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We aimed to evaluate the blood lactate level in response to two bouts of exercise. First, we hypothesized that blood lactate elevation in response to moderate-intensity aerobic exercise (MIAE) would be lower at the end of the second bout of MIAE than the first bout of MIAE. In this context, we also hypothesized that lactate accumulation at the end of resistance exercise (RE) would be reduced if MIAE is performed before RE (i.e., concurrent exercise; CE). If so, we hypothesized that the order of the CE (i.e., RE + MIAE vs. MIAE + RE) influences blood lactate kinetics. To test the hypotheses, forty-three healthy men participated in three studies. In study 1, 20 men (age 21 ± 2 years) performed two bouts of a 20-min MIAE separated by a 20-min rest interval. In study 2, 11 men (age 22 ± 1 years) performed RE only and CE (MIAE + RE; ARCE) with a 20-min rest interval in a crossover design. In study 3, 12 men (age 21 ± 2 years) performed both CEs, which were ARCE and RE + MIAE (RACE), with a 20-min rest interval in a crossover design. We measured blood lactate before and at the end of each exercise session. In study 1, the blood lactate response to the second bout of MIAE was lower than that of the first bout (P < 0.001, r = 0.68). However, the blood lactate response to the ARCE trial was not lower than the response to the RE trial in study 2 (P = 0.475, r = 0.22). The results of study 3 showed that the RACE and ARCE trials induced a similar lactate response (MIAE P = 0.423, r = 0.28; RE P = 0.766, d = 0.03). These observations indicate that whereas lactate accumulation might be diminished by a second bout of MIAE, a different type of exercise (i.e., aerobic/resistance) did not result in a diminished lactate accumulation in response to a second bout of exercise. [ABSTRACT FROM AUTHOR]

Hypoxia has the potential to impair cognitive function; however, it is still uncertain which cognitive domains are adversely affected. We examined the effects of acute hypoxia (∼7 h) on central executive (Go/No‐Go) and non‐executive (memory) tasks and the extent to which impairment was potentially related to regional cerebral blood flow and oxygen delivery (CDO2). Twelve male participants performed cognitive tasks following 0, 2, 4 and 6 h of passive exposure to both normoxia and hypoxia (12% O2), in a randomized block cross‐over single‐blinded design. Middle cerebral artery (MCA) and posterior cerebral artery (PCA) blood velocities and corresponding CDO2 were determined using bilateral transcranial Doppler ultrasound. In hypoxia, MCA DO2 was reduced during the Go/No‐Go task (P = 0.010 vs. normoxia, main effect), and PCA DO2 was attenuated during memorization (P = 0.005 vs. normoxia) and recall components (P = 0.002 vs. normoxia) in the memory task. The accuracy of the memory task was also impaired in hypoxia (P = 0.049 vs. normoxia). In contrast, hypoxia failed to alter reaction time (P = 0.19 vs. normoxia) or accuracy (P = 0.20 vs. normoxia) during the Go/No‐Go task, indicating that selective attention and response inhibition were preserved. Hypoxia did not affect cerebral blood flow or corresponding CDO2 responses to cognitive activity (P > 0.05 vs. normoxia). Collectively, these findings highlight the differential sensitivity of cognitive domains, with memory being selectively vulnerable in hypoxia. New Findings: What is the central question of this study?We sought to examine the effects of acute hypoxia on central executive (selective attention and response inhibition) and non‐executive (memory) performance and the extent to which impairments are potentially related to reductions in regional cerebral blood flow and oxygen delivery.What is the main finding and its importance?Memory was impaired in acute hypoxia, and this was accompanied by a selective reduction in posterior cerebral artery oxygen delivery. In contrast, selective attention and response inhibition remained well preserved. These findings suggest that memory is selectively vulnerable to hypoxia. [ABSTRACT FROM AUTHOR]

The speed and accuracy of decision-making (i.e., executive function (EF) domains) is an integral factor in many sports. At rest, prolonged cognitive load (pCL) impairs reaction time (RT). In contrast, exercise improves RT and EF. We hypothesized that RT and EF during exercise would be diminished by prolonged 'dual tasking' as a consequence of pCL. To test the hypothesis, twenty healthy male participants performed four conditions [resting control (Rest), pCL only (pCLRest), exercise only (EX), and pCL + exercise (pCLEX)] in a randomized-crossover design. Both exercise conditions utilized a 50-min cycling exercise protocol (60% VO2 peak) and the pCL was achieved via a 50-min colour-word Stroop task (CWST). Compared with Rest, pCLRest caused a slowed CWST RT (P < 0.05) and a large SD (i.e., intraindividual variability) of CWST RT (P < 0.01). Similarly, compared with EX, the slowed CWST RT (P < 0.05) and large SD of CWST RT (P < 0.01) were also observed in pCLEX. Whereas the reverse-Stroop interference was not affected in pCLRest (P = 0.46), it was larger (i.e., declined EF) in pCLEX than EX condition (P < 0.05). These observations provide evidence that the effort of pCL impairs RT and EF even during exercise. [ABSTRACT FROM AUTHOR]

