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High‐intensity intermittent exercise (HIIE) has become attractive for presenting a variety of exercise conditions. However, the effects of HIIE on renal function and hemodynamics remain unclear. This study aimed to compare the effects of HIIE and moderate‐intensity continuous exercise (MICE) on renal hemodynamics, renal function, and kidney injury biomarkers. Ten adult males participated in this study. We allowed the participants to perform HIIE or MICE to consider the impact of exercise on renal hemodynamics under both conditions. Renal hemodynamic assessment and blood sampling were conducted before the exercise (pre) and immediately (post 0), 30 min (post 30), and 60 min (post 60) after the exercise. Urine sampling was conducted in the pre, post 0, and post 60 phases. There was no condition‐by‐time interaction (p = 0.614), condition (p = 0.422), or time effect (p = 0.114) regarding renal blood flow. Creatinine‐corrected urinary neutrophil gelatinase‐associated lipocalin concentrations increased at post 60 (p = 0.017), but none exceeded the cut‐off values for defining kidney injury. Moreover, there were no significant changes in other kidney injury biomarkers at any point. These findings suggest that high‐intensity exercise can be performed without decreased RBF or increased kidney injury risk when conducted intermittently for short periods. Visual summary of the current study.

In cycling, critical power (CP) and work above CP (W’) can be estimated through linear and nonlinear models. Despite the concept of CP representing the upper boundary of sustainable exercise, overestimations may be made as the models possess inherent limitations and the protocol design is not always appropriate. To measure and compare CP and W’ through the exponential (CPexp), 3-parameter hyperbolic (CP3-hyp), 2-parameter hyperbolic (CP2-hyp), linear (CPlinear), and linear 1/time (CP1/time) models, using different combinations of TTE trials of different durations (approximately 1–20min). Repeated measures. Thirteen healthy young cyclists (26±3years; 69.0±9.2kg; 174±10cm; 60.4±5.9mLkg−1min−1) performed five TTE trials on separate days. CP and W’ were modeled using two, three, four, and/or five trials. All models were compared against a criterion method (CP3-hyp with five trials; confirmed using the leaving-one-out cross-validation analysis) using smallest worthwhile change (SWC) and concordance correlation coefficient (CCC) analyses. CP was considerably overestimated when only trials lasting less than 10min were included, independent of the mathematical model used. Following CCC analysis, a number of alternative methods were able to predict our criterion method with almost a perfect agreement. However, the application of other common approaches resulted in an overestimation of CP and underestimation of W’, typically these methods only included TTE trials lasting less than 12min. Estimations from CP3-hyp were found to be the most accurate, independently of TTE range. Models that include two trials between 12 and 20min provide good agreement with the criterion method (for both CP and W’).

Redox homeostasis and redox-sensitive protein signaling play a role in exercise-induced adaptation. The effects of sprint-interval exercise (SIE), high-intensity interval exercise (HIIE) and continuous moderate-intensity exercise (CMIE), on post-exercise plasma redox status are unclear. Furthermore, whether post-exercise plasma redox status reflects skeletal muscle redox-sensitive protein signaling is unknown. In a randomized crossover design, eight healthy adults performed a cycling session of HIIE (5×4min at 75% Wmax), SIE (4×30s Wingate’s), and CMIE work-matched to HIIE (30min at 50% of Wmax). Plasma hydrogen peroxide (H2O2), thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD) activity, and catalase activity were measured immediately post, 1h, 2h and 3h post-exercise. Plasma redox status biomarkers were correlated with phosphorylation of skeletal muscle p38-MAPK, JNK, NF-κB, and IκBα protein content immediately and 3h post-exercise. Plasma catalase activity was greater with SIE (56.6±3.8Uml−1) compared to CMIE (42.7±3.2, p<0.01) and HIIE (49.0±5.5, p=0.07). Peak plasma H2O2 was significantly (p<0.05) greater after SIE (4.6±0.6nmol/ml) and HIIE (4.1±0.4) compared to CMIE (3.3±0.5). Post-exercise plasma TBARS and SOD activity significantly (p<0.05) decreased irrespective of exercise protocol. A significant positive correlation was detected between plasma catalase activity and skeletal muscle p38-MAPK phosphorylation 3h post-exercise (r=0.40, p=0.04). No other correlations were detected (all p>0.05). Low-volume SIE elicited greater post-exercise plasma catalase activity compared to HIIE and CMIE, and greater H2O2 compared to CMIE. Plasma redox status did not, however, adequately reflect skeletal muscle redox-sensitive protein signaling.

This study aimed to examine whether a single bout each of high-intensity interval exercise (HIIE) and high-intensity continuous exercise (HICE) could improve inhibitory functions of overweight and obese children, and which mode of exercise was more beneficial. Seventy-two overweight and obese children, with (26.02 ± 1.05 kg/m2), aged 10–14 years (11.56 ± 1.03 years), were randomly assigned to three groups. The HIIE group completed a 30-min treadmill exercise session (5-min warm up, 20-min HIIE, and 5-min cool-down). The HICE group performed 30 min of rope skipping, while the control (CON) group watched a designated cartoon on a tablet computer for the same duration. Reaction time and number of errors in the Stroop test were determined before and after the intervention. The difference between pre- and post-test reaction time scores was higher in the HIIE and HICE groups than in the CON group, while the pre- and post-test difference in the number of errors was similar between groups. Overall, it is likely that both acute HIIE and HICE were similarly efficient in facilitating cognitive and inhibitory functions of children with overweight and obesity conditions, supporting the benefits of acute high-intensity exercise probability for cognitive functions of children in general, as well as of the population with overweight and obesity conditions.

