30-s Sprint Research Articles

A 10-s Sprint Performed After Moderate-Intensity Exercise Neither Increases nor Decreases the Glucose Requirement to Prevent Late-Onset Hypoglycemia in Individuals With Type 1 Diabetes

OBJECTIVETo determine whether performing a 10-s sprint after moderate-intensity exercise increases the amount of carbohydrate required to maintain euglycemia and prevent late-onset postexercise hypoglycemia relative to moderate-intensity exercise alone.RESEARCH DESIGN AND METHODSSeven individuals with type 1 diabetes underwent a hyperinsulinemic-euglycemic clamp and performed 30 min of moderate-intensity exercise on two separate occasions followed by either a 10-s maximal sprint effort or no sprint. During the following 8 h, glucose infusion rate to maintain euglycemia and rates of glucose appearance and disappearance were measured continuously.RESULTSIn response to exercise and throughout the 8-h recovery period, there were no differences in glucose infusion rate, blood glucose levels, plasma insulin concentrations, and rates of glucose appearance and disappearance between the two experimental conditions (P > 0.05).CONCLUSIONSA 10-s sprint performed after 30 min of moderate-intensity exercise does not affect the amount of carbohydrate required to maintain euglycemia postexercise in individuals with type 1 diabetes.

Sprint Interval Training in Hypoxia Stimulates Glycolytic Enzyme Activity

In this study, we compared the effect of sprint interval training (SIT) in normoxia versus hypoxia on muscle glycolytic and oxidative capacity, monocarboxylate transporter content, and endurance exercise performance. Healthy male volunteers (18-30 yr) performed 6 wk of SIT on a cycling ergometer (30-s sprints vs 4.5-min rest intervals; 3 d · wk(-1)) in either normobaric hypoxia (HYP, FiO2 = 14.4%, n = 10) or normoxia (NOR, FiO2 = 20.9%, n = 9). The control group did not train (CON, n = 10). Training load was increased from four sprints per session in week 1 to nine sprints in week 6. Before and after SIT, subjects performed a maximal incremental exercise test plus a 10-min simulated time trial on a cycle ergometer in both normoxia (MAX nor and TT nor) and hypoxia (MAX hyp and TT hyp). A needle biopsy was taken from musculus vastus lateralis at rest 5-6 d after the last exercise session. SIT increased muscle phosphofructokinase activity more in HYP (+59%, P < 0.05) than that in NOR (+17%), whereas citrate synthase activity was similar between groups. Compared with the pretest, power outputs corresponding to 4 mmol blood lactate in HYP during MAX nor (+7%) and MAX hyp (+9%) were slightly increased (P < 0.05), whereas values were constant in NOR. V·O 2max in MAX nor and TT performance in TT nor and TT hyp were increased by ≈ 6%-8% (P < 0.05) in either group. The training elevated monocarboxylate transporter 1 protein content by ≈ 70% (P < 0.05). In CON, all measurements were constant throughout the study. SIT in hypoxia up-regulated muscle phosphofructokinase activity and the anaerobic threshold more than SIT in normoxia but did not enhance endurance exercise performance.