Introduction: High-intensity interval exercise (HIIE) is more effective at increasing metabolic and cardiovascular health compared with moderate-intensity continuous exercise for patients with cardiovascular disease, but exhaustive high-intensity continuous exercise attenuates dynamic cerebral autoregulation (CA). This study assessed the effect of HIIE on dynamic CA. Methods: Nine healthy men (age, 24 ± 3 yr; mean ± SD) warmed up at 50%–60% maximal workload (W max) for 5 min before HIIE including four 4-min bouts of exercise at 80%–90% W max interspaced by four 3-min bouts at 50% to 60% W max. Transcranial Doppler determined middle cerebral artery mean blood velocity (MCA V mean), and brachial artery catheterization determined mean arterial pressure (MAP). Dynamic CA was evaluated by transfer function analysis of changes in MAP and MCA V mean. Results: The HIIE increased MAP (from 92 ± 9 to 104 ± 10 mm Hg; P < 0.0125), whereas MCA V mean did not change. Transfer function phase increased and coherence decreased during HIIE (P < 0.0125 vs rest, respectively), whereas gain was unchanged. Conclusions: The results suggest that dynamic CA is unaffected during HIIE, indicating that the brain is protected from fluctuations in MAP. Thus, we propose that HIIE may be beneficial for brain-related health as maintenance of cerebral perfusion in contrast to high-intensity continuous exercise. [ABSTRACT FROM AUTHOR]

Acute aerobic exercise improves inhibitory control (IC). This improvement is often associated with increases in perceived exertion during exercise. However, listening to music during aerobic exercise mitigates an exercise-induced increase in perceived exertion. Thus, it is hypothesized that such effects of music may interfere with exercise-induced improvements in IC. To test this hypothesis, we examined the effect of music on post-exercise IC improvements that were induced by moderate-intensity exercise. Fifteen healthy young men performed cycle ergometer exercise with music or non-music. The exercise was performed using a moderate-intensity of 60% of VO 2 peak for 30 min. The music condition was performed while listening to self-selected music. The non-music condition involved no music. To evaluate IC, the Stroop task was administered before exercise, immediately after exercise, and during the 30-min post-exercise recovery period. The rate of perceived exertion immediately before moderate-intensity exercise completed was significantly lower in music condition than in non-music condition. The IC significantly improved immediately after exercise and during the post-exercise recovery period compared to before exercise in both music and non-music conditions. The post-exercise IC improvements did not significantly differ between the two conditions. These findings indicate that self-selected music-induced mitigation of the increase in perceived exertion during moderate-intensity exercise dose not interfere with exercise-induced improvements in IC. Therefore, we suggest that listening to music may be a beneficial strategy in mitigating the increase in perceived exertion during aerobic exercise without decreasing the positive effects on IC. [ABSTRACT FROM AUTHOR]

The positive effect of acute resistance exercise on executive function, such as inhibitory control (IC), is poorly understood. Several previous studies have demonstrated this effect using whole-body resistance exercise. However, it remains unclear whether localized resistance exercise performed using only limited muscle groups could also acutely improve IC. Thus, the present study examined the effect of an acute bout of localized resistance exercise on IC. Twelve healthy men performed a color-word Stroop task (CWST) before and immediately after the experimental conditions, which consisted of 2 resistance exercises and a resting control (CON). Bilateral knee extension was used to create 2 resistance exercise conditions: light-intensity resistance exercise (LRE) and high-intensity resistance exercise (HRE) conditions, which were 40% and 80% of one-repetition maximum, respectively. The resistance exercise session was programmed for 6 sets with 10 repetitions per set. The CWST-measured IC was significantly improved immediately after both LRE and HRE, but it did not improve immediately after CON. However, the improved IC was significantly greater in HRE than in LRE. The present findings showed that IC could be rapidly improved by an acute bout of localized resistance exercise, especially with high-intensity. Therefore, we suggest that in addition to whole-body resistance exercise, localized resistance exercise performed using limited muscle groups may be sufficient for improving IC. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?High‐intensity interval exercise (HIIE) is recommended for its favourable haemodynamic stimulation, but excessive haemodynamic fluctuations may stress the brain: is the cerebral vasculature protected against exaggerated systemic blood flow fluctuation during HIIE?What is the main finding and its importance?Time‐ and frequency‐domain indices of aortic–cerebral pulsatile transition were lowered during HIIE. The findings suggest that the arterial system to the cerebral vasculature may attenuate pulsatile transition during HIIE as a defence mechanism against pulsatile fluctuation for the cerebral vasculature. High‐intensity interval exercise (HIIE) is recommended because it provides favourable haemodynamic stimulation, but excessive haemodynamic fluctuations may be an adverse impact on the brain. We tested whether the cerebral vasculature is protected against systemic blood flow fluctuation during HIIE. Fourteen healthy men (age 24 ± 2 years) underwent four 4‐min exercises at 80–90% of maximal workload (Wmax) interspaced by 3‐min active rest at 50–60% Wmax. Transcranial Doppler measured middle cerebral artery blood velocity (CBV). Systemic haemodynamics (Modelflow) and aortic pressure (AoP, general transfer function) were estimated from an invasively recorded brachial arterial pressure waveform. Using transfer function analysis, gain and phase between AoP and CBV (0.39–10.0 Hz) were calculated. Stroke volume, aortic pulse pressure and pulsatile CBV increased during exercise (time effect: P < 0.0001 for all), but a time‐domain index of aortic–cerebral pulsatile transition (pulsatile CBV/pulsatile AoP) decreased throughout the exercise bouts (time effect: P < 0.0001). Furthermore, transfer function gain reduced, and phase increased throughout the exercise bouts (time effect: P < 0.0001 for both), suggesting the attenuation and delay of pulsatile transition. The cerebral vascular conductance index (mean CBV/mean arterial pressure; time effect: P = 0.296), an inverse index of cerebral vascular tone, did not change even though systemic vascular conductance increased during exercise (time effect: P < 0.0001). The arterial system to the cerebral vasculature may attenuate pulsatile transition during HIIE as a defence mechanism against pulsatile fluctuation for the cerebral vasculature. [ABSTRACT FROM AUTHOR]

