Wk Of Sprint Interval Training Research Articles

Cardiorespiratory and Neuromuscular Improvements Plateau after 2 wk of Sprint Interval Training in Sedentary Individuals.

Previous studies ranging from 2 to 12 wk of sprint interval training (SIT) have reported improvements in maximal oxygen uptake (V̇O 2max ) and neuromuscular function in sedentary populations. However, whether the time course of the changes in these variables correlates with greater training volumes is unclear. Thirteen sedentary participants performed three all-out training weekly sessions involving 15-s sprints interspersed with 2 min of recovery on a cycle ergometer. The 6-wk training program was composed of three identical blocks of 2 wk in which training volume was increased from 10 to 14 repetitions over the first four sessions and reduced to 8 in the last session. The power output and the heart rate (HR) were monitored during the sessions. The V̇O 2max , the power-force-velocity profile, and the isometric force were assessed every 2 wk from baseline. A significant increase in V̇O 2max was observed from the second week plateauing thereafter despite four additional weeks of training. The dynamic force production increased from the second week, and the speed production decreased by the end of the protocol. The isometric force and the maximal power output from the power-force-velocity profile did not change. Importantly, the time spent at high percentages of the maximal HR during the training sessions was lower in the second and third training block compared with the first. SIT resulted in an effective approach for rapidly increasing V̇O 2max , and no change in the isometric force was found; cycling-specific neuromuscular adaptations were observed from the second week of training. SIT may be useful in the short term, but further improvement of overall physical fitness might need other training modalities like endurance and/or resistance training.

Effects of a 6-wk Sprint Interval Training Protocol at Different Altitudes on Circulating Extracellular Vesicles.

This study aimed to investigate the modulation of circulating exosome-like extracellular vesicles (ELVs) after 6 wk of sprint interval training (SIT) at sea level and at 2000, 3000, and 4000 m. Thirty trained endurance male athletes (18-35 yr) participated in a 6-wk SIT program (30-s all-out sprint, 4-min 30-s recovery; 4-9 repetitions, 2 sessions per week) at sea level ( n = 8), 2000 m (fraction of inspired oxygen (F io2 ) 0.167, n = 8), 3000 m (F io2 0.145, n = 7), or 4000 m (F io2 0.13, n = 7). Venous blood samples were taken before and after the training period. Plasma ELVs were isolated by size exclusion chromatography, counted by nanoparticle tracking analysis, and characterized according to international standards. Candidate ELV microRNAs (miRNAs) were quantified by real-time polymerase chain reaction. When the three hypoxic groups were analyzed separately, only very minor differences could be detected in the levels of circulating particles, ELV markers, or miRNA. However, the levels of circulating particles increased (+262%) after training when the three hypoxic groups were pooled, and tended to increase at sea level (+65%), with no difference between these two groups. A trend to an increase was observed for the two ELV markers, TSG101 (+65%) and HSP60 (+441%), at sea level, but not in hypoxia. Training also seemed to decrease the abundance of miR-23a-3p and to increase the abundance of miR-21-5p in hypoxia but not at sea level. A 6-wk SIT program tended to increase the basal levels of circulating ELVs when performed at sea level but not in hypoxia. In contrast, ELV miRNA cargo seemed to be modulated in hypoxic conditions only. Further research should explore the potential differences in the origin of ELVs between normoxic and local and systemic hypoxic conditions.

The combined effect of sprint interval training and postexercise blood flow restriction on critical power, capillary growth, and mitochondrial proteins in trained cyclists

Sprint interval training (SIT) combined with postexercise blood flow restriction (BFR) is a novel method to increase maximal oxygen uptake (V̇o2max) in trained individuals and also provides a potent acute stimulus for angiogenesis and mitochondrial biogenesis. The efficacy to enhance endurance performance, however, has yet to be demonstrated. Trained male cyclists ( n = 21) (V̇o2max: 62.8 ± 3.7 ml·min-1·kg-1) undertook 4 wk of SIT (repeated 30-s maximal sprints) either alone (CON; n = 10) or with postexercise BFR ( n = 11). Before and after training V̇o2max, critical power (CP) and curvature constant ( W') were determined and muscle biopsies obtained for determination of skeletal muscle capillarity and mitochondrial protein content. CP increased ( P = 0.001) by a similar extent following CON (287 ± 39 W to 297 ± 43 W) and BFR (296 ± 40 W to 306 ± 36 W). V̇o2max increased following BFR by 5.9% ( P = 0.02) but was unchanged after CON ( P = 0.56). All markers of skeletal muscle capillarity and mitochondrial protein content were unchanged following either training intervention. In conclusion, 4 wk of SIT increased CP; however, this was not enhanced further with BFR. SIT was not sufficient to elicit changes in skeletal muscle capillarity and mitochondrial protein content with or without BFR. However, we further demonstrate the potency of combining BFR with SIT to enhance V̇o2max in trained individuals. NEW & NOTEWORTHY This investigation has demonstrated that 4 wk of sprint interval training (SIT) increased critical power in trained individuals; however, postexercise blood flow restriction (BFR) did not enhance this further. SIT, with or without BFR, did not induce any changes in skeletal muscle capillarity or mitochondrial protein content in our trained population. We do, however, confirm previous findings that SIT combined with BFR is a potent stimulus to enhance maximal oxygen uptake.

