986 resultados para intermittent-sprint exercise


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Purpose: To assess the effects of pre-cooling volume on neuromuscular function and performance in free-paced intermittent-sprint exercise in the heat. Methods: Ten male, teamsport athletes completed four randomized trials involving an 85-min free-paced intermittentsprint exercise protocol in 33°C±33% relative humidity. Pre-cooling sessions included whole body (WB), head+hand (HH), head (H) and no cooling (CONT), applied for 20-min pre-exercise and 5-min mid exercise. Maximal voluntary contractions (MVC) were assessed pre- and postintervention and mid- and post-exercise. Exercise performance was assessed with sprint times, % decline and distances covered during free-paced bouts. Measures of core(Tc) and skin (Tsk) temperatures, heart rate, perceptual exertion and thermal stress were monitored throughout. Venous and capillary blood was analyzed for metabolite, muscle damage and inflammatory markers. Results: WB pre-cooling facilitated the maintenance of sprint times during the exercise protocol with reduced % decline (P=0.04). Mean and total hard running distances increased with pre cooling 12% compared to CONT (P<0.05), specifically, WB was 6-7% greater than HH (P=0.02) and H (P=0.001) respectively. No change was evident in mean voluntary or evoked force pre- to post-exercise with WB and HH cooling (P>0.05). WB and HH cooling reduced Tc by 0.1-0.3°C compared to other conditions (P<0.05). WB Tsk was suppressed for the entire session(P=0.001). HR responses following WB cooling were reduced(P=0.05; d=1.07) compared to CONT conditions during exercise. Conclusion: A relationship between pre-cooling volume and exercise performance seems apparent, as larger surface area coverage augmented subsequent free-paced exercise capacity, in conjunction with greater suppression of physiological load. Maintenance of MVC with pre-cooling, despite increased work output suggests the role of centrally-mediated mechanisms in exercise pacing regulation and subsequent performance.

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This study examined the effects of pre-cooling duration on performance and neuromuscular function for self-paced intermittent-sprint shuttle running in the heat. Eight male, team-sport athletes completed two 35-min bouts of intermittent-sprint shuttle running separated by a 15-min recovery on three separate occasions (33°C, 34% relative humidity). Mixed-method pre-cooling was completed for 20 min (COOL20), 10-min (COOL10) or no cooling (CONT) and reapplied for 5-min mid-exercise. Performance was assessed via sprint times, percentage decline and shuttle-running distance covered. Maximal voluntary contractions (MVC), voluntary activation (VA) and evoked twitch properties were recorded pre- and post-intervention and mid- and post-exercise. Core temperature (T c), skin temperature, heart rate, capillary blood metabolites, sweat losses, perceptual exertion and thermal stress were monitored throughout. Venous blood draws pre- and post-exercise were analyzed for muscle damage and inflammation markers. Shuttle-running distances covered were increased 5.2 ± 3.3% following COOL20 (P < 0.05), with no differences observed between COOL10 and CONT (P > 0.05). COOL20 aided in the maintenance of mid- and post-exercise MVC (P < 0.05; d > 0.80), despite no conditional differences in VA (P > 0.05). Pre-exercise T c was reduced by 0.15 ± 0.13°C with COOL20 (P < 0.05; d > 1.10), and remained lower throughout both COOL20 and COOL10 compared to CONT (P < 0.05; d > 0.80). Pre-cooling reduced sweat losses by 0.4 ± 0.3 kg (P < 0.02; d > 1.15), with COOL20 0.2 ± 0.4 kg less than COOL10 (P = 0.19; d = 1.01). Increased pre-cooling duration lowered physiological demands during exercise heat stress and facilitated the maintenance of self-paced intermittent-sprint performance in the heat. Importantly, the dose-response interaction of pre-cooling and sustained neuromuscular responses may explain the improved exercise performance in hot conditions.