A single bout of aerobic exercise improves executive function (EF), but only for a short period. Compared with a single bout of aerobic exercise, we recently found that high-intensity interval exercise (HIIE) could maintain a longer improvement in EF. However, the mechanism underlying the effect of different exercise modes on the modifications of EF remains unclear. The purpose of the current investigation was to test our hypothesis that the amount of exercise-induced lactate production and its accumulation affects human brain function during and after exercise, thereby affecting post-exercise EF. Ten healthy male subjects performed cycle ergometer exercise. The HIIE protocol consisted of four 4-min bouts at 90% peak VO 2 with a 3-min active recovery period at 60% peak VO 2 . The amount of lactate produced during exercise was manipulated by repeating the HIIE twice with a resting period of 60 min between the 1st HIIE and 2nd HIIE. To evaluate EF, a color-word Stroop task was performed, and reverse-Stroop interference scores were obtained. EF immediately after the 1st HIIE was significantly improved compared to that before exercise, and the improved EF was sustained during 40 min of the post-exercise recovery. However, for the 2nd HIIE, the improved EF was sustained for only 10 min of the post-exercise recovery period, despite the performance of the same exercise. In addition, during and following HIIE, the glucose and lactate accumulation induced by the 2nd HIIE was significantly lower than that induced by the 1st HIIE. Furthermore, there was an inverse relationship between lactate and EF by plotting the changes in lactate levels against changes in EF from pre-exercise during the late phase of post-exercise recovery. These findings suggested the possibility that repeated bouts of HIIE, which decreases lactate accumulation, may dampen the positive effect of exercise on EF during the post-exercise recovery. [ABSTRACT FROM AUTHOR]

Aerobic moderate-intensity continuous exercise (MCE) can improve executive function (EF) acutely, potentially through the activation of both physiological and psychological factors. Recently, high-intensity interval exercise (HIIE) has been reported to be more beneficial for physical adaptation than MCE. Factors for EF improvement can potentially be more enhanced by HIIE than by MCE; but the effects of HIIE on EF remain unknown. Therefore, we aimed to examine to what extent HIIE impacts post-exercise EF immediately after exercise and during post-exercise recovery, compared with traditional MCE. Twelve healthy male subjects performed cycle ergometer exercise based on either HIIE or MCE protocols in a randomized and counterbalanced order. The HIIE protocol consisted of four 4-min bouts at 90% of peak VO 2 with 3-min active recovery at 60% of peak VO 2 . A volume-matched MCE protocol was applied at 60% of peak VO 2 . To evaluate EF, a color-words Stroop task was performed pre- and post-exercise. Improvement in EF immediately after exercise was the same for the HIIE and MCE protocols. However, the improvement of EF by HIIE was sustained during 30 min of post-exercise recovery, during which MCE returned to the pre-exercise level. The EF response in the post-exercise recovery was associated with changes in physiological and psychological responses. The present findings showed that HIIE and MCE were capable of improving EF. Moreover, HIIE could prolong improvement in EF during post-exercise recovery. For the first time, we suggest that HIIE may be more effective strategy than MCE for improving EF. [ABSTRACT FROM AUTHOR]

