Robert Solsona

This research investigated the modulation of autophagy and protein synthesis markers in human peripheral blood mononuclear cells (PBMCs) of moderately trained men following repeated sprint exercises (RSE) performed under hypoxia (HYP, 13% FIO₂), with bilateral blood flow restriction (BFR, 45% of resting arterial occlusive pressure), or normoxia. Using a crossover design, participants completed three sets of five 10-s sprints under each condition. mRNA and protein levels were assessed using qPCR and Western immunoblotting. Exercise significantly increased the microtubule-associated light chain 3B (LC3B)-II/I ratio (p < 0.001, dz = 0.58), with the effect being more pronounced in NOR (p = 0.011, dz = 0.81). Conversely, p62 protein levels were unchanged (p > 0.05). However, a tendency towards a reduced LC3B-II/I ratio was observed in HYP (p = 0.056, dz = 0.34) but not in BFR. No significant effects of exercise or conditions were found for mRNA expression of Atg4B, Beclin, and HIF1-α. Exercise increased the phosphorylation of rpS6 (p < 0.001, dz = 0.96), while the phosphorylation of p70S6K and 4E-BP1 remained unchanged (p > 0.05). These findings demonstrate, for the first time, that a 5 × 10-s RSE protocol induces the early stages of autophagy in PBMCs, whereas hypoxia tended to attenuate this effect. However, the effects on protein synthesis markers were heterogeneous, without influence of HYP and BFR.

Recovery methods, such as thermal interventions, have been developed to promote optimal recovery and maximize long-term training adaptations. However, the beneficial effects of these recovery strategies remain a source of controversy. This narrative review aims to provide a detailed understanding of how cold and heat interventions impact long-term training adaptations. Emphasis is placed on skeletal muscle adaptations, particularly the involvement of signaling pathways regulating protein turnover, ribosome and mitochondrial biogenesis, as well as the critical role of satellite cells in promoting myofiber regeneration following atrophy. The current literature suggests that cold interventions can blunt molecular adaptations (e.g., protein synthesis and satellite cell activation) and oxi-inflammatory responses after resistance exercise, resulting in diminished exercise-induced hypertrophy and lower gains in isometric strength during training protocols. Conversely, heat interventions appear promising for mitigating skeletal muscle degradation during immobilization and atrophy. Indeed, heat treatments (e.g., passive interventions such as sauna-bathing or diathermy) can enhance protein turnover and improve the maintenance of muscle mass in atrophic conditions, although their effects on uninjured skeletal muscles in both humans and rodents remain controversial. Nonetheless, heat treatment may serve as an important tool for attenuating atrophy and preserving mitochondrial function in immobilized or injured athletes. Finally, the potential interplay between exercise, thermal interventions and epigenetics is discussed. Future studies must be encouraged to clarify how repeated thermal interventions (heat and cold) affect long-term exercise training adaptations and to determine the optimal modalities (i.e., method of application, temperature, duration, relative humidity, and timing).

This crossover study evaluated DNA methylation changes in human salivary samples following single sprint interval training sessions performed in hypoxia, with blood flow restriction (BFR), or with gravity‐induced BFR. Global DNA methylation levels were evaluated with an enzyme‐linked immunosorbent assay. Methylation‐sensitive restriction enzymes were used to determine the percentage methylation in a part of the promoter of the gene‐inducible nitric oxide synthase (p‐iNOS), as well as an enhancer (e‐iNOS). Global methylation increased after exercise (p < 0.001; dz = 0.50). A tendency was observed for exercise × condition interaction (p = 0.070). Post hoc analyses revealed a significant increase in global methylation between pre‐ (7.2 ± 2.6%) and postexercise (10.7 ± 2.1%) with BFR (p = 0.025; dz = 0.69). Methylation of p‐iNOS was unchanged (p > 0.05). Conversely, the methylation of e‐iNOS increased from 0.6 ± 0.4% to 0.9 ± 0.8% after exercise (p = 0.025; dz = 0.41), independently of the condition (p > 0.05). Global methylation correlated with muscle oxygenation during exercise (r = 0.37, p = 0.042), while e‐iNOS methylation showed an opposite association (r = −0.60, p = 0.025). Furthermore, p‐iNOS methylation was linked to heart rate (r = 0.49, p = 0.028). Hence, a single sprint interval training increases global methylation in saliva, and adding BFR tends to increase it further. Lower muscle oxygenation is associated with augmented e‐iNOS methylation. Finally, increased cardiovascular strain results in increased p‐iNOS methylation.

This study compared the effects of a brief repeated sprint training (RST) intervention performed with bilateral blood flow restriction (BFR) conditions in normoxia or conducted at high levels of hypoxia on response to exercise. Thirty-nine endurance-trained athletes completed six repeated sprints cycling sessions spread over 2 weeks consisting of four sets of five sprints (10-s maximal sprints with 20-s active recovery). Athletes were assigned to one of the four groups and subjected to a bilateral partial blood flow restriction (45% of arterial occlusion pressure) of the lower limbs during exercise (BFRG), during the recovery (BFRrG), exercised in a hypoxic room simulating hypoxia at FiO₂ ≈ 13% (HG) or were not subjected to additional stress (CG). Peak aerobic power during an incremental test, exercise duration, maximal accumulated oxygen deficit and accumulated oxygen uptake (VO₂) during a supramaximal constant-intensity test were improved thanks to RST (p < 0.05). No significant differences were observed between the groups (p > 0.05). No further effect was found on other variables including time-trial performance and parameters of the force-velocity relationship (p > 0.05). Thus, peak aerobic power, exercise duration, maximal accumulated oxygen deficit, and VO₂ were improved during a supramaximal constant-intensity exercise after six RST sessions. However, combined hypoxic stress or partial BFR did not further increase peak aerobic power.

The regulation of skeletal muscle mass and organelle homeostasis is dependent on the capacity of cells to produce proteins and to recycle cytosolic portions. In this investigation, the mechanisms involved in skeletal muscle mass regulation—especially those associated with proteosynthesis and with the production of new organelles—are presented. Thus, the critical roles of mammalian/mechanistic target of rapamycin complex 1 (mTORC1) pathway and its regulators are reviewed. In addition, the importance of ribosome biogenesis, satellite cells involvement, myonuclear accretion, and some major epigenetic modifications related to protein synthesis are discussed. Furthermore, several studies conducted on the topic of exercise training have recognized the central role of both endurance and resistance exercise to reorganize sarcomeric proteins and to improve the capacity of cells to build efficient organelles. The molecular mechanisms underlying these adaptations to exercise training are presented throughout this review and practical recommendations for exercise prescription are provided. A better understanding of the aforementioned cellular pathways is essential for both healthy and sick people to avoid inefficient prescriptions and to improve muscle function with emergent strategies (e.g., hypoxic training). Finally, current limitations in the literature and further perspectives, notably on epigenetic mechanisms, are provided to encourage additional investigations on this topic.