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This study examined the effects of post-exercise cooling on recovery of neuromuscular, physiological, and cerebral hemodynamic responses after intermittent-sprint exercise in the heat. Nine participants underwent three post-exercise recovery trials, including a control (CONT), mixed-method cooling (MIX), and cold-water immersion (10 °C; CWI). Voluntary force and activation were assessed simultaneously with cerebral oxygenation (near-infrared spectroscopy) pre- and post-exercise, post-intervention, and 1-h and 24-h post-exercise. Measures of heart rate, core temperature, skin temperature, muscle damage, and inflammation were also collected. Both cooling interventions reduced heart rate, core, and skin temperature post-intervention (P < 0.05). CWI hastened the recovery of voluntary force by 12.7 ± 11.7% (mean ± SD) and 16.3 ± 10.5% 1-h post-exercise compared to MIX and CONT, respectively (P < 0.01). Voluntary force remained elevated by 16.1 ± 20.5% 24-h post-exercise after CWI compared to CONT (P < 0.05). Central activation was increased post-intervention and 1-h post-exercise with CWI compared to CONT (P < 0.05), without differences between conditions 24-h post-exercise (P > 0.05). CWI reduced cerebral oxygenation compared to MIX and CONT post-intervention (P < 0.01). Furthermore, cooling interventions reduced cortisol 1-h post-exercise (P < 0.01), although only CWI blunted creatine kinase 24-h post-exercise compared to CONT (P < 0.05). Accordingly, improvements in neuromuscular recovery after post-exercise cooling appear to be disassociated with cerebral oxygenation, rather reflecting reductions in thermoregulatory demands to sustain force production.

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Prolonged intermittent-sprint exercise (i.e., team sports) induce disturbances in skeletal muscle structure and function that are associated with reduced contractile function, a cascade of inflammatory responses, perceptual soreness, and a delayed return to optimal physical performance. In this context, recovery from exercise-induced fatigue is traditionally treated from a peripheral viewpoint, with the regeneration of muscle physiology and other peripheral factors the target of recovery strategies. The direction of this research narrative on post-exercise recovery differs to the increasing emphasis on the complex interaction between both central and peripheral factors regulating exercise intensity during exercise performance. Given the role of the central nervous system (CNS) in motor-unit recruitment during exercise, it too may have an integral role in post-exercise recovery. Indeed, this hypothesis is indirectly supported by an apparent disconnect in time-course changes in physiological and biochemical markers resultant from exercise and the ensuing recovery of exercise performance. Equally, improvements in perceptual recovery, even withstanding the physiological state of recovery, may interact with both feed-forward/feed-back mechanisms to influence subsequent efforts. Considering the research interest afforded to recovery methodologies designed to hasten the return of homeostasis within the muscle, the limited focus on contributors to post-exercise recovery from CNS origins is somewhat surprising. Based on this context, the current review aims to outline the potential contributions of the brain to performance recovery after strenuous exercise.

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The influence of allopurinol on urinary purine loss was examined in 7 active male subjects (age 24.9 ± 3.0 years, weight 82.8 ± 8.3 kg, V˙o2peak 48.1 ± 6.9 mL · kg−1 · min−1). These subjects performed, in random order, a trial with 5 days of prior ingestion of a placebo or allopurinol. Each trial consisted of eight 10-second sprints on an air-braked cycle ergometer and was separated by at least a week. A rest period of 50 seconds separated each repeated sprint. Forearm venous plasma inosine, hypoxanthine (Hx) and uric acid concentrations were measured at rest and during 120 minutes of recovery from exercise. Urinary inosine, Hx, xanthine, and uric acid excretion were also measured before and for 24 hours after exercise. During the first 120 minutes of recovery, plasma Hx concentrations, as well as the urinary Hx and xanthine excretion rates, were higher (P < .05) with allopurinol compared with the placebo trial. In contrast, plasma uric acid concentration and urinary uric acid excretion rates were lower (P < .05) with allopurinol. The total urinary excretion of purines (inosine + Hx + xanthine + uric acid) above basal levels was higher in the allopurinol trial compared with placebo. These results indicate that the total urinary purine excretion after intermittent sprint exercise was enhanced with allopurinol treatment. Furthermore, the composition of urinary purines was markedly affected by this drug.