The Reliability of a 30-s Sprint Test on the Wattbike Cycle Ergometer

To determine the reliability of a 30-s sprint cycle test on the Wattbike cycle ergometer. Over 3 consecutive weeks, 11 highly trained cyclists (mean ± SD; age 31 ± 6 y, mass 74.6 ± 10.6 kg, height 180.5 ± 8.1cm) completed four 30-s maximal sprints on a Wattbike ergometer after a standardized warm-up. The sprint test implemented a "rolling start" that consisted of a 60-s preload (at an intensity of 4.5 W/kg) before the 30-s maximal sprint. Variables determined across the duration of the sprint were peak power (Wpeak), mean power (Wmean), W/kg, mean cadence (rpm), maximum heart rate (n = 10), and postexercise blood lactate. The average intraclass correlation coefficients between trials (2v1, 3v2, 4v3, 4v1) were Wpeak .97 (90%CI .94-.99), Wmean .99 (90%CI .97-1.00), W/kg .96 (90%CI .91-.98), mean cadence .96 (90%CI .92-.99), maximum heart rate .99 (90%CI .97-.99), and postexercise blood lactate .94 (90%CI .87-.98). The average typical error of measurement (expressed as a CV% and absolute value between trials-2v1, 3v2, 4v3, 4v1) was Wpeak 4.9%, 52.7 W; Wmean 2.4%, 19.2 W; W/kg 2.3%, 0.18 W/kg; mean cadence 1.4%, 1.6 rpm; maximum heart rate 0.9%, 1.6 beats/min; and postexercise blood lactate 4.6%, 0.48 mmol/L. A 30-s sprint test on the Wattbike cycle ergometer is highly reproducible in trained cyclists.

Significant Molecular and Systemic Adaptations after Repeated Sprint Training in Hypoxia

While intermittent hypoxic training (IHT) has been reported to evoke cellular responses via hypoxia inducible factors (HIFs) but without substantial performance benefits in endurance athletes, we hypothesized that repeated sprint training in hypoxia could enhance repeated sprint ability (RSA) performed in normoxia via improved glycolysis and O2 utilization. 40 trained subjects completed 8 cycling repeated sprint sessions in hypoxia (RSH, 3000 m) or normoxia (RSN, 485 m). Before (Pre-) and after (Post-) training, muscular levels of selected mRNAs were analyzed from resting muscle biopsies and RSA tested until exhaustion (10-s sprint, work-to-rest ratio 1∶2) with muscle perfusion assessed by near-infrared spectroscopy. From Pre- to Post-, the average power output of all sprints in RSA was increased (p<0.01) to the same extent (6% vs 7%, NS) in RSH and in RSN but the number of sprints to exhaustion was increased in RSH (9.4±4.8 vs. 13.0±6.2 sprints, p<0.01) but not in RSN (9.3±4.2 vs. 8.9±3.5). mRNA concentrations of HIF-1α (+55%), carbonic anhydrase III (+35%) and monocarboxylate transporter-4 (+20%) were augmented (p<0.05) whereas mitochondrial transcription factor A (−40%), peroxisome proliferator-activated receptor gamma coactivator 1α (−23%) and monocarboxylate transporter-1 (−36%) were decreased (p<0.01) in RSH only. Besides, the changes in total hemoglobin variations (Δ[tHb]) during sprints throughout RSA test increased to a greater extent (p<0.01) in RSH. Our findings show larger improvement in repeated sprint performance in RSH than in RSN with significant molecular adaptations and larger blood perfusion variations in active muscles.

Reducing Muscle Temperature Drop after Warm-up Improves Sprint Cycling Performance

This study aimed to determine the effect of passive insulation versus external heating during recovery after a sprint-specific warm-up on thigh muscle temperature and subsequent maximal sprint performance. On three separate occasions, 11 male cyclists (age = 24.7 ± 4.2 yr, height = 1.82 ± 0.72 m, body mass = 77.9 ± 9.8 kg; mean ± SD) completed a standardized 15-min intermittent warm-up on a cycle ergometer, followed by a 30-min passive recovery period before completing a 30-s maximal sprint test. Muscle temperature was measured in the vastus lateralis at 1, 2, and 3 cm depth before and after the warm-up and immediately before the sprint test. Absolute and relative peak power output was determined and blood lactate concentration was measured immediately after exercise. During the recovery period, participants wore a tracksuit top and (i) standard tracksuit pants (CONT), (ii) insulated athletic pants (INS), or (iii) insulated athletic pants with integrated electric heating elements (HEAT). Warm-up increased Tm by approximately 2.5 °C at all depths, with no differences between conditions. During recovery, Tm remained elevated in HEAT compared with INS and CONT at all depths (P < 0.001). Both peak and relative power output were elevated by 9.6% and 9.1%, respectively, in HEAT compared with CONT (both P < 0.05). The increase in blood lactate concentration was greater (P < 0.05) after sprint in HEAT (6.3 ± 1.8 mmol·L(-1)) but not INS (4.0 ± 1.8 mmol·L(-1)) versus CONT (4.1 ± 1.9 mmol·L(-1)). Passive heating of the thighs between warm-up completion and performance execution using pants incorporating electrically heated pads can attenuate the decline in Tm and improve sprint cycling performance.

