Explore the vast range of titles available.

Monitoring core body temperature (Tc) during training and competitions, especially in a hot environment, can help enhance an athlete’s performance, as well as lower the risk for heat stroke. Accordingly, a noninvasive sensor that allows reliable monitoring of Tc would be highly beneficial in this context. One such novel non-invasive sensor was recently introduced onto the market (CORE, greenTEG, Rümlang, Switzerland), but, to our knowledge, a validation study of this device has not yet been reported. Therefore, the purpose of this study was to evaluate the validity and reliability of the CORE sensor. In Study I, 12 males were subjected to a low-to-moderate heat load by performing, on two separate occasions several days apart, two identical 60-min bouts of steady-state cycling in the laboratory at 19 °C and 30% relative humidity. In Study II, 13 males were subjected to moderate-to-high heat load by performing 90 min of cycling in the laboratory at 31 °C and 39% relative humidity. In both cases the core body temperatures indicated by the CORE sensor were compared to the corresponding values obtained using a rectal sensor (Trec). The first major finding was that the reliability of the CORE sensor is acceptable, since the mean bias between the two identical trials of exercise (0.02 °C) was not statistically significant. However, under both levels of heat load, the body temperature indicated by the CORE sensor did not agree well with Trec, with approximately 50% of all paired measurements differing by more than the predefined threshold for validity of ≤0.3 °C. In conclusion, the results obtained do not support the manufacturer’s claim that the CORE sensor provides a valid measure of core body temperature.

With pulmonary symptoms at a centre stage, several exercise training modalities for patients with long-COVID were effectively translated from standard pulmonary rehabilitation [13], while the inspiratory muscle training alone demonstrated no added benefit. [...]the search for safe and effective pulmonary or systemic intervention that would additionally restore pulmonary function continues. [...]future studies should put special emphasis on improving prescription and progression of exercise training, particularly resistance training [20, 21], to counterbalance the cardiopulmonary and skeletal muscle impairments associated with long COVID-19 sequalae [7], which may accelerate sarcopenia in these patient group [2, 6]. [...]the benefits of combined IHC with standard pulmonary rehabilitation [13] should be tested in a longer intervention (8–12 weeks) with extended follow-up (≥ 1 year), to investigate whether IHC effects are maintained over longer period of time or whether long COVID-19 symptoms can present again [2]. After extensive clinical assessment [13, 19], the IHC can be introduced in the early phases of long COVID-19 rehabilitation, preferably immediately after COVID-19 infection hospitalisation for patients with severe symptoms of breathlessness and exercise intolerance. [...]in early phases of rehabilitation (1–4 weeks), IHC can be added to inspiratory muscle training, low-to-moderate intensity continuous aerobic training (40%–60% of peak O2 consumption, 45–60 min) and resistance training (3–5 sets of 15–20 repetitions at 40%–60% of maximal muscle strength), balance training and other cognitive and physical therapy interventions [11, 13].

Premature birth is associated with endothelial and mitochondrial dysfunction, and chronic oxidative stress, which might impair the physiological responses to acute altitude exposure. We assessed peripheral and oxidative stress responses to acute high-altitude exposure in preterm adults compared to term born controls. Post-occlusive skeletal muscle microvascular reactivity and oxidative capacity from the muscle oxygen consumption recovery rate constant ( k ) were determined by Near-Infrared Spectroscopy in the vastus lateralis of seventeen preterm and seventeen term born adults. Measurements were performed at sea-level and within 1 h of arrival at high-altitude (3375 m). Plasma markers of pro/antioxidant balance were assessed in both conditions. Upon acute altitude exposure, compared to sea-level, preterm participants exhibited a lower reperfusion rate (7 ± 31% vs. 30 ± 30%, p  = 0.046) at microvascular level, but higher k (6 ± 32% vs. −15 ± 21%, p  = 0.039), than their term born peers. The altitude-induced increases in plasma advanced oxidation protein products and catalase were higher (35 ± 61% vs. −13 ± 48% and 67 ± 64% vs. 15 ± 61%, p  = 0.034 and p  = 0.010, respectively) and in xanthine oxidase were lower (29 ± 82% vs. 159 ± 162%, p  = 0.030) in preterm compared to term born adults. In conclusion, the blunted microvascular responsiveness, larger increases in oxidative stress and skeletal muscle oxidative capacity may compromise altitude acclimatization in healthy adults born preterm.

