The current study sought to explore the incidence of nonresponders for maximal or submaximal performance following a variety of sprint interval training (SIT) protocols. Data from 63 young adults from 5 previously published studies were utilized in the current analysis. Nonresponders were identified using 2 times the typical error (TE) of measurement for peak oxygen uptake (2 × TE = 1.74 mL/(kg·min)), lactate threshold (2 × TE = 15.7 W), or 500 kcal time-to-completion (TTC; 2 × TE = 306 s) trial. TE was determined on separate groups of participants by calculating the test-retest variance for each outcome. The overall rate of nonresponders for peak oxygen uptake across all participants studied was 22% (14/63) with 4 adverse responders observed. No nonresponders for peak oxygen uptake were observed in studies where participants trained 4 times per week (n = 18), while higher rates were observed in most studies requiring training 3 times per week (30%-50%; n = 45). A nonresponse rate of 44% (8/18) and 50% (11/22) was observed for the TTC test and lactate threshold, respectively. No significant correlations were observed between the changes in peak oxygen uptake and TTC (r = 0.014; p = 0.96) or lactate threshold (r = 0.17; p = 0.44). The current analysis demonstrates a significant incidence of nonresponders for peak oxygen uptake and heterogeneity in the individual patterns of response following SIT. Additionally, these data support the importance of training dose and suggest that the incidence of nonresponse may be mitigated by utilizing the optimal dose of SIT.

The current study examined the contribution of central and peripheral adaptations to changes in maximal oxygen uptake (V̇O) following sprint interval training (SIT). Twenty-three males completed 4 weekly SIT sessions (8 × 20-s cycling bouts at ∼170% of work rate at V̇O, 10-s recovery) for 4 weeks. Following completion of training, the relationship between changes in V̇O and changes in central (cardiac output) and peripheral (arterial-mixed venous oxygen difference (a-vOdiff), muscle capillary density, oxidative capacity, fibre-type distribution) adaptations was determined in all participants using correlation analysis. Participants were then divided into tertiles on the basis of the magnitude of their individual V̇O responses, and differences in central and peripheral adaptations were examined in the top (HI; ∼10 mL·kg·min increase in V̇O, p < 0.05) and bottom (LO; no change in V̇O, p > 0.05) tertiles (n = 8 each). Training had no impact on maximal cardiac output, and no differences were observed between the LO group and the HI group (p > 0.05). The a-vOdiff increased in the HI group only (p < 0.05) and correlated significantly (r = 0.71, p < 0.01) with changes in V̇O across all participants. Muscle capillary density (p < 0.02) and β-hydroxyacyl-CoA dehydrogenase maximal activity (p < 0.05) increased in both groups, with no between-group differences (p > 0.05). Citrate synthase maximal activity (p < 0.01) and type IIA fibre composition (p < 0.05) increased in the LO group only. Collectively, although the heterogeneity in the observed V̇O response following 4 weeks of SIT appears to be attributable to individual differences in systemic vascular and/or muscular adaptations, the markers examined in the current study were unable to explain the divergent V̇O responses in the LO and HI groups.

High-intensity interval training (HIIT) improves peak oxygen uptake (V̇O2peak) and oxygen uptake (V̇O2) kinetics, however, it is unknown whether an optimal intensity of HIIT exists for eliciting improvements in these measures of whole-body oxidative metabolism. The purpose of this study was to (i) investigate the effect of interval intensity on training-induced adaptations in V̇O2peak and V̇O2 kinetics, and (ii) examine the impact of interval intensity on the frequency of nonresponders in V̇O2peak. Thirty-six healthy men and women completed 3 weeks of cycle ergometer HIIT, consisting of intervals targeting 80% (LO), 115% (MID), or 150% (HI) of peak aerobic power. Total work performed per training session was matched across groups. A main effect of training (p < 0.05) and a significant interaction effect was observed for V̇O2peak, with the change in V̇O2peak being greater (p < 0.05) in the MID group than the LO group; however, no differences were observed between the HI group and either the MID or LO groups (ΔV̇O2peak; LO, 2.7 ± 0.7 mL·kg(-1)·min(-1); MID, 5.8 ± 0.7; HI, 4.2 ± 1.0). The greatest proportion of responders was observed in the MID group (LO, 8/12; MID, 12/13; HI, 9/11). A nonsignificant relationship (p = 0.26; r(2) = 0.04) was found between the changes in V̇O2peak and τV̇O2. These results suggest that training at intensities around V̇O2peak may represent a threshold intensity above which further increases in training intensity provide no additional adaptive benefit. The dissociation between changes in V̇O2peak and V̇O2 kinetics also reflects the different underlying mechanisms regulating these adaptations.

