INTRODUCTION & AIMS: High-volume blood flow restriction (BFR) training uses low loads prescribed as a percentage of 1-repetition maximum (1RM), yet performance during these protocols depends on muscular endurance, resulting in variable effort among participants. Measuring concentric velocity during BFR exercise may provide a practical way to monitor performance and effort. This study characterised velocity decline during low-load bench press with BFR, and assessed the reliability of repetition velocity during this exercise. METHODS: Twenty participants completed a bench press 1RM test before two trials of four sets at 30% 1RM with continuous BFR (5 cm cuffs) at 60% arterial occlusion pressure. Sets were structured as 30, 15, 15, and 15+ repetitions (fourth set to failure) with 30 s rest. Mean concentric velocity was measured using a linear position transducer. Velocity decline was profiled for the fourth set, with repetitions divided into deciles to account for varying set lengths. Differences across deciles were analysed via repeated-measures ANOVA. Test–retest reliability for the final 7 repetitions was assessed using ICC and CV, with acceptable reliability defined as ICC ≥ 0.80 and CV ≤ 10%. RESULTS: Velocity declined progressively, with significant differences between deciles (p < 0.05) and an overall reduction of ~69% from first to last decile. Reductions were modest early (≤7% between deciles 2–7) but increased later, with significant drops of ~11%, ~21%, and ~37% across the final three deciles. ICC ranged from 0.54–0.82 and CV from 11.3–26.6%, with no repetitions meeting acceptable reliability thresholds. CONCLUSION: Velocity monitoring clearly reflects performance decrements during low-load BFR bench press, with the largest declines occurring in the final stages of a set. However, mean concentric velocity showed unacceptable reliability for matched repetitions between sessions. While velocity can indicate accumulating fatigue, it should not be used alone to prescribe or adjust BFR resistance training.

Intensive exercise and high-altitude exposure can disrupt neural activity and impair cognitive functioning. Previous research suggests that ketone ester (KE) ingestion may counteract cognitive impairments; however, its impact on neural activity during exercise and hypoxia remains unclear. Therefore, we investigated the impact of KE on electroencephalography (EEG) patterns and cognition during hypoxia and exercise. Twelve healthy males completed three randomized crossover sessions: i) normoxia + placebo, ii) hypoxia + placebo, and iii) hypoxia + KE. Each session included normoxic endurance (ET120') and high-intensity interval training (HIIT80'), followed by a 16-h period including sleep in either normoxia or hypoxia. The next day, participants performed a normoxic 30-min all-out time-trial (TT30'). EEG was recorded during rest and exercise, while cerebral tissue oxygenation index (cTOI) and cognitive performance were evaluated during rest. At rest, KE attenuated hypoxia-induced increases in alpha and beta power and cTOI declines. Nonetheless, cognitive performance remained unaffected. Brain activity rose throughout ET120' and normalized during recovery, while HIIT80' elicited a fluctuating neural response but normalized during recovery. Following TT30', theta, alpha, and gamma power remained elevated during recovery. Altogether, these data, obtained in healthy males, show the potential of KE to stabilize resting-state EEG patterns in hypoxia. Moreover, they shed light on how EEG patterns vary with exercise intensity, with sustained postexercise increases in theta, alpha, and gamma power following high-intensity efforts. These findings suggest that KE can help to preserve neural stability under hypoxia and highlight EEG's potential for monitoring fatigue and tailoring training or recovery strategies.NEW & NOTEWORTHY This study is the first to demonstrate the effects of ketone ester ingestion on hypoxia-induced neural alterations. Moreover, it uniquely combines measurements of cerebral oxygenation, cognitive performance, and electroencephalography (EEG) across low-, high-, and all-out exercise intensities, as well as during rest. Potentially highlighting EEG as a valuable tool for monitoring fatigue and optimizing training strategies.

