Weeks Of Sprint Interval Training Research Articles

Vascular adaptations following an eight-week sprint interval training intervention in healthy men.

Sprint interval training (SIT) has been shown to improve many indices of cardiovascular risk. The effect of SIT on emerging indicators of cardiovascular health, including arterial stiffness and carotid intima media thickness, remains unclear. Thus, the purpose of this study was to assess changes in augmentation index at 75 beats per minute (AIx@75), pulse wave velocity (cfPWV), and carotid intima media thickness (CIMT) at three time points of an 8-week SIT intervention. Eighteen sedentary men (age: 24.7±5.1 years, BMI: 26.7±5.8 kg/m2) participated in the study. Subjects trained 3 times a week for 8 weeks. Training consisted of 3-6 consecutive 30-second bouts of maximal intensity cycling, with 4.5 minutes of active recovery between bouts. Baseline, 4-week, and 8-week vascular assessments were performed. Training effects were analyzed using repeated measures ANOVA. Pearson correlations were used to determine the relationship between baseline values and the change scores (baseline to 8 weeks) of each vascular measure. AIx@75 (BL: -3.6±10.9%, 4W: -5.6±8.3%, 8W: -3.2±9.5%), cfPWV (BL: 5.6±1.0 m/s, 4W: 5.8±0.9 m/s, 8W: 5.6±0.7 m/s), and CIMT (BL: 0.51±0.08 mm, 4W: 0.52±0.08 mm, 8W: 0.51±0.08 mm) did not significantly change (all P>0.05). Baseline cfPWV and AIx@75 were negatively correlated to their change from baseline to 8 weeks (P<0.05). These findings demonstrate that 8 weeks of SIT is an insufficient stimulus to reduce cfPWV, AIx@75, or CIMT in a group of young, healthy men. Baseline arterial stiffness may modulate vascular adaptations to SIT.

Training for Recovery: Impact of Sprint Interval Training on Recovery Dynamics and Aerobic Performance in Kickboxing Athletes

Abstract Purpose Recovery within and between rounds is crucial to combat sports performance. We sought to determine whether sprint interval training (SIT) improves recovery dynamics and aerobic performance. Methods Eleven male kickboxing athletes (26 ± 5 years; body mass index 25 ± 3 kg/m2) were recruited. Participants were tested three times for VO2peak/time to exhaustion and critical power; baseline, 3 weeks control, 3 weeks of SIT (8 × 10 s lower body sprints followed by a maximum of 10 min recovery before completing 8 × 10 s upper body sprints). During SIT session 1 and 9 continuous gas analysis was performed. Results There was a significant reduction in recovery time between lower and upper body sprints with training (session 1: 441 ± 150 s; session 9: 268 ± 10 s; P &lt; 0.01; d = 2.77) and change in oxygen off-kinetics amplitude (session1: 3.0 ± 0.7 L/min, session 9: 3.6 ± 1.0 L/min; P &lt; 0.05; d = − 1.77), VO2 end (session 1: 0.59 ± 0.19 L/min, session 9: 0.81 ± 0.21 L/min; P &lt; 0.05, d = − 0.90), time constant (session 1: 81 ± 21 s; session 9: 60 ± 11 s; P &lt; 0.05; d = 1.03). Following training there was a significant improvement in critical power (P &lt; 0.05; η2p = 0.72) time to exhaustion (P &lt; 0.05; η2p = 0.30) but not VO2peak (P &gt; 0.05). Conclusion SIT improves recovery time associated and aerobic performance associated with improved oxygen off-kinetics. Therefore, training needs to focus on improving oxygen off-kinetics to enhance combat performance.

Five Weeks of Sprint Interval Training Improve Muscle Glycolytic Content and Activity But Not Time to Task Failure in Severe-Intensity Exercise.