No studies have identified the direct effect of changes in cerebral blood flow ( CBF) on cognitive function at rest and during exercise. In this study, we manipulated CBF using hypercapnic gas to examine whether an increase in CBF improves cognitive function during prolonged exercise. The speed and the accuracy of cognitive function were assessed using the Stroop color-word test. After the Stroop test at rest, the subjects began exercising on a cycling ergometer in which the workload was increased by 0.5 kilopond every minute until a target heart rate of 140 beats/min was achieved. Then, the subjects continued to cycle at a constant rate for 50 min. At four time points during the exercise (0, 10, 20, 50 min), the subjects performed a Stroop test with and without hypercapnic respiratory gas (2.0% CO2), with a random order of the exposures in the two tests. Despite a decrease in the mean blood flow velocity in the middle cerebral artery ( MCA Vmean), the reaction time for the Stroop test gradually decreased during the prolonged exercise without any loss of performance accuracy. In addition, the hypercapnia-induced increase in MCA Vmean produced neither changes in the reaction time nor error in the Stroop test during exercise. These findings suggest that the changes in CBF are unlikely to affect cognitive function during prolonged exercise. Thus, we conclude that improved cognitive function may be due to cerebral neural activation associated with exercise rather than global cerebral circulatory condition. [ABSTRACT FROM AUTHOR]

Football players are at increased risk of neurodegeneration, the likely consequence of repetitive mechanical trauma caused by heading the ball. However, to what extent a history of heading the ball affects cerebral blood flow (CBF) regulation and its potential relationship to cognitive impairment is unknown. To address this, we recruited 16 concussion‐free male amateur football players (age: 25 ± 6 y) with a history of heading the ball (18 ± 6 y) and 18 sex, age, education, and activity‐matched controls with no prior history of contact sport participation or concussion. Cerebral perfusion was measured at rest and in response to both hyper/hypocapnia to determine cerebrovascular reactivity to carbon dioxide (CVRCO2HYPER/HYPO) using transcranial Doppler ultrasound and capnography, with the sum reflecting the cerebral vasomotor range. Cognition and visuomotor coordination were assessed using the Montreal cognitive assessment (MoCA) and the Grooved Pegboard Dexterity Test (GPD), respectively. While no differences in cerebral perfusion were observed (p = 0.938), CVRCO2HYPER/HYPO (p = 0.038/p = 0.025), cerebral vasomotor range (p = 0.002), MoCA (p = 0.027), and GPD performance (dominant hand, P ≤ 0.001) were consistently lower in the players compared to controls. These findings are the first to demonstrate that CBF regulation and cognition are collectively impaired in male football players with history of heading the ball, which may contribute to neurodegeneration. [ABSTRACT FROM AUTHOR]

We previously demonstrated that duration of aerobic exercise plays an important role in improving cognitive inhibitory control (IC). Repeated bouts of aerobic exercise (R‐EX), which are performed with a rest interval, is a useful strategy in improving physical health parameters in similar manners to a single bout of aerobic exercise (S‐EX). However, whether R‐EX would be effective in improving IC remains unknown. This study compared the effect of R‐EX versus S‐EX of moderate‐intensity exercise on postexercise IC. Twenty healthy, young males performed both R‐EX and S‐EX in a crossover design. R‐EX consisted of two 20‐min moderate‐intensity bouts (60% of peak oxygen consumption) for 20 min, which were separated by a 20‐min rest interval. S‐EX consisted of a once‐off 40‐min moderate‐intensity bout without rest interval. To evaluate IC, the color‐word Stroop task was administered before exercise, immediately after exercise, and every 10 min during the 30‐min postexercise recovery period. The reverse‐Stroop interference score, which is a parameter of IC, significantly decreased immediately after both R‐EX and S‐EX compared with that before each exercise (both Ps < 0.05). The degree of changes in IC following exercise did not differ between the two protocols. By contrast, the results of the present study showed that R‐EX may have more beneficial effects on cardiac and perceptual responses than S‐EX. Therefore, the present study determined that R‐EX changes postexercise IC similar to S‐EX. We suggest that R‐EX can be used as safe and effective exercise protocol to improve cognitive function in various populations. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?What are the molecular, cerebrovascular and cognitive biomarkers of retired rugby union players with concussion history?What is the main finding and its importance?Retired rugby players compared with matched controls exhibited lower systemic nitric oxide bioavailability accompanied by lower middle cerebral artery velocity and mild cognitive impairment. Retired rugby players are more susceptible to accelerated cognitive decline. Following retirement from sport, the chronic consequences of prior‐recurrent contact are evident and retired rugby union players may be especially prone to accelerated cognitive decline. The present study sought to integrate molecular, cerebrovascular and cognitive biomarkers in retired rugby players with concussion history. Twenty retired rugby players aged 64 ± 5 years with three (interquartile range (IQR), 3) concussions incurred over 22 (IQR, 6) years were compared to 21 sex‐, age‐, cardiorespiratory fitness‐ and education‐matched controls with no prior concussion history. Concussion symptoms and severity were assessed using the Sport Concussion Assessment Tool. Plasma/serum nitric oxide (NO) metabolites (reductive ozone‐based chemiluminescence), neuron specific enolase, glial fibrillary acidic protein and neurofilament light‐chain (ELISA and single molecule array) were assessed. Middle cerebral artery blood velocity (MCAv, doppler ultrasound) and reactivity to hyper/hypocapnia (CVRCO2hyper${\mathrm{CVR}}_{{\mathrm{CO}}_{\mathrm{2}}{\mathrm{hyper}}}$/CVRCO2hypo${\mathrm{CVR}}_{{\mathrm{CO}}_{\mathrm{2}}{\mathrm{hypo}}}$) were assessed. Cognition was determined using the Grooved Pegboard Test and Montreal Cognitive Assessment. Players exhibited persistent neurological symptoms of concussion (U = 109(41), P = 0.007), with increased severity compared to controls (U = 77(41), P < 0.001). Lower total NO bioactivity (U = 135(41), P = 0.049) and lower basal MCAv were apparent in players (F2,39 = 9.344, P = 0.004). This was accompanied by mild cognitive impairment (P = 0.020, 95% CI, −3.95 to −0.34), including impaired fine‐motor coordination (U = 141(41), P = 0.021). Retired rugby union players with history of multiple concussions may be characterised by impaired molecular, cerebral haemodynamic and cognitive function compared to non‐concussed, non‐contact controls. [ABSTRACT FROM AUTHOR]

