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Research regarding the effects of high-intensity interval training (HIIT) on executive function has grown exponentially in recent years. However, there has been no comprehensive review of the current state of literature. Therefore, the aim of this systematic review is to summarize previous research regarding the acute and chronic effects of HIIT on executive function across the lifespan and highlight future research directions. The results indicated that acute bouts of HIIT has a positive effect on inhibition in children/adolescents and adults, and further that chronic HIIT benefits inhibition and working memory in children. More research employing chronic interventions, focusing on middle-aged and older adults, and examining the effects on the working memory and cognitive flexibility domains of executive function are needed. Future research should also focus on a) the use of stronger research designs, b) the effects of HIIT dosage/modality, c) consideration of individual differences, d) possible underlying mechanisms, and e) examining the feasibility of translating HIIT to real-word settings. [ABSTRACT FROM AUTHOR]

Introduction. Children's engagement in vigorous-intensity physical activity is more effective in improving fitness than moderate-intensity physical activity. However, there is limited information about the effect of vigorous-intensity physical education classes on daily physical activity levels. Objective. Compare the contribution of high and moderate-intensity physical education classes by assessing 5 daily physical activity level classifications[sedentary time (ST) and time of light (LPA), moderate (MPA), vigorous (VPA), and moderate-vigorous physical activity (MVPA)] in 9-10-year-old students. Materials and methods. A total of 66 students were recruited with a mean age of 9.48 ± 0.5 years. The participants were assigned to 2 groups: high-intensity activity and moderate-intensity activity. The physical activity level was assessed by accelerometry (Actigraph wGT3X-BT). The Wilcox on signed-rank test was used for the pre and post-intervention statistical analysis. Results. No significant differences were observed in ST (1993.0 min; 1980.5 min, p = 0.429), LPA (800.5 min; 817.3 min, p = 0.191), MPA (67.7 min; 65.4 min, p = 0.299), VPA (18.7 min; 16.5 min, p = 0.098), and MVPA (86.4 min; 82.0 min, p = 0.267) for the high-intensity activity group. For the moderate-intensity activity group, no significant differences were observed neither for ST (1893.5 min; 1959.7 min, p = 0.170) nor for LPA (873.4 min; 845.4 min, p = 0.545). Compared to the high-intensity activity group, the moderate-intensity activity group exhibited a significant reduction in MPA (91.0 min; 63.2 min, p = 0.000), VPA (22.0 min; 11.6 min, p = 0.011), and MPVA (113.0 min; 74.8 min, p = 0.001). Conclusion. High-intensity physical activity did not significantly contribute to an increase in physical activity levels among different intensities (LPA, MPA, VPA, MVPA) but did not decrease them either. Nevertheless, moderate-intensity physical activity decreased the levels of MPA, VPA, and MVPA per day. [ABSTRACT FROM AUTHOR]

Objective: Sleep is an essential component of athletic performance and recovery. This study aimed to investigate the effects of different types of high-intensity exercise on sleep parameters in adolescent speed skaters., Methods: Eighteen male adolescent speed skaters underwent aerobic capacity testing, Wingate testing, and interval training in a randomized crossover design to assess strength output, heart rate, and blood lactate levels during exercise. Sleep quality after each type of exercise was evaluated using the Firstbeat Bodyguard 3 monitor., Results: The results showed that Wingate testing and interval training led to decreased sleep duration, increased duration of stress, decreased RMSSD, and increased LF/HF ratio ( p  < 0.01). Conversely, aerobic capacity testing did not significantly affect sleep ( p  > 0.05). The impact of interval training on sleep parameters was more significant compared to aerobic capacity testing ( p  < 0.01) and Wingate testing ( p  < 0.01)., Conclusion: High-intensity anaerobic exercise has a profound impact on athletes' sleep, primarily resulting in decreased sleep duration, increased stress duration, decreased RMSSD, and increased LF/HF ratio., Competing Interests: XW is employed by Zhejiang Qiangnao Technology Co., Ltd. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Kong, Wei, Shen, Cheng and Feng.)

The intestine functions as a barrier preventing the entry of extrinsic factors into the body. This barrier function is disrupted by oxidative damage along with an impaired mucosal layer. Excessive exercise can generate oxidative stress in the intestinal tissue; however, the effect of exercise-induced oxidative stress on intestinal permeability is unclear. In this study, we examined the involvement of oxidative stress in barrier function of the ileum of mice following high-intensity exercise. Male ICR mice (12-week-old) were divided into sedentary and exercise groups. Mice in the exercise group underwent a single bout of treadmill running, and the ileum was collected for histological and biochemical analyses. Plasma fluorescence intensity level after oral administration of fluorescein isothiocyanate-dextran gradually increased until 30 min after exercise in response to intensity of exercise. Relatively high levels of oxidative proteins and low level of claudin-1, a tight-junction protein, were observed in the exercise group. Treatment with a xanthine oxidase inhibitor suppressed exercise-induced increases in intestinal permeability. Moreover, excessive exercise training for two weeks led to relatively high intestinal permeability at rest. These results suggest that high-intensity exercise increases intestinal permeability and tight junction damage, which may be mediated by oxidative stress., Competing Interests: No potential conflicts of interest were disclosed., (Copyright © 2024 JCBN.)

he purpose of this study was to compare the effects of an experimental versus traditional military run training on 2-mile run ability in Army Reserve Officer Training Corps (ROTC) cadets. Fifty college-aged cadets were randomly placed into two groups and trained for four weeks with either an experimental running program (EXP, n=22) comprised of RPE intensity-specific, energy system based intervals or with traditional military running program (TRA, n=28) utilizing a crossover study design. A 2-mile run assessment was performed just prior to the start, at the end of the first 4 weeks, and again after the second 4 weeks of training following crossover. The EXP program significantly decreased 2-mile run times (961.3s ± 155.8s to 943.4 ± 140.2s, P=0.012, baseline to post 1) while the TRA group experienced a significant increase in run times (901.0 ± 79.2s vs. 913.9 ± 82.9s) over the same training period. There was a moderate effect size (d = 0.61, P=0.07) for the experimental run program to "reverse" the adverse effects of the traditional program within the 4-week training period (post 1 to post 2) following treatment crossover. Thus, for short-term training of military personnel, RPE intensity specific running program comprised of aerobic and anaerobic system development can enhance 2-mile run performance superior of a traditional program while reducing training volume (60 min per session vs. 43.2 min per session, respectively). Future research should extend the training period to determine efficacy of this training approach for long term improvement of aerobic capacity and possible reduction of musculoskeletal injury. [ABSTRACT FROM AUTHOR]