Repeated‐sprint performance and vastus lateralis oxygenation: Effect of limited O2 availability

This study examined the influence of muscle deoxygenation and reoxygenation on repeated-sprint performance via manipulation of O2 delivery. Fourteen team-sport players performed 10 10-s sprints (30-s recovery) under normoxic (NM: FI O2 0.21) and acute hypoxic (HY: FI O2 0.13) conditions in a randomized, single-blind fashion and crossover design. Mechanical work was calculated and arterial O2 saturation (Sp O2 ) was estimated via pulse oximetry for every sprint. Muscle deoxyhemoglobin concentration ([HHb]) was monitored continuously by near-infrared spectroscopy. Differences between NM and HY data were analyzed for practical significance using magnitude-based inferences. HY reduced Sp O2 (-10.7 ± 1.9%, with chances to observe a higher/similar/lower value in HY of 0/0/100%) and mechanical work (-8.2 ± 2.1%; 0/0/100%). Muscle deoxygenation increased during sprints in both environments, but was almost certainly higher in HY (12.5 ± 3.1%, 100/0/0%). Between-sprint muscle reoxygenation was likely more attenuated in HY (-11.1 ± 11.9%; 2/7/91%). The impairment in mechanical work in HY was very largely correlated with HY-induced attenuation in muscle reoxygenation (r = 0.78, 90% confidence limits: 0.49; 0.91). Repeated-sprint performance is related, in part, to muscle reoxygenation capacity during recovery periods. These results extend previous findings that muscle O2 availability is important for prolonged repeated-sprint performance, in particular when the exercise is taken in hypoxia.

Critical role for free radicals on sprint exercise-induced CaMKII and AMPKα phosphorylation in human skeletal muscle

The extremely high energy demand elicited by sprint exercise is satisfied by an increase in O2 consumption combined with a high glycolytic rate, leading to a marked lactate accumulation, increased AMP-to-ATP ratio, and reduced NAD(+)/NADH.H(+) and muscle pH, which are accompanied by marked Thr(172) AMP-activated protein kinase (AMPK)-α phosphorylation during the recovery period by a mechanism not fully understood. To determine the role played by reactive nitrogen and oxygen species (RNOS) on Thr(172)-AMPKα phosphorylation in response to cycling sprint exercise, nine voluntary participants performed a single 30-s sprint (Wingate test) on two occasions: one 2 h after the ingestion of placebo and another after the intake of antioxidants (α-lipoic acid, vitamin C, and vitamin E) in a double-blind design. Vastus lateralis muscle biopsies were obtained before, immediately postsprint, and 30 and 120 min postsprint. Performance and muscle metabolism were similar during both sprints. The NAD(+)-to-NADH.H(+) ratio was similarly reduced (84%) and the AMP-to-ATP ratio was similarly increased (×21-fold) immediately after the sprints. Thr(286) Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and Thr(172)-AMPKα phosphorylations were increased after the control sprint (with placebo) but not when the sprints were preceded by the ingestion of antioxidants. Ser(485)-AMPKα1/Ser(491)-AMPKα2 phosphorylation, a known inhibitory mechanism of Thr(172)-AMPKα phosphorylation, was increased only with antioxidant ingestion. In conclusion, RNOS play a crucial role in AMPK-mediated signaling after sprint exercise in human skeletal muscle. Antioxidant ingestion 2 h before sprint exercise abrogates the Thr(172)-AMPKα phosphorylation response observed after the ingestion of placebo by reducing CaMKII and increasing Ser(485)-AMPKα1/Ser(491)-AMPKα2 phosphorylation. Sprint performance, muscle metabolism, and AMP-to-ATP and NAD(+)-to-NADH.H(+) ratios are not affected by the acute ingestion of antioxidants.

