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Pre-exercise mangiferin–quercetin may enhance athletic performance. This study investigated the effect of mangiferin–quercetin supplementation on high-level male basketball players during a basketball exercise simulation test (BEST) comprising 24 circuits of 30 s activities with various movement distances. The participants were divided into two groups (EXP = 19 and CON = 19) and given a placebo one hour before the BEST (PRE-condition). The following week, the EXP group received mangiferin–quercetin (84 mg/140 mg), while the CON group received a placebo (POST-condition) before the BEST in a double-blind, cross-over design. The mean heart rate (HR) and circuit and sprint times (CT and ST) during the BEST were measured, along with the capillary blood lactate levels (La−), the subjective rating of muscle soreness (RPMS), and the perceived exertion (RPE) during a resting state prior to and following the BEST. The results showed significant interactions for the mean CT (p = 0.013) and RPE (p = 0.004); a marginal interaction for La− (p = 0.054); and non-significant interactions for the mean HR, mean ST, and RPMS. Moreover, the EXP group had significantly lower values in the POST condition for the mean CT (18.17 ± 2.08 s) and RPE (12.42 ± 1.02) compared to the PRE condition (20.33 ± 1.96 s and 13.47 ± 1.22, respectively) and the POST condition of the CON group (20.31 ± 2.10 s and 13.32 ± 1.16, respectively) (p < 0.05). These findings highlight the potential of pre-game mangiferin–quercetin supplementation to enhance intermittent high-intensity efforts in sports such as basketball. [ABSTRACT FROM AUTHOR]

Background: This study compared the effects of low- and moderate-volume supplementary plyometric training in preadolescent female handball players. Methods : Thirty-nine preadolescent handball players (age: 12.9 ± 0.5 years, maturity offset: -1.50 ± 0.56 years) were randomly assigned into three groups: low-volume plyometric training group (LPT, n = 12); moderate-volume plyometric training group (MPT, n = 15); and control group (CG, n = 12). The supplementary plyometric training program was performed twice per week for 10 weeks, along with normal training (3 times/week). Each supplementary session included two upper- and three lower-body exercises performed for two sets (LPT, 36-54 foot contacts, duration 12 min) or four sets (MPT, 72-108 foot contacts, duration 24 min). The CG performed technical handball drills for 20 min. Results: Compared with the control group, both LPT and MPT resulted in similar improvements in modified T-test performance (15.1% and 18.6%, p < 0.01, respectively); linear sprint performance over 5, 10, and 20 m (between 5.1% and 8.8%, p = 0.02 to 0.001); countermovement jump (28.0% and 22.1%, p < 0.05, respectively); and standing long jump (12.6% and 12.5%, p = 0.024, respectively). Handgrip strength and overarm shot ball velocity improved similarly in all groups (CG, MPT, and LPT), by 8-11% ( p < 0.01). Conclusions: Very-low-volume supplementary plyometric training performed for 12 min per session for two sessions per week results in considerable improvements in running speed, change of direction ability, and leg power and is as effective as a moderate-volume program. These findings are important for pre-adolescent female team sports players, who may benefit from a minimal but effective supplementary training, resulting in large benefits in leg speed and power.

Purpose: To reach top performance in cycling, optimizing distribution of energy resources is crucial. The purpose of this study was to investigate power output during 250-m, 500-m, and 1000-m cycling time trials and the characteristics of the adopted pacing strategy. Methods: Nine trained cyclists completed an incremental test and 3 time trials that they were instructed to finish as quickly as possible. Preceding the trials, peak power during short sprints (PPsprint) and gross efficiency (GE) were measured. During the trials, power output and oxygen consumption were measured to calculate the contribution of the aerobic and anaerobic energy sources. After the trial GE was measured again. Results: Peak power during all trials (PPTT) was lower than PPsprint. In the 250-m trial the PPTT was higher in the 1000-m trial (P = .008). The subjects performed a significantly longer time at high intensity in the 250-m than in the 1000-m (P = .029). GE declined significantly during all trials (P < .01). Total anaerobically attributable work was less in the 250-m than in the 500-m (P = .015) and 1000-m (P < .01) trials. Conclusion: The overall pacing pattern in the 250-m trial appears to follow an all-out strategy, although peak power is still lower than the potential maximal power output. This suggests that a true all-out pattern of power output may not be used in fixed-distance events. The 500-m and 1000-m had a more conservative pacing pattern and anaerobic power output reached a constant magnitude. [ABSTRACT FROM AUTHOR]

Purpose: Aortic stiffness may affect shear patterns in the peripheral vasculature. This study examined if sprint exercise, which typically increases aortic stiffness is associated with increased peripheral retrograde blood flow and impaired microvascular function. Methods: Twenty participants (10 women; age: 27 ± 5 years) underwent arterial stiffness, shear rate, and microvascular function assessment at three time points: baseline; following time control; ~ 2 min post a 30-s cycle ergometer sprint against 7.0% body mass. Aortic stiffness was assessed using carotid-femoral pulse wave velocity (cfPWV). Superficial femoral artery (SFA) diameter and blood velocity were assessed using Doppler-ultrasound and were used to calculate shear rates and resistance index (RI). SFA wave reflections were obtained via wave intensity analysis. Vastus medialis microvascular function was measured as tissue saturation index reactivity pre-post exercise via near-infrared spectroscopy. Results: cfPWV increased by + 0.8 ± 0.7 m·s−1 following exercise (p < 0.001). Retrograde shear was reduced following exercise compared with time control (− 4.9 ± 3.8 s−1; p < 0.001), while tissue saturation index was increased post-exercise from baseline (+ 2.3 ± 4.6%; p = 0.04). Reductions in SFA wave reflections (− 1.70 ± 1.96 aU) and RI (− 0.17 ± 0.13 aU) were also noted following exercise (p < 0.001). Conclusion: These data suggest sprint exercise-mediated changes in peripheral shear patterns and microvascular function in the exercised vasculature occur independent from increases in aortic stiffness. Exercise-induced reductions in SFA retrograde shear may be related to decreased wave reflections and peripheral vascular resistance. [ABSTRACT FROM AUTHOR]