This study examined the impact of a 5-wk sprint interval training (SIT) intervention on time to task failure (TTF) during severe-intensity constant work rate (CWR) exercise, as well as in glycolytic enzymatic content and activity, and glycogen content. Fourteen active males were randomized into either a SIT group ( n = 8) composed of 15 SIT sessions over 5 wk, or a control group ( n = 6). At pretraining period, participants performed i) ramp incremental test to measure the cardiorespiratory function; ii) CWR cycling TTF at 150% of the power output (PO) at the respiratory compensation point (RCP-PO) with muscle biopsies at rest and immediately following task failure. After 5 wk, the same evaluations were repeated (i.e., exercise intensities matched to current training status), and an additional cycling CWR matched to pretraining 150% RCP-PO was performed only for TTF evaluation. The content and enzymatic activity of glycogen phosphorylase (GPhos), hexokinase (HK), phosphofructokinase (PFK), and lactate dehydrogenase (LDH), as well as the glycogen content, were analyzed. Content of monocarboxylate transporter isoform 4 (MCT4) and muscle buffering capacity were also measured. Despite improvements in total work performed at CWR posttraining, no differences were observed for TTF. The GPhos, HK, PFK, and LDH content and activity, and glycogen content also improved after training only in the SIT group. Furthermore, the MCT4 concentrations and muscle buffering capacity were also improved only for the SIT group. However, no difference in glycogen depletion was observed between groups and time. Five weeks of SIT improved the glycolytic pathway parameters and total work performed; however, glycogen depletion was not altered during CWR severe-intensity exercise, and TTF remained similar.

Biological sex does not influence the peak cardiac output response to twelve weeks of sprint interval training

Sprint interval training (SIT) increases peak oxygen uptake (V̇O2peak) but the mechanistic basis is unclear. We have reported that 12 wk of SIT increased V̇O2peak and peak cardiac output (Q̇peak) and the changes in these variables were correlated. An exploratory analysis suggested that Q̇peak increased in males but not females. The present study incorporated best practices to examine the potential influence of biological sex on the Q̇peak response to SIT. Male and female participants (n = 10 each; 21 ± 4 y) performed 33 ± 2 sessions of SIT over 12 wk. Each 10-min session involved 3 × 20-s ‘all-out’ sprints on an ergometer. V̇O2peak increased after SIT (3.16 ± 1.0 vs. 2.89 ± 1.0 L/min, η2p = 0.53, p < 0.001) with no sex × time interaction (p = 0.61). Q̇peak was unchanged after training (15.2 ± 3.3 vs. 15.1 ± 3.0 L/min, p = 0.85), in contrast to our previous study. The peak estimated arteriovenous oxygen difference increased after training (204 ± 30 vs. 187 ± 36 ml/L, p = 0.006). There was no effect of training or sex on measures of endothelial function. We conclude that 12 wk of SIT increases V̇O2peak but the mechanistic basis remains unclear. The capacity of inert gas rebreathing to assess changes in Q̇peak may be limited and invasive studies that use more direct measures are needed.

Three-week sprint interval training (SIT) reduces cell-free DNA and low-frequency fatigue but does not induce VO2max improvement in older men.

This study aimed to investigate the impact of sprint interval training (SIT) on both the acute and 3-week modulations of cell-free DNA (cfDNA), as well as its association with neuromuscular fatigue and physical performance in healthy young and old men. Ten young (20-25year old) and nine elderly (63-72year old) healthy men performed nine SIT sessions consisting of 4-to-6-all-out cycling repetitions of 30s interspaced with 4-min rest intervals. We compared the maximal voluntary contractions torque, central activation ratio, low-frequency fatigue (LFF), and cfDNA concentrations between the groups before, immediately after, 1h after, and 24h after the first and ninth SIT sessions. The plasma cfDNA levels were increased post-exercise (from 1.4 ± 0.258 to 1.91 ± 0.278ng/ml (P < 0.01) on a log10 scale), without significant differences between the groups. However, older individuals showed a slight decrease in the baseline cfDNA values, from 1.39 ± 0.176 to 1.29 ± 0.085ng/ml on a log10 scale, after 3weeks (P = 0.043). Importantly, the elevation of the post-exercise cfDNA values was correlated with an increase in LFF in both groups. Three weeks of SIT induced an improvement in the recovery of LFF (main session effect, P = 0.0029); however, only the young group showed an increase in aerobic capacity (VO2max) (from 40.8 ± 6.74 to 43.0 ± 5.80ml/kg/min, P = 0.0039). Three weeks of SIT diminished the baseline cfDNA values in the old group, together with an improvement in the recovery of LFF. However, VO2max was increased only in the young group.