Cold-water immersion following sprint interval training does not alter endurance signaling pathways or training adaptations in human skeletal muscle.

We investigated the underlying molecular mechanisms by which postexercise cold-water immersion (CWI) may alter key markers of mitochondrial biogenesis following both a single session and 6 wk of sprint interval training (SIT). Nineteen men performed a single SIT session, followed by one of two 15-min recovery conditions: cold-water immersion (10°C) or a passive room temperature control (23°C). Sixteen of these participants also completed 6 wk of SIT, each session followed immediately by their designated recovery condition. Four muscle biopsies were obtained in total, three during the single SIT session (preexercise, postrecovery, and 3 h postrecovery) and one 48 h after the last SIT session. After a single SIT session, phosphorylated (p-)AMPK, p-p38 MAPK, p-p53, and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mRNA were all increased (P < 0.05). Postexercise CWI had no effect on these responses. Consistent with the lack of a response after a single session, regular postexercise CWI had no effect on PGC-1α or p53 protein content. Six weeks of SIT increased peak aerobic power, maximal oxygen consumption, maximal uncoupled respiration (complexes I and II), and 2-km time trial performance (P < 0.05). However, regular CWI had no effect on changes in these markers, consistent with the lack of response in the markers of mitochondrial biogenesis. Although these observations suggest that CWI is not detrimental to endurance adaptations following 6 wk of SIT, they question whether postexercise CWI is an effective strategy to promote mitochondrial biogenesis and improvements in endurance performance.

Additive Benefits of β-Alanine Supplementation and Sprint-Interval Training.

The present study investigated the effects of β-alanine supplementation only, and in combination with sprint-interval training (SIT), on training intensity, and energy provision and performance during exhaustive supramaximal-intensity cycling and a 4- and 10-km time trial (TT). Fourteen trained cyclists (V˙O2max = 4.5 ± 0.6 L·min) participated in this placebo-controlled, double-blind study. Subjects performed a supramaximal cycling test to exhaustion (equivalent to 120% V˙O2max) and a 4- and 10-km TT and 4 × 1-km sprints at three time points: before and after 28 d of supplementation loading (6.4 g·d) with β-alanine (n = 7) or a placebo (n = 7), and after a 5-wk supervised, SIT program performed twice weekly (repeated 1-km cycling sprints) while maintaining supplementation with β-alanine (1.2 g·d) or a placebo. After the loading period, sprints 3 and 4 of the 4 × 1-km sprint intervals were improved with β-alanine supplementation (4.5% ± 3.4% and 7.0% ± 4.0%; P < 0.05, respectively). After 5 wk of SIT, training intensity increased in both groups but the change was greater with β-alanine supplementation (9.9% ± 5.0% vs 4.9% ± 5.0%; P = 0.04). β-alanine supplementation also improved supramaximal cycling time to exhaustion to a greater extent than placebo (14.9% ± 9.2% vs 9.0% ± 6.9%; P = 0.04), whereas 4- and 10-km TT performance improved to a similar magnitude in both groups. After SIT, β-alanine also increased anaerobic capacity (5.5% ± 4.2%; P = 0.04), whereas V˙O2peak increased similarly in each group (3.1% ± 2.9% vs 3.5% ± 2.9%; P < 0.05). These findings indicate that β-alanine supplementation enhances training intensity during SIT and provides additional benefits to exhaustive supramaximal cycling compared with SIT alone.

Acute and chronic effects of sprint interval exercise on postprandial lipemia in women at-risk for the metabolic syndrome.