Abstract 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

The Nrf2 transcription factor is induced by reactive oxygen and nitrogen species and is necessary for the adaptive response to exercise in mice. It remains unknown whether Nrf2 signalling is activated by exercise in human skeletal muscle. Here we show that Nrf2 signalling is activated by exercise to exhaustion with similar responses in normoxia (PIO2: 143 mmHg) and severe acute hypoxia (PIO2: 73 mmHg). CaMKII and AMPKα phosphorylation were similarly induced in both conditions. Enhanced Nrf2 signalling was achieved by raising Nrf2 total protein and Ser40 Nrf2 phosphorylation, accompanied by a reduction of Keap1. Keap1 protein degradation is facilitated by the phosphorylation of p62/SQSTM1 at Ser349 by AMPK, which targets Keap1 for autophagic degradation. Consequently, the Nrf2-to-Keap1 ratio was markedly elevated and closely associated with a 2-3-fold increase in Catalase protein. No relationship was observed between Nrf2 signalling and SOD1 and SOD2 protein levels. Application of ischaemia immediately at the end of exercise maintained these changes, which were reverted within 1 min of recovery with free circulation. While SOD2 did not change significantly during either exercise or ischaemia, SOD1 protein expression was marginally downregulated and upregulated during exercise in normoxia and hypoxia, respectively. We conclude that Nrf2/Keap1/Catalase pathway is rapidly regulated during exercise and recovery in human skeletal muscle. Catalase emerges as an essential antioxidant enzyme acutely upregulated during exercise and ischaemia. Post-exercise ischaemia maintains Nrf2 signalling at the level reached at exhaustion and can be used to avoid early post-exercise recovery, which is O2-dependent.

This study investigated the effects of two sodium bicarbonate (NaHCO3) doses on estimated energy system contribution and performance during an intermittent high-intensity cycling test (HICT), and time-to-exhaustion (TTE) exercise. Twelve healthy males (stature: 1.75 ± 0.08 m; body mass: 67.5 ± 6.3 kg; age: 21.0 ± 1.4 years; maximal oxygen consumption: 45.1 ± 7.0 ml.kg.min−1) attended four separate laboratory visits. Maximal aerobic power (MAP) was identified from an incremental exercise test. During the three experimental visits, participants ingested either 0.2 g.kg−1 BM NaHCO3 (SBC2), 0.3 g.kg−1 BM NaHCO3 (SBC3), or 0.07 g.kg−1 BM sodium chloride (placebo; PLA) at 60 min pre-exercise. The HICT involved 3 × 60 s cycling bouts (90, 95, 100% MAP) interspersed with 90 s recovery, followed by TTE cycling at 105% MAP. Blood lactate was measured after each cycling bout to calculate estimates for glycolytic contribution to exercise. Gastrointestinal (GI) upset was quantified at baseline, 30 and 60 min post-ingestion, and 5 min post-exercise. Cycling TTE increased for SBC2 (+20.2 s; p = 0.045) and SBC3 (+31.9 s; p = 0.004) compared to PLA. Glycolytic contribution increased, albeit non-significantly, during the TTE protocol for SBC2 (+7.77 kJ; p = 0.10) and SBC3 (+7.95 kJ; p = 0.07) compared to PLA. GI upset was exacerbated post-exercise after SBC3 for nausea compared to SBC2 and PLA (p < 0.05), whilst SBC2 was not significantly different to PLA for any symptom (p > 0.05). Both NaHCO3 doses enhanced cycling performance and glycolytic contribution, however, higher doses may maximize ergogenic benefits.

Choline is an essential nutrient that has been implicated in athletic performance due to its role in maintaining normal muscle function. The concentration of free choline in serum may decrease during long-distance high-intensity exercise, yet few nutritional strategies to counteract this potentially performance-depleting loss in choline have been investigated outside the laboratory. This exploratory field study was performed to investigate if pre-race supplementation with phosphatidylcholine from krill oil can counteract the expected drop in choline and some of its metabolites during triathlon competitions. Forty-seven triathletes, 12 females and 35 males ranging in age from 25 to 61 years, were recruited from participants in the Ironman-distance Norseman Xtreme triathlon and the Sprint/Olympic-distance Oslo Triathlon. Twenty-four athletes were randomly allocated to the krill oil group, receiving 4 g of SuperbaBoost™ krill oil daily for 5 weeks prior to the race, and 23 athletes were randomly allocated to the placebo group, receiving 4 g of mixed vegetable oil daily. Blood samples were obtained before the race, immediately after completion of the race, and the day after the race for analysis of choline and its metabolites. The results showed that serum choline concentrations significantly decreased from pre-race to race finish in all races, with a more pronounced decrease observed in the Ironman-distance Norseman Xtreme triathlon (34% decrease) relative to the Sprint/Olympic-distance Oslo Triathlon (15% decrease). A reduction in betaine was also observed, while dimethylglycine (DMG) concentrations remained stable across all time points. Significantly higher concentrations of choline (9.4% on average) and DMG (21.4% on average) were observed in the krill oil compared to the placebo group, and the krill oil group showed a significantly greater increase in serum choline following race completion. In conclusion, krill oil may help to prevent that circulating choline concentrations become limiting during endurance competitions.

Abstract 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

During exercise, muscle ATP demand increases with intensity, and at the highest power output, ATP consumption may increase more than 100-fold above the resting level. The rate of mitochondrial ATP production during exercise depends on the availability of O2, carbon substrates, reducing equivalents, ADP, Pi, free creatine, and Ca2+. It may also be modulated by acidosis, nitric oxide and reactive oxygen and nitrogen species (RONS). During fatiguing and repeated sprint exercise, RONS production may cause oxidative stress and damage to cellular structures and may reduce mitochondrial efficiency. Human studies indicate that the relatively low mitochondrial respiratory rates observed during sprint exercise are not due to lack of O2, or insufficient provision of Ca2+, reduced equivalents or carbon substrates, being a suboptimal stimulation by ADP the most plausible explanation. Recent in vitro studies with isolated skeletal muscle mitochondria, studied in conditions mimicking different exercise intensities, indicate that ROS production during aerobic exercise amounts to 1-2 orders of magnitude lower than previously thought. In this review, we will focus on the mechanisms regulating mitochondrial respiration, particularly during high-intensity exercise. We will analyze the factors that limit mitochondrial respiration and those that determine mitochondrial efficiency during exercise. Lastly, the differences in mitochondrial respiration between men and women will be addressed.

Background The present study investigated the effects of chronic sodium bicarbonate (NaHCO3) ingestion on a single bout of high-intensity exercise and on acid-base balance during 7-day high-altitude exposure. Methods Ten recreationally active subjects participated in a pre-test at sea level and a 7-day hiking tour in the Swiss Alps up to 4554 m above sea level. Subjects received either a daily dose of 0.3 g/kg NaHCO3 solution (n = 5) or water as a placebo (n = 5) for 7 days. Anaerobic high-intensity exercise performance was assessed using the portable tethered sprint running (PTSR) test under normoxic and hypoxic conditions (3585 m). PTSR tests assessed overall peak force, mean force, and fatigue index. Blood lactate levels and blood gas parameters were assessed pre- and post-PTSR. Urinary pH and blood gas parameters were further analyzed daily at rest in early morning samples under normoxic and hypoxic conditions. Results There were no significant differences between the bicarbonate and control group in any of the PTSR-related parameters. However, urinary pH (p = 0.003, ηp2 = 0.458), early morning blood bicarbonate concentration (p