Aims: To compare postprandial glucose responses to high-intensity interval exercise (HIE) between obese and lean individuals.Methods: Thirty healthy young adult males (15 obese, 15 lean) ate a standardised meal, then performed HIE (4 × 30-s Wingate cycling/4-min rest) or a no-exercise control trial (CON). Blood glucose was measured preprandially and up to 150 min postprandially.Results: Compared to CON, HIE reduced postprandial glucose concentrations at 120-150 min in obese (p < 0.001) and lean men (p < 0.05), with greater reductions in obese than lean subjects at 120 (-27.0% vs. -8.3%), 135 (-31.9% vs. -15.7%), and 150 min (-21.8% vs. -10.6%). The total glucose area under the curve (AUC) for the testing period was lower with HIE than CON among obese men (p < 0.05), but not lean men (p > 0.05). We found moderate correlations between body mass and postprandial glucose changes (r = 0.39-0.44, p < 0.05), and between glucose AUC and body mass and fat free mass (r = 0.39-0.48, p < 0.05).Conclusions: Our findings suggest that HIE may act as a time-efficient lifestyle intervention strategy for improving obesity-related diabetes risk factors, and might play a role in primary diabetes prevention for the healthy but sedentary population. [ABSTRACT FROM AUTHOR]

Interleukin (IL)-15 stimulates mitochondrial biogenesis, fat oxidation, glucose uptake and myogenesis in skeletal muscle. However, the mechanisms by which exercise triggers IL-15 expression remain to be elucidated in humans. This study aimed at determining whether high-intensity exercise and exercise-induced RONS stimulate IL-15/IL-15Rα expression and its signaling pathway (STAT3) in human skeletal muscle. Nine volunteers performed a 30-s Wingate test in normoxia and hypoxia (PIO2 = 75 mmHg), 2 h after placebo or antioxidant administration (α-lipoic acid, vitamin C and E) in a randomized double-blind design. Blood samples and muscle biopsies (vastus lateralis) were obtained before, immediately after, and 30 and 120 min post-exercise. Sprint exercise upregulated skeletal muscle IL-15 protein expression (ANOVA, P = 0.05), an effect accentuated by antioxidant administration in hypoxia (ANOVA, P = 0.022). In antioxidant conditions, the increased IL-15 expression at 120 min post-exercise (33 %; P = 0.017) was associated with the oxygen deficit caused by the sprint (r = -0.54; P = 0.020); while, IL-15 and Tyr705-STAT3 AUCs were also related (r = 0.50; P = 0.036). Antioxidant administration promotes IL-15 protein expression in human skeletal muscle after sprint exercise, particularly in severe acute hypoxia. Therefore, during intense muscle contraction, a reduced PO2 and glycolytic rate, and possibly, an attenuated RONS generation may facilitate IL-15 production, accompanied by STAT3 activation, in a process that does not require AMPK phosphorylation. [ABSTRACT FROM AUTHOR]

Training has a huge effect on physiological homeostasis. The Thoroughbred racehorse is a valid animal model to investigate such changes for training schedule fine-tuning. As happens in human athletes, it is hypothesized that biochemical and immune response changes and related biomolecular variations could be induced by training programs. The aim of this study was to investigate, for the first time, the long-term metabolic and biomolecular modifications in young untrained Thoroughbred racehorses in the first 4-month timeframe training period. Twenty-nine clinically healthy, untrained, two-year-old Thoroughbred racehorses were followed during their incremental 4-month sprint exercise schedule. Blood collection was performed once a month, five times (T-30, T0, T30, T60, and T90). For each sample, lactate concentration, plasma cell volume (PCV), and hematobiochemical parameters (glucose, urea, creatinine, aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), total bilirubin (Tbil), lactate dehydrogenase (LDH), creatine kinase (CK), cholesterol, triglycerides, albumin (Alb), total proteins (TPs), phosphorus (P), calcium (Ca2+), magnesium (Mg), sodium (Na+), potassium (K−), and chloride (Cl)) were determined. At T-30 and T90, serum protein electrophoresis (SPE), serum amyloid A (SAA), and real-time qPCR were performed on all samples to evaluate the expression of key genes and cytokines related to inflammatory and Th2 immunity responses: Interleukin-4 (IL-4), Interleukin-6 (IL-6), Interleukin-10 (IL-10), Interleukin-1β (IL-1β), Octamer-Binding Transcription Factor 1 (OCT1), B-cell lymphoma/leukemia 11A (BCL11A). Statistical analysis was performed (ANOVA and t test, p < 0.05). Significant modifications were identified compared with T-30 for PCV, glucose, triglycerides, cholesterol, lactate, urea, creatinine, Tbil, ALP, LDH, Na+, K−, Ca2+, SAA, TPs, SPE, IL-6, IL-4, Oct-1, and BCL11A. In conclusion, the first long-term training period was found to induce fundamental systemic changes in untrained Thoroughbreds.

