Giovanni Vinetti

Cyclists from various disciplines may find themselves acutely competing at altitude on mountain roads ( Garvican-Lewis et al. , 2014 ), mountain trails ( Brocherie et al. , 2020 ), and high-elevation velodromes ( Bassett et al. , 1999 ). Moreover, they may live ( Siebenmann et al. , 2012 ; Bejder et al. , 2017 ), train ( Terrados et al. , 1988 ; Montero and Lundby, 2017 ), or both ( Gore et al. , 1998 ; Garvican et al. , 2012 ) at natural or simulated altitude with the aim of enhancing endurance performance at altitude ( Schuler et al. , 2007 ) or near sea level. The effect of altitude on sport performance was first studied in runners ( Daniels and Oldridge, 1970 ; Levine and Stray-Gundersen, 1997 ), but since then several studies on cyclists have accumulated. As compared to running, cycling shows lower ventilatory constraint ( Rice et al. , 2000 ; Tanner et al. , 2014 ) and haemolysis ( Dufaux et al. , 1981 ; Schumacher et al. , 2002 ; Telford et al. , 2003 ), both of which may affect the responses to altitude. In this chapter, only studies involving cyclists, or triathletes studied during cycling, are considered.

Female physiological responses to hypoxia remain underexplored, despite growing participation in mountaineering expeditions. Pulmonary interstitial oedema described during acute hypobaric hypoxia can be exacerbated by prolonged physical exercise. It is unclear whether these factors alter the mechanical properties of the respiratory system. We tested the hypothesis that prolonged exercise at terrestrial high altitude would result in interstitial oedema, quantified as B‐lines by lung ultrasound, decreased respiratory reactance ( X _rs ) and lower respiratory resistance ( R _rs ), probably owing to reduced air density. Seven women, participating in the 2024 K2 female expedition, underwent respiratory oscillometry at Skardu (2228 m), Goro II (4319 m) and K2 Base Camp (5100 m) at 6 h post‐arrival (K2BC1), after 24 h (K2BC2) and post‐descent from camp I–II (K2BCPC; 6060 and 6654 m). The B‐lines and systolic pulmonary artery pressure were assessed at Skardu, K2BC2 and K2BCPC. The inspiratory component of X _rs became more negative with increasing altitude (e.g., Skardu vs. K2BC1, −1.42 ± 0.25 vs. −1.62 ± 0.27 cmH ₂ O·s/L; P = 0.003), indicating reduced lung compliance. Both B‐lines (1.0 ± 1.4 vs. 11.9 ± 9.3; P = 0.039) and systolic pulmonary artery pressure (21.9 ± 6.7 vs. 33.0 ± 2.7 mmHg; P < 0.001) increased significantly from Skardu to K2BCPC. The inspiratory component of R _rs decreased from Skardu to K2BC2 (2.88 ± 0.69 vs. 2.34 ± 0.82 cmH ₂ O·s/L; P = 0.003). In women, prolonged exercise at high altitude promotes the development of interstitial oedema (shown by the increase in B‐lines), which is accompanied by a reduction in inspiratory X _rs , indicative of increased lung stiffness.

We found that a single night spent at simulated moderate altitude (1,900 m) prompts measurable ventilatory acclimatization when ascending to simulated high altitude (3,000 m) in males with coronary artery disease. We also found that, although sleeping at 1,900 m increases the occurrence of apneas and/or hypopneas, this did not modify heart rate variability and baroreflex sensitivity responses at 3,000 m.

A lack of consensus remains on whether normobaric hypoxia (NH) and hypobaric hypoxia (HH) may differentially impact physiological factors affecting cerebrovascular regulation, particularly with an additional strenuous exercise component. We sought to compare the acute effects of NH and HH on global cerebral blood flow (gCBF) at an altitude corresponding to 4000 m. In this randomised, single‐blind crossover study, eight lowlanders (3 females) completed three identical trials inside a hypobaric chamber: the first in normobaric normoxia, for familiarisation, followed in random order by one in NH and one in HH. In each trial, gCBF was measured at two time points via duplex ultrasound, first after 25 min of rest, and second, directly after a graded exercise test (GXT) to volitional exhaustion. Cardiorespiratory responses and cerebral oxygenation () were assessed during all gCBF measurements. At rest, gCBF was higher in HH than in NH (944 ± 230 vs. 883 ± 226 mL min ⁻¹ ; P = 0.027, respectively), whereas remained unchanged. Cardiorespiratory parameters did not differ, except for a reduction in the ratio of dead space to tidal volume in HH compared to NH ( P = 0.028). Post‐GXT, no differential response between the two hypoxic conditions was found. In comparison to NH, at rest gCBF is increased in HH for a given partial pressure of inspired oxygen, a response that is subsequently abolished post maximal cycling exercise. Although subtle, this response indicates that cerebrovascular regulation is affected differently in NH and HH, despite negligible changes in ventilation, and thus, alternative explanations are explored for future investigation.