AIMS:Normative data for cardiopulmonary exercise testing (CPET) provide benchmarks of aerobic fitness that change throughout the lifespan, with new scaling techniques often developed and differing between adults and children/adolescents. Considering the recent interest in the pediatric population for CPET studies, this systematic review aimed to update pediatric-specific CPET reference values. METHODS AND RESULTS:A systematic review was performed according to the PRISMA guidelines from February 1, 2019, to December 31, 2025, from 6 scientific databases. Observational studies in any language, presenting data from maximal CPET, and conducted only on healthy participants <18 years old were included. Primary outcomes included reference values for peak oxygen uptake (V̇O2peak), and secondary outcomes included other variables assessed during CPET. Risk of bias was assessed with the 14-point ATS/ACCP statement for CPET and the 8-point JBI Critical Appraisal Tool. 15 studies conducted on 12,083 participants (5,886 [49.4%] females) were included, of which recruitment was hospital-based in 6 studies, community-based in 8 studies, and athlete-specific in 1 study. 6 studies reported ethnicity, with most participants classified as white, while 1 investigation presented exclusive data for obese/overweight or pediatric athletic cohorts. Normative V̇O2peak ranged between 26.0-56.3 mL·kg-1·min-1, peak heart rate between 175-199 bpm, and peak ventilation between 52.2-96.0 L·min-1. Reference equations were developed in 11 studies, with 5 of these studies validating the derived equations. A high heterogeneity was observed between studies of high- (n=2), moderate- (n=9), and low-quality (n=4), with ATS/ACCP statement and JBI Critical Appraisal Tool often disregarded - although quality level did not influence study outcomes. CONCLUSION:Updated normative values for CPET varied significantly in pediatric cohorts. While female representation matched male, and more studies considering pediatric athletes, showing a positive trend change from previous investigations, obese and overweight children/adolescents, as well as non-white participants, remained underrepresented. Considering the differences in normative data between pediatric cohorts of differing characteristics, clinicians should use reference values derived from cohorts closely matching their patients' characteristics. PROSPERO REGISTRATION NUMBER:CRD420251137402.

Mountain ultra-marathons (MUM) impose multiple stressors on pulmonary function inducing risk of airway epithelial damage. This study aimed to assess the magnitude of pulmonary function changes and the associated risks of airway damage induced by such a race. Thirteen volunteers completed the MUM (330 km, 24,000 m elevation gain). Pulmonary function was assessed using standardized procedures before (pre-) and within 1 h after (post-) the race. Assessments included forced inhalation and exhalation maneuvers, as well as maximal inspiratory pressure (MIP) measurements. Venous blood samples were collected for the analysis of plasma club cell secretory protein 16 (CC16). Blood volume was determined using the carbon monoxide rebreathing method. From pre- to post-, forced vital capacity (FVC) (-7.5

Exogenous ketosis, induced via ketone monoester (KE) ingestion, has been shown to attenuate hypoxia-induced blood, muscle, and brain deoxygenation and augment oxygen uptake (V̇o2) under acute normobaric hypoxia. However, its effects on exercise responses during early acclimatization at terrestrial high-altitude remain unexplored. Thirty-four healthy, active adults completed four exercise sessions: one near sea level and then once per day during a 3 day altitude sojourn (3,375 m), with regular KE or placebo ingestion. Pulmonary gas exchange, minute ventilation, cardiac output, pulse oxygen saturation, skeletal muscle tissue saturation index (TSI), and brain TSI were measured during moderate- and heavy-intensity exercise. KE ingestion induced ketosis at the start of each exercise session (group × time interaction: P < 0.001). However, compared with placebo, KE resulted in a comparable (group × time interaction: P = 0.501) high-altitude-induced slowing of the primary phase time constant of V̇o2 kinetics during heavy-intensity exercise (time effect: P < 0.001). Moreover, both groups exhibited similar (all group × time interactions: P > 0.123) hypoxia-related decreases in gas exchange and increases in minute ventilation, accompanied by reductions in pulse oxygen saturation and brain TSI during both moderate- and heavy-intensity exercise across the 3 days (all time effects: P < 0.015). Notably, KE ingestion increased cardiac output during moderate-intensity exercise on the first altitude day (group × time interaction: P = 0.042). Whole-body energy efficiency was preserved across time at 3,375 m (time effect: P = 0.060) in both groups (group × time interaction: P = 0.084). These data indicate that intermittent exogenous ketosis does not attenuate altitude-induced alternations in V̇o2 kinetics or tissue oxygenation, nor improves whole-body efficiency, during moderate- or heavy-intensity exercise across 3 days at 3,375 m.NEW & NOTEWORTHY This study demonstrates that intermittent exogenous ketosis does not alter the high-altitude slowing of the primary phase of V̇o2 kinetics during the transition to heavy-intensity exercise, nor does it change ventilatory, gas exchange, blood or tissue oxygenation responses, or whole-body efficiency across 3 days at 3,375 m. However, preexercise ketone monoester ingestion increased cardiac output during moderate-intensity exercise on arrival to 3,375 m and after 24 h, but this did not translate to broader physiological benefits.

