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We aim to provide reference values for military aircrews participating in hypoxia awareness training (HAT). We describe several parameters with potential biomedical interest based on selected segments and slopes of the changes in oxygen saturation (SatO2) during a standard HAT. A retrospective analysis of 2298 records of the SatO2 curve was performed, including 1526 military men aged 30.48 ± 6.47 years during HAT in a hypobaric chamber. HAT consisted of pre-oxygenation at 100% and an ascent to 7620 m, followed by O2 disconnection starting the phase of descent of SatO2 until reaching the time of useful consciousness (TUC), and finally reconnection to 100% O2 in the recovery phase. Using an ad hoc computational procedure, the time taken to reach several defined critical values was computed. These key parameters were the time until desaturation of 97% and 90% (hypoxia) after oxygen mask disconnection (D97/D90) and reconnection (R97/R90) phases, the time of desaturation (TUC-D97) and hypoxia (TUC-D90) during disconnection, the total time in desaturation (L97) or hypoxia (L90), and the slopes of SatO2 drop (SDSAT97 and SDSAT90) and recovery (SRSAT97). The mean of the quartiles according to TUC were compared by ANOVA. The correlations between the different parameters were studied using Pearson's test and the effect size was estimated with ω2. Potentially useful parameters for the HAT study were those with statistical significance (p < 0.05) and a large effect size. D97, D90, R97, and R90 showed significant differences with small effect sizes, while TUC-D97, TUC-D90, L97, L90, and SDSAT97 showed significant differences and large effect sizes. SDSAT97 correlated with TUC (R = 0.79), TUC-D97 (R = 0.81), and TUC-D90 (R = 0.81). In conclusion, several parameters of the SatO2 curve are useful for the study and monitoring of HAT. The SDSAT97 measured during the test can estimate the TUC and thus contribute to taking measures to characterize and protect the aircrew members. [ABSTRACT FROM AUTHOR]

Purpose: To analyze the effect of inspiratory muscle training (IMT) on the maximal inspiratory mouth pressure (MIP) and performance of elite swimmers. Methods: Eight participants performed a 3000-m swimming test (T-3000), followed by blood lactate measurements at 1 and 5 minutes postexercise.. The testing protocol was carried out before and after 6 weeks of IMT, in which a high-volume IMT group (HV-IMT) (n = 4) performed IMT twice a day—in the morning in a seated position and in the afternoon in a concurrent session of IMT and core muscle training. Also, a low-volume IMT group (LV-IMT) (n = 4) performed IMT in the morning session only. Results: After the intervention, both groups improved their MIP, HV-IMT (132.75 [27.42] to 156.75 [21.88] cmH2O; P =.010; d = 0.967) and LV-IMT (149.25 [22.82] to 171.50 [23.74] cmH2O; P =.013; d = 0.955), without a significant difference between groups (P =.855). Regarding swimming performance, there were no changes between groups in the T-3000 (P =.472) or lactate removal rate (P =.104). Conclusion: IMT increased inspiratory muscle strength in elite swimmers, but there was no association or meaningful impact on swimming performance. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) generates functional limitations due to functional deterioration and low tolerance to fatigue. Altitudinal hypoxia leads to a deterioration of physical fitness in patients with COPD. The Initiative for Chronic Obstructive Lung Disease recommends prescribed physical exercise programs as an essential element for the treatment of COPD; therefore, cardiopulmonary exercise tests (CPET) should be performed to identify maximum performance thresholds. However, typical CPET protocols may be inadequate for COPD patients residing at >2500 m as altitudinal hypoxia leads to a deterioration of physical fitness in patients with COPD. We present a case report of a COPD patient residing at >2500 m who underwent 3 different CPET protocols until reaching maximum thresholds of physical performance at high altitude. Each test was performed on the same patient two weeks apart between tests. It was found that the CPET protocol for COPD developed at low altitude is not relevant for COPD patients residing in conditions of altitudinal hypoxia, since the minimum criteria of the American Thoracic Society (ATS) are not met, and the values could not be recorded ventilatory and metabolic maximal. We believe that CPET protocols for people with COPD should be adjusted based on environmental conditions. [ABSTRACT FROM AUTHOR]