Compared to normoxia, during sprint exercise in severe acute hypoxia the glycolytic rate is increased leading to greater lactate accumulation, acidification, and oxidative stress. To determine the role played by pyruvate dehydrogenase (PDH) activation and reactive nitrogen and oxygen species (RNOS) in muscle lactate accumulation, nine volunteers performed a single 30-s sprint (Wingate test) on four occasions: two after the ingestion of placebo and another two following the intake of antioxidants, while breathing either hypoxic gas (PIO2 = 75 mmHg) or room air (PIO2 = 143 mmHg). Vastus lateralis muscle biopsies were obtained before, immediately after, 30 and 120 min post-sprint. Antioxidants reduced the glycolytic rate without altering performance or VO2. Immediately after the sprints, Ser293- and Ser300-PDH-E1α phosphorylations were reduced to similar levels in all conditions (~66 and 91%, respectively). However, 30 min into recovery Ser293-PDH-E1α phosphorylation reached pre-exercise values while Ser300-PDH-E1α was still reduced by 44%. Thirty minutes after the sprint Ser293-PDH-E1α phosphorylation was greater with antioxidants, resulting in 74% higher muscle lactate concentration. Changes in Ser293 and Ser300-PDH-E1α phosphorylation from pre to immediately after the sprints were linearly related after placebo (r = 0.74, P < 0.001; n = 18), but not after antioxidants ingestion (r = 0.35, P = 0.15). In summary, lactate accumulation during sprint exercise in severe acute hypoxia is not caused by a reduced activation of the PDH. The ingestion of antioxidants is associated with increased PDH re-phosphorylation and slower elimination of muscle lactate during the recovery period. Ser293 re-phosphorylates at a faster rate than Ser300-PDH-E1α during the recovery period, suggesting slightly different regulatory mechanisms.

It remains unknown whether polyphenols such as luteolin (Lut), mangiferin and quercetin (Q) have ergogenic effects during repeated all-out prolonged sprints. Here we tested the effect of Mangifera indica L. leaf extract (MLE) rich in mangiferin (Zynamite®) administered with either quercetin (Q) and tiger nut extract (TNE), or with luteolin (Lut) on sprint performance and recovery from ischemia-reperfusion. Thirty young volunteers were randomly assigned to three treatments 48 h before exercise. Treatment A: placebo (500mg of maltodextrin/day); B: 140mg of MLE (60% mangiferin) and 50mg of Lut/day; and C: 140mg of MLE, 600mg of Q and 350mg of TNE/day. After warm-up, subjects performed two 30 s Wingate tests and a 60 s all-out sprint interspaced by 4min recovery periods. At the end of the 60 s sprint the circulation of both legs was instantaneously occluded for 20 s. Then, the circulation was re-opened and a 15 s sprint performed, followed by 10 s recovery with open circulation, and another 15 s final sprint. MLE supplements enhanced peak (Wpeak) and mean (Wmean) power output by 5.0-7.0% (P < 0.01). After ischemia, MLE+Q+TNE increased Wpeak by 19.4 and 10.2% compared with the placebo (P < 0.001) and MLE+Lut (P < 0.05), respectively. MLE+Q+TNE increased Wmean post-ischemia by 11.2 and 6.7% compared with the placebo (P < 0.001) and MLE+Lut (P = 0.012). Mean VO2 during the sprints was unchanged, suggesting increased efficiency or recruitment of the anaerobic capacity after MLE ingestion. In women, peak VO2 during the repeated sprints was 5.8% greater after the administration of MLE, coinciding with better brain oxygenation. MLE attenuated the metaboreflex hyperpneic response post-ischemia, may have improved O2 extraction by the Vastus Lateralis (MLE+Q+TNE vs. placebo, P = 0.056), and reduced pain during ischemia (P = 0.068). Blood lactate, acid-base balance, and plasma electrolytes responses were not altered by the supplements. In conclusion, a MLE extract rich in mangiferin combined with either quercetin and tiger nut extract or luteolin exerts a remarkable ergogenic effect, increasing muscle power in fatigued subjects and enhancing peak VO2 and brain oxygenation in women during prolonged sprinting. Importantly, the combination of MLE+Q+TNE improves skeletal muscle contractile function during ischemia/reperfusion. [ABSTRACT FROM AUTHOR]

Compared to normoxia, during sprint exercise in severe acute hypoxia the glycolytic rate is increased leading to greater lactate accumulation, acidification, and oxidative stress. To determine the role played by pyruvate dehydrogenase (PDH) activation and reactive nitrogen and oxygen species (RNOS) in muscle lactate accumulation, nine volunteers performed a single 30-s sprint (Wingate test) on four occasions: two after the ingestion of placebo and another two following the intake of antioxidants, while breathing either hypoxic gas (PIO2 = 75 mmHg) or room air (PIO2 = 143 mmHg). Vastus lateralis muscle biopsies were obtained before, immediately after, 30 and 120min post-sprint. Antioxidants reduced the glycolytic rate without altering performance or VO2. Immediately after the sprints, Ser293- and Ser300-PDH-E1α phosphorylations were reduced to similar levels in all conditions (~66 and 91%, respectively). However, 30min into recovery Ser293-PDH-E1α phosphorylation reached pre-exercise values while Ser300-PDH-E1α was still reduced by 44%. Thirty minutes after the sprint Ser293-PDH-E1α phosphorylation was greater with antioxidants, resulting in 74% higher muscle lactate concentration. Changes in Ser293 and Ser300-PDH-E1α phosphorylation from pre to immediately after the sprints were linearly related after placebo (r = 0.74, P < 0.001; n = 18), but not after antioxidants ingestion (r = 0.35, P = 0.15). In summary, lactate accumulation during sprint exercise in severe acute hypoxia is not caused by a reduced activation of the PDH. The ingestion of antioxidants is associated with increased PDH re-phosphorylation and slower elimination of muscle lactate during the recovery period. Ser293 re-phosphorylates at a faster rate than Ser300-PDH-E1α during the recovery period, suggesting slightly different regulatory mechanisms. [ABSTRACT FROM AUTHOR]