Intermittent exogenous ketosis via ketone monoester (KE) ingestion has been shown to enhance physiological responses and reduce acute mountain sickness (AMS) symptoms during acute normobaric hypoxia. Its effects during early acclimatization to terrestrial high-altitude, however, remain unclear. Thirty-four participants were randomised to an intermittent exogenous ketosis (IEK, n=17) or placebo (PLA, n=17) group and underwent a near sea level trial (295 m) without supplementation, followed by a four-day sojourn at 3375 m during which they received regular KE (IEK) or placebo (PLA) supplements. AMS symptoms, hematological markers, and resting ventilatory, cardiovascular, and cerebral tissue oxygenation responses were assessed each day upon waking, at midday, and before sleep throughout the exposure. KE consistently elevated circulating β-hydroxybutyrate post-ingestion (P<0.001), confirming intermittent exogenous ketosis in the IEK group. AMS incidence peaked at 25–35

This study aimed to examine the physiological mechanisms associated with Voluntary Isocapnic Hyperpnoea (VIH) in severe hypoxia and evaluated whether such respiratory modulation may attenuate hypoxemia and Acute Mountain Sickness (AMS). Eighteen healthy participants (8 females) completed two 2-hour sessions in a normobaric hypoxic chamber simulating 4200 m above sea level, in randomized order: an experimental session including a 5-minute VIH intervention after 1 h, and a control session without VIH. AMS symptoms, arterial oxygen saturation (SpO₂), heart rate, blood pressure and gases were monitored before and during the hypoxic exposure. Separate repeated-measures ANOVAs were employed to analyze the effects of VIH and differences between the sessions. VIH decreased clinical hypoxemia (from 83.3% to 22.2%) and reduced AMS incidence (from 11.1% to 5.5%). This was associated with an increase in SpO₂ (p = 0.011, ηp2 = 0.341, ω2 = 0.159) and blood oxygen partial pressure (p = 0.027, ηp2 = 0.271, ω2 = 0.112). SpO₂ kinetics differed between sessions (p = 0.011, ηp2 = 0.132, ω2 = 0.061), with higher values during the experimental session. This benefit was acute as differences in SpO₂ were not noted at the final timepoint. Substantial intra-individual variability and no sex-related interactions were observed. These preliminary findings suggest that VIH is a feasible method for transiently improving blood oxygen saturation under hypoxia, and has the potential to attenuate AMS. Further research is nevertheless warranted to clarify the role of VIH within the framework of altitude medicine and address potential mechanistic explanations. Methodological insights from the present study should inform future investigations.

Regular physical activity improves vascular function and promotes angiogenesis and erythropoiesis, which are further augmented by hypoxia. Early evidence suggests that long-term exogenous ketosis (EK) can enhance vascular function and angiogenesis. However, the acute responses and underlying mechanisms remain unknown. Moreover, acute and prolonged EK may increase blood erythropoietin (EPO) concentrations in normoxia. Nonetheless, whether this effect is additive to hypoxia is unclear, as an EK-mediated attenuation of blood deoxygenation may counteract the [EPO] increase. In a randomized, placebo-controlled, crossover design, 13 male and two female participants completed four experimental sessions. Each included a high-intensity interval training session, followed by recovery either in normoxia or normobaric hypoxia (3000 m simulated altitude, F I O 2 ${{F}_{{\mathrm{I}}{{{\mathrm{O}}}_2}}}$ : 14.5%), supplemented with placebo or the commercial ketone precursor Ketone-IQ®. Macro- and microvascular function were assessed throughout a vascular occlusion protocol, using femoral artery blood flow and muscle oxygenation, respectively, after 2.5 and 5.5 h recovery. Additionally, serum EPO and endothelin-1 (ET-1) concentrations, and skeletal muscle expression of pro-angiogenic and vascular integrity markers were evaluated. In normoxia and hypoxia, EK increased post-occlusion blood velocity (+15%) and muscle reoxygenation rate (+9%). Furthermore, muscle expression of pro-angiogenic and vascular integrity markers (including vascular endothelial growth factor, peroxisome proliferator-activated receptor γ coactivator 1α, and angiopoietin-1) as well as serum [EPO] (+15%) increased with EK, while serum [ET-1] was reduced (-13%). EK appears as a promising strategy to enhance vascular function and integrity, angiogenic signalling, and circulating [EPO] in response to exercise and hypoxia, thereby facilitating beneficial adaptive responses. KEY POINTS: Exogenous ketosis (EK) enhances macro- and microvascular function during post-exercise recovery, in both normoxia and hypoxia, likely through reducing serum [ET-1]. Moreover, EK upregulates markers of exercise-induced angiogenesis and vascular integrity. Finally, an EK-related, post-exercise increase in serum [EPO] is additive to hypoxic exposure alone.

