ECSS Paris 2023: OP-PN28
INTRODUCTION: Exposure to hypoxia triggers hyperventilation and hypoxic pulmonary vasoconstriction (HPV) which may influence lung diffusing capacity (DL) by modifying pulmonary capillary blood volume (Vc) and/or membrane diffusion (Dm) [1]. These mechanisms are known to affect pulmonary gas exchange. However, their respective time courses during acclimatization, and in particular the relative contributions of Vc versus Dm to changes in DL, remain incompletely characterized, especially in women. Therefore, this study aimed to characterize the changes in pulmonary diffusing capacity and its determinants across 10 days of altitude exposure in women. METHODS: Fifteen healthy young female lowlanders were exposed to normobaric hypoxia (inspired O2 partial pressure: 98 mmHg; ~3500 m) for 10 days. DL was assessed at rest before (pre) and after (post) the exposure, as well as upon arrival (D0), and at day 2 (D2), 4 (D4), 9 (D9) during exposure. DL was also evaluated during steady-state exercise (6-min bouts at 40% of maximal power output) at pre, post and D2, D4, and D9. DL was assessed using the single-breath method with nitric oxide (DLNO) and carbon monoxide corrected for hemoglobin concentration (DLCO) (HypAir, MGC Diagnostics, Saint Paul, MN), following standardized procedures. RESULTS: At rest, alveolar volume (VA) and DLNO remained stable across all time points. Resting DLCO was higher at D9 vs. pre (27.3 ± 3.4 vs 25.6 ± 3.2 mL/min/mmHg, p = 0.022). Vc was greater at D0 (71.3 ± 17.6 mL), D2 (63.8 ± 10.8 mL), and D9 (68.2 ± 12.8 mL) compared with pre (53.2 ± 9.4 mL) and post (51.2 ± 7.9 mL; all p < 0.045). Conversely, DmCO was lower at D4 and D9 (134 ± 21 and 128 ± 17 mL/min/mmHg) compared with pre and post (172 ± 49 and 195 ± 45 mL/min/mmHg, all p < 0.037). During exercise, VA and DLNO did not differ across time points. In contrast, DLCO values were higher at D4 and D9 (36.9 ± 5.3 and 37.6 ± 5.2 mL/min/mmHg) compared with both pre and post (32.0 ± 3.6 and 31.7 ± 2.8 mL/min/mmHg; all p < 0.015). Changes in Vc during exercise followed a similar pattern, while DmCO was lower at D4 and D9 (150 ± 27 and 148 ± 28 mL/min/mmHg) compared with pre- and post-exposure (213 ± 68 and 214 ± 60 mL/min/mmHg, all p < 0.017). There were no differences at rest or during exercise between the normoxic pre-post timepoints. CONCLUSION: Exercising DLCO demonstrated specific acclimatization kinetics across ten days in continuous hypoxia. DL improved after several days, driven by Vc increases that outweighed DmCO reductions. These adaptations likely reflected HPV-mediated elevations in perfusion pressure, leading to capillary distension and recruitment. Collectively, these findings suggest that moderate altitude exposure maintains or slightly enhances DL via Vc increases; an adaptation not maintained upon return to normoxia. 1 Martinot et al. (2013) J Appl Physiol. doi: 10.1152/japplphysiol.01455.2012.
