most important tournament.

Adult↗

PubMed2006

Effect of blood lactate concentration and the level of oxygen uptake immediately before a cycling sprint on neuromuscular activation during repeated cycling sprints.

The purpose of this study was to determine whether neuromuscular activation is affected by blood lactate concentration (La) and the level of oxygen uptake immediately before a cycling sprint (preVO(2)). The tests consisted of ten repeated cycling sprints for 10 sec with 35-sec (RCS(35)) and 350-sec recovery periods (RCS(350)). Peak power output (PPO) was not significantly changed despite an increase in La concentration up to 12 mmol/L in RCS(350). Mean power frequency (MPF) of the power spectrum calculated from a surface electromyogram on the vastus lateralis showed a significantly higher level in RCS(350). In RCS(35), preVO(2) level and La were higher than those in RCS(350) in the initial stage of the RCS and in the last half of the RCS, respectively. Thus, neuromuscular activation during exercise with maximal effort is affected by blood lactate concentration and the level of oxygen uptake immediately before exercise, suggesting a cyclic system between muscle recruitment pattern and muscle metabolites.

Adult↗

PubMed1990

Use of pulmonary artery catheters in patients with acute myocardial infarction. Analysis of experience in 5,841 patients in the SPRINT Registry. SPRINT Study Group.

This study analyzes the use of PAC in a registry comprising 5,841 hospitalized patients with AMI. A total of 371 patients received PAC. In-hospital mortality was higher in patients with CHF who received PAC, while there was no difference in patients with cardiogenic shock or persistent hypotension. Mortality in patients receiving PAC was higher irrespective of the presence or absence of "pump failure." A separate analysis of discharge summaries of 364 patients with CHF showed that PAC was used more frequently in sicker patients and that when severity of CHF was assessed, no difference in mortality was found in patients with mild or moderate CHF. We conclude that while a higher in-hospital mortality is found in patients receiving PAC, this excess is likely related to difference in severity of CHF, which had not been assessed in every individual. It is unlikely that PAC increases mortality.

Adult↗

PubMed1988

Secondary prevention reinfarction Israeli nifedipine trial (SPRINT). A randomized intervention trial of nifedipine in patients with acute myocardial infarction. The Israeli Sprint Study Group.

The efficacy of nifedipine in the prevention of post-infarction morbidity and mortality was evaluated in a double-blind clinical trial of 2276 survivors of acute myocardial infarction recruited from the cardiac departments of 14 Israeli hospitals. The patients were randomized to either nifedipine 30 mg day-1 or placebo between 7 and 21 days after their hospitalization for the acute event. Baseline characteristics of patients in each group were virtually identical for most pertinent variables. Mortality during an average 10-month follow-up period was 5.7% in the placebo group and 5.8% among those receiving nifedipine. Nonfatal recurrent myocardial infarction occurred in 4.8% and 4.4% of placebo and nifedipine patients, respectively. Administration of nifedipine according to the protocol used in the present study had no effect on cardiac events in survivors of acute myocardial infarction.

Clinical Trials as Topic↗

PubMed1998

Power output and muscle metabolism during and following recovery from 10 and 20 s of maximal sprint exercise in humans.

On two separate days eight male subjects performed a 10- or 20-s cycle ergometer sprint (randomized order) followed, after 2 min of recovery, by a 30-s sprint. Muscle biopsies were obtained from the vastus lateralis at rest, immediately after the first sprint and after the 2 min of recovery on both occasions. The anaerobic ATP turnover during the initial 10 s of sprint 1 was 129 +/- 12 mmol kg dry weight-1 and decreased to 63 +/- 10 mmol kg dry weight-1 between the 10th and 20th s of sprint 1. This was a result of a 300% decrease in the rate of phosphocreatine breakdown and a 35% decrease in the glycolytic rate. Despite this 51% reduction in anaerobic ATP turnover, the mean power between 10 and 20 s of sprint 1 was reduced by only 28%. During the same period, oxygen uptake increased from 1.30 +/- 0.15 to 2.40 +/- 0.23 L min-1, which partially compensated for the decreased anaerobic metabolism. Muscle pH decreased from 7.06 +/- 0.02 at rest to 6.94 +/- 0.02 after 10 s and 6.82 +/- 0.03 after 20 s of sprinting (for all changes P < 0.01). Muscle pH did not change following a 2-min recovery period after both the 10- and 20-s sprints, but phosphocreatine was resynthesized to 86 +/- 3 and 76 +/- 3% of the resting value, respectively (n.s. 10- vs. 20-s sprint). Following 2 min of recovery after the 10-s sprint subjects were able to reproduce peak but not mean power. Restoration of both mean and peak power following the 20-s sprint was 88% of sprint 1, and was lower compared with that after the 10-s sprint (P < 0.01). Total work during the second 30-s sprint after the 10- and the 20-s sprint was 19.3 +/- 0.6 and 17.8 +/- 0.5 kJ, respectively (P < 0.01). As oxygen uptake was the same during the 30-s sprints (2.95 +/- 0.15 and 3.02 +/- 0.16 L min-1), and (Phosphocreatine) before the sprint was similar, the lower work may be related to a reduced glycolytic ATP regeneration as a result of the higher muscle acidosis.

Acid-Base Equilibrium↗

PubMed1996

Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise.

This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10- and 30-s sprints. At the end of sprint 1, PCr was 16.9 +/- 1.4% of the resting value, and muscle pH dropped to 6.69 +/- 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 +/- 0.03), but PCr was resynthesized to 78.7 +/- 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 +/- 9 mmol/kg dry muscle during the first sprint but was decreased to 139 +/- 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a approximately 45% decrease in glycolysis. Despite this approximately 41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only approximately 18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 +/- 0.10 vs. 3.17 +/- 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01). These data suggest that aerobic metabolism provides a significant part (approximately 49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.