Abstract Background There is evidence to suggest that postprandial lipemia are is linked to the impairment of endothelial function, which is characterized by an imbalance between the actions of vasodilators and vasoconstrictors. The aim of this study was to determine the effects of a 12-week high-intensity training (HIT) and moderate continuous training (MCT) protocol on postprandial lipemia, vascular function and arterial stiffness in inactive adults after high-fat meal (HFM) ingestion. Methods A randomized clinical trial was conducted in 20 healthy, inactive adults (31.6 ± 7.1 years). Participants followed the two exercise protocols for 12 weeks. To induce a state of postprandial lipemia (PPL), all subjects received a HFM. Endothelial function was measured using flow-mediated vasodilation (FMD), normalized brachial artery FMD (nFMD), aortic pulse wave velocity (PWV) and augmentation index (AIx). Plasma total cholesterol, high-density lipoprotein cholesterol (HDL-c), triglycerides and glucose were also measured. Results The effects of a HFM were evaluated in a fasted state and 60, 120, 180, and 240 min postprandially. A significant decrease in serum glucose between 0 min (fasted state) and 120 min postprandially was found in the HIT group (P = 0.035). Likewise, FMD (%) was significantly different between the fasted state and 60 min after a HFM in the HIT group (P = 0.042). The total cholesterol response expressed as area under curve (AUC)(0–240) was lower following HIT than following MCT, but no significant differences were observed (8%, P > 0.05). Similarly, triglycerides AUC(0–240) was also lower after HIT compared with MCT, which trended towards significance (24%, P = 0.076). The AUC(0–240) for the glucose response was significantly lower following HIT than MCT (10%, P = 0.008). FMD and nFMD AUC(0–240) were significantly higher following HIT than following MCT (46.9%, P = 0.021 and 67.3%, P = 0.009, respectively). PWV AUC(0–240) did not differ following between the two exercise groups (2.3%, P > 0.05). Conclusions Supervised exercise training mitigates endothelial dysfunction and glucose response induced by PPL. Exercise intensity plays an important role in these protective effects, and medium-term HIT may be more effective than MCT in reducing postprandial glucose levels and attenuating vascular impairment. Trial registration ClinicalTrials.gov ID: NCT02738385 Date of registration: April 14, 2016.

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. [ABSTRACT FROM AUTHOR]

Introduction: Endogenous brain-derived neurotrophic factor (BDNF) is thought to be protective against the neurodegeneration seen in Parkinson's disease (PD), and is thought to increase during exercise. This has been proposed as a possible mechanism by which exercise improves outcomes for people with PD. We conducted a pilot study to investigate the role of exercise intensity on BDNF levels in people with PD. Methods: Participants of early- to mid-stage disease were recruited from a single PD service in north-east England, UK into two separate studies of exercise in PD, one involving moderate-intensity continuous training (MICT) and one involving high-intensity interval training (HIIT), both had control groups. In both the interventions, participants exercise three times per week for 12 weeks. Blood samples were taken for BDNF analysis at the start and end of the first session and the start and end of the final session, with corresponding samples taken in controls. Results: Data were available for 27 participants (13 intervention, 14 control) in the MICT intervention and 17 (9 intervention, 8 control) in the HIIT intervention. BDNF level did not rise significantly from the start to end of individual sessions. Across the 12 week period, they rose significantly in the HIIT intervention group, but not in controls or the MICT intervention group. Conclusions: High-intensity interval training appears to have a greater impact on BDNF than MICT. Future work should directly compare exercise modalities and investigate the impact of BDNF levels on disease progression and quality of life. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

About one-third of women of reproductive age are obese, predisposing both mother and baby to unfavourable pregnancy outcomes and initiating an intergenerational cycle of chronic metabolic disorders. Here we summarise recent research on the influence of maternal metabolic health on offspring susceptibility to future cardiometabolic diseases. Current primary lifestyle approaches (i.e., diet and exercise interventions) to halt the succession of inherited and epigenetic metabolic abnormalities have met with limited success due to late implementation, poor adherence, and/or generic guidelines. In our opinion, such interventions must commence prior to conception to improve both maternal and child health outcomes, with new approaches urgently needed to increase adherence to primary lifestyle changes among reproductive-age women. Up to one-third of women of reproductive age are obese, predisposing their offspring to cardiometabolic diseases and initiating an intergenerational cycle of chronic metabolic disorders. Epigenetic modifications in foetal tissue play a mechanistic role in metabolic disease programming through interaction of the pregnancy environment with gene function. Primary lifestyle interventions (i.e.,diet and exercise) to improve maternal health are typically initiated in the second trimester, conferring limited benefits for mother and child. Diet–exercise interventions should commence preconception. Alternative approaches to current guidelines are urgently required to improve adherence and break the intergenerational cycle of inherited and epigenetic abnormalities of metabolism. [ABSTRACT FROM AUTHOR]

Purpose: Enteric-coated sodium bicarbonate (NaHCO3) can attenuate gastrointestinal (GI) symptoms following acute bicarbonate loading, although the subsequent effects on exercise performance have not been investigated. The purpose of this study was to examine the effects of enteric-coated NaHCO3 supplementation on high-intensity exercise performance and GI symptoms.Methods: Eleven trained male cyclists completed three 4 km time trials after consuming; a placebo or 0.3 g∙kg-1 body mass NaHCO3 in enteric-coated or gelatin capsules. Exercise trials were timed with individual peak blood bicarbonate ion concentration ([HCO3-]). Blood acid-base balance was measured pre-ingestion, pre-exercise, and post-exercise, whereas GI symptoms were recorded pre-ingestion and immediately pre-exercise.Results: Pre-exercise blood [HCO3-] and potential hydrogen (pH) were greater for both NaHCO3 conditions (P < 0.0005) when compared to placebo. Performance time was faster with enteric-coated (- 8.5 ± 9.6 s, P = 0.044) and gelatin (- 9.6 ± 7.2 s, P = 0.004) NaHCO3 compared to placebo, with no significant difference between conditions (mean difference = 1.1 ± 5.3 s, P = 1.000). Physiological responses were similar between conditions, although blood lactate ion concentration was higher with gelatin NaHCO3 (2.4 ± 1.7 mmol∙L-1, P = 0.003) compared with placebo. Furthermore, fewer participants experienced GI symptoms with enteric-coated (n = 3) compared to gelatin (n = 7) NaHCO3.Discussion: Acute enteric-coated NaHCO3 consumption mitigates GI symptoms at the onset of exercise and improves subsequent 4 km cycling TT performance. Athletes who experience GI side-effects after acute bicarbonate loading may, therefore, benefit from enteric-coated NaHCO3 supplementation prior to exercise performance. [ABSTRACT FROM AUTHOR]

