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Introduction Ultra-marathon races present a prolonged cardiopulmonary physiological stress but the magnitude, persistence, and impact of race environment on respiratory function are incompletely understood. The aim of this study is to observe the effect of ultra-marathon trail races on both lung function and airway impedance. Methods Fifty-seven individuals (49/8, M/F) participated in either the Courmayeur-Champex-Chamonix (CCC ® , 101.5km), Ultra Trail du Mont-Blanc (UMTB ® , 171.5 km), or the Hong Kong 100 (HK, 100 km) races. Participant demographics were measured pre-race and included: age (40.7±10.3 yrs); height (175.5±7.1 cm), body mass (69.7±8.3 kg). Spirometry, airway impedance (via forced oscillation technique, FOT), maximal inspiratory (MIP) and expiratory pressure (MEP), and exhaled nitric oxide (ExNO) were assessed before, immediately (18–4 hours after), and 188–24 hours post-race. Mixed effects analysis with Dunnett’s post-hoc correction were conducted to evaluate the effects of race and time. Results Results demonstrated significant effects of time for: forced vital capacity (FVC), forced expiratory flow over one second (FEV 1 ), peak expiratory flow (PEF), forced expiratory flow between 25-75% (FEF25-75), forced expiratory flow at 25% and at 50% (FEF 25 and FEF 50 , respectively), MIP, MEP, airway reactance (X) at all frequencies from FOT (X 5 , X 11 , X 19 ), respiratory rate, and ExNO (all p <0.05). A significant effect of race was also observed for ExNO ( p =0.002). Discussion Findings indicate declines in lung function and airway impedance immediately after ultra-marathon races, some of which, persisted up to 24 hours post-race. Further investigations are required to better understand the etiology of changes in lung function following ultra-endurance events.

Abstract Brief inhalation of carbon dioxide (CO 2 ) has been proposed to counteract transient hypocapnia by enhancing oxygen unloading, vasodilation, and sympathetic modulation. Despite these potential ergogenic mechanisms, CO 2 has rarely been investigated in the exercise context. The present study investigated whether brief CO 2 inhalation (iCO 2 ) influences performance and recovery during high‐intensity interval exercise. Nine healthy adults completed two randomized, single‐blinded crossover trials of repeated cycling intervals at 85% peak work rate until volitional exhaustion or cadence dropped below 60 rpm, with a minimum 2‐min interval duration required and 3‐min active recovery between bouts. Participants inhaled 5% CO 2 or room air (15 breaths) before and after each exercise bout. Gas exchange, cardiovascular responses, and perceived exertion were assessed. Total exercise time was similar between trials; however, participants completed more intervals with iCO 2 . During the first interval, iCO 2 increased exercise duration and VO 2 . At matched exercise time, perceived exertion and dyspnea were lower with iCO 2 . During recovery, systolic blood pressure was lower and heart rate was higher following iCO 2 . Brief iCO 2 improved first‐interval performance, altered cardiovascular recovery, and reduced perceptual strain but did not extend overall exercise duration. These findings suggest iCO 2 may transiently modulate tolerance and autonomic‐vascular responses during high‐intensity interval exercise.

Introduction/Aim: Heart failure (HF) is a complex clinical syndrome, characterised by reduced exercise capacity (VO 2 peak) and quality of life leading to premature death. The reduction in VO 2 peak is a key prognostic indicator, and improving exercise capacity remains a critical therapeutic target. In athletes, the use of intermittent hypoxia training to improve VO 2 peak and performance is well established. Changes in VO 2 peak are typically accompanied by improved oxygen carrying capacity with increased haemoglobin (Hb) concentration mediated through increased erythropoietin (EPO) production in the kidney. The purpose of this pilot study was to examine the feasibility of using intermittent hypoxia training in individuals with HF, and examine changes in VO 2 peak, EPO and Hb. We hypothesised that intermittent hypoxia training would be feasible, well tolerated, and improve VO 2 peak, EPO production, Hb concentration in HF with reduced ejection fraction (HFrEF). Methods: Ten male participants with stable, optimally managed HFrEF (Age: 73 ± 5 yr; Ejection Fraction: 37 ± 11%) participated in the study. The training stimulus consisted of 12 x 60-minute sessions of intermittent hypoxia over a 2-week period. During each 60-minute session participants received 6 x 5 minutes of pulsed, reduced FIO 2 exposures interspersed with 5 min of normoxia (total of 30 min hypoxic exposure per session). All participants commenced at 18% FIO 2 , which was decreased to 12% by the 3-4th sesion, as tolerated. Throughout each exposure, oxygen saturation (SpO 2 ), heart rate, blood pressure and dyspnoea (modified Borg scale) were monitored every 5 min. Changes in VO 2 peak were measured using a cycle ergometry, cardiopulmonary exercise test. Changes in VO 2 peak, N-terminal pro B-type natriuretic peptide (NT-proBNP), EPO and Hb concentration were measured pre and immediately post intermittent hypoxic training. Results: All participants completed between 10-12 (median n=12) sessions over the 2-week period. Intermittent hypoxia was well-tolerated with no adverse events. The mean SpO 2 during the hypoxic exposure was 88 ± 4%, and median reported dyspnoea 0 (range 0-1). Following 2 weeks of intermittent hypoxic training, there were significant increases in VO 2 peak (mean difference[MD]: +1.18 mL·kg - ¹·min - ¹, 95% CI 0.47 to 1.89, p = 0.010); EPO (MD: +3.33 IU/L, 95% CI 1.35 to 5.32, p = 0.011); with a modest increase in Hb concentration that approached significance (MD: +4.00 g/L, 95% CI 0.51 to 7.49, p = 0.055). NT-proBNP remained unchanged (MD: –107 pg/mL, 95% CI –356 to 142, p = 0.424). Conclusion The results of this pilot study suggest that in clinically stable HFrEF, 2 weeks of intermittent hypoxic training results in a significant improvement in VO 2 peak, accompanied by increases in EPO and potentially levels of Hb. In our participants, this 60-minute pulsed intermittent hypoxic protocol was extremely well tolerated without any adverse effects, and may improve oxygen carrying capacity of the blood in HFrEF. Further research on the mechanisms of adaptation and the translation of the response into different HF phenotypes is warranted. Supported By: The Prince Charles Hospital Foundation Innovation Grant INN202-049 and Griffith University. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Abstract Introduction Detecting and estimating blood volume loss are important for the diagnosis and management of life-threatening hemorrhage. There is a direct relationship between percent blood volume loss (BVL%) and falling in stroke volume (SV); furthermore, there is a direct relationship between diminishing SV and the corrected flow time of the carotid artery (ccFT). Therefore, we hypothesized that change in ccFT (ccFTΔ) would directly relate with BVL% in a phlebotomy paradigm. Materials and Methods A prospective, convenience sample of healthy volunteers was studied. Volunteers underwent blood donation protocol in a physiology lab. A wireless, wearable Doppler ultrasound system monitored ccFT during blood donation. Traditional vital signs were also measured throughout. The relationship between traditional vital signs as well as ccFTΔ were compared to BVL% using 2 mixed linear regression models. Results Data from 20 subjects and blood donations comprising 46,123 cardiac cycles are included. On average 413.5 ± 39 mL of blood were drawn representing 8.6 ± 1.6% BVL%. There was a significant and strong linear relationship between BVL% and ccFTΔ during blood draw with the regression slope demonstrating that for every 1 ms reduction in ccFT there was a 0.4% reduction in blood volume. Conclusions In healthy subjects and when blood loss is the sole mechanism for falling SV, we estimate that for every 1 ms reduction in ccFT, there is an approximate 0.4 BVL%. Validation of these results in patients with traumatic hemorrhage is underway.