Effect of sprint interval training load on maximal oxygen uptake in trained men.

Sprint interval training (SIT) improves maximal aerobic and anaerobic performance, including oxygen uptake (VO2<inf>max</inf>), power output, and sprint performance. This study aimed to investigate the effect of SIT load on V̇O<inf>2max</inf> in trained subjects. SIT was performed twice a week for three weeks by twenty-four trained men (aged: 20.7±2.7, V̇O<inf>2max</inf> 43.6±6.5) and consisted of seven bouts of 10-s cycling sprints followed by a 4-min rest. Subjects were divided into two groups depending on the relative resistance of the load compared to their body mass (BM): 7.5% (S7.5) and 10% (S10). We measured the peak power, mean power, and peak cadence in SIT during the first and final sessions. V̇O<inf>2max</inf>, maximum aerobic power (MAP), heart rate, and lactate (La) concentration were measured before and after SIT using incremental tests. After 3 weeks of SIT, V̇O<inf>2max</inf>, MAP, and La improved significantly in both S7.5 and S10 groups. In addition, changes in V̇O<inf>2max</inf> in S10 were higher than those in S7.5 (2.2±11.2% vs. 9.23±9.57%, P=0.029, adjusted by pre V̇O<inf>2max</inf>). MAP measurements showed the same results (2.2±11.3% vs. 8.3±10.0%, P=0.015, adjusted by pre-MAP). However, there was no significant interaction between time and group. A significant increase in peak cadence from first session to sixth sessions was observed in S7.5 (P=0.01, ES = 0.93, 95% confidence interval [CI]: 0.02-1.78) but not in S10 (P=0.132, ES = 0.22, 95% [CI]: -0.59-1.01). Our results suggest that 3 weeks of SIT improves endurance performance in trained subjects. It seems that SIT at 10% load may tend to be more effective.

Changes in power-force-velocity profile induced by 2 weeks of sprint interval training.

This study aimed to determine the effects of a running sprint interval training protocol (R-SIT) on the sprint acceleration mechanical properties and jump performance. Eleven young male basketball players performed 6 R-SIT sessions for 2 weeks. Each session consisted of 30-second running bouts repeated 4 to 7 times interspersed by 4 minutes of recovery. Performance was assessed from the individual power-force-velocity profiles (PVFP) over a 20-m sprint and from a countermovement jump at baseline (PRE) and after two weeks of training (POST). Sprint time decreased by 2% over the first 5 and 10 meters (P<0.01) while no significant changes in the time at 20 meters (-0.8%, P=0.09) nor in maximal velocity (-1%, P=0.31) were detected. The average PFVP showed an increase in theoretical maximal force and power output of 5 and 4%, respectively (P<0.05), with no change in theoretical maximal speed (P=0.26). Jump height and power also increased after training (5 and 3% respectively, P<0.01). Players improved their maximal sprint distance covered during the 30-second bouts and became more fatigue-resistant to long sprint events. Six sessions of R-SIT helped to enhance short sprint times, acceleration and power output.

Aerobically trained older adults show impaired resting, but preserved exercise-induced circulating progenitor cell count, which was not improved by sprint interval training

Older adults exhibit a reduced number and function of CD34 + circulating progenitor cells (CPC), a known risk factor for cardiovascular disease. Exercise promotes the mobilisation of CPCs from bone marrow, so whether ageing per se or physical inactivity in older age reduces CPCs is unknown. Thus, this study examined the effect of age on resting and exercise-induced changes in CPCs in aerobically trained adults and the effect of 8 weeks of sprint interval training (SIT) on resting and exercise-induced CPCs in older adults. Twelve young (22–34 years) and nine older (63–70 years) adults participated in the study. Blood was sampled pre and immediately post a graded exercise test to exhaustion in both groups. Older participants repeated the process after 8 weeks of SIT (3 × 20 s ‘all-out’ sprints, 2 × a week). Total CPCs (CD34+) and endothelial progenitor cells (EPCs: CD34+KDR+) were determined by flow cytometry. Older adults exhibited lower basal total CD34+ CPCs (828 ± 314 vs. 1186 ± 272 cells·mL−1, p = 0.0149) and CD34+KDR+ EPCs (177 ± 128 vs. 335 ± 92 cells·mL−1, p = 0.007) than younger adults. The maximal exercise test increased CPCs in young (CD34+: p = 0.004; CD34+KDR+: p = 0.017) and older adults (CD34+: p < 0.001; CD34+KDR+: p = 0.008), without difference between groups (p = 0.211). SIT did not alter resting or exercise-induced changes in CPCs in the older cohort (p > 0.232). This study suggests age per se does not impair exercise-induced CPC counts, but does lower resting CPC counts.