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Background: The present study investigated the effects of chronic sodium bicarbonate (NaHCO3) ingestion on a single bout of high-intensity exercise and on acid-base balance during 7-day high-altitude exposure. Methods: Ten recreationally active subjects participated in a pre-test at sea level and a 7-day hiking tour in the Swiss Alps up to 4554 m above sea level. Subjects received either a daily dose of 0.3 g/kg NaHCO3 solution (n = 5) or water as a placebo (n = 5) for 7 days. Anaerobic high-intensity exercise performance was assessed using the portable tethered sprint running (PTSR) test under normoxic and hypoxic conditions (3585 m). PTSR tests assessed overall peak force, mean force, and fatigue index. Blood lactate levels and blood gas parameters were assessed pre- and post-PTSR. Urinary pH and blood gas parameters were further analyzed daily at rest in early morning samples under normoxic and hypoxic conditions. Results: There were no significant differences between the bicarbonate and control group in any of the PTSR-related parameters. However, urinary pH (p = 0.003, ηp2 = 0.458), early morning blood bicarbonate concentration (p < 0.001, ηp2 = 0.457) and base excess (p = 0.002, ηp2 = 0.436) were significantly higher in the bicarbonate group compared with the control group under hypoxic conditions. Conclusions: These results indicate that oral NaHCO3 ingestion does not ameliorate the hypoxia-induced impairment in anaerobic, high-intensity exercise performance, represented by PTSR-related test parameters, under hypobaric, hypoxic conditions, but the maximal performance measurements may have been negatively affected by other factors, such as poor implementation of PTSR test instructions, pre-acclimatization, the time course of hypoxia-induced renal [HCO3−] compensation, changes in the concentrations of intra- and extracellular ions others than [H+] and [HCO3−], or gastrointestinal disturbances caused by NaHCO3 ingestion. However, chronic NaHCO3 ingestion improves blood bicarbonate concentration and base excess at altitude, which partially represent the blood buffering capacity. [ABSTRACT FROM AUTHOR]

Background: This study aimed to verify the effects of high-intensity aerobic training (HIAT) on BP control and renin-angiotensin system (RAS) components in renal tissue of SHR. Ten SHRs received HIAT or control for 8-weeks. At the end of the training, the SBP showed a reduction of ~ 30mmHg (p <.01) in HIAT and increased by ~ 15 mmHg in the control group. HIAT resulted in a higher release of nitrite, IL-6, ACE2 and ATR2. These results indicated an association between BP, NO and renal RAS. Abbreviations: JAA: writing, carried out all experimental procedures, performed statistical analysis, original draft and revised manuscript DMS: data interpretation, formal analysis, writing, editing and revised manuscript BAP: carried all experimental procedures, revised manuscritpt CPCG: carried all experimental procedures, revised manuscritpt MEN: experimental procedures, revised manuscript and data interpretation RWP: drafted and revised manuscript RCA: writing, experimental procedures, revised manuscript JP: writing, data interpretation and revised manuscript OLF: writing, original draft and revised manuscript. [ABSTRACT FROM AUTHOR]

This study examined the acute performance, cardiovascular and local muscular responses to perceived exertion-based high-intensity interval exercise using either double- or single-leg cycling. Fifteen healthy middle-aged adults completed, on separate occasions, ten 30-s double-leg intervals interspersed with 60 s passive recovery and twenty (ten with each leg) 30-s single-leg intervals interspersed with 60 s passive recovery. Impedance cardiography, blood pressure, muscle oxygenation and total haemoglobin content (near-infrared spectroscopy), oxygen consumption and power output were measured throughout each session. Normalised to the lean mass used during each trial, single-leg cycling resulted in lower power output (single-leg: 8.92 ± 1.74 W kg−1 and double-leg: 10.41 ± 3.22 W kg−1; p < 0.05) but greater oxygen consumption (single-leg: 103 ± 11 mL kg−1 min−1 and double-leg: 84 ± 21 mL kg−1 min−1; p < 0.01) and cardiac output (single-leg: 1407 ± 334 mL kg−1 min−1 and double-leg: 850 ± 222 mL kg−1 min−1; p < 0.01), compared with double-leg cycling. Mean arterial pressure (double-leg: 108 ± 11 mmHg and single-leg: 102 ± 10 mmHg), change in total haemoglobin content (double-leg: 8.76 ± 10.65 µM cm s−1 and single-leg: 13.42 ± 4.10 µM cm s−1) and change in tissue oxygenation index (double-leg: −4.51 ± 3.56% and single-leg: −3.97 ± 3.91%) were not different between double-leg and single-leg cycling. When compared to double-leg cycling, single-leg cycling elicited a higher cardiac output relative to the lean mass, but this did not result in greater power output. The dissociation between blood availability and power output is consistent with an ageing model characterised by a decrease in local oxygen delivery and distribution capability. [ABSTRACT FROM AUTHOR]

Endurance exercise begun with reduced muscle glycogen stores seems to potentiate skeletal muscle protein abundance and gene expression. However, it is unknown whether this greater signaling responses is due to performing two exercise sessions in close proximity—as a first exercise session is necessary to reduce the muscle glycogen stores. In the present study, we manipulated the recovery duration between a first muscle glycogen‐depleting exercise and a second exercise session, such that the second exercise session started with reduced muscle glycogen in both approaches but was performed either 2 or 15 hours after the first exercise session (so‐called "twice‐a‐day" and "once‐daily" approaches, respectively). We found that exercise twice‐a‐day increased the nuclear abundance of transcription factor EB (TFEB) and nuclear factor of activated T cells (NFAT) and potentiated the transcription of peroxisome proliferator‐activated receptor‐ɣ coactivator 1‐alpha (PGC‐1α), peroxisome proliferator‐activated receptor‐alpha (PPARα), and peroxisome proliferator‐activated receptor beta/delta (PPARβ/δ) genes, in comparison with the once‐daily exercise. These results suggest that part of the elevated molecular signaling reported with previous "train‐low" approaches might be attributed to performing two exercise sessions in close proximity. The twice‐a‐day approach might be an effective strategy to induce adaptations related to mitochondrial biogenesis and fat oxidation. [ABSTRACT FROM AUTHOR]

Purpose: To assess the effect of supramaximal intermittent exercise on long-term cardiac autonomic activity, inferred from heart rate variability (HRV). Methods: Eleven healthy males performed a series of two consecutive intermittent 15-s runs at 95% VIFT (i.e., speed reached at the end of the 30-15 Intermittent Fitness Test) interspersed with 15 s of active recovery at 45% VIFT until exhaustion. Beat-to-beat intervals were recorded during two consecutive nights (habituation night and 1st night) before, 10 min before and immediately after exercise, as well as 12 h (2nd night) and 36 h (3rd night) after supramaximal intermittent exercise. The HRV indices were calculated from the last 5 mm of resting and recovery periods, and the first 10 mm of the first estimated slow wave sleep period. Results: Immediate post-supramaximal exercise vagal-related HRV indices were significantly lower than immediate pre-supramaximal exercise values (P < .001). Most vagal-related indices were lower during the 2nd night compared with the 1st night (eg, mean RR intervals, P = .03). Compared with the 2nd night, vagal-related HRV indices were significantly higher during the 3rd night. Variables were not different between the 1st and 3rd nights; however, we noted a tendency (adjusted effect size, aES) for an increased normalized high-frequency component (P = .06 and aES = 0.70) and a tendency toward a decreased low-frequency component (P = .06 and aES = 0.74). Conclusion: Results confirm the strong influence of exercise intensity on short- and long-term postexercise heart rate variability recovery and might help explain the high efficiency of supramaximal training for enhancing indices of cardiorespiratory fitness. [ABSTRACT FROM AUTHOR]