The aim of this study was to determine if reactive oxygen species (ROS) could play a role in blunting Thr172-AMP-activated protein kinase (AMPK)-α phosphorylation in human skeletal muscle after sprint exercise in hypoxia and to elucidate the potential signaling mechanisms responsible for this response. Nine volunteers performed a single 30-s sprint (Wingate test) in two occasions while breathing hypoxic gas PIO2= 75 mmHg): one after the ingestion of placebo and another following the intake of antioxidants (α-lipoic acid, vitamin C, and vitamin E), with a randomized double-blind design. Vastus lateralis muscle biopsies were obtained before, immediately after, and 30- and 120-min postsprint. Compared with the control condition, the ingestion of antioxidants resulted in lower plasma carbonylated proteins, attenuated elevation of the AMP-to-ATP molar ratio, and reduced glycolytic rate (P < 0.05) without significant effects on performance or V̇o2 The ingestion of antioxidants did not alter the basal muscle signaling. Thr172-AMPKα and Thr184/187-transforming growth factor-β-activated kinase 1 (TAK1) phosphorylation were not increased after the sprint regardless of the ingestion of antioxidants. Thr286-CaMKII phosphorylation was increased after the sprint, but this response was blunted by the antioxidants. Ser485-AMPKα1/Ser491-AMPKα2 phosphorylation increased immediately after the sprints coincident with increased Akt phosphorylation. In summary, antioxidants attenuate the glycolytic response to sprint exercise in severe acute hypoxia and modify the muscle signaling response to exercise. Ser485-AMPKα1/Ser491-AMPKα2 phosphorylation, a known mechanism of Thr172-AMPKα phosphorylation inhibition, is increased immediately after sprint exercise in hypoxia, probably by a mechanism independent of ROS.NEW & NOTEWORTHY The glycolytic rate is increased during sprint exercise in severe acute hypoxia. This study showed that the ingestion of antioxidants before sprint exercise in severe acute hypoxia reduced the glycolytic rate and attenuated the increases of the AMP-to-ATP and the reduction of the NAD+-to-NADH.H+ ratios. This resulted in a modified muscle signaling response with a blunted Thr286-CaMKII but similar AMP-activated protein kinase phosphorylation responses in the sprints preceded by the ingestion of antioxidants. [ABSTRACT FROM AUTHOR]

Introduction: Exercise reduces arterial and central venous blood pressures during recovery, which contributes to its valuable anti-hypertensive effects and to facilitating hypervolemia. Repeated sprint exercise potently improves metabolic function, but its cardiovascular effects (esp. hematological) are less well characterised, as are effects of exercising upper versus lower limbs. The purposes of this study were to identify the acute (

Introduction: Exercise reduces arterial and central venous blood pressures during recovery, which contributes to its valuable anti-hypertensive effects and to facilitating hypervolemia. Repeated sprint exercise potently improves metabolic function, but its cardiovascular effects (esp. hematological) are less well-characterized, as are effects of exercising upper versus lower limbs. The purposes of this study were to identify the acute (<24 h) profiles of arterial blood pressure and blood volume for (i) sprint intervals versus endurance exercise, and (ii) sprint intervals using arms versus legs. Methods: Twelve untrained males completed three cycling exercise trials; 50-min endurance (legs), and 5*30-s intervals using legs or arms, in randomized and counterbalanced sequence, at a standardized time of day with at least 8 days between trials. Arterial pressure, hemoglobin concentration and hematocrit were measured before, during and across 22 h after exercise, the first 3 h of which were seated rest. Results: The post-exercise hypotensive response was larger after leg intervals than endurance (AUC: 7540 ± 3853 vs. 3897 ± 2757mm Hg·min, p = 0.049, 95% CI: 20 to 6764), whereas exercising different limbs elicited similar hypotension (arms: 6420 ± 3947mm Hg·min, p = 0.48, CI: -1261 to 3896). In contrast, arterial pressure at 22 h was reduced after endurance but not after leg intervals (-8 ± 8 vs. 0 ± 7mm Hg, p = 0.04, CI: 7 ± 7) or reliably after arm intervals (-4 ± 8mm Hg, p = 0.18 vs. leg intervals). Regardless, plasma volume expansion at 22 h was similar between leg intervals and endurance (both +5 ± 5%; CI: -5 to 5%) and between leg and arm intervals (arms: +5 ± 7%, CI: -8 to 5%). Conclusions: These results emphasize the relative importance of central and/or systemic factors in post-exercise hypotension, and indicate that markedly diverse exercise profiles can induce substantive hypotension and subsequent hypervolemia. At least for endurance exercise, this hypervolemia may not depend on the volume of post-exercise hypotension. Finally, endurance exercise led to reduced blood pressure the following day, but sprint interval exercise did not. [ABSTRACT FROM AUTHOR]

Most sprint interval training (SIT) research involves cycling as the mode of exercise and whether running SIT elicits a similar excess postexercise oxygen consumption (EPOC) response to cycling SIT is unknown. As running is a more whole-body-natured exercise, the potential EPOC response could be greater when using a running session compared with a cycling session. The purpose of the current study was to determine the acute effects of a running versus cycling SIT session on EPOC and whether potential sex differences exist. Sixteen healthy recreationally active individuals (8 males and 8 females) had their gas exchange measured over ∼2.5 h under 3 experimental sessions: ( i) a cycle SIT session, ( ii) a run SIT session, and ( iii) a control (CTRL; no exercise) session. Diet was controlled. During exercise, both SIT modes increased oxygen consumption (cycle: male, 1.967 ± 0.343; female, 1.739 ± 0.296 L·min−1; run: male, 2.169 ± 0.369; female, 1.791 ± 0.481 L·min−1) versus CTRL (male, 0.425 ± 0.065 L·min−1; female, 0.357 ± 0.067; P < 0.001), but not compared with each other ( P = 0.234). In the first hour postexercise, oxygen consumption was still increased following both run (male, 0.590 ± 0.065; female, 0.449 ± 0.084) and cycle SIT (male, 0.556 ± 0.069; female, 0.481 ± 0.110 L·min−1) versus CTRL and oxygen consumption was maintained through the second hour postexercise (CTRL: male, 0.410 ± 0.048; female, 0.332 ± 0.062; cycle: male, 0.430 ± 0.047; female, 0.395 ± 0.087; run: male, 0.463 ± 0.051; female, 0.374 ± 0.087 L·min−1). The total EPOC was not significantly different between modes of exercise or males and females ( P > 0.05). Our data demonstrate that the mode of exercise during SIT (cycling or running) is not important to O2 consumption and that males and females respond similarly. [ABSTRACT FROM AUTHOR]

