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Breaking up periods of sedentary time with brief bouts of high‐intensity interval exercise (HIIE) is suggested as a time‐efficient approach to improve exercise adherence and health. This randomized crossover clinical trial was designed to compare energy expenditure (EE), cardiometabolic, and perceptual responses during HIIE performed in a single session (1xHIIE) or split into three shorter sessions (3xHIIE) throughout the day. Fifteen male participants (48.5 ± 2.9 years) completed two experimental protocols: 1xHIIE protocol consisted of a single 21 min session, whereas the 3xHIIE protocol consisted of three shorter 7 min sessions separated by a 4 h interval between each session. Oxygen consumption (VO2), heart rate (HR), rate of perceived exertion (RPE), and blood lactate were measured during the experimental protocols. The 1xHIIE and 3x HIIE sessions induced similar EE (298.20 ± 51.74 and 299.32 ± 69.18 kcal, respectively; p = 0.88). However, postexercise EE following the 3xHIIE was approximately twice as high as the 1xHIIE (62.97 ± 14.97 vs. 27.42 ± 8.98 kcal, respectively; p < 0.001) or approximately 36 kcal higher. Additionally, compared to 1xHIIE, the 3x HIIE protocol induced lower HR (158 ± 12 and 147 ± 8 bpm, respectively; p = 0.018), rating perceived effort (15.8 ± 1.8 and 14.4 ± 1.7 respectively; p = 0.0012), and blood lactate (7.7 ± 3.7 and 5.4 ± 1.8 mmol/L, respectively; p = 0.013). These findings suggest that multiple brief sessions of HIIE throughout the day result in a greater energy expenditure with less perceived exertion than a single HIIE session in middle‐aged male individuals.

Menopause is associated with increased blood pressure (BP) and vasomotor symptoms (VMS), both elevating cardiovascular risk. Exercise can induce postexercise hypotension (PEH), with responses varying by exercise type and population characteristics. This study aimed to (1) examine the effect of high‐intensity interval exercise (HIIE) and isometric resistance exercise (IRE) compared to control session (CONT) on PEH in normotensive postmenopausal women and (2) examine the VMS effect on PEH responses. A cross‐over randomized controlled trial was conducted in 29 women (15 with moderate‐to‐severe VMS, 14 without), aged 55 ± 3 years. HIIE included 2 sets of 12*15‐s at 100% maximal aerobic power, IRE included 4*2‐min at 30% maximal voluntary contraction, and CONT included a sitting period. PEH was assessed 30 min post‐session and with 24‐h assessment, providing data on dipping profiles and BP variability. Repeated measures ANOVA with Bonferroni post hoc tests were conducted. HIIE induced systolic PEH at +30 min postexercise compared to pre‐exercise (−6.1 mmHg, p = 0.048) and CONT (−8.1 mmHg, p = 0.010). For IRE, nocturnal systolic (SBP) and diastolic (DBP) BP decreased versus CONT (SBP: −3.2 mmHg, p = 0.008; DBP: −2.0 mmHg, p = 0.003) and HIIE (SBP: −3.4 mmHg, p = 0.004; DBP: −2.2 mmHg, p < 0.001), increasing dippers proportion. In women with VMS, nocturnal SBP was lower after IRE than HIIE (−5.6 mmHg, p = 0.002). Both HIIE and IRE induced PEH in postmenopausal women, with HIIE reducing BP +30 min postexercise and IRE improving nocturnal BP and increasing dippers. In women with VMS, the nocturnal BP response varies according to exercise modality. Trial Registration The study is registered on clinicaltrials.gov (n°NCT06533982) Highlights High‐intensity interval exercise reduces systolic blood pressure 30 min postexercise in normotensive postmenopausal women. Isometric resistance exercise improves nocturnal blood pressure and increases the proportion of dippers. In women with vasomotor symptoms, the exercise modality influences nocturnal systolic blood pressure.