The present study compared neuromuscular fatigue profiles between children, untrained adults and adult endurance athletes during repeated maximal muscle contractions. Eighteen prepubertal boys, 19 untrained men and 13 endurance male athletes performed 5-s maximal voluntary isometric knee extensor contractions (MVICs) interspersed with 5-s recovery until MVIC reached 60% of its initial value. Single and doublet magnetic stimulations were delivered to the femoral nerve to quantify the time course of potentiated twitch amplitude (Ttw,pot), high-frequency torque (T100Hz) and the low-to-high frequency torque ratio (T10Hz/T100Hz), i.e., indicators of peripheral fatigue. M-wave-normalized EMG amplitudes (EMG/M) and the maximal voluntary activation level (VA) were calculated to quantify central fatigue. Adults (15.9 ± 3.9 repetitions) performed fewer MVICs than children (40.4 ± 19.7) and endurance athletes (51.7 ± 19.6), however, no difference was observed between children and athletes (P = 0.13). Ttw,pot (∼52%, P < 0.001), T100Hz (∼39%, P < 0.001) and T10Hz/T100Hz (∼23%, P < 0.001) decreased only in adults. Similar decrements in vastus medialis and vastus lateralis EMG/M were observed in children and endurance athletes (range: 40–50%), and these were greater than in adults (∼15%). Whilst VA decreased more in children (-38.4 ± 22.5%, P < 0.001) than endurance athletes (-20.3 ± 10.1%, P < 0.001), it did not change in adults. Thus, children fatigued more slowly than adults and as much as endurance athletes. They developed less peripheral and more central fatigue than adults and, although central fatigue appeared somewhat higher in children than endurance athletes, both children and endurance athletes experienced greater decrements than adults. Therefore, children exhibit a more comparable neuromuscular fatigue profile to endurance athletes than adults.

Background: Currently, endoplasmic reticulum stress is studied utilizing a dephosphorylation inhibitor (Sal). The traditional Chinese patent medicine and simple formulation Shensong Yangxin Capsule is a commonly used medication for the treatment of arrhythmia. However, the efficacy and underlying mechanism of the capsule in treating post-ischemic heart failure in myocardial tissue have not yet been investigated., Objective: The therapeutic effects and the underlying mechanism of the Shensong Yangxin Capsule (SSYX) and the dephosphorylation inhibitor Salubrinal (Sal) on heart failure (HF) induced by high-intensity exercise in rats with acute myocardial infarction (AMI) were investigated., Methods: Male infants of 8 weeks Spragge-Dawley (SD) rats were randomly assigned to one of four groups: sham surgery group, AMI+placebo group, AMI+Shensong Yangxin Capsule group (AMI+SSYX), and AMI+Sal administration group. Rats' myocardial infarction was induced by left coronary artery ligation. Rats were subjected to a 3-week high-intensity exercise program to simulate heart failure after 7 days of postoperative rest. After the fourth postoperative week, echocardiography was applied to determine the left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and left ventricular systolic volume (LVESV) in each group. HE and TUNEL labeling were employed to examine the morphology of cardiac cells and measure the percentage of apoptosis in each group; Western blotting was applied to detect the cardiomyocyte apoptosis-related proteins p-JNK, p-P38, and NOX2, while ELISA was used to detect glutathione(GSH), malondialdehyde (MDA), and superoxide dismutase (SOD) in serum., Results: Following a 4-week drug intervention:(1)LVFS and LVEF in the AMI+placebo group were statistically significantly reduced, while LVESV were significantly higher, compared to those in the sham surgery group (P<0.05); The AMI+SSYX group performed statistically significantly better than the AMI+placebo group(P<0.05). (2) The myocardial cells in the AMI+placebo group exhibited significant swelling and inflammatory cell infiltration; the myocardial cells in the AMI+SSYX group and AMI+Sal group displayed mild swelling and minimal inflammatory cell infiltration; the AMI+SSYX group's myocardial cell morphology was superior to that of the AMI+Sal group; (3) The apoptosis rate of the AMI+placebo group was around 95%, greater than that of the sham surgery group (2.55%). The apoptosis rate of the AMI+SSYX group is approximately 21%, while the apoptosis rate of the AMI+Sal group is about 43%. (4) In the AMI+placebo group, p-JNK, p-P38, and NOX2 protein expression dramatically increased compared to the sham surgery group. The expression of p-P38, NOX2, and p-JNK/t-JNK was considerably reduced in the AMI+Shensong group and AMI+Sal group, compared to the AMI+placebo group. (P<0.01)The AMI+SSYX group's result is superior to that of the AMI+Sal group. (5) Compared to the sham surgery group, the serum levels of SOD and GSH were significantly lower, and MDA was significantly higher in the AMI+placebo group. Compared to the AMI+placebo group, the serum levels of SOD and GSH were significantly higher, and MDA was significantly lower in the AMI+SSYX group and the AMI+Sal group. (P<0.05) Conclusion: In rats with acute myocardial infarction in high-intensity exercise-induced heart failure, Shensong Yangxin Capsule dramatically reduces myocardial cell death and cardiac dysfunction. SSYX has a shorter course of treatment and a better therapeutic effect than Sal., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Monocytes are critical components, not only for innate immunity, but also for the activation of the adaptive immune system. Many studies in animals and humans have demonstrated that monocytes may be closely associated with chronic inflammatory diseases and be proved to be pivotal in the association between high-intensity exercise and anti-inflammation response. However, the underlying molecular mechanisms driving this are barely understood. The present study aimed to screen for potential hub genes and candidate signaling pathways associated with the effects of high-intensity exercise on human monocytes through bioinformatics analysis. Materials and Methods: The GSE51835 gene expression dataset was downloaded from the Gene Expression Omnibus database. The dataset consists of 12 monocyte samples from two groups of pre-exercise and post-exercise individuals. Identifying differentially expressed genes (DEGs) with R software, and functional annotation and pathway analyses were then performed with related web databases. Subsequently, a protein–protein interaction (PPI) network which discovers key functional protein and a transcription factors-DEGs network which predicts upstream regulators were constructed. Results: A total of 146 differentially expressed genes were identified, including 95 upregulated and 51 downregulated genes. Gene Ontology analysis indicated that in the biological process functional group, these DEGs were mainly involved in cellular response to hydrogen peroxide, response to unfolded protein, negative regulation of cell proliferation, cellular response to laminar fluid shear stress, and positive regulation of protein metabolic process. The top five enrichment pathways in a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were the FoxO signaling pathway, protein processing in the endoplasmic reticulum, influenza A, the ErbB signaling pathway, and the MAPK signaling pathway. TNF, DUSP1, ATF3, CXCR4, NR4A1, BHLHE40, CDKN1B, SOCS3, TNFAIP3, and MCL1 were the top 10 potential hub genes. The most important modules obtained in the PPI network were performed KEGG pathway analysis, which showed that these genes were mainly involved in the MAPK signaling pathway, the IL-17 signaling pathway, the TNF signaling pathway, osteoclast differentiation, and apoptosis. A transcription factor (TF) target network illustrated that FOXJ2 was a critical regulatory factor. Conclusions: This study identified the essential genes and pathways associated with exercise and monocytes. Among these, four essential genes (TNF, DUSP1, CXCR4, and NR4A1) and the FoxO signaling pathway play vital roles in the immune function of monocytes. High-intensity exercise may improve the resistance of chronic inflammatory diseases by regulating the expression of these genes.