The effect of acute (24-h) sleep deprivation on exercise-induced growth hormone ( GH) and insulin-like growth factor-1 ( IGF-1) was examined. Ten men (20.6 ± 1.4 years) completed two randomized 24-h sessions including a brief, high-intensity exercise bout following either a night of sleep ( SLEEP) or (24-h) sleep deprivation ( SLD). Anaerobic performance (mean power [ MP], peak power [ PP], minimum power [MinP], time to peak power [ TTPP], fatigue index, [ FI]) and total work per sprint [ TWPS]) was determined from four maximal 30-sec Wingate sprints on a cycle ergometer. Self-reported sleep 7 days prior to each session was similar between SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 h, P = 0.656, respectively) and during the actual SLEEP session in the lab, the total amount of sleep was similar to the 7 days leading up to the lab session (7.72 ± 0.14 h vs. 7.92 ± 0.33 h, respectively) ( P = 0.166). No differences existed in MP, PP, MinP, TTPP, FI, TWPS, resting GH concentrations, time to reach exercise-induced peak GH concentration ( TTP), or free IGF-1 between sessions. GH area under the curve ( AUC) (825.0 ± 199.8 vs. 2212.9 ± 441.9 μg/L*min, P < 0.01), exercise-induced peak GH concentration (17.8 ± 3.7 vs. 39.6 ± 7.1 μg/L, P < 0.01) and Δ GH (peak GH - resting GH) (17.2 ± 3.7 vs. 38.2 ± 7.3 μg/L, P < 0.01) were significantly lower during the SLEEP versus SLD session. Our results indicate that the exercise-induced GH response was significantly augmented in sleep-deprived individuals. [ABSTRACT FROM AUTHOR]

Objective: The goal of this study was to evaluate the effects of creatine (Cr) supplementation on oxidative stress and inflammation markers after acute repeated-sprint exercise in humans. Methods: Twenty-five players under age 20 y were randomly assigned to two groups: Cr supplemented and placebo. Double-blind controlled supplementation was performed using Cr (0.3 g/kg) or placebo tablets for 7 d. Before and after 7 d of supplementation, the athletes performed two consecutive Running-based Anaerobic Sprint Tests (RAST). RAST consisted of six 35-m sprint runs at maximum speed with 10 sec rest between them. Blood samples were collected just prior to start of test (pre), just after the completion (0 h), and 1 h after completion. Results: Average, maximum, and minimum power values were greater in the Cr-supplemented group compared with placebo (P < 0.05). There were significant increases (P < 0.05) in plasma tumor necrosis factor alpha (TNF-α) and C-reactive protein (CRP) up to 1 h after acute sprint exercise in the placebo-supplemented group. Malondialdehyde, lactate dehydrogenase (LDH), catalase, and superoxide dismutase enzymes also were increased after exercise in both groups. Red blood cell glutathione was lower after exercise in both groups. Cr supplementation reversed the increase in TNF-α and CRP as well as LDH induced by acute exercise. Controversially, Cr supplementation did not inhibit the rise in oxidative stress markers. Also, antioxidant enzyme activity was not different between placebo and Cr-supplemented groups. Conclusion: Cr supplementation inhibited the increase of inflammation markers TNF-α and CRP, but not oxidative stress markers, due to acute exercise. [ABSTRACT FROM AUTHOR]

To determine if the muscle signalling response to a 30 s all-out sprint exercise is modulated by the exercise mode and the endocrine response, 27 healthy volunteers were divided in 2 groups that performed isokinetic (10 men and 5 women) and isoinertial (7 men and 5 women) Wingate tests. Blood samples and vastus lateralis muscle biopsies were taken before, immediately after, 30 and 120 min after the sprints. Groups were comparable in age, height, body weight, percentage of body fat, peak power per kg of lower extremities lean mass (Pmax) and muscle fi bre types. However, the isoinertial group achieved a 25 % greater mean power (Pmean). Sprint exercise elicited marked increases in the musculus vastus lateralis AMPK?, ACC?, STAT3, STAT5 and ERK1/2 phosphorylation (all P < 0.05). The AMPK?, STAT3, and ERK1/2 phosphorylation responses were more marked after the isoinertial than isokinetic test (interaction: P < 0.01). The diff erences in muscle signalling could not be accounted for by diff erences in Pmax, although Pmean could explain part of the diff erence in AMPK? phosphorylation. The leptin, insulin, glucose, GH, IL-6, and lactate response were similar in both groups. In conclusion, the muscle signalling response to sprint exercise diff ers between isoinertial and isokinetic sprints. [ABSTRACT FROM AUTHOR]

This study examined the acute effect of sprint interval exercise (SIE) on postexercise oxygen consumption, substrate oxidation, and blood pressure. The participants were 10 healthy males aged 21-27 years. Following overnight fasts, each participant undertook 2 trials in a random balanced order: ( i) four 30-s bouts of SIE on a cycle ergometer, separated by 4.5 min of recovery, and ( ii) resting (control) in the laboratory for an equivalent period. Time-matched measurements of oxygen consumption, respiratory exchange ratio, and blood pressure were made for 2 h into recovery. Total 2-h oxygen consumption was significantly higher in the SIE than in the control trial (mean ± SD: Control: 31.9 ± 6.7 L vs Exercise: 45.5 ± 6.8 L, p < 0.001). The rate of fat oxidation was 75% higher 2 h after the exercise trial compared with the control trial (Control: 0.08 ± 0.05 g·min−1 vs Exercise: 0.14 ± 0.06 g·min−1, p = 0.035). Systolic blood pressure (Control: 117 ± 8 mm Hg vs Exercise: 109 ± 8 mm Hg, p < 0.05) and diastolic blood pressure (Control: 84 ± 6 mm Hg vs Exercise: 77 ± 5 mm Hg, p < 0.05) were significantly lower 2 h after the exercise trial compared with the control trial. These data showed a 42% increase in oxygen consumption (∼13.6 L) over 2 h after a single bout of SIE. Moreover, the rate of fat oxidation increased by 75%, whereas blood pressure was reduced by ∼8 mm Hg 2 h after SIE. Whether these acute benefits of SIE can translate into long-term changes in body composition and an improvement in vascular health needs investigation. [ABSTRACT FROM AUTHOR]

