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).

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.

Muscle activation and the change in peroxisome proliferator‐activated receptor y co‐activator 1α (PGC‐1α) mRNA expression following high‐intensity interval exercise (HIIE) were examined in healthy men (n=8; age, 21.9 ± 2.2 yrs; VO2peak, 53.1 ± 6.4 ml/min/kg; peak WR, 317 ± 23.5 watts). Participants reported to the lab for 3 experimental visits. On each visit HIIE was performed on a cycle ergometer with a target intensity of either 73 (LO), 100 (MI), or 133% (HI) of peak WR. Muscle biopsies were taken at rest and 3 hours after each exercise condition. There were no differences in total work between conditions (~730 kJ) while average power output (LO, 237 ± 21; MI, 323 ± 26; HI, 384 ± 35 watts) and EMG derived muscle activation (LO, 1262 ± 605; MI, 2089 ± 737; HI, 3029 ± 1206 total integrated EMG per interval) increased in an intensity dependent fashion. PGC‐1α mRNA was elevated (p<0.05) after all 3 conditions, with the increase observed following MI (~9 fold) being greater (p<0.05) than that observed following both LO and HI (~4 fold). When expressed relative to muscle activation, the change in PGC‐1α for HI was less than (p<0.05) that for LO and MI. These findings suggest that intensity dependent increases in PGC‐1α mRNA following submaximal exercise are largely due to increases in muscle recruitment. Interestingly, intensity, muscle activation and PGC‐1α mRNA were dissociated following HI. This research was supported by NSERC.