Gq/11 protein-coupled human histamine H1 receptors in Chinese hamster ovary cells stimulated with histamine undergo clathrin-dependent endocytosis followed by proteasome/lysosome-mediated down-regulation. In this study, we evaluated the effects of a sustained increase in intracellular Ca2+ concentrations induced by a receptor-bypassed stimulation with ionomycin, a Ca2+ ionophore, on the endocytosis and down-regulation of H1 receptors in Chinese hamster ovary cells. All cellular and cell-surface H1 receptors were detected by the binding of [3H]mepyramine to intact cells sensitive to the hydrophobic and hydrophilic H1 receptor ligands, mepyramine and pirdonium, respectively. The pretreatment of cells with ionomycin markedly reduced the mepyramine- and pirdonium-sensitive binding sites of [3H]mepyramine, which were completely abrogated by the deprivation of extracellular Ca2+ and partially by a ubiquitin-activating enzyme inhibitor ( UBEI-41), but were not affected by inhibitors of calmodulin (W-7 or calmidazolium) and protein kinase C (chelerythrine or GF109203X). These ionomycin-induced changes were also not affected by inhibitors of receptor endocytosis via clathrin (hypertonic sucrose) and caveolae/lipid rafts (filipin or nystatin) or by inhibitors of lysosomes (E-64, leupeptin, chloroquine, or NH4Cl), proteasomes (lactacystin or MG-132), and a Ca2+-dependent non-lysosomal cysteine protease (calpain) ( MDL28170). Since H1 receptors were normally detected by confocal immunofluorescence microscopy with an antibody against H1 receptors, even after the ionomycin treatment, H1 receptors appeared to exist in a form to which [3H]mepyramine was unable to bind. These results suggest that H1 receptors are apparently down-regulated by a sustained increase in intracellular Ca2+ concentrations with no process of endocytosis and lysosomal/proteasomal degradation of receptors. [ABSTRACT FROM AUTHOR]

High‐altitude (HA) hypoxia may alter the structural–functional integrity of the neurovascular unit (NVU). Herein, we compared male lowlanders (n = 9) at sea level (SL) and after 14 days acclimatization to 4300 m (chronic HA) in Cerro de Pasco (CdP), Péru (HA), against sex‐, age‐ and body mass index‐matched healthy highlanders (n = 9) native to CdP (lifelong HA). Venous blood was assayed for serum proteins reflecting NVU integrity, in addition to free radicals and nitric oxide (NO). Regional cerebral blood flow (CBF) was examined in conjunction with cerebral substrate delivery, dynamic cerebral autoregulation (dCA), cerebrovascular reactivity to carbon dioxide (CVRCO2) and neurovascular coupling (NVC). Psychomotor tests were employed to examine cognitive function. Compared to lowlanders at SL, highlanders exhibited elevated basal plasma and red blood cell NO bioavailability, improved anterior and posterior dCA, elevated anterior CVRCO2 and preserved cerebral substrate delivery, NVC and cognition. In highlanders, S100B, neurofilament light‐chain (NF‐L) and T‐tau were consistently lower and cognition comparable to lowlanders following chronic‐HA. These findings highlight novel integrated adaptations towards regulation of the NVU in highlanders that may represent a neuroprotective phenotype underpinning successful adaptation to the lifelong stress of HA hypoxia. Key points: High‐altitude (HA) hypoxia has the potential to alter the structural–functional integrity of the neurovascular unit (NVU) in humans.For the first time, we examined to what extent chronic and lifelong hypoxia impacts multimodal biomarkers reflecting NVU structure and function in lowlanders and native Andean highlanders.Despite lowlanders presenting with a reduction in systemic oxidative–nitrosative stress and maintained cerebral bioenergetics and cerebrovascular function during chronic hypoxia, there was evidence for increased axonal injury and cognitive impairment.Compared to lowlanders at sea level, highlanders exhibited elevated vascular NO bioavailability, improved dynamic regulatory capacity and cerebrovascular reactivity, comparable cerebral substrate delivery and neurovascular coupling, and maintained cognition. Unlike lowlanders following chronic HA, highlanders presented with lower concentrations of S100B, neurofilament light chain and total tau.These findings highlight novel integrated adaptations towards the regulation of the NVU in highlanders that may represent a neuroprotective phenotype underpinning successful adaptation to the lifelong stress of HA hypoxia. [ABSTRACT FROM AUTHOR]