Abstract Aims Monitoring pulmonary congestion in chronic heart failure (HF) reduces decompensation and hospitalization, but conventional methods such as weight and symptom tracking are often unreliable. As fluid accumulation affects the lungs and vocal tract, subtle voice alterations may serve as a non-invasive signal for early detection of worsening HF. Methods and results The Voice Analysis for Monitoring Patients with HF trial (VAMP-HF, NCT06566911) prospectively enrolled 104 patients hospitalized with acute decompensated HF (ADHF) across two academic centres in the USA and Germany. Daily voice recordings were collected from admission to discharge, with breathing features extracted from speech and acoustic features from sustained vowels. A machine-learning model was trained to classify recordings as admission-phase vs. discharge-phase using leave-one-patient-out. Patients with clinical deterioration, insufficient audio quality, or short length of stay were excluded. Seventy-nine patients were included in the final dataset. The model classified admission and discharge with an F1-score of 0.83 (95% CI: 0.77–0.90; AUC = 0.90). In patients with higher audio volume (N = 54), performance reached 0.89 (95% CI: 0.82–0.94; AUC = 0.91). When applied to intermediate hospitalization days, model-predicted scores showed progressive increases from admission towards discharge. Performance remained robust irrespective of significant weight loss during hospitalization. Conclusion In this pilot study, structured voice and breathing analysis discriminated hospitalization phase from admission through discharge in patients with ADHF. This non-invasive approach captured progressive changes during the hospital course and warrants further investigation with concurrent objective congestion markers to establish physiological specificity.

Background: Exhaled volatile organic compounds (VOCs) can provide insight into various physiological and metabolic processes. Aim: The purpose of this study was to determine if exhaled VOCs would differ across disease severity in heart failure (HF) patients. Methods: We recruited 62 individuals who were classified as healthy control (CTL), admissions with fluid overload (DHF), NYHA class I-II or NYHA class II-III. Breath samples were collected using the ReCIVA Breath Sampler (Owlstone Medical Ltd) and analyzed using mass spectrometry and gas chromatography. Typical clinical characteristics were documented at the time of exhaled breath collection. Results: Data were obtained on 16 CTL, 21 DHF, 15 NYHA I-II and 10 NYHA II-III (characteristics shown in Table). For the HF groups, DHF, NYHA I-II and NYHA II-III, the %HPEFF were 32, 63 and 63% respectively. Regarding exhaled VOCs, we observed a stepwise increase in VOCs potentially linked to lipid peroxidation or fatty acid metabolism, such as pent-3-en-2-one, 2-pentanone, and 4-heptanone, as disease severity worsened. A similar trend was seen for sulphur containing compounds (methyl propyl sulfide, allyl methyl sulfide and 1(methyl thiol)-1 propene)), potentially providing insight into impaired hepatic or renal clearance in more advanced HF. The level of methyl pyruvate on breath also rose with increasing disease severity, which may reflect altered energy metabolism. Finally, gut microbiome-related VOCs (acetoin, 2,3-butanediol, and butyric anhydride) increased across severity groups, potentially reflecting dysbiosis in advanced disease. Conclusions: In a small pilot study aiming to identify potential exhaled breath biomarkers in HF, we observed significant differences in VOCs across disease severity. These compounds have been linked to lipid peroxidation, energy metabolism, liver and kidney function as well as microbial fermentation and short-chain fatty acid metabolism. Collectively, these data demonstrate the ability of breath omics to potentially stratify disease severity and provide additional biological insights into HF pathophysiology. Larger studies are needed to determine whether a breath biomarker panel could be established to quantify disease severity and predict decompensation risk in HF.