Introduction: Regular exercise can reduce the risk of developing cardiovascular disease through risk factor modification, with high-intensity exercise and more recently small muscle mass training providing alternatives to moderate-intensity exercise. Methods: This study randomly assigned 53 healthy middle-age adults (age, 62 ± 6 yr) to complete 24 sessions (8 wk; 3 d·wk−1) of exercise training, using either high-intensity double-leg cycling (n = 17; HITDL), high-intensity single-leg cycling (n = 18; HITSL), or moderate-intensity double-leg cycling (n = 18; MCTDL). Biomarkers of cardiovascular risk (total cholesterol, triglycerides, HDL-c, LDL-c, apo-B48, and glucose), anthropometry measures (body mass, body mass index, waist circumference, and waist-to-hip ratio), resting blood pressure, and aerobic capacity were assessed pre- and postintervention. Results: Total work completed was greater (P < 0.01) in MCTDL (5938 ± 1462 kJ) compared with the HITDL (3462 ± 1063 kJ) and HITSL (4423 ± 1875 kJ). Pre- to posttraining differences were observed for waist-to-hip ratio (0.84 ± 0.09 vs 0.83 ± 0.09; P < 0.01), resting systolic blood pressure (129 ± 11 vs 124 ± 12 mm Hg; P < 0.01), total cholesterol (5.87 ± 1.17 vs 5.55 ± 0.98 mmol·L−1; P < 0.01), and LDL-c (3.70 ± 1.04 vs 3.44 ± 0.84 mmol·L−1; P < 0.01), with no differences between conditions. In addition, aerobic capacity increased after training (22.3 ± 6.4 vs 24.9 ± 7.6 mL·kg−1·min−1; P < 0.01), with no differences between conditions. Conclusion: These findings suggest that all three modes of exercise can be prescribed to achieve cardiovascular risk reduction in an aging population. [ABSTRACT FROM AUTHOR]

The current study examined the effect of acute caffeine ingestion on mean and peak power production, fatigue index and rating of perceived exertion (RPE) during upper body and lower body Wingate anaerobic test (WANT) performance. Using a double-blind design, 22 males undertook one upper body and one lower body WANT, 60 min following ingestion of caffeine (5 mg*kg−1) and one upper body and one lower body WANT following ingestion of placebo (5 mg*kg−1 Dextrose). Peak power was significantly higher (P =.001) following caffeine ingestion in both upper and lower body WANT. Peak power and mean power was also significantly higher during lower body, compared to upper body WANTs irrespective of substance ingested. However, caffeine ingestion did not enhance mean power neither in upper nor lower-body WANT. There were no significant differences in mean fatigue index as a consequence of substance ingested or mode of exercise (all P > 0.05). For RPE there was also a significant substance ingested X mode interaction (P =.001) where there were no differences in RPE between caffeine and placebo conditions in lower body WANTs but significantly lower RPE during upper body WANT in the presence of caffeine compared to placebo (P =.014). This is the first study to compare the effects of caffeine ingestion on upper and lower body 30-second WANT performance and suggests that caffeine ingestion in the dose of 5 mg*kg−1 ingested 60 min prior to exercise significantly enhances peak power when data from upper and lower body WANTs are combined. [ABSTRACT FROM AUTHOR]

The O2-kinetic response to constant work rate exercise provides an insight into the adjustment of systemic oxygen transport and muscle metabolism. Whether O2-kinetics measured in laboratory conditions reflect O2-kinetics in field conditions has not yet been analysed. The aim of this study was to compare O2-kinetics between field and laboratory conditions. Thirteen competitive male cyclists (mean±SD age 23.3±4.1 years; V̇O2peak 68.2±4.7 mL. min−1. kg−1) completed two 6-min severe-intensity trials at 60 and 90 rev. min−1 in both conditions. Power output was measured with an SRM power meter and V̇O2 was measured with a portable gas analyser. The time constant (τ), the time delay (TD) and the amplitude (Amp) were resolved by least square regression, and the V̇O2 slow component (SC) was calculated as the difference between the end-exercise V̇O2 and Amp. To determine differences between the trials, a repeated-measure ANOVA was conducted. The Amp and end-exercise V̇O2 were significantly higher during field cycling whereas the SC were significantly higher during laboratory cycling (all at p<0.001). No significant differences were found for τ (p=0.24). Laboratory measures tend to underestimate the oxygen demand in field cycling. A higher cadence leads to greater oxygen demand in laboratory and field cycling. [ABSTRACT FROM AUTHOR]

The focus of the investigation was to examine the effects of citrulline malate (CM) on muscular fatigue in healthy, recreationally trained participants. Twelve participants (men = 6 and women = 6) (24.1 ± 3.9 years) visited the laboratory on 3 separate days, all separated by 1 week. Each visit consisted of consuming 1 of 3 treatments: placebo, CM (8 g), and control in which no drink mixture was consumed. For each day of testing, participants consumed assigned treatment and performed 1 high-intensity exercise trial consisting of squats, lunge jumps, squat jumps, and lateral jumps. Participants performed the exercises in the listed order, which was designated as 1 round. Each participant performed 3 rounds, with the work-to-rest ratio being 20 seconds of work and 30 seconds of rest. A 1-minute rest was given between rounds. A pre/post-exercise isokinetic leg extension test was performed to measure for peak power, peak torque, and rate of fatigue. In addition, blood lactate was obtained pre/post-exercise. There were no treatment or interaction effects (p > 0.05) for peak torque, peak power, rate of fatigue, or blood lactate accumulation. However, there was a statistical significant decrease from pre/post-exercise for peak torque (p = 0.003), peak power (p = 0.003), and rate of fatigue (p = 0.001). In addition, lactate accumulation did increase significantly from pre/post-exercise (p = 0.0001). Finally, neither total work nor final heart rate was statistically significant between the treatments (p > 0.05). Citrulline malate was not effective in improving performance or alleviating fatigue after a high-intensity exercise session. [ABSTRACT FROM AUTHOR]

Recent data demonstrate improved locomotion with high-intensity locomotor training (LT) in individuals with incomplete spinal cord injury (iSCI), although concerns remain regarding reinforcement of abnormal motor strategies. The present study evaluated the effects of LT intensity on kinematic and neuromuscular coordination in individuals with iSCI. Using a randomized, crossover design, participants with iSCI received up to 20 sessions of high-intensity LT, with attempts to achieve 70–85% of age-predicted maximum heart rate (HRmax), or low-intensity LT (50–65% HRmax), following which the other intervention was performed. Specific measures included spatiotemporal variables, sagittal-plane gait kinematics, and neuromuscular synergies from electromyographic (EMG) recordings. Correlation analyses were conducted to evaluate associations between variables. Significant improvements in sagittal-plane joint excursions and intralimb hip-knee coordination were observed following high- but not low-intensity LT when comparing peak treadmill (TM) speed before and after LT. Neuromuscular complexity (i.e., number of synergies to explain >90% of EMG variance) was also increased following high- but not low-intensity LT. Comparison of speed-matched trials confirmed significant improvements in the knee excursion of the less impaired limb and intralimb hip-knee coordination, as well as improvements in neuromuscular complexity following high-intensity LT. These findings suggest greater neuromuscular complexity may be due to LT and not necessarily differences in speeds. Only selected kinematic changes (i.e., weak hip excursion) was correlated to improvements in treadmill speed. In conclusion, LT intensity can facilitate gains in kinematic variables and neuromuscular synergies in individuals with iSCI. [ABSTRACT FROM AUTHOR]