Purpose: No study has assessed the acute effect of caffeine supplementation on 100-m sprint running in athletics and caffeine's net ergogenicity on 100-m sprint running remains unclear. We investigated the acute effects of caffeine supplementation on 100-m sprint running performance in a field test. Methods: Thirteen male collegiate sprinters were subjected to 100-m sprint running time trials (TT) after the ingestion of 6 mg·kg−1 body weight caffeine or placebo supplementation in a double-blind, counterbalanced, randomized, and crossover design. Sprint velocity was measured with a laser system, and sprint time was calculated from the data in which the effects of environmental factors that would act as confounding factors on sprint time during TT were eliminated. Results: The corrected 100-m sprint time was significantly shortened by 0.14 s with caffeine supplementation compared with placebo (placebo: 11.40 ± 0.39 s, caffeine: 11.26 ± 0.33 s; P = 0.007, g = −0.33). The corrected sprint time up to 60 m during TT was also significantly shorter with caffeine supplementation than with placebo (P = 0.002). Furthermore, the mean sprint velocity for splits of 0–10 and 10–20 m was significantly increased by caffeine supplementation (all P < 0.05). Conclusions: Acute caffeine supplementation enhanced the corrected 100-m sprint time by improving the sprint performance in the first 60 m after more explosive acceleration in the early stage of the acceleration phase. Thus, for the first time, we directly demonstrated caffeine's ergogenicity on 100-m sprint performance in athletics. [ABSTRACT FROM AUTHOR]

