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BACKGROUND Sprint interval training is a popular workout modality. Studies have eluded to a positive effect on maximal oxygen uptake, however little is known about the mechanistic basis of this adaptation. Therefore, the purpose of this study was to determine the effects of a short-term high-intensity sprint interval training (SIT) intervention on VO2max through quantification of both the respiratory and hemodynamic responses. METHODS Thirty-six physically active participants undertook 4 weeks of either cycling-based SIT (8×20 s at 170% P-VO2max with 10 s recovery) or continuous exercise training (CET) (30 min at 70% P-VO2max) 3 times per week. VO2max, blood-based markers and hemodynamic responses were assessed pre and post the intervention period. VO2max was assessed using breath-by-breath open circuit spirometry, while hemodynamic responses were monitored using thoracic impedance cardiography. RESULTS VO2max exhibited a non-significant 4.1% increase (ES=0.24) for SIT with 7.0% P=0.007 (ES=0.40) increase for CET. Hemodynamic responses (maximal cardiac output, maximal stroke volume) displayed non-significant responses for CET and SIT while a-vO2dif-max increased from 15.8±4.8 to 18.3±2.9 mL/100 mL) (P=0.02) (ES=0.63) in SIT. CONCLUSIONS VO2max is a function of maximal cardiac output and a-vO2dif-max, so for a meaningful change to occur in cardiorespiratory fitness, there must be a concomitant increase in O2 delivery. This study demonstrates that a low volume SIT intervention evokes peripherally mediated responses (a-vO2dif) and anaerobic substrate utilization rather than O2 delivery components. Future works should address the time course of the responses and when assessing VO2max-based responses that due attention be given to the hemodynamic responses as means of quantification of the response.

The aim of this systematic review and meta-analysis was to identify a list of common, candidate genes associated with the three components of fitness, specifically cardiovascular fitness, muscular strength, and anaerobic power, and how these genes are associated with exercise response phenotype variability, in previously untrained participants. A total of 3,969 potentially relevant papers were identified and processed for inclusion. After eligibility and study selection assessment, 24 studies were selected for meta-analysis, comprising a total of 3,012 participants (male n = 1,512; females n = 1,239; not stated n = 261; age 28 ± 9 years). Meta-Essentials spreadsheet 1.4 (Microsoft Excel) was used in creating the forest plots and meta-analysis. IBM SPSS statistics V24 was implemented for the statistical analyses and the alpha was set at p ≤ 0.05. 13 candidate genes and their associated alleles were identified, which were associated with the phenotypes of interest. Analysis of training group data showed significant differential phenotypic responses. Subgroup analysis showed; 44%, 72% and 10% of the response variance in aerobic, strength and power phenotypes, respectively, were explained by genetic influences. This analysis established that genetic variability explained a significant proportion of the adaptation differences across the three components of fitness in the participants post-training. The results also showed the importance of analysing and reporting specific gene alleles. Information obtained from these findings has the potential to inform and influence future exercise-related genes and training studies.

This study investigates heart rate (HR), in 11 young adults (22.4±3.21yr), at V̇O2max, to ascertain whether measured maximal heart rate (HRmax), as determined by a plateau in HR (HRplat), can reliably confirm V̇O2max. V̇O2max and HRplat were determined, using the parameters of a V̇O2≤50 ml•min−1 and a ∆HR≤2b•min−1, respectively, over the final 60 s of sampling. V̇O2 was also independently determined using a verification phase protocol. A HRplat was achieved by 91% of participants (∆HR=1.3±1b•min−1) and critically the time at which HRmax was reached coincided with that at which V̇O2max was achieved. Moreover RER and ΔRER criteria were reached significantly earlier (p