Effects of single bout of very high-intensity exercise on metabolic health biomarkers in overweight/obese sedentary men

This study aimed to investigate the effects of a single session of sprint interval training (SIT) and a single extended sprint (ES), matched for total work, on metabolic health biomarkers. Ten overweight/obese men aged 26.9±6.2years participated. Following a pre-trial incremental exercise test and SIT familiarization, each participant undertook three 2-day trials in randomized order. On Day 1 participants either undertook no exercise (CON), four maximal 30-s sprints, with 4.5min recovery between each (SIT), or a single maximal extended sprint (ES) matched with SIT for work done. On Day 2, participants had a fasting blood sample taken, undertook an oral glucose tolerance test to determine insulin sensitivity index (ISI), and had blood pressure measured. Total work done during exercise did not differ between SIT and ES (61.7±2.9 vs. 61.3±2.8kJ; p=0.741). Mean power was higher in SIT than ES (518±21 vs. 306±16W, p<0.0005), resulting in a shorter high-intensity exercise duration in SIT (120±0 vs. 198±10s, p<0.0005). ISI was 44.6% higher following ES than CON (9.4±2.1 vs. 6.5±1.3; p=0.022), but did not differ significantly between SIT and CON (6.6±0.9 vs. 6.5±1.3; p=0.208). However, on the day following exercise fat oxidation in the fasted state was increased by 63% and 38%, compared to CON, in SIT and ES, respectively (p<0.05 for both), with a concomitant reduction in carbohydrate oxidation (p<0.05). A single ES, which may represent a more time-efficient alternative to SIT, can increase insulin sensitivity and increase fat oxidation in overweight overweight/obese sedentary men.

Different responses of selected hormones to three types of exercise in young men

Exercise is a potent stimulus for release of growth hormone (GH), cortisol, testosterone and prolactin, and prolonged exercise inhibits insulin secretion. These responses seem to be specific to the type of exercise but this has been poorly characterised primarily because they have not been compared during exercise performed by the same individuals. We investigated hormone responses to resistance, sprint and endurance exercise in young men using a repeated measures design in which each subject served as their own control. Eight healthy non-obese young adults (18-25 years) were studied on four occasions in random order: 30-s cycle ergometer sprint (Sprint), 30-min resistance exercise bout (Resistance), 30-min cycle at 70 % VO(2max) (Endurance), and seated rest in the laboratory (Rest). Cortisol, GH, testosterone, prolactin, insulin and glucose concentrations were measured for 60 min after the four different interventions. Endurance and sprint exercise significantly increased GH, cortisol, prolactin and testosterone. Sprint exercise also increased insulin concentrations, whereas this decreased in response to endurance exercise. Resistance exercise significantly increased only testosterone and glucose. Sprint exercise elicited the largest response per unit of work, but the smallest response relative to mean work rate in all hormones. In conclusion, the nature and magnitude of the hormone response were influenced by exercise type, perhaps reflecting the roles of these hormones in regulating metabolism during and after resistance, sprint and endurance exercise.

Increased oxidative stress and anaerobic energy release, but blunted Thr172-AMPKα phosphorylation, in response to sprint exercise in severe acute hypoxia in humans