ABSTRACT We compared neuromuscular fatigue induced by cycling at a fixed perceived effort in normoxic condition (NOR) and three purported hypoxia modalities: systemic hypoxia (SyH, FiO 2 = 0.13), blood flow restriction (BFR, 50% arterial occlusion pressure) and airflow restriction mask (ARM, calibrated to ~3500 m). Seventeen healthy young participants cycled for 20 min at a self‐selected power output corresponding to a hard effort (15/20, Borg scale) on an innovative cycle ergometer allowing immediate neuromuscular evaluation. Isometric maximum voluntary contraction of the knee extensors (IMVC), central (voluntary activation, VA) and peripheral fatigue were measured before and every 5 min during cycling. Power output, peripheral oxygen saturation (SpO 2 ), quadriceps oxygenation (near‐infrared spectroscopy, TSI) and pain were assessed throughout cycling. Power output was lower in BFR and SyH compared to NOR and ARM and was lower in BFR compared to SyH. SpO 2 was reduced only in SyH (mean 77% ± 4%). In all conditions, IMVC decreased from minute 5 and subsequently plateaued (~−10% to −20%), except in BFR, wherein it further declined to −40% ± 14% at minute 20 in the presence of lowered VA and exacerbated muscle pain compared to other conditions. Muscle TSI was further decreased in SyH compared to other conditions. Our results confirm the inability of ARM to induce hypoxia. Compared to other conditions, BFR showed a greater reduction in IMVC and VA, in the presence of a higher quadriceps pain and no greater muscle deoxygenation. These results underline the psychophysiological impact of quadriceps pain on both maximal and submaximal motor output.

The ergogenic effects of caffeine for endurance performance at sea level are well established. However, whether caffeine enhances exercise capacity or modulates cardiorespiratory responses in hypoxia remains unclear. Twenty-nine healthy, active volunteers (14 women) completed four tests in a pseudorandomized order, comprising 10 min of steady-state cycling (40% normoxic maximal aerobic power) followed by incremental exercise tests to exhaustion. Participants consumed 6 mg/kg body mass anhydrous caffeine, or placebo, 45 min before exercise. Tests were performed while breathing room air or a hypoxic gas mixture (simulating ∼3,500 m). At peak exercise intensity, oxygen uptake was affected by condition (hypoxia vs. normoxia; 44.8 ± 7.3 vs. 51.4 ± 7.9 ml·kg −1 ·min −1 ; p < .001) but not supplement (caffeine vs. placebo; 48.2 ± 8.2 vs. 48.0 ± 8.4 ml·kg −1 ·min −1 ; p = .501). Maximal aerobic power and pulse oxygen saturation were lower in hypoxia (both p < .001), but unaffected by caffeine ( p = .061 and .898, respectively). Pulmonary ventilation was unaffected by hypoxia ( p = .154) or caffeine ( p = .117). Heart rate was higher in normoxia and with caffeine (both p < .001). During steady-state cycling, hypoxia ( p < .001) and caffeine ( p = .026) increased pulmonary ventilation. However, the hypoxia-induced pulse oxygen saturation decrease ( p < .001) was not attenuated with caffeine (interaction p = .283). Perceived exertion was higher in hypoxia ( p < .001) and lower with caffeine ( p = .026). Caffeine increased vastus lateralis oxygenation in hypoxia (caffeine vs. placebo; 52 ± 8 vs. 50 ± 10%; p = .020) but not in normoxia (caffeine vs. placebo; 59 ± 7 vs. 59 ± 8%; p > .999). Overall, caffeine did not enhance exercise capacity in either environmental condition. However, during steady-state cycling, caffeine enhanced pulmonary ventilation, reduced perceived exertion, and mitigated hypoxia-induced muscle oxygenation reductions.

