Citations

Abstract The sections in this article are: Regulation of the Upper Airway During Exercise Anatomy and Physiology of the Upper Airway Contractile Properties and Endurance of Upper Airway Muscles Changes in Upper Airway Flow Resistance During Exercise Upper Airway Muscle Activities during Exercise Oronasal Distribution of Respiratory Airflow Effects of Exercise on Passive Respiratory Mechanics Elastic Properties Total Lung Capacity Expiratory Flow Rates, Vital Capacity, and Residual Volume Breathing Pattern During Exercise Mechanical Breathing Pattern Methods of Assessment of Respiratory Muscle Contraction Pattern of Respiratory Muscle Contraction Influence of Sensory Feedback on Breathing Pattern Influence of Respiratory Mechanics on Breathing Pattern Influence of Duration of Exercise on Breathing Pattern Influence of Mode of Exercise on Breathing Pattern Breathing Pattern during Recovery from Exercise Physiological Implications of Exercise Breathing Pattern Importance of Respiratory Load in Regulation of Exercise Hyperpnea Helium‐Oxygen Unloading Unloading with Pressure Assist Conclusion Locomotor‐Respiration Interdependence Entrainment—the Most Obvious Locomotor‐Respiratory Interaction How Does Entrainment Effect Ventilation? Is there Stronger Evidence to Support a Significant Biomechanical Effect of Locomotion on Respiration in Dogs? Are Biomechanical Effects Important in Entrainment in Humans? Locomotory: Respiratory Interactions, Independent of Entrainment Conclusion Respiratory Muscle Perfusion and Energetics Oxygen Cost of Hyperpnea Respiratory Muscle Blood Flow Exercise‐Induced Respiratory Muscle Fatigue Respiratory System Design Assessment of Diaphragm Fatigue in Animal Models Glycogen Depletion Fiber Type Recruitment Definition of Fatigue Task Failure vs. Objective Assessment of Fatigue Contractile Changes with Fatigue Predicting Respiratory Muscle Fatigue During Exercise Application of Resting Tests to Respiratory Muscle Function During Exercise Assessment of Respiratory Muscle Fatigue in Humans Volitional Tests Volitional Tests Applied to Exercise Nonvolitional Tests Bilateral Phrenic Nerve Stimulation ( BPNS ) Characteristics of Diaphragm Fatigue High‐ vs. Low‐Frequency Fatigue Sites and Mechanisms of Respiratory Muscle Fatigue Central Fatigue in Humans Neurotransmission Fatigue Bilateral Phrenic Nerve Stimulation Applied to Exercise Short‐Term Exercise Endurance Exercise Factors Contributing to the Decline in Twitch Pdi Following Exercise Role of Diaphragmatic Force Output in Fatigue Consequences of Exercise‐Induced Diaphragmatic Fatigue Fatigue vs. Task Failure Does Training of Respiratory Muscles Affect Exercise Performance? Altered Respiratory Muscle Recruitment with Fatigue Physical Training Effects on Respiratory Muscles Respiratory Muscle Morphology and Contractile Properties Whole‐Body Training: Effects on Rodent Respiratory Muscles Whole‐Body Exercise: Effects on Human Respiratory Muscle Performance Specific Respiratory Muscle Training Respiratory Sensation During Exertion Mechanisms of Respiratory Sensations during Exercise Methods of Assessing Respiratory Sensations Respiratory Movements An Urge to Breathe A Sense of Respiratory Effort Respiratory Sensation as a Respiratory Controller during Exercise Respiratory Sensation as a Limiting Factor during Exercise Conclusions Summary—Pulmonary System Limitations and Their Effects on Exercise Performance Absence of Pulmonary System Limitations in the Normally Fit Contrasting Adaptabilities: Demand vs. Capacity Alveolar Capillary Diffusion Surface of the Lung Ventilatory Limitations/Constraints Inadequate Alveolar Ventilation and Limitations Endurance Exercise Performance Special Circumstances Favoring Pulmonary Limitations to Exercise Performance in Health Hypoxia of High Altitudes Aging Effects on Pulmonary Limitations