AMP-activated protein kinase (AMPK) is a major mediator of the exercise response and a molecular target to improve insulin sensitivity. To determine if the anaerobic component of the exercise response, which is exaggerated when sprint is performed in severe acute hypoxia, influences sprint exercise-elicited Thr(172)-AMPKα phosphorylation, 10 volunteers performed a single 30-s sprint (Wingate test) in normoxia and in severe acute hypoxia (inspired Po(2): 75 mmHg). Vastus lateralis muscle biopsies were obtained before and immediately after 30 and 120 min postsprint. Mean power output and O(2) consumption were 6% and 37%, respectively, lower in hypoxia than in normoxia. O(2) deficit and muscle lactate accumulation were greater in hypoxia than in normoxia. Carbonylated skeletal muscle and plasma proteins were increased after the sprint in hypoxia. Thr(172)-AMPKα phosphorylation was increased by 3.1-fold 30 min after the sprint in normoxia. This effect was prevented by hypoxia. The NAD(+)-to-NADH.H(+) ratio was reduced (by 24-fold) after the sprints, with a greater reduction in hypoxia than in normoxia (P < 0.05), concomitant with 53% lower sirtuin 1 (SIRT1) protein levels after the sprint in hypoxia (P < 0.05). This could have led to lower liver kinase B1 (LKB1) activation by SIRT1 and, hence, blunted Thr(172)-AMPKα phosphorylation. Ser(485)-AMPKα(1)/Ser(491)-AMPKα(2) phosphorylation, a known negative regulating mechanism of Thr(172)-AMPKα phosphorylation, was increased by 60% immediately after the sprint in hypoxia, coincident with increased Thr(308)-Akt phosphorylation. Collectively, our results indicate that the signaling response to sprint exercise in human skeletal muscle is altered in severe acute hypoxia, which abrogated Thr(172)-AMPKα phosphorylation, likely due to lower LKB1 activation by SIRT1.

Extremely short duration high-intensity training substantially improves endurance performance in triathletes

High-intensity training (HIT) involving 30-s sprints is an effective training regimen to improve aerobic performance. We tested whether 6-s HITs can improve aerobic performance in triathletes. Six subelite triathletes (age, 40 ± 9 years; weight, 86 ± 11 kg; body mass index, 26 ± 3 kg·m⁻²) took part in cycle HIT and 6 endurance-trained subelite athletes (age, 36 ± 9 years; weight, 82 ± 11 kg; BMI, 26 ± 3 kg·m⁻²) maintained their normal training routine. Before and after 2 weeks of HIT, involving 10 × 6-s sprints or normal activity, participants performed a self-paced 10-km time trial and a time to exhaustion test on a cycle ergometer. Finger prick blood samples were taken throughout the time to exhaustion test to determine blood lactate concentration. Two weeks of HIT resulted in a 10% decrease in self-paced 10-km time trial (p = 0.03) but no significant change in time to exhaustion. The time taken to reach onset of blood lactate accumulation (OBLA, defined as the point where blood lactate reaches 4 mmol·L⁻¹) was significantly increased following 2 weeks of HIT (p = 0.003). The change in time trial performance was correlated to the change in time taken to reach OBLA (R² = 0.63; p = 0.001). We concluded that a very short duration HIT is a very effective training regimen to improve aerobic performance in subelite triathletes and this is associated with a delay in blood lactate build-up.

EFFECTS OF BLOOD LACTATE ON OXYGEN UPTAKE KINETICS DURING RECOVERY AFTER SPRINT IN HUMANS

The purpose of this study was to examine the effects of blood lactate level (La) on oxygen uptake ( · VO2) kinetics during recovery after short-term exercise with maximal effort (sprint). Three sprints were performed on a cycle ergometer with a load of 8% of body weight at maximal rotation rate. · VO2 kinetics and oxygen debt were determined after three sprint tests: one 10-s cycling sprint, five repeated 10-s cycling sprints with 6-min intervals and one 30-s cycling sprint. There was no significant difference between peak power outputs in the 10-s sprint and five sprints. There was no difference in · VO2 kinetics during recovery from one sprint and during recovery after five sprints. La peaked at 5 min. The peak value of La was significantly lower in one sprint (4.41 ± 0.9 mM) than in five sprints (7.01 ± 2.2 mM). Thus, despite a difference in La, there was no difference between · VO2 kinetics during recovery after one sprint and after five sprints. There was a significant difference in · VO2 between the five sprints and 30-s sprint from 70 s to 320 s during recovery, but there were no significant differences in La after 5 min of recovery. There were two phases in · VO2. They consisted of fast oxygen debt and slow oxygen debt. There were also no differences in slow and fast oxygen debts between the two 10-s sprints despite significant differences in blood lactate during recovery. Peak La in the five sprints was not significantly different from that in the 30-s sprint (8.68 ± 1.2 mM). However, slow oxygen debt was significantly greater in the 30-s sprint than in the five sprints. It is concluded that · VO2 kinetics during recovery are not affected by an increase in blood lactate.