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The aim of the present study was to examine the effect of creatine supplementation (CrS) on sprint exercise performance and skeletal muscle anaerobic metabolism during and after sprint exercise. Eight active, untrained men performed a 20-s maximal sprint on an air-braked cycle ergometer after 5 days of CrS [30 g creatine (Cr) + 30 g dextrose per day] or placebo (30 g dextrose per day). The trials were separated by 4 wk, and a double-blind crossover design was used. Muscle and blood samples were obtained at rest, immediately after exercise, and after 2 min of passive recovery. CrS increased the muscle total Cr content (9.5 ± 2.0%, P < 0.05, mean ± SE); however, 20-s sprint performance was not improved by CrS. Similarly, the magnitude of the degradation or accumulation of muscle (e.g., adenine nucleotides, phosphocreatine, inosine 5′-monophosphate, lactate, and glycogen) and plasma metabolites (e.g., lactate, hypoxanthine, and ammonia/ammonium) were also unaffected by CrS during exercise or recovery. These data demonstrated that CrS increased muscle total Cr content, but the increase did not induce an improved sprint exercise performance or alterations in anaerobic muscle metabolism.

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In order to examine the influence of sprint training on metabolism and exercise performance during sprint exercise, 16 recreationally-active, untrained, men (TO2peak= 3.8+/-0.1 1.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

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Purpose: To investigate the effects of an acute multinutrient supplement on game-based running performance, peak power output, anaerobic by-products, hormonal profiles, markers of muscle damage, and perceived muscular soreness before, immediately after, and 24 h following competitive rugby union games. Methods: Twelve male rugby union players ingested either a comprehensive multinutrient supplement (SUPP), [RE-ACTIVATE:01], or a placebo (PL) for 5 d. Participants then performed a competitive rugby union game (with global positioning system tracking), with associated blood draws and vertical jump assessments pre, immediately post and 24 h following competition. Results: SUPP ingestion resulted in moderate to large effects for augmented 1st half very high intensity running (VHIR) mean speed (5.9 ± 0.4 vs 4.8 ± 2.3 m·min–1; d= 0.93). Further, moderate increases in 2nd half VHIR distance (137 ± 119 vs 83 ± 89 m; d= 0.73) and VHIR mean speed (5.9 ± 0.6 v 5.3 ± 1.7 m·min–1; d= 0.56) in SUPP condition were also apparent. Postgame aspartate aminotransferase (AST; 44.1 ± 11.8 vs 37.0 ± 3.2 UL; d= 1.16) and creatine kinase (CK; 882 ± 472 vs. 645 ± 123 UL; d= 0.97) measures demonstrated increased values in the SUPP condition, while AST and CK values correlated with 2nd half VHIR distance (r= –0.71 and r= –0.76 respectively). Elevated C-reactive protein (CRP) was observed postgame in both conditions; however, it was significantly blunted with SUPP (P= .05). Conclusions: These findings suggest SUPP may assist in the maintenance of VHIR during rugby union games, possibly via the buffering qualities of SUPP ingredients. However, correlations between increased work completed at very high intensities and muscular degradation in SUPP conditions, may mask any anticatabolic properties of the supplement.