Individuals diagnosed with the metabolic syndrome (MetS) exhibit elevated postprandial lipemia (PPL). The aims of this investigation were to determine 1) if an acute bout of sprint interval training (SIT) attenuates PPL; and 2) if the attenuation of PPL following 6 wk of SIT is magnified compared with a single session of SIT prior to training in women at-risk for MetS (n = 45; 30-65 yr). Women were randomized to SIT (n = 22) or a nonexercise control (n = 23; CON) for 6 wk. Postprandial responses to a high-fat meal challenge (HFMC) were assessed in the CON group before (B-HFMC) and after (Post-HFMC) without prior exercise and in the SIT group at baseline (B-HFMC) without prior exercise, after an acute bout of SIT (four 30-s all-out sprints with 4-min recovery) prior to (Pre-HFMC), and after the 6-wk intervention (Post-HFMC). Responses to the HFMC were assessed by collecting venous blood samples in the fasted state and at 0, 30, 60, 120, and 180 min postprandial. Compared with baseline, an acute bout of SIT before (Pre-HFMC) and after the 6-wk intervention (Post-HFMC) significantly attenuated fasted TG (P < 0.05; 16.6% and 12.3%, respectively) and postprandial area under the curve (13.1% and 9.7%, respectively; tAUC) TG responses. There was no difference in fasted or tAUC TG responses between Pre-HFMC and Post-HFMC. SIT is an effective mode of exercise to reduce fasted and postprandial TG concentrations in women at-risk for MetS. Six weeks of SIT does not magnify the attenuation of PPL in response to a single session of SIT.

Sprint Interval Training in Hypoxia Stimulates Glycolytic Enzyme Activity

In this study, we compared the effect of sprint interval training (SIT) in normoxia versus hypoxia on muscle glycolytic and oxidative capacity, monocarboxylate transporter content, and endurance exercise performance. Healthy male volunteers (18-30 yr) performed 6 wk of SIT on a cycling ergometer (30-s sprints vs 4.5-min rest intervals; 3 d · wk(-1)) in either normobaric hypoxia (HYP, FiO2 = 14.4%, n = 10) or normoxia (NOR, FiO2 = 20.9%, n = 9). The control group did not train (CON, n = 10). Training load was increased from four sprints per session in week 1 to nine sprints in week 6. Before and after SIT, subjects performed a maximal incremental exercise test plus a 10-min simulated time trial on a cycle ergometer in both normoxia (MAX nor and TT nor) and hypoxia (MAX hyp and TT hyp). A needle biopsy was taken from musculus vastus lateralis at rest 5-6 d after the last exercise session. SIT increased muscle phosphofructokinase activity more in HYP (+59%, P < 0.05) than that in NOR (+17%), whereas citrate synthase activity was similar between groups. Compared with the pretest, power outputs corresponding to 4 mmol blood lactate in HYP during MAX nor (+7%) and MAX hyp (+9%) were slightly increased (P < 0.05), whereas values were constant in NOR. V·O 2max in MAX nor and TT performance in TT nor and TT hyp were increased by ≈ 6%-8% (P < 0.05) in either group. The training elevated monocarboxylate transporter 1 protein content by ≈ 70% (P < 0.05). In CON, all measurements were constant throughout the study. SIT in hypoxia up-regulated muscle phosphofructokinase activity and the anaerobic threshold more than SIT in normoxia but did not enhance endurance exercise performance.

Improving Acceleration and Repeated Sprint Ability in Well-Trained Adolescent Handball Players: Speed Versus Sprint Interval Training

The aim of the current study was to compare the effects of speed/agility (S/A) training with sprint interval training (SIT) on acceleration and repeated sprint ability (RSA) in well-trained male handball players. In addition to their normal training program, players performed either S/A (n = 7) or SIT (n = 7) training for 4 wk. Speed/agility sessions consisted of 3 to 4 series of 4 to 6 exercises (eg, agility drills, standing start and very short sprints, all of <5 s duration); each repetition and series was interspersed with 30 s and 3 min of passive recovery, respectively. Sprint interval training consisted of 3 to 5 repetitions of 30-s all-out shuttle sprints over 40 m, interspersed with 2 min of passive recovery. Pre- and posttests included a countermovement jump (CMJ), 10-m sprint (10m), RSA test and a graded intermittent aerobic test (30-15 Intermittent Fitness Test, V(IFT)). S/A training produced a very likely greater improvement in 10-m sprint (+4.6%, 90% CL 1.2 to 7.8), best (+2.7%, 90% CL 0.1 to 5.2) and mean (+2.2%, 90% CL -0.2 to 4.5) RSA times than SIT (all effect sizes [ES] greater than 0.79). In contrast, SIT resulted in an almost certain greater improvement in V(IFT) compared with S/A (+5.2%, 90% CL 3.5 to 6.9, with ES = -0.83). In well-trained handball players, 4 wk of SIT is likely to have a moderate impact on intermittent endurance capacity only, whereas S/A training is likely to improve acceleration and repeated sprint performance.