Ovarian hormones may modulate key physiological functions that play a crucial role in the acute response to hypoxia. Women remain underrepresented in high-altitude physiology research. This exploratory study aimed to investigate the impact of menstrual cycle (MC) phases on resting skeletal muscle oxygen consumption and post-occlusive microvascular reactive hyperemia in the lower limbs during acute high-altitude exposure in eumenorrheic women. Microvascular function was assessed via vascular occlusion test in combination with near-infrared spectroscopy on the vastus lateralis muscle. Measurements were conducted at low altitude (1224 m) and after one night at 3375 m (inspired O2 pressure: 96 ± 1 mmHg) during both the early follicular (EF) and mid-luteal (ML) phases. At high altitude, baseline tissue saturation index (TSI) (65.0 ± 4.8 vs. 66.1 ± 2.7 %; p = 0.559), desaturation rate (-0.086 ± 0.061 vs. -0.080 ± 0.039 %·s-1; p = 0.920), normalized reperfusion slope (0.013 ± 0.010 vs. 0.014 ± 0.005 %·s-1; p = 0.100) and minimum TSI (52.9 ± 6.8 vs. 53.9 ± 3.9 %; p = 0.647) did not differ significantly between EF and ML. Reperfusion rate decreased significantly from low (0.894 ± 0.320) to high altitude during both EF (0.661 ± 0.424; p = 0.027) and ML (0.722 ± 0.253; p = 0.027). These findings suggest that microvascular function is not significantly modulated by the MC at 3375 m. This study adds further evidence suggesting that no specific recommendation regarding the optimal menstrual cycle phase for acute high-altitude exposure is warranted.

High-altitude (HA) exposure induces an integrated physiological response to mitigate hypoxemia. Exogenous ketosis at simulated HA was previously shown to accentuate sympathetic activation and attenuate pulse oxygen saturation ([Formula: see text]) decreases through hyperventilation. The aim of this study was to extend these findings by investigating the effects of intermittent exogenous ketosis (IEK) across 2 days at terrestrial HA (3,375 m) on baroreflex sensitivity, heart rate variability, and hypoxic/hypercapnic ventilatory responses. Thirty-four healthy active adults completed neutral, hypoxic, and hypercapnic (0.03 [Formula: see text]) exposures, each comprising 6 min of seated rest, once at sea level (SL) and once after 2 days at HA. Across the 2 days, participants intermittently ingested either ketone monoester supplements (IEK) or placebo (PLA). During each exposure, blood pressure, ventilation, [Formula: see text], and end-tidal CO2 pressure ([Formula: see text]) were continuously recorded, and arterialized capillary blood gas content was measured in the final 30 s. Baroreflex sensitivity and time-domain metrics of heart rate variability were reduced at HA (P = 0.006-0.043) but unaffected by group (P = 0.288-0.525). However, ventilation at HA under all three conditions was significantly higher in IEK compared with PLA (all P < 0.001). In hypoxia, this induced a higher [Formula: see text] (P = 0.038) and capillary O2 pressure (P = 0.003). In hypercapnia, this induced a lower [Formula: see text] and capillary CO2 tension (both P < 0.001). These results extend previous findings, suggesting that IEK enhances ventilation at terrestrial HA after 2 days of exposure, with this effect being independent from baroreflex sensitivity or heart rate variability changes.NEW & NOTEWORTHY This study demonstrates that 2 days of intermittent exogenous ketosis at 3,375 m terrestrial altitude does not alter baroreflex sensitivity or heart rate variability but significantly increases pulmonary ventilation under neutral, hypoxic, and hypercapnic conditions, improving oxygenation and lowering carbon dioxide retention. These findings suggest that ketone supplementation may enhance ventilatory acclimatization to high altitude via metabolic acidosis-driven respiratory stimulation, offering a nonpharmacological alternative to typical interventions used to support acclimatization.

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 ( S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ ) dynamics and assessed the predictive potential of nocturnal S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ -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 S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ 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 S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ (mean ± SD; 77% ± 3% vs. 77% ± 4%; P = 0.661), minimum S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ (median[IQR]; 67[4]% vs. 69[5]%; P = 0.223), relative time spent with S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$  < 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 S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ 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 S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ , minimum S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ , morning S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ and relative time spent with S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$  < 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 S p O 2 ${{S}_{{\mathrm{p}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ dynamics and influence AMS prediction in severe hypoxia.