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This study investigated the effects of alcohol ingestion on lower body strength and power, and physiological and cognitive recovery following competitive Rugby League matches. Nine male Rugby players participated in two matches, followed by one of two randomized interventions; a control or alcohol ingestion session. Four hours post-match, participants consumed either beverages containing a total of 1g of ethanol per kg bodyweight (vodka and orange juice; ALC) or a caloric and taste matched non-alcoholic beverage (orange juice; CONT). Pre, post, 2 h post and 16 h post match measures of countermovement jump (CMJ), maximal voluntary contraction(MVC), voluntary activation (VA), damage and stress markers of creatine kinase (CK), C-reactive protein (CRP), cortisol, and testosterone analysed from venous blood collection, and cognitive function (modified Stroop test) were determined. Alcohol resulted in large effects for decreased CMJ height(-2.35 ± 8.14 and -10.53 ± 8.36 % decrement for CONT and ALC respectively; P=0.15, d=1.40), without changes in MVC (P=0.52, d=0.70) or VA (P=0.15, d=0.69). Furthermore, alcohol resulted in a significant slowing of total time in a cognitive test (P=0.04, d=1.59), whilst exhibiting large effects for detriments in congruent reaction time (P=0.19, d=1.73). Despite large effects for increased cortisol following alcohol ingestion during recovery (P=0.28, d=1.44), post-match alcohol consumption did not unduly affect testosterone (P-0.96, d=0.10), CK (P=0.66, d=0.70) or CRP(P=0.75, d=0.60). It appears alcohol consumption during the evening following competitive rugby matches may have some detrimental effects on peak power and cognitive recovery the morning following a Rugby League match. Accordingly, practitioners should be aware of the potential associated detrimental effects of alcohol consumption on recovery and provide alcohol awareness to athletes at post-match functions.

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PURPOSE: This study examined the effects of overnight sleep deprivation on recovery following competitive rugby league matches. METHODS: Eleven male, amateur rugby league players performed two competitive matches, followed by either a normal night's sleep (~8h; CONT) or a sleep deprived night (~0h; SDEP) in a randomised fashion. Testing was conducted the morning of the match, and immediately post-match, 2h post and the next morning (16h post-match). Measures included counter-movement jump (CMJ) distance, knee extensor maximal voluntary contraction (MVC), voluntary activation (VA), venous blood creatine kinase (CK) and C-reactive protein (CRP), perceived muscle soreness and a word-colour recognition cognitive function test. Percent change between post- and 16h post-match was reported to determine the effect of the intervention the next morning. RESULTS: Large effects indicated a greater post- to 16h post-match percentage decline in CMJ distance following SDEP compared to CONT (P=0.10-0.16; d=0.95-1.05). Similarly, the percentage decline in incongruent word-colour reaction times were increased in SDEP trials (P=0.007; d=1.75). Measures of MVC did not differ between conditions (P=0.40-0.75; d=0.13-0.33), though trends for larger percentage decline in VA were detected in SDEP (P=0.19; d=0.84). Further, large effects indicated higher CK and CRP responses 16h post-match during SDEP compared to CONT (P=0.11-0.87; d=0.80-0.88). CONCLUSIONS: Sleep deprivation negatively affected recovery following a rugby league match, specifically impairing CMJ distance and cognitive function. Practitioners should promote adequate post-match sleep patterns or adjust training demands the next day to accommodate the altered physical and cognitive state following sleep deprivation.

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Hamstring strain injuries (HSI) are the predominant non-contact injury in many sports. Intermittent running has been shown to result in preferential reductions in eccentric hamstring strength, which increase the risk of sustaining a HSI. The eccentric specific nature of this decline in hamstring function implicates central mechanisms, as peripheral fatigue mechanisms tend to impact upon both concentric and eccentric contractions modes. However, neural function of the hamstrings, such as the median power frequency (MPF) of the surface electromyography signal has yet to be examined in the fatigued hamstring following intermittent sprint running. AIM: To determine the impact of fatigue induced by intermittent sprinting on the MPF of the medial and lateral hamstring muscles. METHODS: Fifteen recreationally active males completed 18 × 20m overground sprints. Maximal strength (concentric and eccentric knee flexor and concentric knee extensor) was determined isokinetically at the velocities of ±180.s-1 and ±60.s- while hamstring muscle activation was assessed using surface electromyography, before and 15 minutes after the running protocol. RESULTS: Overground intermittent running caused a significant reduction in eccentric knee flexor strength (27.2 Nm; 95% CI = 11.2 to 43.3; p=0.0001) but not concentric strength (9.3 Nm; 95% CI = -6.7 to 25.3; P=0.6361). Following the overground running, MPF of the lateral hamstrings showed a significant decline eccentrically (0.86; 95% CI = 0.59 to 1.54; P=0.038) and concentrically (0.76; 95%CI = 0.66 to 0.83; P=0.039). Similar declines in MPF were also noted in the medial hamstrings eccentrically (1.54; 95% CI = 0.59 to 7.9; P=0.005) and concentrically (1.18; 95% CI = 0.44 to 6.8; P=0.040). CONCLUSION: Whilst sprint running induced fatigue led to a eccentric specific reduction in knee flexor torque, MPF was suppressed across both contraction modes. This would indicate that factors associated with the decline in MPF do not appear to explain the contraction mode-specific loss of strength after intermittent sprints. This would implicate other central mechanisms, such as declines in voluntary activation, in explaining the eccentric specific decline in strength seen following sprint running.