Calsequestrin (CSQ) is the main Ca binding protein inside the sarcoplasmic reticulum (SR) of skeletal and cardiac muscle. The present study demonstrates the specific effects of different training regimens on CSQ isoform 1 (CSQ1, the primary isoform) and SR Ca-ATPase (SERCA1, 2) expression in various skeletal muscles of mouse. CSQ1, SERCA1, and SERCA2 protein expression was determined with Western blot in m. soleus (SOL), m. extensor digitorum longus (EDL), m. gastrocnemius (GAS), m. rectus femoris (RF), and m. tibialis anterior (TA) muscles after completing a 6-week endurance or sprint training program. Endurance training induced decrease in CSQ1 concentration in SOL ( p < 0.001) and in SERCA1 levels in GAS ( p < 0.05), whereas increase in CSQ1 expression was detected in EDL ( p < 0.01). After sprint training the concentration of CSQ1 increased in GAS ( p < 0.01) and EDL ( p < 0.01). Additionally, sprint exercise induced an increase in SERCA1 in GAS ( p < 0.001) and a decline in TA ( p < 0.05). SERCA2 was up-regulated with sprint training in GAS ( p < 0.01). Myosin heavy chain (MHC) based fibre type composition altered differently depending on the muscle and the training regimen.These results indicate that (1) diverse training strategies used affect differently CSQ1 and SERCA1 concentrations in the skeletal muscle, (2) the regulation of CSQ1 and SERCA1 does not necessary follow the fast-slow definition despite the correlation between MHC isoforms, and (3) the changes in CSQ1 concentration occur prior to SERCA1 or SERCA2. [ABSTRACT FROM AUTHOR]

Peripheral arterial distensibility is improved with sprint interval exercise training in young healthy participants (Rakobowchuk et al. in Am J Physiol Regul Integr Comp Physiol 295:R236-R242, 2008). To fully understand the mechanisms contributing to these training effects it is useful to examine the acute responses to sprint interval exercise. Following supine rest, nine healthy males completed either a single sprint interval (Wingate test) or a multiple sprint interval exercise session (4 Wingate tests each separated by 4.5 min). Following exercise, participants recovered for 60 min while central and peripheral arterial distensibility measurements were conducted at discrete time points, using applanation tonometry and ultrasound imaging and continuously, using central and peripheral pulsewave velocity (PWV). Single and multiple sprint interval exercise sessions caused similar changes in all variables. Heart rate was increased throughout recovery (p < 0.05), while central artery PWV was increased until 20 min of recovery (p < 0.05) and lower extremity PWV was decreased until ~45 min (p < 0.05). Distensibility of the superficial femoral artery showed a trend for a reduction at 2 min post-exercise (p = 0.06). These results indicate that extremely high intensity exercise transiently increases central artery stiffness, while metabolite induced vasodilation reduces peripheral stiffness in exercised limbs well into recovery. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine the effect of oral administration of sodium bicarbonate (NaHCO3) on surface electromyogram (SEMG) activity from the vastus lateralis (VL) during repeated cycling sprints (RCS). Subjects performed two RCS tests (ten 10-s sprints) interspersed with both 30-s and 360-s recovery periods 1 h after oral administration of either NaHCO3 (RCSAlk) or CaCO3 (RCSPla) in a random counterbalanced order. Recovery periods of 360 s were set before the 5th and 9th sprints. The rate of decrease in plasma HCO3- concentration during RCS was significantly greater in RCSAlk than in RCSPla, but the rates of decline in blood pH during the two RCS tests were similar. There was no difference between change in plasma lactate concentration in RCSAlk and that in RCSPla. Performance during RCSAlk was similar to that during RCSPla. There were no differences in oxygen uptake immediately before each cycling sprint (preVO2) and in SEMG activity between RCSAlk and RCSPla. In conclusion, oral administration of NaHCO3 did not affect SEMG activity from the VL. This suggests that the muscle recruitment strategy during RCS is not determined by only intramuscular pH. [ABSTRACT FROM AUTHOR]

The article presents a study that assesses the effects of the intensity of short recoveries on performance by a Wingate test and on the deoxyhemoglobin variations. The test performed after active recovery areas were significantly higher than mean power and peak power performed after active recovery. It demonstrates that when two Wingate tests are performed almost successively but with a short recovery between the two, passive recovery is more appropriate than active recovery to restore the performance level.

Summary: This study assessed whether an eccentric chainring that increases crank arm length at the downstroke and decreases it during the upstroke improves performance in a track cycling event: the 1000m time trial. It also determined whether selected physical and physiological variables and the velocity profile are associated with eccentric chainring performance. Twelve cyclists performed an outdoor 1000m time trial on a 333m banked, cement-surfaced track using two different chainrings, round and eccentric, in randomised order. The important findings of this study were that (1) performance did not significantly differ between chainrings; (2) neither the physiological variables (lactate and heart rate) nor the velocity profile (lap times) were affected by use of the eccentric design; (3) when time was saved with the eccentric chainring, it was significantly correlated with estimated lower limb muscle volume (r =−0.605), circumference (r =−0.739), estimated calf muscle volume (r =−0.772) and cross-sectional area (r =−0.745). Moreover, estimated lower limb muscle volume (r =−0.703), estimated calf muscle volume (r =−0.772) and cross-sectional area (r =−0.871) significantly predicted performance with the eccentric chainring. The physical variables associated with eccentric chainring performance were muscle anthropometric parameters. We have interpreted our results cautiously and suggest that the subjects who had greater lower limb muscle volume and greater calf muscle volume, seem to have had a significant advantage in performing with the eccentric chainring. Further testing with track specialists performing at national or international level would be helpful to define the maximal possibilities of this chainring. [Copyright &y& Elsevier]