Separate and combined influence of posture and sprint running on plasma volume changes

It is currently unknown whether any changes in plasma volume (PV) after sprint running are inherent to sprint running per se or are due to other confounding factors such as changes in posture. The purpose of the present study was to examine the independent effects of sprint running on PV changes. Eight females completed two trials on separate days: (1) a 30-s sprint on a non-motorised treadmill and (2) a control trial where no exercise was undertaken but blood samples were taken at identical time points as in the exercise trial. Changes in PV were calculated using haematocrit and haemoglobin. Post-sprint PV reductions were greater in the sprint than the control trial (mean: −17.7, SD=3.1% vs. mean: −7.5, s = 4.9, P<0.05, n=8). There were greater changes in PV in the sprint than the control trial in most sampling points. These data show that sprint running of only 30 s induces transient reductions in PV independently of posture change. The present findings suggest that PV changes due to sprint running should be routinely reported as well as the posture and the exact time in this posture.

Changes of Whole-Body Power, Muscle Function, and Jump Performance With Prolonged Cycling to Exhaustion

To quantify how whole-body power, muscle-function, and jump-performance measures change during prolonged cycling and recovery and determine whether there are relationships between the different fatigue measures. Ten competitive or recreationally active male cyclists underwent repeated 20-min stages of prolonged cycling at 70% VO2peak until exhaustion. Whole-body peak power output (PPO) was assessed using an all-out 30-s sprint 17 min into each cycle stage. Ratings of perceived exertion (RPE) were recorded throughout. Isometric and isokinetic muscle-function tests were made between cycle stages, over ~6 min, and during 30-min recovery. Drop-jump measures were tested at exhaustion and during recovery. PPO initially increased or was maintained in some subjects but fell to 81% of maximum at exhaustion. RPE was near maximal (18.7) at exhaustion, with the time to exhaustion related to the rate of rise of RPE. PPO first started to decline only when RPE exceeded 16 (ie, hard). Peak isometric and concentric isokinetic torque (180°/s) for the quadriceps fell to 86% and 83% of pretest at exhaustion, respectively. In contrast, the peak concentric isokinetic torque (180°/s) of the hamstrings increased by 10% before declining to 93% of maximum. Jump height fell to 92% of pretest at exhaustion and was correlated with the decline in PPO (r = .79). Muscle-function and jump-performance measures did not recover over the 30-min postexercise rest period. At exhaustion, whole-body power, muscle-function, and jump-performance measures had all fallen by 7-19%. PPO and drop-jump decrements were linearly correlated and are appropriate measures of maximal performance.

Four weeks of normobaric “live high-train low” do not alter muscular or systemic capacity for maintaining pH and K+ homeostasis during intense exercise

It was investigated if athletes subjected to 4 wk of living in normobaric hypoxia (3,000 m; 16 h/day) while training at 800-1,300 m ["live high-train low" (LHTL)] increase muscular and systemic capacity for maintaining pH and K(+) homeostasis as well as intense exercise performance. The design was double-blind and placebo controlled. Mean power during 30-s all-out cycling was similar before and immediately after LHTL (650 ± 31 vs. 628 ± 32 W; n = 10) and placebo exposure (658 ± 22 vs. 660 ± 23 W; n = 6). Supporting the performance data, arterial plasma pH, lactate, and K(+) during submaximal and maximal exercise were also unaffected by the intervention in both groups. In addition, muscle buffer capacity (in mmol H(+)·kg dry wt(-1)·pH(-1)) was similar before and after in both the LHTL (140 ± 12 vs. 140 ± 16) and placebo group (145 ± 2 vs. 140 ± 3). The expression of sarcolemmal H(+) transporters (Na(+)/H(+) exchanger 1, monocarboxylate transporters 1 and 4), as well as expression of Na(+)-K(+) pump subunits-α(1), -α(2), and -β(1) was also similar before and after the intervention. In conclusion, muscular and systemic capacity for maintaining pH and K(+) balance during exercise is similar before and after 4 wk of placebo-controlled normobaric LHTL. In accordance, 30-s all-out sprint ability was similar before and after LHTL.