The physiological sequelae of pre‐term birth might influence the responses of this population to hypoxia. Moreover, identifying variables associated with development of acute mountain sickness (AMS) remains a key practically significant area of altitude research. We investigated the effects of pre‐term birth on nocturnal oxygen saturation (SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$ ) dynamics and assessed the predictive potential of nocturnal SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$ ‐related metrics for morning AMS in 12 healthy adults with gestational age < 32 weeks (pre‐term) and 12 term‐born control participants. Participants spent one night at a simulated altitude of ∼4200 m (normobaric hypoxia; fraction of inspired O2 = 0.141), with nocturnal SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$and heart rate recorded continuously at the fingertip using pulse oximetry and with morning AMS assessed using the Lake Louise scale. Pre‐term and term‐born participants had similar nocturnal mean SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$(mean ± SD; 77% ± 3% vs. 77% ± 4%; P = 0.661), minimum SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$(median[IQR]; 67[4]% vs. 69[5]%; P = 0.223), relative time spent with SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$  < 80% (72% ± 29% vs. 70% ± 27%; P = 0.879) and mean heart rate (79 ± 12 vs. 71 ± 7 beats/min; P = 0.053). However, the increase in SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$between the two halves of the night was blunted with prematurity (−0.12% ± 1.51% vs. 1.11% ± 0.78%; P = 0.021). Moreover, the cumulative relative desaturation‐based hypoxic ‘load’ was higher with prematurity (32[26]%min/h vs. 7[25]%min/h; P = 0.039), underpinned by increased desaturation frequency (69[49] vs. 21[35] counts/h; P = 0.009). Mean SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$ , minimum SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$ , morning SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$and relative time spent with SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$  < 80% predicted AMS incidence better than a random classifier exclusively in the pre‐term group, with no other variables predictive of AMS in the two groups separately or combined. Overall, pre‐term birth might alter nocturnal SpO2 ${{S}_{{\\mathrm{p}}{{{\\mathrm{O}}}_{\\mathrm{2}}}$dynamics and influence AMS prediction in severe hypoxia. What is the central question of this study? Does pre‐term birth impact nocturnal pulse oxygen saturation dynamics and acute mountain sickness during simulated high‐altitude exposure equivalent to 4200 m? What is the main finding and its importance? Despite no influence of pre‐term birth on composite nocturnal pulse oxygen saturation metrics, an increased desaturation‐induced hypoxic burden was observed in this group. Composite pulse oxygen saturation metrics predicted acute mountain sickness exclusively in pre‐term adults, suggesting a more direct connection between nocturnal hypoxaemia and altitude‐related illness. These findings advance our understanding of prematurity‐related physiology, particularly in relationship to acute prediction of mountain sickness.

Recent reports suggest that high‐altitude residence may be beneficial in the novel coronavirus disease (COVID‐19) implicating that traveling to high places or using hypoxic conditioning thus could be favorable as well. Physiological high‐altitude characteristics and symptoms of altitude illnesses furthermore seem similar to several pathologies associated with COVID‐19. As a consequence, high altitude and hypoxia research and related clinical practices are discussed for potential applications in COVID‐19 prevention and treatment. We summarize the currently available evidence on the relationship between altitude/hypoxia conditions and COVID‐19 epidemiology and pathophysiology. The potential for treatment strategies used for altitude illnesses is evaluated. Symptomatic overlaps in the pathophysiology of COVID‐19 induced ARDS and high altitude illnesses (i.e., hypoxemia, dyspnea…) have been reported but are also common to other pathologies (i.e., heart failure, pulmonary embolism, COPD…). Most treatments of altitude illnesses have limited value and may even be detrimental in COVID‐19. Some may be efficient, potentially the corticosteroid dexamethasone. Physiological adaptations to altitude/hypoxia can exert diverse effects, depending on the constitution of the target individual and the hypoxic dose. In healthy individuals, they may optimize oxygen supply and increase mitochondrial, antioxidant, and immune system function. It is highly debated if these physiological responses to hypoxia overlap in many instances with SARS‐CoV‐2 infection and may exert preventive effects under very specific conditions. The temporal overlap of SARS‐CoV‐2 infection and exposure to altitude/hypoxia may be detrimental. No evidence‐based knowledge is presently available on whether and how altitude/hypoxia may prevent, treat or aggravate COVID‐19. The reported lower incidence and mortality of COVID‐19 in high‐altitude places remain to be confirmed. High‐altitude illnesses and COVID‐19 pathologies exhibit clear pathophysiological differences. While potentially effective as a prophylactic measure, altitude/hypoxia is likely associated with elevated risks for patients with COVID‐19. Altogether, the different points discussed in this review are of possibly some relevance for individuals who aim to reach high‐altitude areas. However, due to the ever‐changing state of understanding of COVID‐19, all points discussed in this review may be out of date at the time of its publication. We reviewed the differences and similarities in the pathological responses, symptoms, mechanisms, treatments associated to altitude and to COVID‐19.