Read CV Antoine RaberinECSS Paris 2023: OP-PN28
INTRODUCTION: Ventilatory acclimatization is a form of respiratory plasticity that enables successful acclimatization to high altitude by progressively increasing chemoreceptor-driven ventilation at a given altitude to protect oxygenation. For unknown reasons, ventilatory acclimatization is impaired in individuals with a patent foramen ovale (PFO), which is an intracardiac shunt present in ~30% of the population (Lovering et al., 2022). Recently, the steady-state chemoreceptor drive (SSCD) has been proposed as an integrative index of prevailing respiratory drive, derived non-invasively as minute ventilation divided by a stimulus index (SI), defined as the ratio of end-tidal CO₂ to peripheral oxygen saturation (Johnson et al., 2025). In the present study, we used SSCD derived from direct arterial measures to quantify respiratory drive after 16 days of acclimatization to 5260m in participants with and without a PFO. METHODS: Resting measures were assessed in twenty participants with (PFO+; 11 (7 females) and without a PFO (PFO-: 9 (2 females) at sea level (SL) and at day 16 (ALT16) after rapid ascent to 5,260 m. The SSCD was derived from calculated alveolar ventilation (V̇A), arterial saturation (SaO₂), and partial pressure of arterial carbon dioxide (PaCO₂) derived from direct arterial blood gas and co-oximeter analyses. Two-way repeated-measures mixed-model ANOVAs with Tukey corrections for multiple comparisons were conducted for all variables on the factors time (SL, ALT16) and PFO (presence/absence). RESULTS: As a group, all variables demonstrated significant time effects (all p < 0.0001) with increased V̇A (+5 L min-1), reduced PaCO2 (-17 mmHg) and SaO2 (-16.7 mmHg) at ALT16, and a resulting increased SSCD (+29.5 a.u.). Pair-wise comparisons showed no group differences at SL, but there were significant main effects of PFO and PFO x Time for SSCD (p = 0.0227, p = 0.0111 respectively). However, PFO+ participants had a lower V̇A (-3.2 L min-1) and consequently a lower SaO2 (-4%) at ALT16, which resulted in a significantly lower SSCD (-23 a.u.) than PFO- participants. CONCLUSION: We found that the presence of a patent foramen ovale (PFO) was associated with a reduced SSCD, quantified directly from arterial blood draws. This reduced SSCD limited the expected improvement in SaO2 with acclimatization to high altitude after 16 days. The reason(s) SSCD was attenuated remains unknown, although it is possible that PFO+ participants require more time to effectively acclimatize to 5260m, potentially due to impairments in V̇/Q̇-matching and O2-exchange. Nevertheless, the relative attenuation in ventilatory drive after acclimatization in PFO+ may constrain expected improvements in exercise and cognitive performance at altitude. In applied settings, SSCD represents a promising metric for monitoring health and performance during high-altitude acclimatization. Johnson (2025), Proc Natl Acad Sci, DOI: 10.1073/pnas.241256112 Lovering (2022), J Physiol, DOI: 10.1113/JP281108
Read CV Fabian MöllerECSS Paris 2023: OP-PN28
INTRODUCTION: During maximal ramp-incremental exercise (RIE), whole-body oxygen uptake (VO2) may increase disproportionately near exhaustion, complicating the determination of maximal oxygen consumption (VO2max) during athlete performance testing. These increases may reflect skeletal muscle VO2 demand but may also include substantial contributions from the respiratory and postural musculature, thereby increasing the VO2 cost of ventilation (VO2VENT). Such variability complicates traditional confirmation of VO2max based on the presence of a VO2 plateau. Consequently, the absence of a VO2 plateau may not indicate a failure to reach physiological maximum but instead reflect intensity-dependent shifts in the contributors to whole-body VO2. While VO2VENT has been quantified in recreational populations, its influence on VO2max determination remains poorly defined in highly trained endurance athletes. Quantifying this contribution is therefore critical for isolating skeletal muscle VO2 and improving interpretation of VO2max in applied testing. METHODS: Eight highly trained male endurance athletes (Age, 35 +/- 7 yrs; VO2max 5.75 +/- 0.620 L min-1) performed a maximal RIE cycling test. Breath-by-breath pulmonary gas-exchange was measured using a calibrated fast-response turbine flow transducer (Hans Rudolph-430) and rapid response electronic gas analyzers (AEI Technologies, Model S-3 A and Model CD-3H). VO2max was defined as the highest 15-breath average. VO2VENT was measured during separate voluntary hyperpnoea trials at rest (50-95% of maximal inspired ventilation; MaxVI) with hypercapnic gas (FICO2 = 3.7%; FIO2 = 21%; balance N2) used to prevent hypocapnia. Individual VI-VO2 relationships were modelled and extrapolated to estimate VO2VENT at 100% MaxVI, then applied to RIE data. Whole-body VO2 was corrected for VO2VENT (VO2VCORR), and linear slopes of the final 30 s of exercise were compared between measured VO2 and VO2VCORR using paired t-tests (p<0.05). RESULTS: At VO2max, VO2VENT accounted for 11.1% +/- 2.1% (range 8.4-13.9%) of whole-body VO2. Individual VI-VO2 regressions were highly linear (R2 = 0.90 +/- 0.10). Correcting for VO2VENT significantly decreased the final 30 s VO2 slope (0.320 +/- 0.178 vs. 0.171 +/- 0.135 mL min-1 W-1; p < 0.0001). Participants exhibited increased breathing frequency and reduced tidal volume prior to and near exhaustion. CONCLUSION: Respiratory work imposes a substantial metabolic load in highly trained endurance athletes and significantly increases VO2 near exhaustion. Accounting for VO2VENT refines estimates of skeletal muscle VO2 demand, improves VO2max accuracy and interpretation, and enhances athlete performance test interpretation. This work establishes VO2VENT as a measurable and modifiable contributor to VO2max, warranting targeted investigation of respiratory training strategies to improve ventilatory efficiency and endurance performance.
Read CV Bridgette OMalleyECSS Paris 2023: OP-PN28