Targeted Lipidomics and Inflammation Response to Six Weeks of Sprint Interval Training in Male Adolescents.

Lipids play an important role in coordinating and regulating metabolic and inflammatory processes. Sprint interval training (SIT) is widely used to improve sports performance and health outcomes, but the current understanding of SIT-induced lipid metabolism and the corresponding systemic inflammatory status modification remains controversial and limited, especially in male adolescents. To answer these questions, twelve untrained male adolescents were recruited and underwent 6 weeks of SIT. The pre- and post-training testing included analyses of peak oxygen consumption (VO2peak), biometric data (weight and body composition), serum biochemical parameters (fasting blood glucose, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triacylglycerol, testosterone, and cortisol), inflammatory markers, and targeted lipidomics. After the 6-week SIT, the serum C-reactive protein (CRP), interleukin (IL)-1β, IL-2, IL-4, IL-10, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β significantly decreased (p < 0.05), whereas IL-6 and IL-10/TNF-α significantly increased (p < 0.05). In addition, the targeted lipidomics revealed changes in 296 lipids, of which 33 changed significantly (p < 0.05, fold change > 1.2 or <1/1.2). The correlation analysis revealed that the changes in the inflammatory markers were closely correlated with the changes in some of the lipids, such as LPC, HexCer, and FFA. In conclusion, the 6-week SIT induced significant changes in the inflammatory markers and circulating lipid composition, offering health benefits to the population.

Exploring interindividual differences in fasting and postprandial insulin sensitivity adaptations in response to sprint interval exercise training

ABSTRACT Previous studies have concluded that wide variance in changes in insulin sensitivity markers following exercise training demonstrates heterogeneity in individual trainability. However, these studies frequently don’t account for technical, biological, and random within-subject measurement error. We used the standard deviation of individual responses (SDIR) to determine whether interindividual variability in trainability exists for fasting and postprandial insulin sensitivity outcomes following low-volume sprint interval training (SIT). We pooled data from 63 untrained participants who completed 6 weeks of SIT (n = 49; VO2max: 35 (7) mL⋅kg−1⋅min−1) or acted as no-intervention controls (n = 14; VO2max: 34 (6) mL⋅kg−1⋅min−1). Fasting and oral glucose tolerance test (OGTT)-derived measures of insulin sensitivity were measured pre- and post-intervention. SDIR values were positive and exceeded a small effect size threshold for changes in fasting glucose (SDIR = 0.27 [95%CI 0.07,0.38] mmol⋅L−1), 2-h OGTT glucose (SDIR = 0.89 [0.22,1.23] mmol⋅L−1), glucose area-under-the-curve (SDIR = 66.4 [−81.5,124.3] mmol⋅L−1⋅120min−1) and The Cederholm Index (SDIR = 7.2 [−16.0,19.0] mg⋅l2⋅mmol−1⋅mU−1⋅min−1), suggesting meaningful individual responses to SIT, whilst SDIR values were negative for fasting insulin, fasting insulin resistance and insulin AUC. For all variables, the 95% CIs were wide and/or crossed zero, highlighting uncertainty about the existence of true interindividual differences in exercise trainability. Only 2–22% of participants could be classified as responders or non-responders with more than 95% certainty. Our findings demonstrate it cannot be assumed that variation in changes in insulin sensitivity following SIT is attributable to inherent differences in trainability, and reiterate the importance of accounting for technical, biological, and random error when examining heterogeneity in health-related training adaptations. Highlights This study tested whether true interindividual variability exists for changes in insulin sensitivity and glyceamic control following 6-weeks of low volume sprint interval training (SIT). The high level of technical, biological, and random error associated with repeated measurements of insulin sensitivity and glycaemic control, means we can neither confidently conclude that there is evidence of true interindividual differences in the trainability of these outcomes following SIT, nor confidently identify responders or non-responders for such parameters. Researchers contrasting responders vs. non-responders for a given parameter, either to understand mechanisms of adaptation and/or develop physiological/genetic/epigenetic predictors of response, need to be aware that identification of responders and non-responders with sufficient certainty may not be achievable for parameters with a high level of technical, biological, and random error.