The purpose of this study was to investigate whether hypoxia can alter anaerobic energy release during supramaximal exercise. Seven male subjects performed 12 submaximal cycling tests to establish the relationship between workload and O2 demand. The subjects also performed 40 s Wingate tests (WT) under normoxia (room air), two levels of moderate hypoxia of 16.4% O2 and 12.7% O2. We measured the power output and oxygen uptake ( VO2) during each test and estimated the O2 demand, O2 deficit and percentage of anaerobic energy release (%AnAER). These data were analyzed for each 20 s interval. At all intervals, there were no differences in Pmean·body mass (BM)−1, O2 demand·BM−1 or O2 deficit·BM−1 among the three O2 conditions. However, under hypoxia of 12.7%, VO2·BM−1 was significantly decreased and %AnAER was significantly increased in the late phase (20–40 s) of the WT, compared to normoxia ( P<0.05). There were no such significant differences between normoxia and hypoxia of 16.4%. Thus, the present results show that the degree of hypoxia affects the magnitude of the hypoxia-induced increase in anaerobic energy release in the late phase of the WT and suggest that certain degrees of hypoxia induce significant increases in the amount of anaerobic energy released, compared to normoxia. [ABSTRACT FROM AUTHOR]

This study was aimed to investigate changes in blood markers of oxidative damage induced by short-term supramaximal anaerobic exercise and to determine whether oxidative stress was associated to activation of the redox-sensitive transcription factor nuclear factor-?B (NF-?B). Both a single Wingate test (WAnT) test and series of four WAnTs separated by 60?min rest intervals were carried out by eight professional cyclists. Leukocyte 8-OH-2-deoxyguanosine levels were significantly elevated 24?h after both exercise protocols. A significant decrease in blood reduced glutathione (GSH) concentration was observed immediately after and at 15, 60 and 120?min of the single WAnT, followed by a return to basal value after 24?h. This decrease was parallel to a significant increase of the oxidised/reduced glutathione (GSSG/GSH) ratio, to an activation of NF-?B and to a significant decrease in the protein level of its inhibitor I?B. GSH concentration and the GSSG/GSH ratio changed significantly for the first three of the WAnTs series and normalised thereafter. A significant activation of NF-?B and a decrease in the I?B protein level were also detected. We conclude that short-term supramaximal anaerobic exercise induces oxidative stress, as evidenced by non cumulative damage to macromolecules and changes in the glutathione status. Our data also indicate that high intensity anaerobic work gives rise to an activation of the transcription factor NF-?B accompanied by a degradation of I?B. [ABSTRACT FROM AUTHOR]

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) μmol 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) μg l-1, P<0.05], and mean integrated serum hGH concentrations were 55% lower after training [567 (158) vs 256 (121) min μg 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. [ABSTRACT FROM AUTHOR]

The popularity of intermittent fasting (IF) and high intensity (sprint) interval training (SIT) has increased in recent years amongst the general public due to their purported health benefits and feasibility of incorporation into daily life. The number of scientific studies investigating these strategies has also increased, however, very few have examined the combined effects, especially on body composition and cardiometabolic biomarkers, which is the primary aim of this investigation. A total of thirty-four male and female participants (age: 35.4 ± 8.4 y, body mass index (BMI): 31.3 ± 3.5 kg/m2, aerobic capacity (VO2peak) 27.7 ± 7.0 mL·kg−1·min−1) were randomized into one of three 16-week interventions: (1) 5:2 IF (2 non-consecutive days of fasting per week, 5 days on ad libitum eating), (2) supervised SIT (3 bouts per week of 20s cycling at 150% VO2peak followed by 40 s of active rest, total 10 min duration), and (3) a combination of both interventions. Body composition, haemodynamic and VO2peak were measured at 0, 8 and 16 weeks. Blood samples were also taken and analysed for lipid profiles and markers of glucose regulation. Both IF and IF/SIT significantly decreased body weight, fat mass and visceral fat compared to SIT only (p < 0.05), with no significant differences between diet and diet + exercise combined. The effects of diet and/or exercise on cardiometabolic biomarkers were mixed. Only exercise alone or with IF significantly increased cardiorespiratory fitness. The results suggest that energy restriction was the main driver of body composition enhancement, with little effect from the low volume SIT. Conversely, to achieve benefits in cardiorespiratory fitness, exercise is required.

Simple Summary: Sport training leads to adaptation to physical effort that is reflected by changes in blood parameters. The Thoroughbred racehorse is a valid animal model to investigate such changes. Twenty-nine clinically healthy, two-year-old Thoroughbred racehorses were followed during their first 4-month sprint training. Blood collection was performed at rest, once a month, five times. For each sample, blood parameters were determined. Moreover, before the beginning and at the end of the experimental period, serum protein electrophoresis and genetic analysis to evaluate the expression of key genes related to inflammatory and immunity responses were performed on all samples. Significant modifications were identified compared with the beginning of training for numerous metabolites and genes related to immunity response. In conclusion, the first long-term training period induces fundamental systemic changes in untrained Thoroughbreds probably as the result of the onset of physiologic adaptation to training. Training has a huge effect on physiological homeostasis. The Thoroughbred racehorse is a valid animal model to investigate such changes for training schedule fine-tuning. As happens in human athletes, it is hypothesized that biochemical and immune response changes and related biomolecular variations could be induced by training programs. The aim of this study was to investigate, for the first time, the long-term metabolic and biomolecular modifications in young untrained Thoroughbred racehorses in the first 4-month timeframe training period. Twenty-nine clinically healthy, untrained, two-year-old Thoroughbred racehorses were followed during their incremental 4-month sprint exercise schedule. Blood collection was performed once a month, five times (T-30, T0, T30, T60, and T90). For each sample, lactate concentration, plasma cell volume (PCV), and hematobiochemical parameters (glucose, urea, creatinine, aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), total bilirubin (Tbil), lactate dehydrogenase (LDH), creatine kinase (CK), cholesterol, triglycerides, albumin (Alb), total proteins (TPs), phosphorus (P), calcium (Ca2+), magnesium (Mg), sodium (Na+), potassium (K−), and chloride (Cl)) were determined. At T-30 and T90, serum protein electrophoresis (SPE), serum amyloid A (SAA), and real-time qPCR were performed on all samples to evaluate the expression of key genes and cytokines related to inflammatory and Th2 immunity responses: Interleukin-4 (IL-4), Interleukin-6 (IL-6), Interleukin-10 (IL-10), Interleukin-1β (IL-1β), Octamer-Binding Transcription Factor 1 (OCT1), B-cell lymphoma/leukemia 11A (BCL11A). Statistical analysis was performed (ANOVA and t test, p < 0.05). Significant modifications were identified compared with T-30 for PCV, glucose, triglycerides, cholesterol, lactate, urea, creatinine, Tbil, ALP, LDH, Na+, K−, Ca2+, SAA, TPs, SPE, IL-6, IL-4, Oct-1, and BCL11A. In conclusion, the first long-term training period was found to induce fundamental systemic changes in untrained Thoroughbreds. [ABSTRACT FROM AUTHOR]