The Effects of 4 Different Recovery Strategies on Repeat Sprint-Cycling Performance

To evaluate the effectiveness of different recovery strategies on repeat cycling performance where a short duration between exercise bouts is required. Eleven highly trained cyclists (mean ± SD; age = 31 ± 6 y, mass = 74.6 ± 10.6 kg, height = 180.5 ± 8.1 cm) completed 4 trials each consisting of three 30-s maximal sprints (S1, S2, S3) on a cycle ergometer, separated by 20-min recovery periods. In a counterbalanced, crossover design, each trial involved subjects performing 1 of 4 recovery strategies: compression garments (COMP), electronic muscle stimulation (EMS), humidification therapy (HUM), and a passive control (CON). The sprint tests implemented a 60-s preload (at an intensity of 4.5 W/kg) before a 30-s maximal sprint. Mean power outputs (W) for the 3 sprints, in combination with perceived recovery and blood lactate concentration, were used to examine the effect of each recovery strategy. In CON, S2 and S3 were (mean ± SD) -2.1% ± 3.9% and -3.1% ± 4.2% lower than S1, respectively. Compared with CON, COMP resulted in a higher mean power output from S1 to S2 (mean ± 90%CL: 0.8% ± 1.2%; possibly beneficial) and from S1 to S3 (1.2% ± 1.9%; possibly beneficial), while HUM showed a higher mean power output from S1 to S3 (2.2% ± 2.5%; likely beneficial) relative to CON. The authors suggest that both COMP and HUM may be effective strategies to enhance recovery between repeated sprint-cycling bouts separated by ~30 min.

Sprint exercise enhances skeletal muscle p70S6k phosphorylation and more so in women than in men

Sprint exercise is characterized by repeated sessions of brief intermittent exercise at a high relative workload. However, little is known about the effect on mTOR pathway, an important link in the regulation of muscle protein synthesis. An earlier training study showed a greater increase in muscle fibre cross-sectional area in women than men. Therefore, we tested the hypothesis that the activation of mTOR signalling is more pronounced in women than in men. Healthy men (n=9) and women (n=8) performed three bouts of 30-s sprint exercise with 20-min rest in between. Multiple blood samples were collected over time, and muscle biopsy specimens were obtained at rest and 140 min after the last sprint. Serum insulin increased by sprint exercise and more so in women than in men [gender (g) × time (t)]: P=0.04. In skeletal muscle, phosphorylation of Akt increased by 50% (t, P=0.001) and mTOR by 120% (t, P=0.002) independent of gender. The elevation in p70S6k phosphorylation was larger in women (g × t, P=0.03) and averaged 230% (P=0.006) as compared to 60% in men (P=0.04). Phosphorylation rpS6 increased by 660% over time independent of gender (t, P=0.003). Increase in the phosphorylation of p70S6k was directly related to increase in serum insulin (r=0.68, P=0.004). It is concluded that repeated 30-s all-out bouts of sprint exercise separated by 20 min of rest increases Akt/mTOR signalling in skeletal muscle. Secondly, signalling downstream of mTOR was stronger in women than in men after sprint exercise indicated by the increased phosphorylation of p70S6k.