Recurrent contact and concussion in rugby union remains a significant public health concern given the potential increased risk of neurodegeneration in later life. This study determined to what extent prior‐recurrent contact impacts molecular‐hemodynamic biomarkers underpinning cognition in current professional rugby union players with a history of concussion. Measurements were performed in 20 professional rugby union players with an average of 16 (interquartile range [IQR] 13–19) years playing history reporting 3 (IQR 1–4) concussions. They were compared to 17 sex‐age‐physical activity‐and education‐matched non‐contact controls with no prior history of self‐reported concussion. Venous blood was assayed directly for the ascorbate free radical (A•− electron paramagnetic resonance spectroscopy) nitric oxide metabolites (NO reductive ozone‐based chemiluminescence) and select biomarkers of neurovascular unit integrity (NVU chemiluminescence/ELISA). Middle cerebral artery blood flow velocity (MCAv doppler ultrasound) was employed to determine basal perfusion and cerebrovascular reactivity (CVR) to hyper/hypocapnia (CVRCO2Hyper/Hypo). Cognition was assessed by neuropsychometric testing. Elevated systemic oxidative‐nitrosative stress was confirmed in the players through increased A•− (p < 0.001) and suppression of NO bioavailability (p < 0.001). This was accompanied by a lower CVR range (CVRCO2Range; p = 0.045) elevation in neurofilament light‐chain (p = 0.010) and frontotemporal impairments in immediate‐memory (p = 0.001) delayed‐recall (p = 0.048) and fine‐motor coordination (p < 0.001). Accelerated cognitive decline subsequent to prior‐recurrent contact and concussion history is associated with a free radical‐mediated suppression of CVR and neuronal injury providing important mechanistic insight that may help better inform clinical management. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?To what extent do hypoxia‐induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral oxygen delivery, with corresponding implications for susceptibility to acute mountain sickness?What is the main finding and its importance?We provide evidence for site‐specific regulation of cerebral blood flow in hypoxia that preserves oxygen delivery in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. External carotid artery vasodilatation might prove to be an alternative haemodynamic risk factor that predisposes to acute mountain sickness. The aim of the present study was to determine the extent to which hypoxia‐induced changes in the peripheral and central respiratory chemoreflex modulate anterior and posterior cerebral blood flow (CBF) and oxygen delivery (CDO2), with corresponding implications for the pathophysiology of the neurological syndrome, acute mountain sickness (AMS). Eight healthy men were randomly assigned single blind to 7 h of passive exposure to both normoxia (21% O2) and hypoxia (12% O2). The peripheral and central respiratory chemoreflex, internal carotid artery, external carotid artery (ECA) and vertebral artery blood flow (duplex ultrasound) and AMS scores (questionnaires) were measured throughout. A reduction in internal carotid artery CDO2 was observed during hypoxia despite a compensatory elevation in perfusion. In contrast, vertebral artery and ECA CDO2 were preserved, and the former was attributable to a more marked increase in perfusion. Hypoxia was associated with progressive activation of the peripheral respiratory chemoreflex (P < 0.001), whereas the central respiratory chemoreflex remained unchanged (P > 0.05). Symptom severity in participants who developed clinical AMS was positively related to ECA blood flow (Lake Louise score, r = 0.546–0.709, P = 0.004–0.043; Environmental Symptoms Questionnaires‐Cerebral symptoms score, r = 0.587–0.771, P = 0.001–0.027, n = 4). Collectively, these findings highlight the site‐specific regulation of CBF in hypoxia that maintains CDO2 selectively in the posterior but not the anterior cerebral circulation, with minimal contribution from the central respiratory chemoreflex. Furthermore, ECA vasodilatation might represent a hitherto unexplored haemodynamic risk factor implicated in the pathophysiology of AMS. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?How does recurrent contact incurred across a season of professional rugby union impact molecular, cerebrovascular and cognitive function?What is the main findings and its importance?A single season of professional rugby union increases systemic oxidative–nitrosative stress (OXNOS) confirmed by a free radical‐mediated suppression in nitric oxide bioavailability. Forwards encountered a higher frequency of contact events compared to backs, exhibiting elevated OXNOS and lower cerebrovascular function and cognition. Collectively, these findings provide mechanistic insight into the possible cause of reduced cognition in rugby union subsequent to impairment in the redox regulation of cerebrovascular function. Contact events in rugby union remain a public health concern. We determined the molecular, cerebrovascular and cognitive consequences of contact events during a season of professional rugby. Twenty‐one male players aged 25 (mean) ± 4 (SD) years were recruited from a professional rugby team comprising forwards (n = 13) and backs (n = 8). Data were collected across the season. Pre‐ and post‐season, venous blood was assayed for the ascorbate free radical (A•–, electron paramagnetic resonance spectroscopy) and nitric oxide (NO, reductive ozone‐based chemiluminescence) to quantify oxidative–nitrosative stress (OXNOS). Middle cerebral artery velocity (MCAv, Doppler ultrasound) was measured to assess cerebrovascular reactivity (CVR), and cognition was assessed using the Montreal Cognitive Assessment (MoCA). Notational analysis determined contact events over the season. Forwards incurred more collisions (Mean difference [MD] 7.49; 95% CI, 2.58–12.40; P = 0.005), tackles (MD 3.49; 95% CI, 0.42–6.56; P = 0.028) and jackals (MD 2.21; 95% CI, 0.18–4.24; P = 0.034). Forwards suffered five concussions while backs suffered one concussion. An increase in systemic OXNOS, confirmed by elevated A•– (F2,19 = 10.589, P = 0.004) and corresponding suppression of NO bioavailability (F2,19 = 11.492, P = 0.003) was apparent in forwards and backs across the season. This was accompanied by a reduction in cerebral oxygen delivery (cDO2, F2,19 = 9.440, P = 0.006) and cognition (F2,19 = 4.813, P = 0.041). Forwards exhibited a greater decline in the cerebrovascular reactivity range to changes in PETCO2 (CVRCO2RANG compared to backs (MD 1.378; 95% CI, 0.74–2.02; P < 0.001). [ABSTRACT FROM AUTHOR]

Purpose: Blood flow restriction (BFR) walking is recognized as a beneficial strategy for increasing skeletal muscle mass and strength. No study has examined the effect of BFR exercise on cognitive functions, including executive function (EF). In this study, we examined the effect of BFR walking on EF. Methods: We performed two studies, at rest and exercise, with BFR or non-BFR (NBFR) in a crossover design. Sitting rest was performed for 15 min (study 1, n = 8). Exercise was programmed at five sets of 2-min walking at 5 km·h−1 with 1-min rest intervals (study 2, n = 16). The BFR condition was achieved using 200 mm Hg pressure cuffs placed around the proximal region of the thighs. The NBFR condition involved no pressure cuffs. EF was assessed using the color–word Stroop task before and after each condition. Results: In study 1, there were no significant effects on EF parameters for both BFR and NBFR conditions, suggesting that BFR alone does not improve EF. In study 2, incongruent reaction time shortened after BFR walking compared with that before walking (P = 0.001). Furthermore, the reverse Stroop interference score decreased after BFR walking compared with that before walking (P < 0.001). Conclusion: These findings suggest that, even with a mild exercise, BFR walking improves EF independently of the effect of BFR alone or walking alone. [ABSTRACT FROM AUTHOR]

