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High-intensity exercise in athletes results in mainly the production of excess reactive oxygen species (ROS) in skeletal muscle, and thus athletes should maintain greater ROS scavenging activity in the body. We investigated the changes in six different ROS-scavenging activities in athletes following high-intensity anaerobic exercise. A 30-s Wingate exercise test as a form of high-intensity anaerobic exercise was completed by 10 male university track and field team members. Blood samples were collected before and after the exercise, and the ROS-scavenging activities (OH•, O2•−, 1O2, RO• and ROO•, and CH3•) were evaluated by the electron spin resonance (ESR) spin-trapping method. The anaerobic exercise significantly increased RO• and ROO• scavenging activities, and the total area of the radar chart in the ROS-scavenging activities increased 178% from that in pre-exercise. A significant correlation between the mean power of the anaerobic exercise and the 1O2 scavenging activity was revealed (r = 0.72, p < 0.05). The increase ratio in OH• scavenging activity after high-intensity exercise was significantly greater in the higher mean-power group compared to the lower mean-power group (n = 5, each). These results suggest that (i) the scavenging activities of some ROS are increased immediately after high-intensity anaerobic exercise, and (ii) an individual’s OH• scavenging activity responsiveness may be related to his anaerobic exercise performance. In addition, greater pre-exercise 1O2 scavenging activity might lead to the generation of higher mean power in high-intensity anaerobic exercise.

Cold temperatures (<−15°C) increase exercise‐induced bronchoconstriction (EIB), while hypoxic‐induced hyperventilation exacerbates respiratory muscle fatigue for a given exercising task. This study aimed to determine the individual and combined effects of cold and normobaric hypoxia on the respiratory system responses to high‐intensity exercise. Fourteen trained male runners (V̇O2max ${{\\dot{V}}_{{{\\mathrm{O}}}_2}{\\mathrm{max}}}$ : 64 ± 5 mL/kg/min) randomly performed an incremental cardiopulmonary exercise test (CPET) to volitional exhaustion under four environmental conditions: normothermic (18°C) normoxia (FIO2 ${{F}_{{\\mathrm{I}}{{{\\mathrm{O}}}_2}}}$ : 20.9%) and hypoxia (FIO2 ${{F}_{{\\mathrm{I}}{{{\\mathrm{O}}}_2}}}$ : 13.5%), and cold (−20°C) normoxia and hypoxia. Ventilatory responses during exercise and lung function (LF), maximal inspiratory (MIP) and expiratory (MEP) pressure measurements before and after exercise were evaluated. Volume of air forcefully exhaled in 1 s (FEV1), FEV1/forced vital capacity (FVC), peak expiratory flow, forced expiratory flow during the mid (25–75%) portion of the FVC, and maximal expiratory flow at 50% of FVC were affected by cold exposure. No significant pre‐ to post‐exercise change in MIP and MEP was found, independent of environmental conditions. Greater LF impairments in cold‐normoxia and coldhypoxia were associated with the lowest peak ventilatory responses during exercise. Cold exposure was found to negatively impact peak ventilatory responses and post‐exercise LF, further highlighting a relationship between EIB presence and the blunted ventilatory response in the cold. Respiratory muscle strength remained unchanged after exercise regardless of the environmental condition, suggesting no detrimental effect of hypoxia on this parameter when intermittent short‐duration high‐intensity exercises are performed. Future studies should investigate the combined cold‐hypoxic effect on longer exercise durations at a sustained high intensity, accounting for differences between normobaric and hypobaric hypoxia exposures. What is the central question of this study? What are the independent and combined effects of cold and normobaric hypoxia on respiratory responses to high‐intensity exercise? What is the main finding and its importance? Cold exposure impaired lung function and peak ventilatory responses during high‐intensity exercise, with greater impairments observed under combined cold‐hypoxia condition. The findings highlight a link between exercise‐induced bronchoconstriction and reduced ventilatory capacity in cold environments. Respiratory muscle strength remained unaffected post‐exercise across all conditions, suggesting no detrimental impact of hypoxia during short‐duration high‐intensity tasks.

Moderately trained male subjects (mean age 25 years; range 19–33 years) completed an 8‐week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30‐sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts. A single exercise bout seems to increase autophagosome number, and exercise training seems to increase the capacity for autophagy and mitophagy regulation in human skeletal muscle. In addition, the present findings provide evidence that these effects are unaffected by interspersed sprint bouts, although regulation of some autophagy markers appear to be inhibited by short lasting high‐intensity bouts.