This study investigated whether VO peak is reproducible across repeated tests before (PRE) and after (POST) training, and whether variability across tests impacts how individual responses are classified following 3 weeks of aerobic exercise training (cycle ergometry). Data from 45 young healthy adults (age: 20·1 ± 0·9 years; VO peak, 42·0 ± 6·7 ml·min ) from two previously published studies were utilized in the current analysis. Non-responders were classified as individuals who failed to demonstrate an increase or decrease in VO peak that was greater than 2·0 times the typical error of measurement (107 ml·min ) away from zero, while responders and adverse responders were above and below this cut-off, respectively. VO peak tests at PRE (three total) and POST (three total) were highly reproducible (PRE and POST average and single measures ICCs: range 0·938-0·992), with low coefficients of variation (PRE:4·9 ± 3·1%, POST: 4·8 ± 2·7%). However, a potential learning effect was observed in the VO peak tests prior to training, as the initial pretraining test was significantly lower than the third (p = 0·010, PRE 1: 2 946 ± 924 ml·min , PRE 3: 3 042 ± 919 ml·min ). This resulted in fewer individuals classified as adverse responders for Test 3 compared to any combination of tests that included Test 1, suggesting that a single ramp test at baseline may not be sufficient to accurately classify the VO peak response in young recreationally active individuals. Thus, it is our recommendation that the initial VO peak test be used as a familiarization visit and not included for analysis.

Considerable interindividual differences in the Q˙−V˙normalO2 relationship during exercise have been documented but implications for submaximal exercise tolerance have not been considered. We tested the hypothesis that these interindividual differences were associated with differences in exercising muscle deoxygenation and ratings of perceived exertion (RPE) across a range of submaximal exercise intensities. A total of 31 (21 ± 3 years) healthy recreationally active males performed an incremental exercise test to exhaustion 24 h following a resting muscle biopsy. Cardiac output (trueQ˙ L/min; inert gas rebreathe), oxygen uptake (V˙normalO2 L/min; breath‐by‐breath pulmonary gas exchange), quadriceps saturation (near infrared spectroscopy) and exercise tolerance (6–20; Borg Scale RPE) were measured. The Q˙−V˙normalO2 relationship from 40 to 160 W was used to partition individuals post hoc into higher (n = 10; 6.3 ± 0.4) versus lower (n = 10; 3.7 ± 0.4, P < 0.001) responders. The Q˙−V˙normalO2 difference between responder types was not explained by arterial oxygen content differences (P = 0.5) or peripheral skeletal muscle characteristics (P from 0.1 to 0.8) but was strongly associated with stroke volume (P < 0.05). Despite considerable Q˙−V˙normalO2 difference between groups, no difference in quadriceps deoxygenation was observed during exercise (all P > 0.4). Lower cardiac responders had greater leg (P = 0.027) and whole body (P = 0.03) RPE only at 185 W, but this represented a higher %peak V˙normalO2 in lower cardiac responders (87 ± 15% vs. 66 ± 12%, P = 0.005). Substantially lower Q˙−V˙normalO2 in the lower responder group did not result in altered RPE or exercising muscle deoxygenation. This suggests substantial recruitment of blood flow redistribution in the lower responder group as part of protecting matching of exercising muscle oxygen delivery to demand.