EFFECT OF DIFFERENT INTERVAL SPEED TRAINING ON ATHLETE REACTION

ABSTRACT Introduction: High-intensity Intermittent Training (HIIT) ranked first in the ACSM “2013 Global Training Methodology Survey”. Objective: To explore the influence of different speed training intervals on athlete reaction speed. Methods: Sixteen male bicycle athletes were randomly divided into two groups. The two groups then completed a six-week training routine (NT). The two groups then completed a six-week training routine , started 6 weeks of Sprint Interval Training (SIT) (a total of 12 lessons), with SIT instead of Normal Training (NT) live endurance training, and another training remains unchanged. Results: After 6 weeks of NT, Pmax GXT in the CG and DG groups decreased by 0.7% and 1.7%, respectively,as compared to the pre-training numbers. The difference was not statistically significant (P&gt;0.05). And after 6 weeks of SIT, Pmax GXT increased significantly (P&lt;0.05) in both experimental groupss,with increases of 9.2% and 10.2% for the CG and DG groups, respectively. Conclusions: The results show that intermittent training can effectively improve the aerobic metabolism of short-haul cyclists. As the power bicycle load and the training intensity and volume of the deceleration intermittent training program increase, the more significant the changes in aerobic capacity that can result in adaptability. Level of evidence II; Therapeutic studies - investigation of treatment results.

Subcutaneous adipose tissue sclerostin is reduced and Wnt signaling is enhanced following 4-weeks of sprint interval training in young men with obesity.

Sclerostin is a Wnt/β‐catenin antagonist, mainly secreted by osteocytes, and most known for its role in reducing bone formation. Studies in rodents suggest sclerostin can also regulate adipose tissue mass and metabolism, representing bone–adipose tissue crosstalk. Exercise training has been shown to reduce plasma sclerostin levels; but the effects of exercise on sclerostin and Wnt/β‐catenin signaling specifically within adipose tissue has yet to be examined. The purpose of this study was to examine subcutaneous WAT (scWAT) sclerostin content and Wnt signaling in response to exercise training in young men with obesity. To this end, 7 male participants (BMI = 35 ± 4; 25 ± 4 years) underwent 4 weeks of sprint interval training (SIT) involving 4 weekly sessions consisting of a 5‐min warmup, followed by 8 × 20 s intervals at 170% of work rate at VO2peak, separated by 10 s of rest. Serum and scWAT were sampled at rest both pre‐ and post‐SIT. Despite no changes in serum sclerostin levels, we found a significant decrease in adipose sclerostin content (−37%, p = 0.04), an increase in total β‐catenin (+52%, p = 0.03), and no changes in GSK3β serine 9 phosphorylation. There were also concomitant reductions in serum TNF‐α (−0.36 pg/ml, p = 0.03) and IL‐6 (−1.44 pg/ml, p = 0.05) as well as an increase in VO2peak (+5%, p = 0.03) and scWAT COXIV protein content (+95%, p = 0.04). In conclusion, scWAT sclerostin content was reduced and β‐catenin content was increased following SIT in young men with excess adiposity, suggesting a role of sclerostin in regulating human adipose tissue in response to exercise training.

Improvements in Maximal Oxygen Uptake After Sprint-Interval Training Coincide with Increases in Central Hemodynamic Factors.