Adenosine Triphosphate↗

PubMed2005

Human growth hormone responses to repeated bouts of sprint exercise with different recovery periods between bouts.

This study examined the growth hormone (GH) response to repeated bouts of sprint cycling. Eight healthy men completed three trials consisting of two 30-s sprints on a cycle ergometer separated by either 60 min (Trial A) or 240 min (Trial B) of recovery and a single 30-s sprint carried out the day after Trial B (Trial C). Trials A and B were separated by at least 7 days. Blood samples were obtained at rest and during recovery from each sprint. In Trial A, GH was elevated immediately before sprint 2, and there was no further increase in GH following the second sprint [area under the curve: 460 (SD 348) vs. 226 min.mug(-1).l(-1) (SD 182), P = 0.05]. Free insulin-like growth factor I tended to be lower immediately before sprint 2 than sprint 1 (P = 0.06). Serum free fatty acids were not different immediately before each of the sprints. In Trial B, there was a trend for a smaller GH response to the second sprint [GH area under the curve: 512 (SD 396) vs. 242 min.mug(-1).l(-1) (SD 190), P = 0.09]. Free insulin-like growth factor I tended to be lower (P = 0.06), and serum free fatty acids were higher (P = 0.01) immediately before sprint 2 than sprint 1. There was no difference in the GH response to sprinting on consecutive days (Trials B and C). In conclusion, repeated bouts of sprint cycling on the same day result in an attenuation or even ablation of the exercise-induced increase in GH, depending on the recovery interval between sprints.

Acceleration↗

PubMed2001

Neural influences on sprint running: training adaptations and acute responses.

Performance in sprint exercise is determined by the ability to accelerate, the magnitude of maximal velocity and the ability to maintain velocity against the onset of fatigue. These factors are strongly influenced by metabolic and anthropometric components. Improved temporal sequencing of muscle activation and/or improved fast twitch fibre recruitment may contribute to superior sprint performance. Speed of impulse transmission along the motor axon may also have implications on sprint performance. Nerve conduction velocity (NCV) has been shown to increase in response to a period of sprint training. However, it is difficult to determine if increased NCV is likely to contribute to improved sprint performance. An increase in motoneuron excitability, as measured by the Hoffman reflex (H-reflex), has been reported to produce a more powerful muscular contraction, hence maximising motoneuron excitability would be expected to benefit sprint performance. Motoneuron excitability can be raised acutely by an appropriate stimulus with obvious implications for sprint performance. However, at rest H-reflex has been reported to be lower in athletes trained for explosive events compared with endurance-trained athletes. This may be caused by the relatively high, fast twitch fibre percentage and the consequent high activation thresholds of such motor units in power-trained populations. In contrast, stretch reflexes appear to be enhanced in sprint athletes possibly because of increased muscle spindle sensitivity as a result of sprint training. With muscle in a contracted state, however, there is evidence to suggest greater reflex potentiation among both sprint and resistance-trained populations compared with controls. Again this may be indicative of the predominant types of motor units in these populations, but may also mean an enhanced reflex contribution to force production during running in sprint-trained athletes. Fatigue of neural origin both during and following sprint exercise has implications with respect to optimising training frequency and volume. Research suggests athletes are unable to maintain maximal firing frequencies for the full duration of, for example, a 100m sprint. Fatigue after a single training session may also have a neural manifestation with some athletes unable to voluntarily fully activate muscle or experiencing stretch reflex inhibition after heavy training. This may occur in conjunction with muscle damage. Research investigating the neural influences on sprint performance is limited. Further longitudinal research is necessary to improve our understanding of neural factors that contribute to training-induced improvements in sprint performance.

Adaptation, Physiological↗

PubMed1996

Effects of oral creatine supplementation on multiple sprint cycle performance.

This study examined the influence of oral creatine monohydrate supplementation on repeated 10 s cycle ergometer sprint performance. Seventeen recreationally active males (mean +/- SD age, body mass, height, and peak oxygen uptake = 20.5 +/- 1.2 yr, 72.1 +/- 10.3 kg, 176.8 +/- 6.6 cm and 3.87 +/- 0.91 l.min-1, respectively) participated in the 16 day experiment. All subjects initially completed a VO2peak test and were then administered glucose (4 x 10 g per day) in a single blind fashion for four days, after which they completed the first series of multiple sprints (7 x 10 s). Following the sprints, subjects were matched on sprint performance and divided into two groups (n = 8, placebo (Pl); and n = 9, creatine (Cr)). For the following four days, diets were supplemented with either Cr (4 x 70 mg.kg-1 body mass per day mixed with 5 g glucose) or glucose (4 x 10 g per day); supplementation during this phase was double-blind. Subjects then repeated the multiple sprint and VO2peak tests. Measures of peak power output (PPO), mean power output (MPO), end-power output (EPO), and percent power decline were recorded during the sprints. Each 10 s sprint was separated by 30 s of passive recovery except for sprints five and six which were separated by five minutes. Venous blood was sampled at rest, immediately after sprint five, before sprint six, and following sprint seven for the analysis of plasma lactate and blood pH. Expired air was sampled for five minutes following sprint seven for the calculation of post-exercise VO2. Analysis of variance revealed that four days of Cr supplementation did not influence multiple sprint performance, plasma lactate, blood pH and excess post-sprint oxygen consumption. Furthermore, VO2peak was unchanged following Cr supplementation. The data suggest that either the four day period of Cr supplementation failed to significantly raise resting muscle [Cr], or that multiple sprint performance was not enhanced by increases in resting muscle [Cr].

Adult↗