As more women engage in high-altitude activities, understanding how ovarian hormone fluctuations affect their cardiorespiratory system is essential for optimizing acclimatization to these environments. This study investigates the effects of menstrual cycle (MC) phases on physiological responses at rest, during and after submaximal exercise, at high-altitude (barometric pressure 509 ± 6 mmHg; partial pressure of inspired oxygen 96 ± 1 mmHg; ambient temperature 21 ± 2 °C and relative humidity 27 ± 4%) in 16 eumenorrheic women. Gas exchange, hemodynamic responses, heart rate variability and heart rate recovery (HRR) were monitored at low altitude, and then at 3375 m on the Mont Blanc (following nocturnal exposure) during both the early-follicular (EF) and mid-luteal (ML) phases. Significant differences were observed between low and high-altitude in ventilation, heart rate and cardiac output. Resting ventilation (15.2 ± 1.9 vs. 13.2 ± 2.5 L.min -1 ; p  = 0.039) and tidal volume (812 ± 217 vs. 713 ± 190 mL; p  = 0.027) were higher during EF than ML at high-altitude. These differences between EF and ML were no longer evident during exercise, with comparable responses in oxygen uptake kinetics, cycling efficiency and HRR. The MC had negligible effects on physiological responses to high-altitude. An individualized approach, tailored to each woman’s specific responses to hypoxia across the MC, may be more beneficial in optimizing high-altitude sojourns than general guidelines.

Preterm born (PTB) infants are at risk for injuries related to oxidative stress. We investigated the association between antioxidant and neurodevelopmental gene polymorphisms and oxidative stress parameters in PTB male young adults and their term-born counterparts at rest and during exercise. Healthy young PTB (N = 22) and full-term (N = 15) males underwent graded exercise tests in normobaric normoxic (F i O 2  = 0.21) and hypoxic (F i O 2  = 0.13) conditions. CAT rs1001179 was associated with decrease in nitrites in the whole group and in PTB individuals (P = 0.017 and P = 0.043, respectively). GPX1 rs1050450 was associated with decrease in ferric reducing antioxidant power in the whole group and in full-term individuals (P = 0.017 and P = 0.021, respectively). HIF1A rs11549465 was associated with decrease in nitrotyrosine and increase in malondialdehyde (P = 0.022 and P = 0.018, respectively). NOTCH4 rs367398 was associated with increase in advanced oxidation protein products and nitrites (P = 0.002 and P = 0.004, respectively) in hypoxia. In normoxia, NOTCH4 rs367398 was associated with increase in malondialdehyde in the whole group (P = 0.043). BDNF rs6265 was associated with decreased nitrites/nitrates in the whole group and in PTB individuals (P = 0.009 and P = 0.043, respectively). Polymorphisms in investigated genes and PTB might influence oxidative stress response after exercise in normoxic or hypoxic conditions far beyond the neonatal period in young male adults.

As differential physiological responses to hypoxic exercise between adults and children remain poorly understood, we aimed to comprehensively characterise cardiorespiratory and muscle oxygenation responses to submaximal and maximal exercise in normobaric hypoxia between the two groups. Following familiarisation, fifteen children (Age = 9 ± 1 years) and fifteen adults (Age = 22 ± 2 years) completed two graded cycling exercise sessions to exhaustion in a randomized and single-blind manner in normoxia (NOR; FiO2 = 20.9) and normobaric hypoxia (HYP; FiO2 = 13.0) exercises conditions. Age-specific workload increments were 25 W·3 min−1 for children and 40 W·3 min−1 for adults. Gas exchange and vastus lateralis oxygenation parameters were measured continuously via metabolic cart and near-infrared spectroscopy, respectively. Hypoxia provoked significant decreases in maximal power output PMAX (children = 29%; adults 16% (F = 39.3; p < 0.01)) and power output at the gas exchange threshold (children = 10%; adults:18% (F = 8.08; p = 0.01)) in both groups. Comparable changes were noted in most respiratory and gas exchange parameters at similar power outputs between groups. Children, however, demonstrated, lower PETCO2 throughout the test at similar power outputs and during the maintenance of V˙CO2 at the maximal power output. These data indicate that, while most cardiorespiratory responses to acute hypoxic exercise are comparable between children and adults, there exist age-related differential responses in select respiratory and muscle oxygenation parameters.