We sought to investigate whether the magnitude of differences in cycling critical power between normoxia and hypoxia (∆CP) is associated with fitness level or haematological status in highly trained endurance athletes. Thirty-three triathletes and longtrack speed skaters (11 females) completed two 3-minute CP cycling tests: one in normoxia (FiO2 = 20.8%) and the other in normobaric hypoxia (FiO2 = 14.2%). This cross-sectional study analysed ∆CP regarding performance, physiological, and haematological indices using correlation and regression analyses. Significant correlations were found between ∆CP and baseline CP in normoxia (r = -0.366, p = 0.047), V ˙ O 2 max (r = -0.437, p = 0.018), and MCH (r = 0.487, p = 0.012). Only a few significant associations were found between the indices obtained from venous blood sampling and ∆CP, different for females and males. In females, ∆CP was correlated with Hbmass (r = -0.761, p = 0.017), erythrocyte volume (r = -0.783, p = 0.013), plasma volume (r = -0.745, p = 0.021), and blood volume (r = -0.870, p = 0.002), all established with the CO rebreathing method. The best-performing regression model (R2 = 0.501, RMSE = 0.033, p = 0.002, Cohen's F2 = 1.004) included MCH, V ˙ O 2 max , and Hbmass. A higher fitness level is associated with a greater CP decrease in hypoxia among the homogeneous cohort of highly trained endurance athletes. Haematological status plays a more prominent role in females, and the CO rebreathing method should be considered a preferred approach for assessing haematological status in highly trained athletes.

Novel wearable near-infrared spectroscopy devices allow for a better understanding of muscle oxygenation kinetics during exercise. A muscle oxygen saturation (SmO2) plateau is often applied in the scientific literature, but clear criteria for its definition remain unestablished to date. The aim of this study was to develop criteria allowing for definition of SmO2 plateaus. Multiple variables associated with physiological plateaus during exercise were assessed to develop a framework for an SmO2 plateau. Subsequently, the existence of an SmO2 plateau during 3 min all-out cycling trials (critical oxygenation plateau) was tested in different conditions of oxygen availability (i.e., normoxia and hypoxia) in vastus lateralis and triceps brachii among 30 endurance athletes. Plateau determination methods based on a threshold of change of ±5 arbitrary units (a.u.) of SmO2 and expert visual assessment showed almost perfect agreement. However, a threshold of 10 a.u. yielded high SmO2 variability associated with a large number of possibly false-positive detections. Conversely, relative changes (thresholds of 5% and 10%) did not align with other methods, corresponding to low absolute changes, limiting their applicability. The inter-rater agreement between individual visual assessments exhibited a higher reliability among expert versus non-expert raters. The determination of an SmO2 plateau depends on the applied methodology. Overall, a critical oxygenation plateau was observed in the vastus lateralis in both normoxia and hypoxia in >90% of cases. The results of this study allow recommendation either for the use of a threshold of change corresponding to 5 a.u. of SmO2 or expert visual assessment, using 30 s segments.

Epidemiological evidence suggests that living at a moderate altitude (i.e. between 1000 and 2500 m) is associated with lower overall mortality, particularly from cardiovascular diseases. The underlying mechanisms have been scarcely investigated, although environmental and lifestyle factors likely play prominent roles. This review aims to shed light on two important modulators of cardiovascular health and mortality, that is, physical activity and body mass, and to explore how these factors interact with altitude. The lifestyle habits of people living at moderate altitudes have been shown to differ from individuals living at low altitudes. In addition the environmental conditions, notably the hypobaric hypoxia, at moderate altitudes influence the physiological parameters associated with these habits. Specifically engaging in the same physical activity at moderate altitude compared to low altitude results in enhanced cardiovascular responses and specific metabolic responses, potentially imparting benefits related to the cardiovascular system and body composition. Conversely mild hypobaric hypoxia can suppress appetite and food intake, leading to lower overall body mass and decreased risk of obesity. Exercise or sleep can accentuate the hypoxic stimuli at moderate altitudes and, like hypoxia conditioning, elicit adaptations such as improved oxygen supply, reduced dependence on oxygen and increased cellular/tissue resilience. These effects may prove beneficial for the cardiovascular and metabolic systems and contribute to lower mortality rates observed in moderate altitude residents.