This research examined the effects of single-dose molecular hydrogen (H2) supplements on acid-base status and local muscle deoxygenation during rest, high-intensity intermittent training (HIIT) performance, and recovery. Ten healthy, trained subjects in a randomized, double-blind, crossover design received H2-rich calcium powder (HCP) (1500 mg, containing 2.544 μg of H2) or H2-depleted placebo (1500 mg) supplements 1 h pre-exercise. They performed six bouts of 7 s all-out pedaling (HIIT) at 7.5% of body weight separated by 40 s pedaling intervals, followed by a recovery period. Blood gases’ pH, PCO2, and HCO3− concentrations were measured at rest. Muscle deoxygenation (deoxy[Hb + Mb]) and tissue O2 saturation (StO2) were determined via time-resolved near-infrared spectroscopy in the vastus lateralis (VL) and rectus femoris (RF) muscles from rest to recovery. At rest, the HCP group had significantly higher PCO2 and HCO3− concentrations and a slight tendency toward acidosis. During exercise, the first HIIT bout’s peak power was significantly higher in HCP (839  ±  112 W) vs. Placebo (816  ±  108 W, p = 0.001), and HCP had a notable effect on significantly increased deoxy[Hb + Mb] concentration during HIIT exercise, despite no differences in heart rate response. The HCP group showed significantly greater O2 extraction in VL and microvascular (Hb) volume in RF during HIIT exercise. The HIIT exercise provided significantly improved blood flow and muscle reoxygenation rates in both the RF and VL during passive recovery compared to rest in all groups. The HCP supplement might exert ergogenic effects on high-intensity exercise and prove advantageous for improving anaerobic HIIT exercise performance.

Exercise as a medical intervention is effective to help prevent and manage many chronic and complex diseases, including dementia. There is evidence to suggest that regular aerobic exercise protects against age‐related brain atrophy and reduces the risk of cognitive decline. The mechanisms by which exercise infers a neuroprotective effect remain to be established but may be related to a maintenance of brain volume and neuronal survival, improved cerebrovascular density and function, and/or increased synaptic plasticity. In addition, there is growing evidence to suggest the beneficial effects of exercise on brain health and cognitive function are, at least in part, mediated by factors released by skeletal muscle during contraction. The fact that the brain responds to exercise suggests that muscle‐derived peripheral factors, or “myokines,” may play a key role in muscle–brain crosstalk and exercise neuroprotection. However, the most effective “dose” of aerobic exercise to promote beneficial changes in these myokine pathways is currently unknown. Specifically, most of the evidence to date is from studies that have used moderate‐intensity exercise, and research investigating the merit of high‐intensity exercise is scarce. Considering the well‐established role of high‐intensity interval training in protecting against numerous medical conditions, more research is needed to identify the most effective “dose” of exercise to improve the beneficial effects of these myokines. Highlights Neuroprotection through exercise: Regular aerobic exercise mitigates age‐related brain atrophy and cognitive decline via multiple mechanisms, including brain volume maintenance, improved cerebrovascular function, and synaptic plasticity. Myokines as mediators: Muscle‐derived factors (myokines) play a crucial role in muscle–brain crosstalk, significantly contributing to the neuroprotective effects of exercise. Intensity matters: The review underscores the necessity to define and study exercise intensity, revealing high‐intensity exercise may be as effective, if not more, in promoting neuroprotective myokine levels compared to moderate‐intensity exercise. Future research directions: This review emphasizes the need for well‐controlled studies to explore the optimal exercise dose for enhancing myokine pathways and their implications for neurodegenerative disease prevention.

