ECSS Paris 2023: OP-PN33
INTRODUCTION: Physical exertion under acute hypoxic conditions leads to a progressive reduction in oxygen saturation (SpO₂). This event, in turn, further exacerbates oxidative stress and inflammatory responses, often leading to cellular oxidative damage at different organ/tissue levels. Exposure above 4,000 m altitude is frequently associated with the so-called acute mountain sickness (AMS), a syndrome reflecting the substantial physiological strain imposed by high-altitude environments, yet its neuro-endocrine and molecular mechanisms remain elusive. METHODS: Using a non-invasive saliva and urine sampling approach, we tested the impact of high altitude on a neuroendocrine portfolio (cortisol, dopamine, and BDNF levels) and a redox-inflammatory portfolio. The latter consisted of the evaluation of redox markers, such as lipid peroxidation, 8-isoprostane, total antioxidant capacity (TAC), and glycation: RAGE, and pro-inflammatory and bactericidal proteins, such as interleukin 6 (IL-6) and surfactant Protein D (SP-D), respectively. Italian Air Force (AF) specialists (all males; n=9) were enrolled in the study during their mission (Artemis 4554) in the Italian Alps. The team walked from Alagna (T0) to the Rifugio Gnifetti (T1), then continued to Capanna Margherita (T2–T3), and finally returned to Alagna (T4). To assess the extent of AMS sickness, we used the subjective scale (VAS), and the Lake Louise Score (LLS). RESULTS: The AF specialists exhibited a marked increase in the extent of oxidative stress (8-iso =+151%; TAC=-41%) and inflammation (IL-6 = +244%) that peaked at 4558 m, when SaO2 plummeted. Concomitantly, cortisol levels rose (+13%), whereas dopamine and BDNF declined by -40 and 28%, respectively. During the mission, 4 cases (44%) of AMS (score >3) were reported, including 1 case at Rifugio Gnifetti that interrupted the ascent, and 3 cases at Capanna Margherita. CONCLUSION: Our data indicate that high-altitude exposure, i.e., hypobaric hypoxia, engages neuroendocrine pathways, resulting in reduced dopamine levels and BDNF concentrations that could underscore loss of cognitive capacity. At the same time, elevated cortisol levels, in conjunction with a pro-oxidative/inflammatory milieu, attest to stress conditions. When combined and prolonged, these factors can impair alertness, thus affecting the operational readiness/performance of military personnel operating at high altitudes.
Read CV Manuel MarzolaECSS Paris 2023: OP-PN33
INTRODUCTION: Continuous hypoxic exposure induces systemic cardiovascular and cellular adaptations that may influence tolerance to other environmental stressors [1]. Whether such adaptations confer cross-adaptation to exercise-induced heat stress – particularly in women who remain under-represented in thermoregulatory research [2] – remains poorly understood [3]. METHODS: Healthy, active women were studied before and after a ten-day intervention. The experimental group participants (n=14) continuously resided in normobaric hypoxia (PiO2=98 mmHg; ~3500 m), while control participants (n=13) were free-living in normoxia. At baseline and post-intervention, participants cycled for 45 min at 40% maximal aerobic power (Mean±SD; 102±14 W) under heat-stress conditions induced via insulated clothing in a thermoneutral ambient environment (24±2°C ambient temperature, 51±6% relative humidity). Core body temperature (rectal; pill backup) was measured continuously, alongside gas exchange (metabolic cart) and heart rate (chest strap). Capillary blood samples were obtained at rest and during the final three minutes of exercise for blood lactate analysis. Subjective ratings of perceived exertion (RPE; 6 to 20) and thermal sensation (TS; -4 to 4) were recorded in the final minute. Circulating heat shock proteins (HSP) were measured in resting venous blood samples. Data were analysed using two-way ANOVA (group [hypoxia, control] x time [baseline, post]); interaction effects guided interpretation with significance accepted at