Key points: Low‐volume high‐intensity exercise training promotes muscle mitochondrial adaptations that resemble those associated with high‐volume moderate‐intensity exercise training. These training‐induced mitochondrial adaptations stem from the cumulative effects of transient transcriptional responses to each acute exercise bout. However, whether metabolic stress is a key mediator of the acute molecular responses to high‐intensity exercise is still incompletely understood. Here we show that, by comparing different work‐matched low‐volume high‐intensity exercise protocols, more marked metabolic perturbations were associated with enhanced mitochondrial biogenesis‐related muscle mRNA responses. Furthermore, when compared with high‐volume moderate‐intensity exercise, only the low‐volume high‐intensity exercise eliciting severe metabolic stress compensated for reduced exercise volume in the induction of mitochondrial biogenic mRNA responses. The present results, besides improving our understanding of the mechanisms mediating exercise‐induced mitochondrial biogenesis, may have implications for applied and clinical research that adopts exercise as a means to increase muscle mitochondrial content and function in healthy or diseased individuals. The aim of the present study was to examine the impact of exercise‐induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance‐trained men performed three cycling exercise protocols characterized by different metabolic profiles in a randomized, counter‐balanced order. Specifically, two work‐matched low‐volume supramaximal‐intensity intermittent regimes, consisting of repeated‐sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high‐volume continuous moderate‐intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3 h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post‐exercise plasma adrenaline levels in comparison with RS and CM. Exercise‐induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise‐induced PGC‐1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF‐2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise‐induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high‐intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations.

The present study examined muscle adaptations and alterations in performance of highly trained soccer players with intensified training or training cessation. Eighteen elite soccer players were, for a 2-wk period, assigned to either a group that performed high-intensity training with a reduction in the amount of training (HI, n = 7), or an inactivity group without training (IN, n = 11). HI improved ( P < 0.05) performance of the 4th, 6th, and 10th sprint in a repeated 20-m sprint test, and IN reduced ( P < 0.05) performance in the 5th to the 10th sprints after the 2-wk intervention period. In addition, the Yo-Yo intermittent recovery level 2 test performance of IN was lowered from 845 ± 48 to 654 ± 30 m. In HI, the protein expression of the Na⁺-K⁺pump α₂-isoform was 15% higher ( P < 0.05) after the intervention period, whereas no changes were observed in α₁- and β₁-isoform expression. In IN, Na⁺-K⁺pump expression was not changed. In HI, the FXYD1ser68-to-FXYD1 ratio was 27% higher ( P < 0.01) after the intervention period, and, in IN, the AB_FXYD1ser68 signal was 18% lower ( P < 0.05) after inactivity. The change in FXYD1ser68-to-FXYD1 ratio was correlated ( r²= 0.35; P < 0.05) with change in performance in repeated sprint test. The present data suggest that short-term intensified training, even for trained soccer players, can increase muscle Na⁺-K⁺pump α₂-isoform expression, and that cessation of training for 2 wk does not affect the expression of Na⁺-K⁺pump isoforms. Resting phosphorylation status of the Na⁺-K⁺pump is changed by training and inactivity and may play a role in performance during repeated, intense exercise.

Moderately trained male subjects (mean age 25 years; range 19-33 years) completed an 8-week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30-sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts.

The present study examined muscle adaptations and alterations in work capacity in endurance-trained runners after a change from endurance to sprint training. Fifteen runners were assigned to either a sprint training (ST, n = 8) or a control (CON, n = 7) group. ST replaced their normal training by 30-s sprint runs three to four times a week, whereas CON continued the endurance training (∼45 km/wk). After the 4-wk sprint period, the expression of the muscle Na⁺-K⁺ pump α₁-subunit and Na⁺/H⁺-exchanger isoform 1 was 29 and 30% higher ( P < 0.05), respectively. Furthermore, plasma K⁺ concentration was reduced ( P < 0.05) during repeated intense running. In ST, performance in a 30-s sprint test, Yo-Yo intermittent recovery test, and two supramaximal exhaustive runs was improved ( P < 0.05) by 7, 19, 27, and 19%, respectively, after the sprint training period, whereas pulmonary maximum oxygen uptake and 10-k time were unchanged. No changes in CON were observed. The present data suggest a role of the Na⁺-K⁺ pump in the control of K⁺ homeostasis and in the development of fatigue during repeated high-intensity exercise. Furthermore, performance during intense exercise can be improved and endurance performance maintained even with a reduction in training volume if the intensity of training is very high.

Purpose: To examine the degree of neuromuscular fatigue development along with changes in muscle metabolism during two work-matched high-intensity intermittent exercise protocols in trained individuals.Methods: In a randomized, counter-balanced, crossover design, 11 endurance-trained men performed high-intensity intermittent cycle exercise protocols matched for total work and including either multiple short-duration (18 × 5 s; SS) or long-duration (6 × 20 s; LS) sprints. Neuromuscular fatigue was determined by preexercise to postexercise changes in maximal voluntary contraction force, voluntary activation level and contractile properties of the quadriceps muscle. Metabolites and pH were measured in vastus lateralis muscle biopsies taken before and after the first and last sprint of each exercise protocol.Results: Peak power output (11% ± 2% vs 16% ± 8%,P< 0.01), maximal voluntary contraction (10% ± 5% vs 25% ± 6%,P< 0.05), and peak twitch force (34% ± 5% vs 67% ± 5%,P< 0.01) declined to a lesser extent in SS than LS, whereas voluntary activation level decreased similarly in SS and LS (10% ± 2% vs 11% ± 4%). Muscle [phosphocreatine] before the last sprint was 1.5-fold lower in SS than LS (P< 0.001). Preexercise to postexercise intramuscular accumulation of lactate and H⁺was twofold and threefold lower, respectively, in SS than LS (P< 0.001), whereas muscle glycogen depletion was similar in SS and LS. Rate of muscle glycolysis was similar in SS and LS during the first sprint, but twofold higher in SS than LS during the last sprint (P< 0.05).Conclusions: These findings indicate that, in endurance-trained individuals, multiple long-sprints induce larger impairments in performance along with greater degrees of peripheral fatigue compared to work-matched multiple short-sprints, with these differences being possibly attributed to more extensive intramuscular accumulation of lactate/H⁺and to lower rates of glycolysis during multiple long-sprint exercise.