Sprint-interval training has been shown to improve maximal oxygen uptake, in part through peripheral muscle adaptations that increase oxygen utilization. In contrast, the adaptations of central hemodynamic factors in this context remain unexplored. The aim of the current study was to explore the effects of sprint-interval training on maximal oxygen uptake and central hemodynamic factors. Healthy men and women (n = 29; mean age, 27 ± 5 yr; height, 175 ± 8 cm; body mass, 72.5 ± 12.0 kg) performed 6 wk of sprint-interval training consisting of three weekly sessions of 10-min low-intensity cycling interspersed with 3 × 30-s all-out sprints. Maximal oxygen uptake, total blood volume, and maximal cardiac output were measured before and after the intervention. Maximal oxygen uptake increased by 10.3% (P < 0.001). Simultaneously, plasma volume, blood volume, total hemoglobin mass, and cardiac output increased by 8.1% (276 ± 234 mL; P < 0.001), 6.8% (382 ± 325 mL; P < 0.001), 5.7% (42 ± 41 g; P < 0.001), and 8.5% (1.0 ± 0.9 L·min-1; P < 0.001), respectively. Increased total hemoglobin mass along with measures of body surface area had a significant impact on the improvements in maximal oxygen uptake. Six weeks of sprint-interval training results in significant increases in hemoglobin mass, blood volume, and cardiac output. Because these changes were associated with marked improvements in maximal oxygen uptake, we conclude that central hemodynamic adaptations contribute to the improvement in maximal oxygen uptake during sprint-interval training.

Acetylsalicylic acid-induced alterations in male reproductive parameters in Wistar rats and the effect of sprint interval training.

The present study investigated the effect of a 5-week ASA treatment on male reproductive parameters in Wistar rats; moreover, the potential benefits of a 4-week sprint interval training (SIT) on these measures following ASA treatment were investigated. A total of 25 male rats were obtained and randomly assigned to the control group (C, n=10) and the ASA treatment group (EP, n=15). After 5weeks, five rats from each group were killed and the effect of ASA treatment on the reproductive parameters was assessed. Then, the ASA treatment terminated and the remaining 10 ASA-treated rats were divided into the non-treatment group (NT, n=5) and the exercise training group (ET, n=5), which performed SIT 3 sessions/week for 4weeks. Five weeks of ASA treatment resulted in a statistically significant decrease in serum testosterone level, Leydig cell number, sperm count, sperm motility, sperm viability, TDI, SI and RI, and it resulted in a significant increase in sperm nucleus maturity and sperm DNA fragmentation (p˂0.05). Furthermore, 4weeks of SIT reversed all the ASA-induced changes in male reproductive parameters (p<0.05), but not the number of seminiferous tubules and the sperm motility (p>0.05). A subchronic dose of ASA could lead to adverse alterations in male reproductive parameters and SIT is beneficial in reversing those alterations.

Vitamin C and E Treatment Blocks Changes in Kynurenine Metabolism Triggered by Three Weeks of Sprint Interval Training in Recreationally Active Elderly Humans.

The kynurenine pathway (KP) is gaining attention in several clinical fields. Recent studies show that physical exercise offers a therapeutic way to improve ratios of neurotoxic to neuroprotective KP metabolites. Antioxidant supplementation can blunt beneficial responses to physical exercise. We here studied the effects of endurance training in the form of sprint interval training (SIT; three sessions of 4–6 × 30 s cycling sprints per week for three weeks) in elderly (~65 years) men exposed to either placebo (n = 9) or the antioxidants vitamin C (1 g/day) and E (235 mg/day) (n = 11). Blood samples and muscle biopsies were taken under resting conditions in association with the first (untrained state) and last (trained state) SIT sessions. In the placebo group, the blood plasma level of the neurotoxic quinolinic acid was lower (~30%) and the neuroprotective kynurenic acid to quinolinic acid ratio was higher (~50%) in the trained than in the untrained state. Moreover, muscle biopsies showed a training-induced increase in kynurenine aminotransferase (KAT) III in the placebo group. All these training effects were absent in the vitamin-treated group. In conclusion, KP metabolism was shifted towards neuroprotection after three weeks of SIT in elderly men and this shift was blocked by antioxidant treatment.