Key points Muscle injuries are the leading cause of sports casualties. Because of its high plasticity, skeletal muscle can respond to different stimuli to maintain and improve functionality. Intermittent hypobaric hypoxia (IHH) improves muscle oxygen delivery and utilization. Hypobaria coexists with cold in the biosphere, opening the possibility to consider the combined use of both environmental factors to achieve beneficial physiological adjustments. We studied the effects of IHH and cold exposure, separately and simultaneously, on muscle regeneration. Adult male rats were surgically injured in one gastrocnemius and randomly assigned to the following groups: (1) CTRL: passive recovery; (2) COLD: intermittently exposed to cold (4°C); (3) HYPO: submitted to IHH (4500 m); (4) COHY: exposed to intermittent simultaneous cold and hypoxia. Animals were subjected to these interventions for 4 h/day for 9 or 21 days. COLD and COHY rats showed faster muscle regeneration than CTRL, evidenced after 9 days at histological (dMHC‐positive and centrally nucleated fibre reduction) and functional levels after 21 days. HYPO rats showed a full recovery from injury (at histological and functional levels) after 9 days, while COLD and COHY needed more time to induce a total functional recovery. IHH can be postulated as an anti‐fibrotic treatment since it reduces collagen I deposition. The increase in the pSer473Akt/total Akt ratio observed after 9 days in COLD, HYPO and COHY, together with the increase in the pThr172AMPKα/total AMPKα ratio observed in the gastrocnemius of HYPO, provides clues to the molecular mechanisms involved in the improved muscle regeneration. Only intermittent hypobaric exposure accelerated muscle recovery as early as 9 days following injury at histological and functional levels. Injured muscles from animals treated with intermittent (4 h/day) cold, hypobaric hypoxia or a simultaneous combination of both stimuli regenerated histological structure and recovered muscle function 21 days after injury. The combination of cold and hypoxia showed a blunting effect as compared to hypoxia alone in the time course of the muscle recovery. The increased expression of the phosphorylated forms of Akt observed in all experimental groups could participate in the molecular cascade of events leading to a faster regeneration. The elevated levels of phosphorylated AMPKα in the HYPO group could play a key role in the modulation of the inflammatory response during the first steps of the muscle regeneration process. [ABSTRACT FROM AUTHOR]

Simple Summary: Damage to the spinal cord affects the voluntary control of skeletal muscles and also the control of the autonomic nervous system, thus affecting the cardiorespiratory system and the magnitude of the impact that is related to the level and complete or incomplete nature of the spinal cord injury. Associated with spinal cord damage are a sedentary lifestyle, increased adipose tissue, and low-grade inflammation/oxidative damage at the systemic level and in the lung. Lung malfunction has been recurrently described in this pathological context in both epidemiological and experimental studies. Physical exercise (PE) seems to be a potential therapeutic strategy, which involves a large mass of muscle tissue, thus potentially improving both lung functionality and the control of systemic and pulmonary inflammation. Furthermore, it is hypothesized that specific PE for the respiratory musculature per se or in association with other general exercise protocols may positively contribute to the function of this tissue. Chronic spinal cord injury affects several respiratory-function-related parameters, such as a decrease in respiratory volumes associated with weakness and a tendency to fibrosis of the perithoracic muscles, a predominance of vagal over sympathetic action inducing airway obstructions, and a difficulty in mobilizing secretions. Altogether, these changes result in both restrictive and obstructive patterns. Moreover, low pulmonary ventilation and reduced cardiovascular system functionality (low venous return and right stroke volume) will hinder adequate alveolar recruitment and low O2 diffusion, leading to a drop in peak physical performance. In addition to the functional effects described above, systemic and localized effects on this organ chronically increase oxidative damage and tissue inflammation. This narrative review describes both the deleterious effects of chronic spinal cord injury on the functional effects of the respiratory system as well as the role of oxidative damage/inflammation in this clinical context. In addition, the evidence for the effect of general and respiratory muscular training on the skeletal muscle as a possible preventive and treatment strategy for both functional effects and underlying tissue mechanisms is summarized. [ABSTRACT FROM AUTHOR]