The optimal exercise intensity and modality for maximizing cerebral blood flow (CBF) and hence potential exposure to positive, hemodynamically derived cerebral adaptations is yet to be fully determined. This study compared CBF velocity responses between running and cycling across a range of exercise intensities. Twenty‐six participants (12 females; age: 26 ± 8 years) completed four exercise sessions; two mode‐specific maximal oxygen consumption (VO2max) tests, followed by (order randomized) two incremental exercise protocols (3‐min stages at 35%, 50%, 65%, 80%, 95% VO2max). Continuous measures of middle cerebral artery velocity (MCAv), oxygen consumption, end‐tidal CO2 (PETCO2), and heart rate were obtained. Modality‐specific MCAv changes were observed for the whole group (interaction effect: p = .01). Exercise‐induced increases in MCAvmean during cycling followed an inverted‐U pattern, peaking at 65% VO2max (Δ12 ± 7 cm/s from rest), whereas MCAvmean during running increased linearly up to 95% VO2max (change from rest: Δ12 ± 13 vs. Δ7 ± 8 cm/s for running vs. cycling at 95% VO2max; p = .01). In contrast, both modalities had an inverted‐U pattern for PETCO2 changes, although peaked at different intensities (running: 50% VO2max, Δ6 ± 2 mmHg; cycling: 65% VO2max, Δ7 ± 2 mmHg; interaction effect: p = .01). Further subgroup analysis revealed that the running‐specific linear MCAvmean response was fitness dependent (Fitness*modality*intensity interaction effect: p = .04). Above 65% VO2max, fitter participants (n = 16; male > 45 mL/min/kg and female > 40 mL/min/kg) increased MCAvmean up to 95% VO2max, whereas in unfit participants (n = 7, male < mL/min/kg and female < 35 mL/min/kg) MCAvmean returned toward resting values. Findings demonstrate that modality‐ and fitness‐specific profiles for MCAvmean are seen at exercise intensities exceeding 65% VO2max. This study compared cerebral blood flow (CBF) responses between running and cycling across a range of exercise intensities. Our findings demonstrate that exercise‐induced increases in CBF (as indexed from Doppler‐based measures of middle cerebral artery velocity, MCAv) during incremental running and cycling differ at higher exercise intensities, with the pattern of the MCAv response during running for fitter individuals dissociating from the regulatory influence of PCO2 at near maximal intensity (95% VO2max). Thus, modality‐specific differences in beat‐to‐beat flow patterns may alter CBF regulation processes and affect the complex integration of factors regulating CBF during exercise.

This study aimed to examine sex differences in acute caffeine intake on repeated sprint performance. Fifty‐two resistance‐trained individuals (age: 24.6 ± 4.5 years and sex (female/male): 26/26) participated in a randomized, triple‐blind, cross‐over, and placebo‐controlled study. Participants ingested 3 mg/kg caffeine or placebo and, after 60 min, performed 4 Wingate tests (Wt), consisting of a 30 s all‐out lower‐body sprint against an individualized resisted load, with 90 s rest periods between sprints. Mean (Wmean) and peak (Wpeak) power showed an interaction between sprint and supplement (P = 0.038, ηp2 = 0.095 and P < 0.001, ηp2 = 0.157, respectively), but only Wpeak reported a supplement and sex interaction (P = 0.049 and ηp2 = 0.166). Caffeine increased Wmean in Wt3 (3.5%, P = 0.004, and g = 1.059) and Wt4 (3.9%, P = 0.012, and g = 1.091) compared to placebo. Whereas, for Wpeak, caffeine increased Wpeak in the Wt1 (2.9%, P = 0.050 and g = 1.01) and Wt2 (3.2%, P = 0.050, and g = 1.01) in males and in Wt3 (5.2%, P = 0.008, and g = 1.79) and Wt4 (8.1%, P = 0.004, and g = 2.27) in female participants compared to placebo. No statistically significant sex differences were found in time to reach Wpeak, fatigue index. Acute caffeine intake stimulated a similar ergogenic effect on repeated sprint performance in men and women, except in peak power output, where caffeine increased performance during the first sprints in males and the last sprints in female participants. Highlights A four‐repeated Wingate test is a valuable protocol for assessing and improving anaerobic capacity and power, tailoring training programs, monitoring recovery from injury, and evaluating the ability to sustain high‐intensity efforts over multiple bouts, which are critical components of many sports (e.g., cycling or soccer). Low doses (3 mg/kg) of caffeine consumed acutely improve repeated sprint performance in both male and female athletes. The pattern of the ergogenic effect seems to differ between sexes only in peak power output. In males, caffeine increases this variable in the first two sprints, whereas in women, it does it in the last two sprints.