Neuromuscular Adjustments Following Sprint Training with Ischemic Preconditioning in Endurance Athletes: Preliminary Data.

This preliminary study examined the effect of chronic ischemic preconditioning (IPC) on neuromuscular responses to high-intensity exercise. In a parallel-group design, twelve endurance-trained males (VO2max 60.0 ± 9.1 mL·kg−1·min−1) performed a 30-s Wingate test before, during, and after 4 weeks of sprint-interval training. Training consisted of bi-weekly sessions of 4 to 7 supra-maximal all-out 30-s cycling bouts with 4.5 min of recovery, preceded by either IPC (3 × 5-min of compression at 220 mmHg/5-min reperfusion, IPC, n = 6) or placebo compressions (20 mmHg, PLA, n = 6). Mechanical indices and the root mean square and mean power frequency of the electromyographic signal from three lower-limb muscles were continuously measured during the Wingate tests. Data were averaged over six 5-s intervals and analyzed with Cohen’s effect sizes. Changes in peak power output were not different between groups. However, from mid- to post-training, IPC improved power output more than PLA in the 20 to 25-s interval (7.6 ± 10.0%, ES 0.51) and the 25 to 30-s interval (8.8 ± 11.2%, ES 0.58), as well as the fatigue index (10.0 ± 2.3%, ES 0.46). Concomitantly to this performance difference, IPC attenuated the decline in frequency spectrum throughout the Wingate (mean difference: 14.8%, ES range: 0.88–1.80). There was no difference in root mean square amplitude between groups. These preliminary results suggest that using IPC before sprint training may enhance performance during a 30-s Wingate test, and such gains occurred in the last 2 weeks of the intervention. This improvement may be due, in part, to neuromuscular adjustments induced by the chronic use of IPC.

Difference in total workload during sprint interval training for adults living with or without obesity.

The primary objective of the study was to compare the implications of body composition on work volume, power outputs (peak, mean, and minimum), and relative drop load throughout 4 weeks of sprint interval training (SIT) in individuals living with and without obesity. Thirty-four participants living with (n = 16) and without (n = 18) obesity took part in 12 sessions of SIT over 4 weeks. SIT consisted of repeated 30-s Wingate with a drop load of 7.5% of the participant's body mass separated by 4 min of active recovery. Fat-free mass was estimated using a BODPOD. Work volume, drop load, and power output(peak, mean, and minimum) relative to body mass and fat-free mass were calculated using a Monark 874E Weight cycle ergometer. Individuals living with obesity had a significantly larger drop load relative to fat-free mass (p < 0.001) and absolute drop load (p < 0.001) as well as a lower cycling cadence (p < 0.001) compared to individuals without obesity. No significant difference was observed in work volume (p = 0.167) as well as mean (p = 0.903), peak (p = 0.294), and minimum (p = 0.103) power relative to fat-free mass between groups. The findings suggest that individuals living with obesity work at a higher relative drop load when utilizing a percentage of body mass; however, a reduced cycling cadence results in similar total work volume throughout SIT.

Effects of sprint interval training on substrate oxidation in adults living with and without obesity: The i-FLEX study.

Metabolic flexibility is the ability to adapt substrate oxidation according to metabolic demand. Exercise increases fat oxidation responses in individuals living with obesity; however, limited research exists on the relationship between substrate oxidation and insulin sensitivity after sprint interval training (SIT). The primary objective was to investigate changes in substrate oxidation at rest and during submaximal exercise, and in insulin sensitivity after 4 weeks of SIT in individuals living with or without obesity. The secondary objective was to investigate correlations between changes in substrate oxidation and insulin sensitivity following SIT. Adults living with obesity (n = 16, body mass index (BMI) = 34.1 kg/m2 ± 3.8) and without obesity (n = 18, BMI = 22.9 kg/m2 ± 1.6) took part in a 4‐week SIT intervention. Participants completed three sessions of SIT per week, consisting of repeated sets of a 30‐s Wingate separated by 4 m of active recovery. Substrate oxidation at rest and during submaximal exercise was measured using VCO2/VO2. Insulin sensitivity was calculated using the Matsuda index. No difference in substrate oxidation at rest was observed for either group (p > 0.05), while a significant increase in fat oxidation was observed in individuals living with obesity [F(1,31) = 14.55, p = 0.001] during the submaximal exercise test. A significant decrease in insulin sensitivity was observed among individuals without obesity [F(1,31) = 5.010, p = 0.033]. No correlations were observed between changes in substrate oxidation and insulin sensitivity (p > 0.05). Following SIT, individuals living with obesity increased submaximal fat oxidation compared to individuals without obesity. No correlations were observed between substrate oxidation and insulin sensitivity. Thus, SIT impacts fat oxidation during exercise in individuals living with obesity while having no such influence on insulin sensitivity.