Dynamic cerebral autoregulation (CA) refers to the brain's ability to maintain stable cerebral blood flow despite fluctuations in blood pressure (BP). Impaired CA has been associated with cardiovascular disease severity and cognitive decline. On the other hand, enhanced cardiorespiratory fitness appears to be protective against both cerebrovascular dysregulation and cognitive decline, with an unclear link between the two. However, among individuals with cardiovascular disease, the impact of exercise-based cardiac rehabilitation (CR) on CA remains unclear. Therefore, the aim of this study was to test the hypothesis that a 12-week CR program would improve dynamic CA in adults with CVD. To address this question, data were collected from 14 patients enrolled in the Mayo Clinic CR program following a cardiac-related hospital admission (age: 43-70 yrs; n=3 females), which included moderate-high intensity aerobic exercise 3 times/week for 12-weeks. Continuous measures of middle cerebral artery velocity (MCAv; transcranial doppler) and finger BP (photoplethysmography) were obtained during 3-minutes of rest and a 3-minute sit-to-stand protocol (0.025Hz frequency) pre- and post the CR program. Transfer function analyses were used to provide an index of dynamic CA. BP-MCAv coherence in the low frequency (LF) and very low frequency (vLF) domains at rest were not different pre- and post- CR (LF: 0.48±0.19 vs 0.43±0.16; P=0.54; vLF: 0.51±0.12 vs 0.47±0.16; P=0.14). Similarly, gain and phase values at rest were not different pre- and post- CR (gain LF: 0.66±0.37 vs 0.58±0.33; P=0.16; vLF: 0.87±0.53 vs 0.74±0.43; P=0.21; phase LF: 0.41±0.30 vs 0.43±0.26; P=0.64; vLF: 0.72±0.53 vs 0.66±0.16; P=0.18). In contrast, during the sit-to-stand protocol, coherence was lower following CR (pre vs post LF: 0.81±0.13 vs 0.79±0.16; p<0.01; vLF: 0.80±0.09 vs 0.79±0.14; p<0.01). In addition, gain was reduced post CR (pre vs post LF: 0.59±0.35 vs 0.55±0.31; P=0.02; vLF: 0.76±0.33 vs 0.61±0.37; p<0.01), suggesting CR-induced improvements in CA efficiency. However, phase remained unchanged pre- and post- CR during the sit-to-stand protocol (LF: 1.01±0.71 vs 0.84±0.58; P=0.17; vLF: 1.16±0.69 vs 1.08±0.60; P=0.19). Taken together, these findings demonstrate that a 12-week exercise-based CR program improves dynamic CA efficiency after a cardiac event. These novel results highlight the potential role of exercise training in improving cerebrovascular regulation. Funding: NIH AG073726 and Mayo Clinic This abstract was presented at the American Physiology Summit 2025 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 Rationale: Volatile organic compounds (VOCs) in exhaled breath change significantly after ultramarathons and could help monitor athletes’ physiological status to optimize training. While VOCs can reflect metabolic changes, the connection between VOCs and clinical blood and respiratory data remains unknown. In this study, we investigated how breath VOCs are linked to clinical variables that reflect the cardiovascular and respiratory system. Methods: Correlation analysis was performed between respiratory data collected in pre- and post-race samples from 24 runners who participated in the 2019 Ultra-Trail du Mont Blanc (UTMB®) ultra-marathon. Correlation analysis was then performed between these clinical data and previously published breath VOC data collected from the same individuals. Results: Clinical data indicated a slight decrease in runner's lung function post-race. Interestingly, in post-race samples, respiratory parameters vital capacity (VC) and forced expiratory volume in one second (FEV1) formed a moderate positive correlation with 2,3-butanediol (r = 0.53, r = 0.63, respectively), a compound produced by bacterial metabolism. We hypothesize that production of 2,3-butanediol results from the effect of exhaustive exercise on the gut microbiome, which may provide protection to ameliorate lung injury. Additionally, a strengthened correlation from moderate (r = 0.5 – 0.7) to strong (r &gt; 0.7) between VC and FEV1 (r = 0.67 to r = 0.84), forced vital capacity (FVC) and maximal expiratory pressure (MEP) (r = 0.57 to r = 0.75), was observed from pre-race to post-race samples. Finally, FEV1 and MEP shifted from no correlation (r &lt; 0.5) in pre-race to a strong correlation (r = 0.73) in post-race. Conclusion: The strengthened correlation between respiratory data in post-race samples suggests that the gut microbiome, under the effect of exercise, may have an indirect impact on both lung function and respiratory muscle function changes. Our findings support the notion that there is an intricate relationship between exhaustive exercise, altered gut microbiome activity, and lung function, and together they can influence athlete performance.

