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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.

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]

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]

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.

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]

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.