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.

We examined maximal oxygen consumption responses following exercise training to demonstrate the limitations associated with threshold‐based dichotomous classification of responders and non‐responders and proposed alternative methods for classification. Specifically, we: 1) calculated individual probabilities of response, and 2) classified individuals using response confidence intervals (CI) and reference points of zero and a smallest worthwhile change of 0.5 METs. Our findings support the use of individual probabilities and individual CIs to improve the accuracy in non‐response classification.

The purpose of this study was to test the hypotheses that: 1) inter-individual variability in acute blood lactate responses during exercise at 65% of peak work rate (WRPEAK; REL) will predict variability in the chronic responses to exercise training, and 2) exercising at an intensity that causes uncomfortable speech production (negative [NEG] talk test [TT] stage) elicits high acute blood lactate responses and large adaptations to training. Twenty-eight participants competed four weeks of exercise training consisting of REL (n: 14) NEG (TT, n: 14). Fifteen additional participants were assigned to a no-exercise control group (CTL, n: 15). In REL, acute blood lactate responses during the first training session significantly predicted changes in VO2peak (r=0.69) after training. TT resulted in consistently high acute blood lactate responses. REL and TT improved (p<0.05) maximal oxygen consumption (VO2peak), WRPEAK, and work rate at the onset of blood lactate accumulation (WROBLA). Despite non-significance, small to medium between-group effect sizes for changes in VO2peak, WRPEAK, and WROBLA, and a higher WR, heart rate, RPE, and blood lactate during training at NEG, support the potential superiority of TT over REL. When exercise is prescribed using a traditional method (%WRPEAK; REL), acute metabolic stress may partly explain the variance in the adaptations to training. Additionally, TT elicited significant increases in VO2peak, WRPEAK, WROBLA, and although our small sample size limits the ability to confidently compare training adaptations between groups, our preliminary results suggest that future investigations with larger sample sizes should assess the potential superiority of TT over REL.

The purpose of the present study was to determine if acute responses in PGC-1α, VEGFA, SDHA, and GPD1-2 mRNA expression predict their associated chronic skeletal muscle molecular (SDH-GPD activity and substrate storage) and morphological (fibre-type composition and capillary density) adaptations following training. Skeletal muscle biopsies were collected from 14 recreationally active men (age: 22.0 ± 2.4 years) before (PRE) and 3 h after (3HR) the completion of an acute bout of sprint interval training (SIT) (eight 20-s intervals at ∼170% peak oxygen uptake work rate separated by 10 s of recovery). Participants then completed 6 weeks of SIT 4 times per week with additional biopsies after 2 (MID) and 6 (POST) weeks of training. Acute increases in PGC-1α mRNA strongly predicted increases in SDH activity (a marker of oxidative capacity) from PRE and MID to POST (PRE-POST: r = 0.81, r = 0.65, p < 0.01; MID-POST: r = 0.79, r = 0.62, p < 0.01) and glycogen content from MID to POST (r = 0.60, r = 0.36, p < 0.05). No other significant relationships were found between acute responses in PGC-1α, VEGFA, SDHA, and GPD1-2 mRNA expression and chronic adaptations to training. These results suggest that acute upregulation of PGC-1α mRNA relates to the magnitude of subsequent training-induced increases in oxidative capacity, but not other molecular and morphological chronic skeletal muscle adaptations. Additionally, acute mRNA responses in PGC-1α correlated with VEGFA, but not SDHA, suggesting a coordinated upregulation between PGC-1α and only some of its proposed targets in human skeletal muscle.

Wearable technology and live video conferencing: The development of an affordable virtual teaching platform to enhance clinical skills education during the COVID-19 pandemic Technologie portable et vidéoconférence en direct : élaboration d'une plateforme d'enseignement virtuel abordable pour améliorer l'enseignement des habiletés cliniques pendant la pandémie de la COVID-19