Abstract Rationale: Heart failure (HF) is often characterized by elevated left ventricular filling pressures (LVFP) and pulmonary congestion. However, LVFP may not always predict congestion. Pulmonary congestion can be quantified by computed tomography (CT) imaging. We hypothesized that extravascular lung water quantified by CT may differ in HF groups such as HF with preserved ejection fraction (HFpEF) vs HF with reduced ejection fraction (HFrEF), inpatients with acute decompensated heart failure (ADHF) vs stable and this would be related to echocardiography (echo) derived estimates of LVFP. Methods: We enrolled and studied 83 patients with HF who were either admitted or had a clinic visit at Mayo Clinic, Rochester, MN from May 2018 through March 2019. All subjects underwent comprehensive echo and supine thoracic CT scans. CT lung fluid was quantified and reported as proportion (%) of total lung volume. CT attenuation in lung tissue was also measured. LVFP was evaluated according to standardized echo diagnostic algorithms. Patients were stratified based on clinical diagnosis of HF as inpatients with HFpEF (n=26, 75.6±8.5yrs, M=50%, BMI=36.2±8.9kg/m2) inpatients with HFrEF (n=33, 75.6±14yrs, M=79%, BMI=31.1±9.1kg/m2), inpatients with ADHF (n=14, 72.6±14.5yrs, m=64.2%, BMI= 32.2±7.6Kg/m2) and stable outpatient HF controls (n=10, 65±13 yrs, m=90%, BMI= 29.5±5.2Kg/m2). All four groups were compared using one-way ANOVA followed by a post-hoc analysis. A correlation between lung fluid % and LVFP was performed using Spearman's correlation test. Results: When HF groups were compared according to CT % lung fluid, significant differences were found between HF groups (p=0.004). Post-hoc analysis revealed a significant difference in % lung fluid as HFrEF group had higher mean value in % lung fluid compared to HF control group (p=0.004). Similarly, ADHF group had higher mean % lung fluid compared to HF control group (p= 0.007). However, we found no correlation between LVFP and % lung fluid. The rightward shift in CT attenuation for HFpEF, HFrEF, and ADHF subjects, as displayed in figure 1, suggests greater levels of % lung water in these subjects compared to controls. Conclusion: These data suggest that CT measures of lung water differ in subgroups of HF patients and may not correlate with LVFP.

AbstractIntermittent hypoxia has been used to enhance oxygen delivery in athletes and patients; however, it is unclear whether acute exposure is sufficient to elicit lasting physiologic adaptation(s). The purpose of this study was to evaluate physiologic response(s) to hypobaric‐hypoxic (HH) exercise. Nine participants (4 M/5F; 37.9 ± 12.7 yrs.; 174.3 ± 9.4 cm; 75.3 ± 15.9 kg; 24.4 ± 3.4 kg/m2) were exposed to progressively higher simulated altitudes and completed two HH submaximal exercise sessions (~30 min ea., ≥72 h apart) on a cycle ergometer at the first altitude that posed a significant challenge to them. Altitude was dependent on individual response as determined from heart rate (HR), peripheral oxygenation (SpO2), and the ratio of HR response to SpO2 (HR/SpO2). Statistical analyses included paired samples t‐test (p ≤ 0.05). No significant change in SpO2 (HH‐1: 85 ± 4% vs. HH‐2: 85 ± 4%, p = 0.684) was observed between sessions. However, there were significant decreases in: HR (HH‐1: 150 ± 18 bpm vs. HH‐2: 133 ± 27 bpm, p = 0.001) of 18 bpm (11%); HR/SpO2 (HH‐1: 1.76 ± 0.22 vs. HH‐2: 1.57 ± 0.33, p = 0.012); and RPE (HH‐1: 15 ± 2 vs. HH‐2: 11 ± 4, p = 0.017). While workload significantly increased (HH‐1: 89 ± 36 W vs. HH‐2: 105 ± 36 W, p = 0.024). Some participants had a threshold/challenging altitude, but from a single bout there is evidence of improved tolerance that can last over a week. Further investigation is required to replicate and understand possible mechanisms.

AbstractAimWe investigated whether a commercial bi‐level positive airway pressure (BPAP) device, would improve peripheral oxygen saturation (SpO2) during recreational aviation up to 12,500 feet without supplemental oxygen. Ten adults with recreational flight experience (age:47 ± 14; female = 5) completed a standardized flight profile in an unpressurised aircraft, involving randomized crossover design at 8,000 feet and 12,500 feet with BPAP or control. SpO2, middle cerebral artery velocity (MCAv), heart rate (HR), respiratory rate (RR), and relative tidal volume (TV) index were measured continuously. Psychomotor vigilance test (3‐min) assessed reaction time halfway through taxi and altitude stages. Altitude significantly (p < 0.05) decreased mean SpO2, MCAv, and RR, and increased TV index and HR. There was no effect of altitude (p > 0.05) on reaction time. BPAP increased mean SpO2 at 8,000 feet [Control: 92 ± 1%; BPAP: 94 ± 2%; mean difference (MD) = 2 ± 2%; p = 0.002] and 12,500 feet [Control: 86 ± 4%; BPAP: 89 ± 4%; MD = 2 ± 3%; p = 0.013]. BPAP lowered MCAv at 8,000 feet [Control: 53 ± 10 cm/s; BPAP: 50 ± 9 cm/s; MD = ‐3 ± 2 cm/s; p = 0.001] and 12,500 feet [Control: 52 ± 10 cm/s; BPAP: 50 ± 8 cm/s; MD = ‐2 ± 3 cm/s; p = 0.041]. BPAP increased TV index at 8,000 feet (Control: 6.6 ± 1.3; BPAP:8.1 ± 1.8; MD = 1.9 ± 0.8; p < 0.001) but not 12,500 feet, without effect on RR or reaction time. This study provides preliminary results that BPAP may improve mean SpO2 for recreational aviators up to 12,500 feet without supplemental oxygen.