This study aimed to examine the effects of hydrogen gas (H2) produced by intestinal microbiota on participant conditioning to prevent intense exercise-induced damage. In this double-blind, randomized, crossover study, participants ingested H2-producing milk that induced intestinal bacterial H2 production or a placebo on the trial day, 4 h before performing an intense exercise at 75% maximal oxygen uptake for 60 min. Blood marker levels and respiratory variables were measured before, during, and after exercise. Visual analog scale scores of general and lower limb muscle soreness evaluated were 3.8- and 2.3-fold higher, respectively, on the morning after treatment than that before treatment during the placebo trial, but not during the test beverage consumption. Urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) concentrations and production rates significantly increased with placebo consumption; no changes were observed with test beverage consumption. After exercise, relative blood lactate levels with H2-producing milk consumption were lower than those with placebo consumption. A negative correlation was observed between the variation of 8-OHdG and the area under the curve (AUC) of breath H2 concentrations. Lipid oxidation AUC was 1.3-fold higher significantly with H2-producing milk than with placebo consumption. Conclusively, activating intestinal bacterial H2 production by consuming a specific beverage may be a new strategy for promoting recovery and conditioning in athletes frequently performing intense exercises.

Although systemic sex‐specific differences in cardiovascular responses to exercise are well established, the comparison of sex‐specific cerebrovascular responses to exercise has gone under‐investigated especially, during high intensity exercise. Therefore, our purpose was to compare cerebrovascular responses in males and females throughout a graded exercise test (GXT). Twenty‐six participants (13 Females and 13 Males, 24 ± 4 yrs.) completed a GXT on a recumbent cycle ergometer consisting of 3‐min stages. Each sex completed 50W, 75W, 100W stages. Thereafter, power output increased 30W/stage for females and 40W/stage for males until participants were unable to maintain 60‐80 RPM. The final stage completed by the participant was considered maximum workload(Wmax). Respiratory gases (End‐tidal CO2, EtCO2), middle cerebral artery blood velocity (MCAv), heart rate (HR), non‐invasive mean arterial pressure (MAP), cardiac output (CO), and stroke volume (SV) were continuously recorded on a breath‐by‐breath or beat‐by‐beat basis. Cerebral perfusion pressure, CPP = MAP (0. 7,355 distance from heart‐level to doppler probe) and cerebral vascular conductance index, CVCi = MCAv/CPP 100mmHg were calculated. The change from baseline (Δ) in MCAv was similar between the sexes during the GXT (p = .091, ωp2 = 0.05). However, ΔCPP (p < .001, ωp2 = 0.25) was greater in males at intensities ≥ 80% Wmax and ΔCVCi (p = .005, ωp2 = 0.15) was greater in females at 100% Wmax. Δ End‐tidal CO2 (ΔEtCO2) was not different between the sexes during exercise (p = .606, ωp2 = −0.03). These data suggest there are sex‐specific differences in cerebrovascular control, and these differences may only be identifiable at high and severe intensity exercise. We examined cerebrovascular responses to exercise over a wide range of exercise intensities. Our data found that blood velocity responses are not particularly different between the sexes, however, the vascular control is. During high intensity exercise, females vasodilate more than men and men generate more pressure.

Postdiagnosis physical activity is associated with improved cancer outcomes, but biological mechanisms mediating anticancer effects remain unclear. Recent findings suggest that physiological adaptations to acute exercise comprise potential anticancer effects, but these remain poorly explored in clinical settings. The objective of this study was to explore the effects of a single exercise bout on tumor oxygenation and immune cell infiltration in patients with prostate cancer. Thirty patients with localized prostate cancer were randomized (2:1) to either one high‐intensity interval training bout or no exercise on the day before radical prostatectomy. Immunohistochemical analyses were performed on prostatic tissue from surgery and assessed for tumor hypoxia, natural killer (NK) cell infiltration, and microvessel density (MVD). Acute systemic response in blood lymphocytes, epinephrine, norepinephrine, IL‐6, tumor necrosis factor, cortisol, lactate, and glucose was also evaluated. We did not find between‐group differences in tumor hypoxia (Mann–Whitney U test, U = 83.5, p = 0.604) or NK cell infiltration (U = 77.0, p = 0.328). Also, no significant correlation was found between MVD and tumor hypoxia or NK cell infiltration. One exercise bout is likely insufficient to modulate tumor hypoxia or NK cell infiltration. Future studies may elucidate if an accumulation of several exercise bouts can impact these outcomes (NCT03675529, www.clinicaltrials.gov). Biological mechanisms mediating anti‐cancer effects of physical exercise in humans are unclear, but physiological adaptations to acute exercise have been shown to hold anti‐cancer potential in preclinical studies. We explored the effects of one exercise bout on tumor oxygenation and immune cell infiltration in patients with prostate cancer and report that one exercise bout is not enough to impact these outcomes in a human setting, and the accumulation of several exercise bouts may be required to impact tumor biology.