Introduction. – A recent study (Groussard et al., personal communication) demonstrated that a single sprint exercise (30 s) induced an increase in lipid radical production and an alteration of blood enzymatic antioxidant system. So we hypothesised that the same exercise may also affect plasma non enzymatic antioxidant status.Method and results. – Eight students in physical education performed a Wingate test. Plasma nonenzymatic antioxidant status (uric acid, vitamins C and E, β-carotene) was determined at rest (R), after the warm up (E), after the exercise (P0), and at 5 (P5), 10 (P10), 20 (P20) and 40 (P40) minutes of recovery. We observed an increase in plasma uric acid and vitamin C respectively since P10 et P20. Inversely, the Wingate test induced a decrease in plasma vitamin E concentration at P5 and P10 which then return to basal values and a decrease in plasma β-carotene concentration since P5.Conclusion. – These results demonstrated that a short (30 s) single sprint exercise alters plasma non-enzymatic antioxidant status. [Copyright &y& Elsevier]

The natural components of the pomegranate fruit may provide additional benefits for endothelial function and microcirculation. It was hypothesized that supplementation with pomegranate extract might improve glycocalyx properties and microcirculation during acute high-intensity sprint interval cycling exercise. Eighteen healthy and recreationally active male volunteers 22-28 years of age were recruited randomly to the experimental and control groups. The experimental group was supplemented with pomegranate extract 20 mL (720 mg phenolic compounds) for two weeks. At the beginning and end of the study, the participants completed a high-intensity sprint interval cycling-exercise protocol. The microcirculation flow and density parameters, glycocalyx markers, systemic hemodynamics, lactate, and glucose concentration were evaluated before and after the initial and repeated (after 2 weeks supplementation) exercise bouts. There were no significant differences in the microcirculation or glycocalyx over the course of the study ( p < 0.05). The lactate concentration was significantly higher in both groups after the initial and repeated exercise bouts, and were significantly higher in the experimental group compared to the control group after the repeated bout: 13.2 (11.9-14.8) vs. 10.3 (9.3-12.7) mmol/L, p = 0.017. Two weeks of supplementation with pomegranate extract does not influence changes in the microcirculation and glycocalyx during acute high-intensity sprint interval cycling-exercise. Although an unexplained rise in blood lactate concentration was observed.

It remains unknown whether polyphenols such as luteolin (Lut), mangiferin and quercetin (Q) have ergogenic effects during repeated all-out prolonged sprints. Here we tested the effect of Mangifera indica L. leaf extract (MLE) rich in mangiferin (Zynamite®) administered with either quercetin (Q) and tiger nut extract (TNE), or with luteolin (Lut) on sprint performance and recovery from ischemia-reperfusion. Thirty young volunteers were randomly assigned to three treatments 48 h before exercise. Treatment A: placebo (500 mg of maltodextrin/day); B: 140 mg of MLE (60% mangiferin) and 50 mg of Lut/day; and C: 140 mg of MLE, 600 mg of Q and 350 mg of TNE/day. After warm-up, subjects performed two 30 s Wingate tests and a 60 s all-out sprint interspaced by 4 min recovery periods. At the end of the 60 s sprint the circulation of both legs was instantaneously occluded for 20 s. Then, the circulation was re-opened and a 15 s sprint performed, followed by 10 s recovery with open circulation, and another 15 s final sprint. MLE supplements enhanced peak (Wpeak) and mean (Wmean) power output by 5.0-7.0% ( P < 0.01). After ischemia, MLE+Q+TNE increased Wpeak by 19.4 and 10.2% compared with the placebo ( P < 0.001) and MLE+Lut ( P < 0.05), respectively. MLE+Q+TNE increased Wmean post-ischemia by 11.2 and 6.7% compared with the placebo ( P < 0.001) and MLE+Lut ( P = 0.012). Mean VO 2 during the sprints was unchanged, suggesting increased efficiency or recruitment of the anaerobic capacity after MLE ingestion. In women, peak VO 2 during the repeated sprints was 5.8% greater after the administration of MLE, coinciding with better brain oxygenation. MLE attenuated the metaboreflex hyperpneic response post-ischemia, may have improved O 2 extraction by the Vastus Lateralis (MLE+Q+TNE vs. placebo, P = 0.056), and reduced pain during ischemia ( P = 0.068). Blood lactate, acid-base balance, and plasma electrolytes responses were not altered by the supplements. In conclusion, a MLE extract rich in mangiferin combined with either quercetin and tiger nut extract or luteolin exerts a remarkable ergogenic effect, increasing muscle power in fatigued subjects and enhancing peak VO 2 and brain oxygenation in women during prolonged sprinting. Importantly, the combination of MLE+Q+TNE improves skeletal muscle contractile function during ischemia/reperfusion.