Sprint interval and traditional endurance training induce similar improvements in peripheral arterial stiffness and flow-mediated dilation in healthy humans

Low-volume sprint interval training (SIT), or repeated sessions of brief, intense intermittent exercise, elicits metabolic adaptations that resemble traditional high-volume endurance training (ET). The effects of these different forms of exercise training on vascular structure and function remain largely unexplored. To test the hypothesis that SIT and ET would similarly improve peripheral artery distensibility and endothelial function and central artery distensibility, we recruited 20 healthy untrained subjects (age: 23.3 +/- 2.8 yr) and had them perform 6 wk of SIT or ET (n = 5 men and 5 women per group). The SIT group completed four to six 30-s "all-out" Wingate tests separated by 4.5 min of recovery 3 days/wk. The ET group completed 40-60 min of cycling at 65% of their peak oxygen uptake (Vo2peak) 5 days/wk. Popliteal endothelial function, both relative and normalized to shear stimulus, was improved after training in both groups (main effect for time, P < 0.05). Carotid artery distensibility was not statistically altered by training (P = 0.29) in either group; however, popliteal artery distensibility was improved in both groups to the same degree (main effect, P < 0.05). We conclude that SIT is a time-efficient strategy to elicit improvements in peripheral vascular structure and function that are comparable to ET. However, alterations in central artery distensibility may require a longer training stimuli and/or greater initial vascular stiffness than observed in this group of healthy subjects.

Divergent response of metabolite transport proteins in human skeletal muscle after sprint interval training and detraining

Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22 +/- 1 yr; peak oxygen uptake = 50 +/- 2 ml.kg(-1).min(-1)) performed 4-6 x 30 s all-out cycling efforts with 4-min recovery, 3 days/wk for 6 wk. Needle muscle biopsy samples (vastus lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT, and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by approximately 35% after 1 wk of SIT and remained higher compared with Pre, even after 6 wk of detraining (P < 0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained approximately 20% higher compared with baseline during detraining (P < 0.05). The monocarboxylate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared with Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining (P < 0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) (P > 0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate, and fatty acid transport.

Seven High-Intensity Interval Training Sessions Increases Aerobic Capacity and Blunts the Metabolic and Hormonal Responses to Intense Exercise

Numerous studies have shown that traditional endurance exercise (∼55–70% VO2peak) improves aerobic capacity. Alternately, a recent study reported that 2 wk of sprint interval training (>100% VO2peak) also improved aerobic capacity and exercise performance. Interval training at an intermediate, but still intense power output (∼90% VO2peak), may offer a more practical training protocol to improve aerobic capacity and high intensity performance for the general population. PURPOSE: Our aim was to investigate the effects of a short term, high intensity interval training (HIT) program on aerobic capacity and to quantify the short-term changes in the cardiovascular, metabolic and hormonal responses to exercise at ∼90% VO2peakM METHODS: Eight females participated in the study (mean ± SE: 22.1 ± 0.2 yrs, 65.0 ±0.8 kg, 2.36 ± 0.17 VO2peak). Subjects performed a VO2peak test prior and following training. Training consisted of 7 HIT sessions over 2 wk. Subjects trained every other day performing ten 4 min bouts at 90% VO2peak with 2 min of rest between bouts. On the 2nd and 7th training session, heart rate (HR) and respiratory and blood samples were collected before and after bouts 1, 3, 5 and 10. The 7th training session was at the same absolute power output as the 2nd session. RESULTS: On average, subjects reached 90% VO2peak by the end of each exercise bout (session 2 (S2): 90.3 ± 3.6, session 7 (S7): 90.5 ± 4.0% VO2peak). Exercising workloads increased throughout training, with an average increase of 10% from the 1 * to 6th training session. VO2peak significantly increased (p < 0.05) following training (2.36 ± 0.17 to 2.66 ± 021 l/min). Lactate decreased with training following the 3rd bout (S2: 3.37 ± 0.08 vs. S7: 2.96 ± 0.18 mM) and following the 5th bout (S2: 3.63 ±0.12 vs. S7: 3.27 ± 0.18 mM). Plasma epinephrine significantly decreased with training following the 3rd bout (S2: 1.80 ±0.08 vs. S7: 0.95 ± 0.06 nM) and the 10th bout (S2: 3.11 ±0.24 vs. S7: 1.39 ±0.03 nM). The highest HR reached during exercise significantly decreased following training (S2: 179.6 ± 1.4, S7: 173.9 ± 1.7 beats/min). HR recovery during rest periods decreased on average from 128.1 ± 3.0 to 122.8 ± 3.5 beats/min. Plasma free fatty acids (S2: 0.38 ±011 vs. S7: 0.27 ± 0.03 mM) and glycerol(S2: 127.7 ± 13.5 vs. S7: 97.6 ± 5.9 mM) following bout 10 were significantly decreased following training. CONCLUSION: Aerobic capacity was increased and cardiovascular, hormonal and metabolic responses to high intensity exercise were blunted with 2 wk of HIT. HIT at ∼90% VO2peak may offer a realistic and practical training protocol to improve aerobic capacity and high intensity performance for the general population.