BACKGROUND: There are alterations in strength in relation to menstrual cycle phase but little data attributing these responses to female sex hormone levels using a pseudo-menstrual cycle group as control. OBJECTIVE: Examining the effects of menstrual cycle phase on the development of peak torque across a range of isokinetic speeds. METHOD: 17 well trained females, 11 formed the non-oral contraceptive group (n-OC) (age 20.7 ± 1.4 yrs, mass 59.2 ± 6.9 kg, height 166.8 ± 7.1 cm) and 6 the oral contraceptive control group (OC) (age 20.3 ± 0.5 yrs, mass 60.5 ± 4.2 kg, height 164.8 ± 4.8 cm). Concentric strength of the knee flexors and extensors (60–240°/s) was assessed, corresponding to menstruation (MEN), mid-follicular (mFOL), mid-luteal (mLUT) and pre-menstrual (pMEN). RESULTS: For n-OC significant decreases in peak torque production of the extensors at 120°/s (P=0.0207) (MEN) and of the flexors at 60°/s (P=0.0116) (MEN) and 120°/s (P=0.0282) (MEN) were observed compared to pMEN. No significant differences were observed across any menstrual cycle phase and peak torque for the OC group (p> 0.05). Significant positive correlations were observed (mLUT) between peak torque and oestrogen at 60°/s (P=0.040) and 120°/s (P=0.031). CONCLUSIONS: There are significant fluctuations in peak torque of the knee extensors in response to phases of the menstrual cycle associated with variances in the female sex hormones. The findings have implications for the planning of strength training in female athletes.

The purpose of this study was to determine the effect of exercise modality on the incidence of plateau at VO2max. Twelve recreationally active men (age, 21·7 ± 2·3 year; mass, 74·8 ± 6·5 kg; height, 177·6 ± 5·6 cm) completed four incremental tests to volitional exhaustion, of which two were completed on a treadmill (TRE) and two were completed using a cycle ergometer (CYC). The work rate employed for CYC was 1 W·2 s(-1) from an initial loading of 100 W with cadence being maintained at 60 rpm. For TRE, the workload (gradient) increased at a rate of 0·5% · 30 s(-1) while maintaining a constant running speed of 10 kph. Throughout all the trials, VO2 was determined on a breath-by-breath basis using a precalibrated metabolic cart. The criteria adopted for determination of a plateau was a Δ VO2 over the final two consecutive 30-s sampling periods of ≤50 ml · min(-1). Averaging across the two trials per each exercise modality showed a significant difference for plateau incidence between CYC (8%) and TRE (58%) (P = 0·017). This was aligned with a significant difference in the slope of the regression line during the final 60 s of the VO2max test, CYC (99·9 ± 49·7 ml · min(-1)) and TRE (49·6 ± 42·6 ml · min(-1)) (P = 0·017). Repeat measures ANOVA of these data suggests that plateau incidence rates at VO2max differ between treadmill- and cycle ergometry-based exercises. Future studies need to address whether these response rates are replicated in well-trained athletes.

The purpose of this study was to determine the effect of 6 min of prior-priming exercise on the incidence of plateau at VO(2max). Twelve trained cyclists (age, 21 ± 3 years; height, 175·0 ± 8·0 cm; weight, 69·0 ± 10·4 kg; maximal oxygen uptake (VO(2max)), 56·3 ± 6·9 ml kg(-1) min(-1)) completed three incremental tests to volitional exhaustion, which were classified as unprimed (UP), heavy-primed (HP) and severe-primed (SP), at a work rate of 1 W 2 s(-1), from an initial workload of 100 W, for the determination of VO(2max). VO(2max) trial in the HP and SP conditions was preceded by a period of 4-min unloaded cycling followed by a further 6 min of constant load cycling at Δ50% VO(2) gas exchange threshold (GET)-VO(2max) (HP) and Δ75% VO(2) GET-VO(2max) (SP). Expired air was recorded on a breath-by-breath basis during all trials. The criteria adopted for a plateau in VO(2max) was a ΔVO(2) over the final two consecutive 30-s sampling periods ≤ 2·1 ml kg(-1) min(-1). There was a significant increase in plateau responses between the UP (50%) and HP (100%) conditions (P = 0·001) coupled with a significant change in the slope of the regression line during the final 60 s of the VO(2max) test, UP and HP (P = 0·0299) and UP and SP (P = 0·0296). These data suggest that a bout of prior-priming exercise promotes an increased incidence of plateau responses at VO(2max) . It is suggested that future studies address how such an approach can be adopted without prior knowledge of GET.