Twelve weeks of sprint interval training increases peak cardiac output in previously untrained individuals.

Sprint interval training (SIT), characterized by brief bouts of 'supramaximal' exercise interspersed with recovery periods, increases peak oxygen uptake ([Formula: see text]) despite a low total exercise volume. Per the Fick principle, increased [Formula: see text] is attributable to increased peak cardiac output ([Formula: see text]) and/or peak arterio-venous oxygen difference (a-vO2diff). There are limited and equivocal data regarding the physiological basis for SIT-induced increases in [Formula: see text], with most studies lasting ≤ 6 weeks. To determine the effect of 12 weeks of SIT on [Formula: see text], measured using inert gas rebreathing, and the relationship between changes in [Formula: see text] and [Formula: see text]. 15 healthy untrained adults [6 males, 9 females; 21 ± 2 y (mean ± SD)] performed 28 ± 3 training sessions. Each session involved a 2-min warm-up at 50 W, 3 × 20-s 'all-out' cycling bouts (581 ± 221 W) interspersed with 2-min of recovery, and a 3-min cool-down at 50 W. Measurements performed before and after training showed that 12 weeks of SIT increased [Formula: see text] (17.0 ± 3.7 vs 18.1 ± 4.6 L/min, p = 0.01, partial η2 = 0.28) and [Formula: see text] (2.63 ± 0.78 vs 3.18 ± 1.1 L/min, p < 0.01, partial η2 = 0.58). The changes in these two variables were correlated (r2 = 0.46, p < 0.01). Calculated peak a-vO2diff also increased after training (154 ± 22 vs 174 ± 23 ml O2/L; p < 0.01) and was correlated with the change in [Formula: see text] (r2 = 0.33, p = 0.03). Exploratory analyses revealed an interaction (p < 0.01) such that [Formula: see text] increased in male (+ 10%, p < 0.01) but not female participants (+ 0.6%, p = 0.96), suggesting potential sex-specific differences. Twelve weeks of SIT increased [Formula: see text] by 6% in previously untrained participants and the change was correlated with the larger 21% increase in [Formula: see text].

The Effects of 15 or 30 s SIT in Normobaric Hypoxia on Aerobic, Anaerobic Performance and Critical Power.

Sprint interval training (SIT) is a concept that has been shown to enhance aerobic-anaerobic training adaptations and induce larger effects in hypoxia. The purpose of this study was to examine the effects of 4 weeks of SIT with 15 or 30 s in hypoxia on aerobic, anaerobic performance and critical power (CP). A total of 32 male team players were divided into four groups: SIT with 15 s at FiO2: 0.209 (15 N); FiO2: 0.135 (15 H); SIT with 30 s at FiO2: 0.209 (30 N); and FiO2: 0.135 (30 H). VO2max did not significantly increase, however time-to-exhaustion (TTE) was found to be significantly longer in the post test compared to pre test (p = 0.001) with no difference between groups (p = 0.86). Mean power (MPw.kg) after repeated wingate tests was significantly higher compared to pre training in all groups (p = 0.001) with no difference between groups (p = 0.66). Similarly, CP was increased in all groups with 4 weeks of SIT (p = 0.001) with no difference between groups (p = 0.82). This study showed that 4 weeks of SIT with 15 and 30 s sprint bouts in normoxia or hypoxia did not increased VO2max in trained athletes. However, anerobic performance and CP can be increased with 4 weeks of SIT both in normoxia or hypoxia with 15 or 30 s of sprint durations.