Objectives: The optic nerve sheath expands with elevated intracranial pressure, and its diameter is a sensitive proxy measure. While 2D transorbital ultrasound is well-established for detecting elevated intracranial pressure (>20 mm Hg), it shows limited sensitivity to modest or gradual changes, potentially due to geometric assumptions and imaging misalignment. This study introduces freehand 3D ultrasound imaging of the optic nerve sheath to reduce measurement ambiguity and enhance the fidelity of optic nerve sheath assessment as a noninvasive marker of intracranial pressure. Materials and Methods: Twelve healthy participants (28.7 ± 8.2 y; 6 females) underwent freehand 3D optic nerve sheath imaging during 24 hours of normobaric hypoxia in an environmental chamber (FiO ₂ = 13.1%). Scans were acquired in a head-raised (30 degrees) position at baseline, 6, 12, and 24 hours. Cardiorespiratory parameters, cerebral blood flow, and end-tidal gases were recorded. In 6 participants, postural effects were also assessed at baseline. Nutrition and hydration were standardized to 75% of daily requirements. Results: The optic nerve sheath’s curved, noncircular shape makes the 2D diameter measurement of the sheath a geometric mismatch and an inadequate descriptor. Probe misalignments of 1.2 mm or 15 degrees led to 2D diameter errors (9%/18.7%) exceeding observer variability (2.6%/3.4%). Freehand 3D imaging was reproducible and yielded more informative metrics, including sheath area and thickness. Internal sheath thickness was more responsive to posture and hypoxia than internal 2D diameter (+31.5%, P = 0.01 vs +2.4%, P = 0.9; +8.2%, P = 0.04 vs +1.8%, P = 0.9). A time effect was observed for internal sheath thickness ( P = 0.04), and both area and thickness correlated with internal carotid artery velocity (area: r = 0.9, P = 0.05; thickness: r = 0.8, P = 0.07), consistent with physiological expectations. Conclusion: By eliminating geometric assumptions and misalignment, freehand 3D ultrasound improves the fidelity and sensitivity of optic nerve sheath measurements at the bedside.

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Purpose: Dynamic apnea with fins (DYN) involves swimming the longest distance relying solely on the body’s oxygen and anaerobic energy stores. The energy cost per unit distance ( C ) is therefore an important determinant of DYN performance, yet it has never been measured. This study aimed to assess the C of DYN and its aerobic (EO ₂ ), anaerobic lactic (ELa), and alactic (EPCr) energy contributions. Methods: In a 50-m swimming pool, 22 freedivers (3 females; 10 using bi-fins, 6 using monofin, 6 using both) performed a 50-m DYN, and 7 performed a 100-m DYN. Net C (above resting) was calculated from the O ₂ debt measured at emersion plus ELa (calculated from the blood lactate increase). In nine subjects (six of whom performed also the 100-m DYN), determination of hemoglobin mass and total lung capacity allowed the estimation of EO ₂ and, by subtraction, EPCr. Results: C was unchanged between the 100-m and the 50-m DYN ( P = 0.81) and resulted higher with bi-fins than with the monofin (7.4 ± 2.2 vs 5.5 ± 1.6 J·kg ⁻¹ ·m ⁻¹ , P = 0.02) due to a higher O ₂ debt and ELa. DYN personal best correlated better with the distance swum per unit of EO ₂ at 50 m ( R ² = 0.70) than with C ( R ² = 0.25). From 50 to 100 m, fractional EO ₂ decreased (58% ± 19% to 47% ± 13%, P = 0.02), ELa increased (10% ± 5% to 21% ± 5%, P < 0.001), and EPCr was unchanged (31% ± 20% to 32% ± 15%, P = 0.83). Conclusions: The C of DYN seems compatible with published values for surface swimming with fins at the same speed. At 100 m, ELa and EPCr were disproportionately high for the exercise intensity, possibly due to a diving response. Sparing EO ₂ is at least as important as C in determining DYN performance.

Purpose: There is controversy whether there are meaningful physiological differences between hypobaric (HH) and normobaric hypoxia (NH). This study aimed to compare the cardiorespiratory responses to acute HH and NH under strictly controlled conditions. We hypothesized no differences at rest and during submaximal exercise, whereas during maximal exercise, a higher maximal ventilation (V̇_Emax), peripheral oxygen saturation (SpO₂) and maximal oxygen consumption (V̇O_2max) in HH than in NH. Methods: In a randomized, single-blind, crossover design, eight young healthy subjects (three females) were studied in an environmental chamber in which either the barometric pressure (HH) or the inspired oxygen fraction (NH) was reduced to the equivalent of ~4000 m altitude. Measurements were taken at rest, during submaximal (moderate and high intensity) and maximal cycling exercise. Results: All resting parameters were similar between HH and NH, except for a lower root mean square of the successive R-R interval differences in HH (p < 0.05). SpO₂ was 2% higher in HH at all exercise intensities (p < 0.05). During submaximal exercise, minute ventilation was similar between HH and NH. However, HH yielded a 7% lower tidal volume during moderate-intensity exercise (p < 0.05) and a lower respiratory exchange ratio during high-intensity exercise (p < 0.01). V̇_Emax and V̇O_2max were 11% and 6% higher in HH, respectively (p < 0.01 for both). SpO₂ at maximal exercise was positively correlated with V̇_Emax, V̇_Emax/V̇O_2max and V̇O_2max. Conclusions: The higher V̇O_2max found in HH than in NH can be attributed to the higher V̇_Emax counteracting desaturation at maximal exercise. Conversely, submaximal SpO₂ improved in HH through mechanisms other than increased ventilation. These findings are likely due to respiratory muscle unloading in HH, which operated through different mechanisms depending on exercise intensity.