This study, employing an exercise versus control crossover design, was conducted to investigate the influence of acute high-intensity exercise on salivary nitric oxide (NO) levels. Nine healthy males (aged 23.8 ± 1.4 years) performed ergometer exercise at 80%VO2peak for 60 min, whereas controls sat at rest for 60 min. Saliva samples were collected before (Pre: 0800 h) and after (Post 0-h: 0900 h, Post 1-h: 1000 h, Post 2-h: 1100 h, Post 3-h: 1200 h) the interventions. Salivary NO levels were determined by colorimetric assay. It was found that the salivary NO levels in controls were decreased (P < 0.05) at Post 0-h (-94 ± 15), Post 1-h (-80 ± 20), Post 2-h (-92 ± 34) and Post 3-h (-145 ± 39) relative to the Pre values. Under exercise conditions, salivary NO levels did not change after high-intensity ergometer exercise relative to the Pre values. Thus, the response of salivary NO levels appeared to differ between high-intensity ergometer exercise and inactivity, that exercise-related stress induces the production of salivary NO. [ABSTRACT FROM AUTHOR]

The aim of this study was to perform a systematic review and meta-analysis on the acute and chronic effects of sodium bicarbonate (NaHCO3) ingestion on Wingate performance. Following a search through PubMed, Scopus and Web of Science, 9 studies were found meeting inclusion criteria (6 acute and 3 chronic). Random-effects meta-analysis of standardized mean difference (SMD) for peak and mean power was performed. Study quality was assessed using the QualSyst. Results of the meta-analysis showed that acute ingestion of NaHCO3 did not improve Wingate test peak (weighted average effect size Hedges's g = 0.02, 95%CI: - 0.19 to 0.23, P = 0.87) or mean power (weighted average effect size Hedges's g = 0.15, 95%CI: −0.06 to 0.36, P = 0.92). However, chronic ingestion of NaHCO3 improved Wingate test peak (weighted average effect size Hedges's g = 1.21, 95%CI: 0.83 to 1.42, P = 0.001) and mean power (weighted average effect size Hedges's g = 1.26, 95%CI: 0.96 to 1.56, P = 0.001). Quality assessment of selected articles was classified as strong. This meta-analysis provides evidence that chronic, but not acute, ingestion of NaHCO3 increases both Wingate test peak and mean power. [ABSTRACT FROM AUTHOR]

The current study examined the effect of acute caffeine ingestion on mean and peak power production during upper body Wingate test (WANT) performance, rating of perceived exertion, readiness to invest effort and cognitive performance. Using a double-blind design, 12 males undertook upper body WANTs, following ingestion of caffeine (5 mg*kg−1) or placebo. Pre-substance ingestion, 60 mins post substance ingestion and post exercise participants completed measures of readiness to invest physical and mental effort and cognitive performance. Peak power was significantly higher (P = .026), fatigue index greater (P = .02) and rating of perceived exertion lower (P = .025) in the presence of caffeine. Readiness to invest physical effort was also higher (P = .016) in the caffeine condition irrespective of time point (pre, 60 mins post ingestion and post exercise). Response accuracy for incongruent trials on the Flanker task was superior in the presence of caffeine (P = .006). There was a significant substance × time interaction for response speed in both congruent and incongruent conditions (both P = .001) whereby response speeds were faster at 60 mins post ingestion and post exercise in the caffeine condition, compared to placebo. This is the first study to examine the effects of caffeine ingestion on this modality of exercise and suggests that caffeine ingestion significantly enhances peak power, readiness to invest physical effort, and cognitive performance during WANT performance. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study was to assess the acute cardiorespiratory as well as muscle and cerebral tissue oxygenation responses to submaximal constant-load (CL) and high-intensity interval (HII) cycling exercise performed in normoxia and in hypoxia at similar intensity, reproducing whole-body endurance exercise training sessions as performed in sedentary and clinical populations.Methods: Healthy subjects performed two CL (30 min, 75% of maximal heart rate, n = 12) and two HII (15 times 1-min high-intensity exercise-1-min passive recovery, n = 12) cycling exercise sessions in normoxia and in hypoxia [mean arterial oxygen saturation 76 ± 1% (clamped) during CL and 77 ± 5% (inspiratory oxygen fraction 0.135) during HII]. Cardiorespiratory and near-infrared spectroscopy parameters as well as the rate of perceived exertion were continuously recorded.Results: Power output was 21 ± 11% and 15% (according to protocol design) lower in hypoxia compared to normoxia during CL and HII exercise sessions, respectively. Heart rate did not differ between normoxic and hypoxic exercise sessions, while minute ventilation was higher in hypoxia during HII exercise only (+ 13 ± 29%, p < 0.05). Quadriceps tissue saturation index did not differ significantly between normoxia and hypoxia (CL 60 ± 8% versus 59 ± 5%; HII 59 ± 10% versus 56 ± 9%; p > 0.05), while prefrontal cortex deoxygenation was significantly greater in hypoxia during both CL (66 ± 4% versus 56 ± 6%) and HII (58 ± 5% versus 55 ± 5%; p < 0.05) sessions. The rate of perceived exertion did not differ between normoxic and hypoxic CL (2.4 ± 1.7 versus 2.9 ± 1.8) and HII (6.9 ± 1.4 versus 7.5 ± 0.8) sessions (p > 0.05).Conclusion: This study indicates that at identical heart rate, reducing arterial oxygen saturation near 75% does not accentuate muscle deoxygenation during both CL and HII exercise sessions compared to normoxia. Hence, within these conditions, larger muscle hypoxic stress should not be expected. [ABSTRACT FROM AUTHOR]

Graphical abstract Highlights • Caffeine intake attenuates inflammation induced by high-intensity exercise. • Caffeine prevented the increase in IL-6 levels induced by exercise. • Lymphocyte proliferation occurred in trained animals treated with caffeine. • Caffeine prevented alterations in ATP hydrolysis induced by exercise. • Intense exercise increased the acetylcholinesterase activity in lymphocytes. Abstract This study evaluated the effects of caffeine in combination with high-intensity interval training (HIIT) on sensitivity to glucocorticoids and proliferation of lymphocytes, IL-6 and IL-10 levels and NTPDase, adenosine deaminase (ADA) and acetylcholinesterase (AChE) activity in rat lymphocytes. The animals were divided into groups: control, caffeine 4 mg/kg, caffeine 8 mg/kg, HIIT, HIIT plus caffeine 4 mg/kg and HIIT plus caffeine 8 mg/kg. The rats were trained three times a week for 6 weeks for a total workload 23% of body weight at the end of the experiment. Caffeine was administered orally 30 min before the training session. When lymphocytes were stimulated with phytohaemagglutinin no changes were observed in proliferative response between trained and sedentary animals; however, when caffeine was associated with HIIT an increase in T lymphocyte proliferation and in the sensitivity of lymphocytes to glucocorticoids occurred. ATP and ADP hydrolysis was decreased in the lymphocytes of the animals only trained and caffeine treatment prevented alterations in ATP hydrolysis. HIIT caused an increase in the ADA and AChE activity in lymphocytes and this effect was more pronounced in rats trained and supplemented with caffeine. The level of IL-6 was increased while the level of IL-10 was decreased in trained animals (HIIT) and caffeine was capable of preventing this exercise effect. Our findings suggest that caffeine ingestion attenuates, as least in part, the immune and inflammatory alterations following a prolonged HIIT protocol. [ABSTRACT FROM AUTHOR]

