Systemic and muscular responses to effort-matched short intervals and long intervals in elite cyclists.

The purpose of this study was to compare the acute effects of time- and effort-matched high-intensity intervals on physiological, endocrine, and skeletal muscle molecular variables in elite cyclists. Eight elite cyclists performed short intervals (SI: 30-seconds) and long intervals (LI: 5-minutes) with work:recovery ratio 2:1, using a randomized crossover design. SI was associated with 14% ± 3% higher mean power output (SI; 421 ± 27 vs LI; 371 ± 22 W), and longer working time above 90% of maximal oxygen uptake (VO2max , 54% ± 76%) and 90% peak heart rate (HRpeak , 153% ± 148%) than LI (all P < .05), despite similar degrees of perceived exertion, blood lactate levels and muscle activation measured using EMG root mean square (EMG rms). In blood, SI was associated with more pronounced increases in testosterone and testosterone-to-sex hormone-binding globulin (SHBG) ratios, as well as prolonged cortisol responses (P < .05). In skeletal muscle (m. Vastus lateralis), SI and LI led to similar changes in mRNA abundance for a range of transcripts, with the exception of NHE1 mRNA, which decreased after SI (P < .05). Overall, SI was associated with more pronounced physiological and endocrine responses than LI in elite cyclists, suggesting that such training might lead to superior adaptations in elite cyclists.

Effect of speed endurance training and reduced training volume on running economy and single muscle fiber adaptations in trained runners.

The aim of the present study was to examine whether improved running economy with a period of speed endurance training and reduced training volume could be related to adaptations in specific muscle fibers. Twenty trained male (n = 14) and female (n = 6) runners (maximum oxygen consumption (VO2 -max): 56.4 ± 4.6 mL/min/kg) completed a 40-day intervention with 10 sessions of speed endurance training (5-10 × 30-sec maximal running) and a reduced (36%) volume of training. Before and after the intervention, a muscle biopsy was obtained at rest, and an incremental running test to exhaustion was performed. In addition, running at 60% vVO2 -max, and a 10-km run was performed in a normal and a muscle slow twitch (ST) glycogen-depleted condition. After compared to before the intervention, expression of mitochondrial uncoupling protein 3 (UCP3) was lower (P < 0.05) and dystrophin was higher (P < 0.05) in ST muscle fibers, and sarcoplasmic reticulum calcium ATPase 1 (SERCA1) was lower (P < 0.05) in fast twitch muscle fibers. Running economy at 60% vVO2 -max (11.6 ± 0.2 km/h) and at v10-km (13.7 ± 0.3 km/h) was ~2% better (P < 0.05) after the intervention in the normal condition, but unchanged in the ST glycogen-depleted condition. Ten kilometer performance was improved (P < 0.01) by 3.2% (43.7 ± 1.0 vs. 45.2 ± 1.2 min) and 3.9% (45.8 ± 1.2 vs. 47.7 ± 1.3 min) in the normal and the ST glycogen-depleted condition, respectively. VO2 -max was the same, but vVO2 -max was 2.0% higher (P < 0.05; 19.3 ± 0.3 vs. 18.9 ± 0.3 km/h) after than before the intervention. Thus, improved running economy with intense training may be related to changes in expression of proteins linked to energy consuming processes in primarily ST muscle fibers.