We previously demonstrated that a traditional high-volume (HV) high-intensity interval exercise (HIIE) was more effective in improving post-exercise inhibitory control (IC) than moderate-intensity continuous exercise (MCE). Nevertheless, because HV-HIIE is performed with a higher volume and longer duration, it may result in decreased adherence to this exercise for some individuals. In this study, we compared the effect of a practical low-volume (LV) HIIE to that of MCE on post-exercise IC improvements. Twenty healthy males performed both LV-HIIE and MCE on a cycle ergometer in a crossover design. LV-HIIE was consisted of ten 1-min bouts at 90% of the peak oxygen consumption (VO 2 peak) with 1-min active recovery at 30% of VO 2 peak , which had a total duration of 20 min. MCE was performed for 40 min at 60% of VO 2 peak. To evaluate IC, the Stroop test was administered before exercise, immediately after exercise, and every 10 min during the 30-min post-exercise recovery period. IC significantly improved immediately after LV-HIIE and MCE compared with that before each exercise (both P s < 0.05). The improved IC remained significant until the 20-min post-exercise recovery period for both protocols (all P s < 0.05). The degrees of post-exercise IC improvements throughout the 30-min post-exercise recovery period did not differ significantly between protocols. These findings demonstrated that despite lower exercise volume and shorter exercise duration, LV-HIIE could improve post-exercise IC similar to MCE. • High-intensity interval exercise (HIIE) significantly improves post-exercise inhibitory control (IC). • This study compared the effect of low-volume (LV) HIIE and moderate-intensity continuous exercise (MCE) on post-exercise IC. • Despite lower exercise volume and shorter exercise duration, LV-HIIE could improve post-exercise IC similar to MCE. [ABSTRACT FROM AUTHOR]

We previously determined that improvement in cognitive inhibitory control (IC) immediately after localized resistance exercise was greater for high‐intensity resistance exercise (HRE) than for low‐intensity resistance exercise (LRE). However, our previous study used the same total repetitions (i.e., same repetitions per set) between HRE and LRE; therefore, the difference in postexercise IC improvement might be due to a difference in work volume (i.e., intensity × total repetitions). In this study, we compared the effect of high‐volume (HV)‐LRE to that of volume‐matched HRE on postexercise IC improvements. Twenty‐two healthy, young males performed both HV‐LRE and HRE in a crossover design. Exercise loads for HV‐LRE and HRE were set at 35% and 70% of one‐repetition maximum, respectively. The bilateral knee extension exercises for HV‐LRE and HRE were programmed for six sets with 20 and 10 repetitions, respectively, per set. IC was measured using the color‐word Stroop task (CWST) at six time points; baseline, pre‐exercise, immediate postexercise, and every 10 min during the 30‐min postexercise recovery period. The reverse‐Stroop interference score decreased significantly immediately after HV‐LRE and HRE compared with that before each exercise (decreasing rate >34 and >38%, respectively, vs. baseline and pre‐exercise; all ps <.05), and the decreased score remained significant until 20 min after both protocols (decreasing rate >40 and >38%, respectively, vs. baseline and pre‐exercise; all ps <.05). The degree of the postexercise IC improvements did not differ significantly between the two protocols. These findings suggest that HV‐LRE improves IC in a similar manner to volume‐matched HRE. [ABSTRACT FROM AUTHOR]

• To what extent regular exercise confers neuroprotection in females remains less established than in males. • Compared to their male counterparts, untrained females are characterized by improved cerebrovascular function. • Despite this, regular exercise conferred equivalent neuroprotection across sexes in the form of elevated CVR CO2. • These findings highlight the neuroprotective benefits of regular exercise that do not appear to be sex-specific. • Regular exercise could help combat the accelerated trajectory towards cerebrovascular disease in females in later life. Females are more prone to cognitive decline, stroke and neurodegenerative disease, possibly due to more marked reductions in cerebral blood flow and cerebrovascular reactivity to CO 2 (CVR CO2HYPER) in later life. To what extent regular exercise confers selective neuroprotection in females remains unestablished. To examine this, 73 adults were prospectively assigned to 1 of 4 groups based on sex (male, ♂ vs. female, ♀) and physical activity status (trained, ≥150 min of moderate-vigorous intensity aerobic exercise/week; n = 18♂ vs. 18♀ vs. untrained, no formal exercise; n = 18♂ vs. 19♀). Middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound), mean arterial pressure (MAP, finger photoplethysmography) and end-tidal CO 2 (capnography) were assessed at rest during normocapnea and hypercapnea (5% CO 2) enabling CVR CO2HYPER to be assessed. Cerebrovascular resistance/conductance indices (CVRi/CVCi) were calculated as MAP/MCAv and MCAv/MAP. Maximal oxygen uptake (VO 2MAX) was determined during incremental semi-recumbent cycling ergometry to volitional exhaustion. Despite having a lower VO 2MAX , females were characterized by selective elevations in MCAv, CVR CO2HYPER and lower CVRi (P < 0.05), but the training responses were similar across sexes. Linear relationships were observed between VO 2MAX and CVR CO2HYPER (pooled untrained and trained data; ♂ r = 0.70, ♀ r = 0.51; both P < 0.05) with a consistent elevation in the latter equivalent to ∼1.50%.mmHg−1 compared to males across the spectrum of cardiorespiratory fitness. These findings indicate that despite having comparatively lower levels of cardiorespiratory fitness, the neuroprotective benefits of regular exercise translate into females and may help combat cerebrovascular disease in later life. [ABSTRACT FROM AUTHOR]