Long‐term, intense endurance exercise training can occasionally induce endothelial micro‐damage and cardiac fibrosis. The underlying mechanisms are incompletely understood. Twenty healthy, well‐trained male participants (10 runners and 10 cyclists) performed a strenuous high‐intensity interval training (HIIT) session matched by age, height, weight and maximal oxygen consumption. We assessed the acute exercise response of novel cardiac biomarkers of fibrosis [e.g., galectin‐3 (Gal‐3) and soluble suppression of tumorigenicity 2 (sST2)] per exercise modality and their relationship with haemodynamic contributors, such as preload, afterload and cardiac contractility index (CTi), in addition to endothelial damage by sustained activation and shedding of endothelial cells (ECs). Serum Gal‐3 and sST2 concentrations were investigated by enzyme‐linked immunosorbent assays; haemodynamics were analysed via impedance plethysmography and circulating ECs by flow cytometry. The Gal‐3 and sST2 concentrations and ECs were elevated after exercise (P < 0.001), without interaction between exercise modalities. Circulating Gal‐3 and sST2 concentrations both showed a positive relationship with ECs (rrm = 0.68, P = 0.001 and rrm = 0.57, P = 0.010, respectively, both n = 18). The EC association with Gal‐3 was significant only in cyclists, but equally strong for both modalities. Gal‐3 was also related to exercise‐induced CTi (rrm = 0.57, P = 0.011, n = 18). Cardiac wall stress is increased after an acute HIIT session but does not differ between exercise modalities. Exercise‐released Gal‐3 from cardiac macrophages could very probably drive systemic endothelial damage, based on an enhanced CTi. The importance of acute exercise‐induced vascular resistances and cardiac contractility for the release of fibrotic biomarkers and any long‐term pathological endothelial adaptation should be investigated further, also relative to the exercise modality. What is the central question of this study? Circulating biomarkers of cardiac wall stress and fibrosis are influenced by physical exercise. The underlying mechanisms per exercise modality are still unclear. What is the main finding and its importance? We show that galectin‐3 (Gal‐3) and soluble suppression of tumorigenicity 2 (sST2) are increased after acute exercise but do not differ between running and cycling. One haemodynamic contributor to the secretion of Gal‐3 is an enhanced cardiac contractility. Acute exercise‐released Gal‐3 and sST2 are linked to sustained endothelial activation and cell shedding. This could be relevant in the context of fibrosis development and could identify athletes at risk for pathological endothelial adaptations.

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.

High‐intensity interval (HII) exercise elicits distinct vascular responses compared to a matched dose of moderate intensity continuous (MOD) exercise. However, the acute effects of HII compared to MOD exercise on arterial stiffness are incompletely understood. Circulating microRNAs (ci‐miRs) may contribute to the vascular effects of exercise. We sought to determine exercise intensity‐dependent changes in ci‐miR potentially underlying changes in arterial stiffness. Ten young, healthy men underwent well‐matched, 30‐min HII and MOD exercise bouts. RT‐qPCR was used to determine the levels of seven vascular‐related ci‐miRs in serum obtained immediately before and after exercise. Arterial stiffness measures including carotid to femoral pulse wave velocity (cf‐PWV), carotid arterial compliance and β‐stiffness, and augmentation index (AIx and AIx75) were taken before, 10min after and 60min after exercise. Ci‐miR‐21‐5p, 126‐3p, 126‐5p, 150‐5p, 155‐5p, and 181b‐5p increased after HII exercise (p < .05), while ci‐miR‐150‐5p and 221‐3p increased after MOD exercise (p = .03 and 0.056). One hour after HII exercise, cf‐PWV trended toward being lower compared to baseline (p = .056) and was significantly lower compared to 60min after MOD exercise (p = .04). Carotid arterial compliance was increased 60min after HII exercise (p = .049) and was greater than 60min after MOD exercise (p = .02). AIx75 increased 10 min after both HII and MOD exercise (p < .05). There were significant correlations between some of the exercise‐induced changes in individual ci‐miRs and changes in cf‐PWV and AIx/AIx75. These results support the hypotheses that arterial stiffness and ci‐miRs are altered in an exercise intensity‐dependent manner, and ci‐miRs may contribute to changes in arterial stiffness. We identified a reduction in central artery stiffness and an increase in carotid arterial compliance one hour after acute high intensity interval (HII) cycling exercise, that was not seen after moderate intensity continuous cycling (MOD). HII and MOD elicited distinct increases in the concentrations of circulating microRNAs (ci‐miRs) with potential regulatory roles in arterial stiffness. Significant correlations between some of the changes in ci‐miRs and measures of arterial stiffness suggest potential mechanistic roles for ci‐miRs.