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Purpose: Given the widespread use of water immersion during recovery from exercise, we aimed to investigate the effect of contrast water immersion on recovery of sprint cycling performance, HR and, blood lactate.

Methods: Two groups completed high-intensity sprint exercise before and after a 30-min randomized recovery. The Wingate group (n = 8) performed 3 x 30-s Wingate tests (4-min rest periods). The repeated intermittent sprint group (n = 8) cycled for alternating 30-s periods at 40% of predetermined maximum power and 120% maximum power, until exhaustion. Both groups completed three trials using a different recovery treatment for each trial (balanced randomized application). Recovery treatments were passive rest, 1:1 contrast water immersion (2.5 min of cold (8-C) to 2.5 min of hot (40-C)), and 1:4 contrast water immersion (1 min of cold to 4 min of hot). Blood lactate and HR were recorded throughout, and peak power and total work for pre- and postrecovery Wingate performance and exercise time and total work for repeated sprinting were recorded.

Results: Recovery of Wingate peak power was 8% greater after 1:4 contrast water immersion than after passive rest, whereas both contrast water immersion ratios provided a greater recovery of exercise time (È10%) and total work (È14%) for repeated sprinting than for passive rest. Blood lactate was similar between trials. Compared with passive rest, HR initially declined more slowly during contrast water immersion but increased with each transition to a cold immersion phase.

Conclusions: These data support contrast water immersion being effective in maintaining performance during a short-term recovery from sprint exercise. This effect needs further investigation but is likely explained by cardiovascular mechanisms, shown here by an elevation in HR upon each cold immersion.

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Few studies have focused on the metabolic responses to alternating high- and low-intensity exercise and, specifically, compared these responses to those seen during constant-load exercise performed at the same average power output. This study compared muscle metabolic responses between two patterns of exercise during which the intensity was either constant and just below critical power (CP) or that oscillated above and below CP. Six trained males (mean +/- SD age 23.6 +/- 2.6 y) completed two 30-minute bouts of cycling (alternating and constant) at an average intensity equal to 90% of CR The intensity during alternating exercise varied between 158% CP and 73% CP. Biopsy samples from the vastus lateralis muscle were taken before (PRE), at the midpoint and end (POST) of exercise and analysed for glycogen, lactate, PCr and pH. Although these metabolic variables in muscle changed significantly during both patterns of exercise, there were no significant differences (p > 0.05) between constant and alternating exercise for glycogen (PRE: 418.8 +/- 85 vs. 444.3 +/- 70; POST: 220.5 +/- 59 vs. 259.5 +/- 126mmol.kg(-1) dw), lactate (PRE: 8.5 +/- 7.7 vs. 8.5 +/- 8.3; POST: 49.9 +/- 19.0 vs. 42.6 +/- 26.6 mmol.kg(-1)dw), phosphocreatine (PRE: 77.9 +/- 11.6 vs. 75.7 +/- 16.9; POST: 65.8 +/- 12.1 vs. 61.2 +/- 12.7mmol.kg(-1)dw) or pH (PRE: 6.99 +/- 0.12 vs. 6.99 +/- 0.08; POST: 6.86 +/- 0.13 vs. 6.85 +/- 0.06), respectively. There were also no significant differences in blood lactate responses to the two patterns of exercise. These data suggest that, when the average power output is similar, large variations in exercise intensity exert no significant effect on muscle metabolism.