Warm-up effects on muscle oxygenation, metabolism and sprint cycling performance

To investigate the effects of warm-up intensity on all-out sprint cycling performance, muscle oxygenation and metabolism, 8 trained male cyclists/triathletes undertook a 30-s sprint cycling test preceded by moderate, heavy or severe warm up and 10-min recovery. Muscle oxygenation was measured by near-infrared spectroscopy, with deoxyhaemoglobin ([HHb]) during the sprint analysed with monoexponential models with time delay. Aerobic, anaerobic-glycolytic and phosphocreatine energy provision to the sprint were estimated from oxygen uptake and lactate production. Immediately prior to the sprint, blood [lactate] was different for each warm up and higher than resting for the heavy and severe warm ups (mod. 0.94±0.36, heavy 1.92±0.64, severe 4.37±0.93mmoll(-1) P<0.05), although muscle oxygenation was equally raised above rest. Mean power during the sprint was lower following severe compared to moderate warm up (mod. 672±54, heavy 666±56, severe 655±59W, P<0.05). The [HHb] kinetics during the sprint were not different among conditions, although the time delay before [HHb] increased was shorter for severe versus moderate warm up (mod. 5.8±0.6, heavy 5.6±0.9, severe 5.2±0.7s, P<0.05). The severe warm up was without effect on estimated aerobic metabolism, but increased estimated phosphocreatine hydrolysis, the latter unable to compensate for the reduction in estimated anaerobic-glycolytic metabolism. It appears that despite all warm ups equally increasing muscle oxygenation, and indicators of marginally faster oxygen utilisation at the start of exercise following a severe-intensity warm up, other energy sources may not be able to fully compensate for a reduced glycolytic rate in sprint exercise with potential detrimental effects on performance.

Sprint exercise enhances skeletal muscle p70S6k phosphorylation and more so in females than in males

Aim: Sprint exercise is characterized by repeated sessions of brief intermittent exercise at a high relative workload. However, little is known about the effect on mTOR pathway, an important link in regulation of muscle protein synthesis. An earlier training study showed a greater increase in muscle fibre cross sectional area in females than males. Therefore, we tested the hypothesis that activation of mTOR signalling is more pronounced in females than in males. Healthy males (n=9) and females (n=8) performed three bouts of 30-s sprint exercise with 20 min rest between. Methods: Multiple blood samples were collected over time and muscle biopsy specimens were obtained at rest and 140 min after the last sprint. Results: Serum insulin increased by sprint exercise and more so in females than in males (gender (g) x time (t):P=0.04. In skeletal muscle, phosphorylation of Akt increased by 50% (t, P=0.001) and mTOR by 120% (t, P=0.002) independent of gender. The elevation in p70S6k phosphorylation was larger in females (g x t, P=0.03) and averaged 230% (P=0.006) as compared to 60% in males (P=0.04). Phosphorylation rpS6 increased by 660% over time independent of gender (t, P=0.003). Increase in phosphorylation of p70S6k was directly related to increase in serum insulin (r=0.68, P=0.004). Conclusion: It is concluded that repeated 30-s all out bouts of sprint exercise separated by 20 min of rest, increases Akt/mTOR signalling in skeletal muscle. Secondly, signalling downstream of mTOR was stronger in females than in males after sprint exercise indicated by increased phosphorylation of p70S6k.

The Effect of Pre-Exercise Carbohydrate Supplementation on Anaerobic Exercise Performance in Adolescent Males

Carbohydrate (CHO) consumption before anaerobic exercise was studied in 13 adolescent boys (15.2 ± 0.9 yrs). A within subjects design was employed where subjects consumed a 22% CHO or volume-matched placebo (PL) beverage 30-min before anaerobic exercise on two separate days. Exercise consisted of a Wingate Anaerobic Test (WAnT), ten by 10-s-sprints, and a second WAnT. Fatigue index and peak power (PP) were similar while mean power (MP) was higher (p < .025) in CHO trial; however this difference was ascribed to initial WAnT performance. PP and MP for the 10-s sprints were similar between trials. Intravenous blood glucose and insulin concentrations were higher (p < .05) in the CHO trial while lactate and catecholamine concentrations were similar. Improved performance on a single WAnT was apparent with CHO consumption before exercise; however, this strategy did not attenuate fatigue over time in adolescent boys.