Athletes train to improve strength and endurance to demonstrate maximum performance during competitions. Training methods vary but most focus on strength, endurance, or both. Concurrent training is a combination of two different modes of training. In this study, we combined resistance exercise (RE) and high‐intensity interval exercise (HIIE) to investigate the influence of the order of the concurrent training on signal molecules on hypertrophy and glycolysis in the skeletal muscle. The phosphorylation levels of mechanistic target of rapamycin (mTOR) signals, p70 S6 kinase (p70S6 K), ribosomal protein S6 (S6), and glycogen synthase kinase beta (GSK‐3β) were significantly increased in the HIIE first group compared with the control group. The combined training course did not affect the glycogen content and expression levels of proteins concerning glycolytic and metabolic capacity, suggesting that a combination of HIIE and RE on the same day, with HIIE prior to RE, improves hypertrophy response and glycolysis enhancement. In this study, we performed concurrent training combining RE and HIIE and examined the expression dynamics of mTOR signaling and signaling molecules of glycolytic metabolism. As a result, it was suggested that the expression of the signaling molecules was enhanced by resistance exercise first in order to increase the effect of both exercises.

Abstract Aims High-intensity interval training (HIIT) improves peak oxygen uptake and left ventricular diastology in patients with heart failure with preserved ejection fraction (HFpEF). However, its effects on myocardial strain in HFpEF remain unknown. We explored the effects of HIIT and moderate-intensity aerobic continuous training (MI-ACT) on left and right ventricular strain parameters in patients with HFpEF. Furthermore, we explored their relationship with peak oxygen uptake (VO2peak). Methods and results Fifteen patients with HFpEF (age = 70 ± 8.3 years) were randomized to either: (i) HIIT (4 × 4 min, 85–90% peak heart rate, interspersed with 3 min of active recovery; n = 9) or (ii) MI-ACT (30 min at 70% peak heart rate; n = 6). Patients were trained 3 days/week for 4 weeks and underwent VO2peak testing and 2D echocardiography at baseline and after completion of the 12 sessions of supervised exercise training. Left ventricular (LV) and right ventricular (RV) average global peak systolic longitudinal strain (GLS) and peak systolic longitudinal strain rate (GSR) were quantified. Paired t-tests were used to examine within-group differences and unpaired t-tests used for between-group differences (α = 0.05). Right ventricular average global peak systolic longitudinal strain improved significantly in the HIIT group after training (pre = −18.4 ± 3.2%, post = −21.4 ± 1.7%; P = 0.02) while RV-GSR, LV-GLS, and LV-GSR did not (P > 0.2). No significant improvements were observed following MI-ACT. No significant between-group differences were observed for any strain measure. ΔLV-GLS and ΔRV-GLS were modestly correlated with ΔVO2peak (r = −0.48 and r = −0.45; P = 0.1, respectively). Conclusions In patients with HFpEF, 4 weeks of HIIT significantly improved RV-GLS.

The purpose of this study was to test the hypothesis that high‐intensity interval exercise (HIE) significantly increases growth hormone (GH) secretion to a greater extent than moderate‐intensity continuous exercise (MOD) in young women. Five young, sedentary women (mean ± SD; age: 22.6±1.3 years; BMI: 27.4±3.1 kg/m2) were tested during the early follicular phase of their menstrual cycle on three occasions. For each visit, participants reported to the laboratory at 1700 h, exercised from 1730–1800 h, and remained in the laboratory until 0700 h the following morning. The exercise component consisted of either 30‐min of moderate‐intensity continuous cycling at 50% of measured peak power (MOD), four 30‐s “all‐out” sprints with 4.5 min of active recovery (HIE), or a time‐matched sedentary control using a randomized, cross‐over design. The overnight GH secretory profile of each trial was determined from 10‐min sampling of venous blood from 1730–0600 h, using deconvolution analysis. Deconvolution GH parameters were log transformed prior to statistical analyses. Calculated GH AUC (0–120 min) was significantly greater in HIE than CON (P = 0.04), but HIE was not different from MOD. Total GH secretory rate (ng/mL/12.5 h) was significantly greater in the HIE than the CON (P = 0.05), but MOD was not different from CON or HIE. Nocturnal GH secretion (ng/mL/7.5 h) was not different between the three trials. For these women, in this pilot study, a single bout of HIE was sufficient to increase 12.5 h pulsatile GH secretion. It remains to be determined if regular HIE may contribute to increased daily GH secretion. Growth hormone (GH) is a potent lipolytic hormone that is secreted primarily at night and in a dose‐dependent response to exercise. We aimed to determine if high‐intensity interval exercise increased both total and overnight GH secretion compared to moderate‐ intensity exercise or no exercise. It was determined that an acute bout of high‐intensity interval exercise increases GH secretion compared to no exercise, but it was not different from moderate‐intensity exercise.