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.

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.

The positive effects of physical exercise (EX) are well known to be mediated by cerebral BDNF (brain-derived neurotrophic factor), a neurotrophin involved in learning and memory, the expression of which could be induced by circulating irisin, a peptide derived from Fibronectin type III domain-containing protein 5 (FNDC5) produced by skeletal muscle contraction. While the influence of EX modalities on cerebral BDNF expression was characterized, their effect on muscle FNDC5/Irisin expression and circulating irisin levels remains to be explored. The present study involved Wistar rats divided into four experimental groups: sedentary (SED), low- (40% of maximal aerobic speed, MAS), intermediate- (50% of MAS) and high- (70% of MAS) intensities of treadmill EX (30 min/day, 7 days). Soleus (SOL) versus gastrocnemius (GAS) FNDC5 and hippocampal BDNF expressions were evaluated by Western blotting. Additionally, muscular FNDC5/Irisin localization and serum/hippocampal irisin levels were studied by immunofluorescence and ELISA, respectively. Our findings revealed that (1) serum irisin and hippocampal BDNF levels vary with EX intensity, showing a threshold intensity at 50% of MAS; (2) hippocampal BDNF levels positively correlate with serum irisin but not with hippocampal FNDC5/Irisin; and (3) GAS, in response to EX intensity, overexpresses FNDC5/Irisin in type II muscle fibers. Altogether, peripheral FNDC5/Irisin levels likely explain EX-dependent hippocampal BDNF expression.

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.

Type 2 diabetes (T2D) risk is lower in females than males. It has been reported that females have greater pancreatic 𝛽‐cell function than males, which may at least in part contribute to the T2D risk in females. 𝛽‐cell function is influenced by exercise training; however, previous trials comparing 𝛽‐cell function between the sexes have not included participants matched for training status. Furthermore, the acute effects of different modes of exercise on 𝛽‐cell function, and whether sex inherently influences these effects, are largely unexamined. Males and females (12/sex) completed a 120‐min oral glucose tolerance test (OGTT) at rest (CON) and following acute bouts of high‐intensity interval exercise (HIIE), moderate intensity continuous (MIC) exercise, and low‐load high‐repetition (LLHR) resistance exercise to assess whether sex inherently influences baseline and/or post‐exercise pancreatic function in the absence of pathology. We found no sex differences in basal pancreatic 𝛽‐cell function. Females had greater basal insulin clearance following MIC exercise compared to males (p = 0.01) and males tended to have a higher potentiation ratio following HIIE (p = 0.07). Females also had lower glucose sensitivity following MIC exercise compared to HIIE (p = 0.007) and LLHR (p = 0.003). Insulin clearance during the OGTT was greater following HIIE as compared with CON and MIC exercise (p = 0.02). 2‐H oral glucose insulin sensitivity was greater following LLHR compared to CON (p = 0.01). Acute bouts of different modes of exercise do not differentially influence 𝛽‐cell function but do influence insulin clearance and insulin sensitivity. Therefore, sex and exercise mode interact to differentially influence insulin clearance and glucose sensitivity. The findings of this study indicate that sex and exercise mode interact to differentially influence insulin clearance and glucose sensitivity. There were no sex differences in pancreatic function. However, exercise mode influenced insulin clearance and oral glucose insulin sensitivity. Furthermore, following an acute bout of moderate intensity continuous exercise, insulin clearance was greater in females than males. Additionally, in females only, glucose sensitivity and insulin clearance were higher following high intensity interval exercise compared with moderate intensity continuous exercise.

Abstract Objectives To compare 12 weeks of exercise training at two intensities on oxidative stress, antioxidants and inflammatory biomarkers in patients with type 2 diabetes (T2D). Design Randomized trial. Methods Thirty-six participants with T2D were randomized to complete either 12 weeks of treadmill based high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT), followed by 40 weeks of home-based training at the same intensities. Plasma inflammation, oxidative stress and antioxidant biomarkers (total F2-isoprostanes, protein carbonyls, total antioxidant capacity, glutathione peroxidase activity, interleukin-10, interleukin-6, interleukin-8 and TNF-α) were measured at baseline, 12-weeks and 1-year. Results There were no significant changes (p > 0.05) in oxidative stress and inflammation biomarkers from baseline to 12-weeks in either intervention. A decrease in total antioxidant capacity in the MICT group from baseline to 1-year by 0.05 mmol/L (p = 0.05) was observed. There was a significant difference (p < 0.05) when groups were separated by sex with females in the MICT group having a 22.1% (p < 0.05) decrease in protein carbonyls from baseline to 1-year. Conclusions HIIT and MICT had no acute effect on oxidative stress and inflammatory biomarkers in patients with T2D.