The Effect of Training Intensity on VO2max in Young Healthy Adults: A Meta-Regression and Meta-Analysis.

Exercise training at a variety of intensities increases maximal oxygen uptake (VO2max), the strongest predictor of cardiovascular and all-cause mortality. The purpose of the present study was to perform a systematic review, meta-regression and meta-analysis of available literature to determine if a dose-response relationship exists between exercise intensity and training-induced increases in VO2max in young healthy adults. Twenty-eight studies involving human participants (Mean age: 23±1 yr; Mean VO2max: 3.4±0.8 l·min-1) were included in the meta-regression with exercise training intensity, session dose, baseline VO2max, and total training volume used as covariates. These studies were also divided into 3 tertiles based on intensity (tertile 1: ~60-70%; 2: ~80-92.5%; 3: ~100-250%VO2max), for comparison using separate meta-analyses. The fixed and random effects meta-regression models examining training intensity, session dose, baseline VO2max and total training volume was non-significant (Q4=1.36; p=0.85; R2=0.05). There was no significant difference between tertiles in mean change in VO2max (tertile 1:+0.29±0.15 l/min, ES (effect size) =0.77; 2:+0.26±0.10 l/min, ES=0.68; 3:+0.35±0.17 l/min, ES=0.80), despite significant (p<0.05) reductions in session dose and total training volume as training intensity increased. These data suggest that exercise training intensity has no effect on the magnitude of training-induced increases in maximal oxygen uptake in young healthy human participants, but similar adaptations can be achieved in low training doses at higher exercise intensities than higher training doses of lower intensity (endurance training).

Reducing the volume of sprint interval training does not diminish maximal and submaximal performance gains in healthy men.

PURPOSE: The present study examined the effect of reducing sprint interval training (SIT) work-interval duration on increases in maximal and submaximal performance. METHODS: Subjects (n = 36) were assigned to one of three training groups: endurance training (ET; 60 min per session for weeks 1-2, increasing to 75 min per session for weeks 3-4), or sprint interval training consisting of either repeated 30 (SIT 30) or 15 (SIT 15) second all-out intervals (starting with 4 bouts per session for weeks 1-2, increasing to 6 intervals per session for weeks 3-4). Training consisted of cycling 3 times per week for 4 weeks. RESULTS: While there was a significant main effect of training on VO2peak such that VO2peak was elevated post-training, no significant difference was observed in the improvements observed between groups (ET ~13%, SIT 30-4%, SIT 15-8%). A significant main effect of training was observed such that lactate threshold and critical power were higher during post-testing across all groups (p < 0.05). There was a main effect of training (p < 0.05) on Wingate peak power with no differences observed between groups at post-training. CONCLUSIONS: Together, these results indicate that reducing SIT work-interval duration from 30 to 15 s had no impact on training-induced increases in aerobic or anaerobic power, or on increases in lactate threshold (absolute) and critical power.

Dissociation of increases in PGC-1α and its regulators from exercise intensity and muscle activation following acute exercise.

Muscle activation as well as changes in peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) following high-intensity interval exercise (HIIE) were examined in young healthy men (n  = 8; age, 21.9±2.2 yrs; VO2peak, 53.1±6.4 ml/min/kg; peak work rate, 317±23.5 watts). On each of 3 visits HIIE was performed on a cycle ergometer at a target intensity of 73, 100, or 133% of peak work rate. Muscle biopsies were taken at rest and three hours after each exercise condition. Total work was not different between conditions (∼730 kJ) while average power output (73%, 237±21; 100%, 323±26; 133%, 384±35 watts) and EMG derived muscle activation (73%, 1262±605; 100%, 2089±737; 133%, 3029±1206 total integrated EMG per interval) increased in an intensity dependent fashion. PGC-1α mRNA was elevated after all three conditions (p<0.05), with a greater increase observed following the 100% condition (∼9 fold, p<0.05) compared to both the 73 and 133% conditions (∼4 fold). When expressed relative to muscle activation, the increase in PGC-1α mRNA for the 133% condition was less than that for the 73 and 100% conditions (p<0.05). SIRT1 mRNA was also elevated after all three conditions (∼1.4 fold, p<0.05), with no difference between conditions. These findings suggest that intensity-dependent increases in PGC-1α mRNA following submaximal exercise are largely due to increases in muscle recruitment. As well, the blunted response of PGC-1α mRNA expression following supramaximal exercise may indicate that signalling mediated activation of PGC-1α may also be blunted. We also indentify that increases in PDK4, SIRT1, and RIP140 mRNA following acute exercise are dissociated from exercise intensity and muscle activation, while increases in EGR1 are augmented with supramaximal HIIE (p<0.05).