Background Rheumatoid arthritis (RA) is a chronic inflammatory disease in which adults have significant joint issues leading to poor health. Poor health is compounded by many factors, including exercise avoidance and increased risk of opportunistic infection. Exercise training can improve the health of patients with RA and potentially improve immune function; however, information on the effects of high-intensity interval training (HIIT) in RA is limited. We sought to determine whether 10 weeks of a walking-based HIIT program would be associated with health improvements as measured by disease activity and aerobic fitness. Further, we assessed whether HIIT was associated with improved immune function, specifically antimicrobial/bacterial functions of neutrophils and monocytes. Methods Twelve physically inactive adults aged 64 ± 7 years with either seropositive or radiographically proven (bone erosions) RA completed 10 weeks of high-intensity interval walking. Training consisted of 3 × 30-minute sessions/week of ten ≥ 60-second intervals of high intensity (80–90% VO 2reserve ) separated by similar bouts of lower-intensity intervals (50–60% VO 2reserve ). Pre- and postintervention assessments included aerobic and physical function; disease activity as measured by Disease Activity score in 28 joints (DAS28), self-perceived health, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR); plasma interleukin (IL)-1β, IL-6, chemokine (C-X-C motif) ligand (CXCL)-8, IL-10, and tumor necrosis factor (TNF)-α concentrations; and neutrophil and monocyte phenotypes and functions. Results Despite minimal body composition change, cardiorespiratory fitness increased by 9% (change in both relative and absolute aerobic capacity; p  < 0.001), and resting blood pressure and heart rate were both reduced (both p  < 0.05). Postintervention disease activity was reduced by 38% (DAS28; p  = 0.001) with significant reductions in ESR and swollen joints as well as improved self-perceived health. Neutrophil migration toward CXCL-8 ( p  = 0.003), phagocytosis of Escherichia coli ( p  = 0.03), and ROS production ( p  < 0.001) all increased following training. The frequency of cluster of differentiation 14-positive (CD14 + )/CD16 + monocytes was reduced ( p  = 0.002), with both nonclassical (CD14 dim /CD16 bright ) and intermediate (CD14 bright /CD16 positive ) monocytes being reduced (both p  < 0.05). Following training, the cell surface expression of intermediate monocyte Toll-like receptor 2 (TLR2), TLR4, and HLA-DR was reduced (all p  < 0.05), and monocyte phagocytosis of E. coli increased ( p  = 0.02). No changes were observed for inflammatory markers IL-1β, IL-6, CXCL-8, IL-10, CRP, or TNF-α. Conclusions We report for the first time, to our knowledge, that a high-intensity interval walking protocol in older adults with stable RA is associated with reduced disease activity, improved cardiovascular fitness, and improved innate immune functions, indicative of reduced infection risk and inflammatory potential. Importantly, the exercise program was well tolerated by these patients. Trial registration ClinicalTrials.gov, NCT02528344 . Registered on 19 August 2015.

A single bout of exercise can result in inflammatory responses, increased oxidative stress and upregulation of enzymatic antioxidant mechanisms. Although low-volume high-intensity interval training (HIIT) has become popular, its acute responses on the above mechanisms have not been adequately studied. The present study evaluated the effects of HIIT on hematological profile and redox status compared with those following traditional continuous aerobic exercise (CET). Twelve healthy young men participated in a randomized crossover design under HIIT and CET. In HIIT session, participants performed four 30-sec sprints on a cycle-ergometer with 4 min of recovery against a resistance of 0.375 kg/kg of body mass. CET consisted of 30-min cycling on a cycle-ergometer at 70% of their VO . Blood was drawn at baseline, immediately post, 24h, 48h and 72h post-exercise and was analyzed for complete blood count and redox status (thiobarbituric acid reactive substances, [TBARS]; protein carbonyls, [PC]; total antioxidant capacity, [TAC]; catalase and uric acid). White blood cells (WBC) increased after both exercise protocols immediately post-exercise (HIIT: 50% and CET: 31%, respectively). HIIT increased (+22%) PC post-exercise compared to baseline and CET (p < 0.05). HIIT increased TAC immediately post-exercise (16%) and at 24h post-exercise (11%, p < 0.05), while CET increased TAC only post-exercise (12%, p < 0.05) compared to baseline, and TAC was higher following HIIT compared to CET (p < 0.05). Both HIIT and CET increased uric acid immediately post- (21% and 5%, respectively, p < 0.05) and 24h (27% and 5%, respectively, p < 0.05) post-exercise and the rise was greater following HIIT (p < 0.05). There were no significant changes (p > 0.05) for TBARS and catalase following either exercise protocol. Low-volume HIIT is associated with a greater acute phase leukocyte count and redox response than low-volume CET, and this should be considered when an exercise training program is developed and complete blood count is performed for health purposes.