p<0.05. RESULTS: During the 45-min exercise, core temperature rise did not differ between groups or time (hypoxia: 1.2±0.4 to 0.9±0.4°C; control: 1.0±0.5 to 0.9±0.4°C; interaction p=0.083). From pre- to post-, relative oxygen uptake exhibited a significant group x time interaction (p=0.002), decreasing more markedly following hypoxic residence (35±4 vs. 32±2 ml/kg/min) than in control (31±4 vs. 29±3 ml/kg/min). Similar interaction effects indicated greater hypoxia-group decreases for heart rate (173±16 to 159±15 bpm vs. 163±13 to 160±11 bpm, interaction p<0.001), blood lactate concentration (4.5±2.5 to 1.8±1.6 mmol/L vs. 2.5±0.9 to 2.0±1.1 mmol/L, interaction p<0.001), RPE (14.3±1.9 to 12.1±1.5 vs. 13.3±2.2 to 13.0±2.2, interaction p=0.001) and TS (3.2±1.0 to 2.2±1.2 vs. 3.0±0.8 to 2.8±0.9, interaction p=0.014). Circulating HSP72 and HSP90a concentrations were unaffected by hypoxic residence (interaction p=0.459 and 0.405, respectively). CONCLUSION: Overall, ten days of continuous normobaric hypoxic residence attenuated the metabolic, cardiovascular, and perceptual responses to exercise heat stress in women, without a corresponding reduction in core temperature rise. This pattern suggests enhanced tolerance to sustained exercise under thermal stress following hypoxic residence, potentially mediated by peripheral thermoregulatory adaptations. 1. Sotiridis et al. (2022) Am J Physiol Regu 2. Hutchins et al. (2021) Sports Med Open 3. Sotiridis et al. (2018) J Appl Physiol
Read CV Tadej DebevecECSS Paris 2023: OP-PN33
INTRODUCTION: Satellite cells participate to myogenesis and contribute to skeletal muscle regeneration and hypertrophy. Amongst other stimuli, satellite cells can be activated by exercise and hypoxia. However, the cumulative effect of those conditions on myogenesis is not well understood yet, certainly in human. Furthermore, whether satellite cells activation and myogenesis differs between environmental hypoxia and blood flow restriction is not known. The purpose of this study was to analyse satellite cell and myogenic markers in response to an acute eccentric resistance exercise in normoxia, normobaric environmental hypoxia and with blood flow restriction (local hypoxia). METHODS: Thirty-eight healthy young men were allocated to one of the three experimental conditions: normoxia (n=13), normobaric environmental hypoxia (n=12) and blood flow restriction (n=13). They all performed 5 series of 15 repetitions at 60°/s for the knee extension and 30°/s for the knee flexion on an isokinetic dynamometer. Vastus lateralis muscle biopsies and blood samples were taken before, 1 h, 24 h and 72 h after exercise. In addition, human skeletal muscle myotubes were stimulated with electrical pulse stimulation at 21%, 5% and 1% O2 and directly harvested. RESULTS: Pax7 and myogenic regulatory factor expression were upregulated after exercise to a greater extent in the normoxic group than in the hypoxic group and almost blunted in the blood flow restriction group. Additionally, compared to pre-exercise, circulating creatine kinase levels increased at 72 h post-exercise by about 5-fold in normoxia and by about 20-fold in normobaric environmental hypoxia but did not change with blood flow restriction. Despite differential regulation of myogenic regulatory factor expression and circulating creatine kinase levels, none of the regulators of myogenesis investigated such as immediate early genes, inflammatory markers and the mitogen-activated protein kinase pathway was differently regulated between the groups. In vitro experiments showed no changes in myogenic regulatory factors between conditions. CONCLUSION: Contrary to our hypothesis, satellite cell activation and myogenesis were not potentiated by the combination of eccentric resistance exercise and hypoxic conditions. Satellite cell and myogenic markers were expressed in a lesser extent when exercising with blood flow restriction than in environmental hypoxia.
Read CV Sophie van Doorslaer de te RyenECSS Paris 2023: OP-PN33