Purpose: The aim of the present study was to investigate the effect of exercise intensity on energy intake post-exercise and its relationship with enjoyment and rating of perceived exertion (RPE) generated by exercise.Methods: For this, nine sedentary overweight men performed high-intensity intermittent exercise and steady-state exercise, totaling 30 min for both exercise sessions, and energy intake post-exercise was evaluated. Rating of perceived exertion and enjoyment scores were also measured immediately post-exercise.Results: There was no difference in the amount of calories ingested post-exercise between conditions, enjoyment scores and RPE. There was a negative correlation between enjoyment and energy intake (r = − 0.552 [strong]; p = 0.018).Conclusions: These data demonstrated that independent of exercise intensity, enjoyment scores were related to post-exercise energy intake. [ABSTRACT FROM AUTHOR]

In this study, we evaluated the effects of high-intensity swimming in an experimental model of acute lung injury (ALI) induced by lipopolysaccharide (LPS) on lung inflammation and antioxidant defenses. Balb/C male mice were submitted to exercise (30 min/day, 5 days/week, for a period of 3 weeks) prior to LPS instillation in the lung. Twenty-four hours after delivery of LPS (10 μg/animal), mice were euthanized and bronchoalveolar fluid (BALF) was obtained for cell counting and analysis of cytokines by ELISA. Lung tissue was used to evaluate antioxidant defenses. LPS instillation resulted in an increase in total and mononuclear cells, IL-1β, TNF-α, and IL-6 in BALF. LPS instillation also altered IL-10 and IL-ra levels in BALF and induced antioxidant defenses (glutathione, superoxide dismutase, catalase, and glutathione peroxidase) in the lung. Protein carbonyl increased in the LPS-treated animals. High-intensity swimming prevented all these changes induced by LPS. Significance: Therefore, this experimental protocol of high-intensity swimming showed a protective effect on ALI, decreasing inflammatory processes and preventing disturbances in antioxidant defenses into the lungs. [ABSTRACT FROM AUTHOR]

High-intensity exercise/training, especially interval exercise/training, has gained popularity in recent years. Hypoxic training was introduced to elite athletes half a century ago and has recently been adopted by the general public. In the current review, we have summarised the molecular adaptive responses of skeletal muscle to high-intensity exercise/training, focusing on mitochondrial biogenesis, angiogenesis, and muscle fibre composition. The literature suggests that (peroxisome proliferator-activated receptor gamma coactivator 1-alpha) PGC-1α, vascular endothelial growth factor (VEGF), and hypoxia-inducible factor 1-alpha (HIF1-α) might be the main mediators of skeletal muscle adaptations to high-intensity exercises in hypoxia. Exercise is known to be anti-inflammatory, while the effects of hypoxia on inflammatory signalling are more complex. The anti-inflammatory effects of a single session of exercise might result from the release of anti-inflammatory myokines and other cytokines, as well as the downregulation of Toll-like receptor signalling, while training-induced anti-inflammatory effects may be due to reductions in abdominal and visceral fat (which are main sources of pro-inflammatory cytokines). Hypoxia can lead to inflammation, and inflammation can result in tissue hypoxia. However, the hypoxic factor HIF1-α is essential for preventing excessive inflammation. Disease-induced hypoxia is related to an upregulation of inflammatory signalling, but the effects of exercise-induced hypoxia on inflammation are less conclusive. The effects of high-intensity exercise under hypoxia on skeletal muscle molecular adaptations and inflammatory signalling have not been fully explored and are worth investigating in future studies. Understanding these effects will lead to a more comprehensive scientific basis for maximising the benefits of high-intensity exercise.

Nowadays, new types of vinegar have been developed using various raw materials and biotechnological processes. The fruit of Prunus mume has been extensively distributed in East Asia and used as a folk medication for fatigue. In this study, the Prunus mume vinegar (PV) was produced by a two-step fermentation and was evaluated for its anti-fatigue activity by C2C12 myoblasts and high-intensity exercised rats. The administration of PV significantly improved running endurance and glycogen accumulation in the liver and muscle of PV supplemented rats compared to sedentary and exercised control groups. In addition, PV supplementation elicited lower fatigue-related serum biomarkers, for instance, ammonia, inorganic phosphate, and lactate. PV administered rats exhibited higher lactate dehydrogenase activity and glutathione peroxidase activity, and lower creatine kinase activity and malondialdehyde levels. Furthermore, phenolic compounds in PV were identified using HPLC analysis. The phenolic acids analyzed in PV were protocatechuic acid, syringic acid, chlorogenic acid, and its derivates. These results indicate that the administration of PV with antioxidative property contributes to the improvement of fatigue recovery in exhausted rats. The findings of this study suggest that the PV containing various bioactive constituents can be used as a functional material against fatigue caused by high-intensity exercise.

Consumption of low-glycemic index (GI) carbohydrates (CHO) may be superior to high-GI CHO before exercise by increasing fat oxidation and decreasing carbohydrate oxidation. We compared the effects of pre-exercise feeding of a low-GI lentil-based sports nutrition bar with a high-GI bar on metabolism and performance during a simulated soccer match. Using a randomized, double-blind, counterbalanced, crossover design, participants (n = 8) consumed 1.5 g/kg available CHO from a low-GI bar (GI = 45) or high-GI bar (GI = 101) two hours before a 90 min simulated soccer match, and 0.38 g/kg body mass during a 15 min half-time break. The test involved alternating 6 min intervals of paced jogging, running, walking, and sprinting, and 3 min intervals of soccer-specific skills (timed ball dribbling, agility running, heading, kicking accuracy). Carbohydrate oxidation rate was lower during the match after consuming the low-GI compared to high-GI bar (2.17 ± 0.6 vs. 2.72 ± 0.4 g/min; p < 0.05). Participants performed better during the low-GI versus high-GI bar condition on the agility test (5.7 ± 0.4 versus 6.1 ± 0.6 s; p < 0.01) and heading (i.e., jumping height 24.7 ± 4.3 versus 22.2 ± 4.5 cm; p < 0.01) late in the soccer match (72 min). A low-GI lentil-based sports nutrition bar provides a metabolic benefit (lower carbohydrate oxidation rate) and a modest improvement in agility running and jumping height (heading) late in the test.