Distinguishing science from pseudoscience in commercial respiratory interventions: an evidence-based guide for health and exercise professionals.

Respiratory function has become a global health priority. Not only is chronic respiratory disease a leading cause of worldwide morbidity and mortality, but the COVID-19 pandemic has heightened attention on respiratory health and the means of enhancing it. Subsequently, and inevitably, the respiratory system has become a target of the multi-trillion-dollar health and wellness industry. Numerous commercial, respiratory-related interventions are now coupled to therapeutic and/or ergogenic claims that vary in their plausibility: from the reasonable to the absurd. Moreover, legitimate and illegitimate claims are often conflated in a wellness space that lacks regulation. The abundance of interventions, the range of potential therapeutic targets in the respiratory system, and the wealth of research that varies in quality, all confound the ability for health and exercise professionals to make informed risk-to-benefit assessments with their patients and clients. This review focuses on numerous commercial interventions that purport to improve respiratory health, including nasal dilators, nasal breathing, and systematized breathing interventions (such as pursed-lips breathing), respiratory muscle training, canned oxygen, nutritional supplements, and inhaled L-menthol. For each intervention we describe the premise, examine the plausibility, and systematically contrast commercial claims against the published literature. The overarching aim is to assist health and exercise professionals to distinguish science from pseudoscience and make pragmatic and safe risk-to-benefit decisions.

Exercise Is Medicine? The Cardiorespiratory Implications of Ultra-marathon.

Regular physical activity decreases the risk of cardiovascular disease, type II diabetes, obesity, certain cancers, and all-cause mortality. Nevertheless, there is mounting evidence that extreme exercise behaviors may be detrimental to human health. This review collates several decades of literature on the physiology and pathophysiology of ultra-marathon running, with emphasis on the cardiorespiratory implications. Herein, we discuss the prevalence and clinical significance of postrace decreases in lung function and diffusing capacity, respiratory muscle fatigue, pulmonary edema, biomarkers of cardiac injury, left/right ventricular dysfunction, and chronic myocardial remodeling. The aim of this article is to inform risk stratification for ultra-marathon and to edify best practice for personnel overseeing the events (i.e., race directors and medics).

Mechanical-ventilatory responses to peak and ventilation-matched upper- versus lower-body exercise in normal subjects.

NEW FINDINGS: What is the central question of this study? To what extent are the mechanical-ventilatory responses to upper-body exercise influenced by task-specific locomotor mechanics? What is the main finding and its importance? When compared with lower-body exercise performed at similar ventilations, upper-body exercise was characterized by tidal volume constraint, dynamic lung hyperinflation and an increased propensity towards neuromechanical uncoupling of the respiratory system. Importantly, these responses were independent of respiratory dysfunction and flow limitation. Thus, the mechanical ventilatory responses to upper-body exercise are attributable, in part, to task-specific locomotor mechanics (i.e. non-respiratory loading of the thorax). ABSTRACT: The aim of this study was to determine the extent to which the mechanical ventilatory responses to upper-body exercise are influenced by task-specific locomotor mechanics. Eight healthy men (mean ± SD: age, 24 ± 5 years; mass, 74 ± 11 kg; and stature, 1.79 ± 0.07 m) completed two maximal exercise tests, on separate days, comprising 4 min stepwise increments of 15 W during upper-body exercise (arm-cranking) or 30 W during lower-body exercise (leg-cycling). The tests were repeated at work rates calculated to elicit 20, 40, 60, 80 and 100% of the peak ventilation achieved during arm-cranking ( V̇E,UBE ). Exercise measures included pulmonary ventilation and gas exchange, oesophageal pressure-derived indices of respiratory mechanics, operating lung volumes and expiratory flow limitation. Subjects exhibited normal resting pulmonary function. Arm-crank exercise elicited significantly lower peak values for work rate, O2 uptake, CO2 output, minute ventilation and tidal volume (p < 0.05). At matched ventilations, arm-crank exercise restricted tidal volume expansion relative to leg-cycling exercise at 60% V̇E,UBE (1.74 ± 0.61 versus 2.27 ± 0.68 l, p < 0.001), 80% V̇E,UBE (2.07 ± 0.70 versus 2.52 ± 0.67 l, p < 0.001) and 100% V̇E,UBE (1.97 ± 0.85 versus 2.55 ± 0.72 l, p = 0.002). Despite minimal evidence of expiratory flow limitation, expiratory reserve volume was significantly higher during arm-cranking versus leg-cycling exercise at 100% V̇E,UBE (39 ± 8 versus 29 ± 8% of vital capacity, p = 0.002). At any given ventilation, arm-cranking elicited greater inspiratory effort (oesophageal pressure) relative to thoracic displacement (tidal volume). Arm-cranking exercise is sufficient to provoke respiratory mechanical derangements (restricted tidal volume expansion, dynamic hyperinflation and neuromechanical uncoupling) in subjects with normal pulmonary function and expiratory flow reserve. These responses are likely to be attributable to task-specific locomotor mechanics (i.e. non-respiratory loading of the thorax).

Pulmonary and respiratory muscle function in response to 10 marathons in 10 days.

PURPOSE: Marathon and ultramarathon provoke respiratory muscle fatigue and pulmonary dysfunction; nevertheless, it is unknown how the respiratory system responds to multiple, consecutive days of endurance exercise. METHODS: Nine trained individuals (six male) contested 10 marathons in 10 consecutive days. Respiratory muscle strength (maximum static inspiratory and expiratory mouth-pressures), pulmonary function (spirometry), perceptual ratings of respiratory muscle soreness (Visual Analogue Scale), breathlessness (dyspnea, modified Borg CR10 scale), and symptoms of Upper Respiratory Tract Infection (URTI), were assessed before and after marathons on days 1, 4, 7, and 10. RESULTS: Group mean time for 10 marathons was 276 ± 35 min. Relative to pre-challenge baseline (159 ± 32 cmH2O), MEP was reduced after day 1 (136 ± 31 cmH2O, p = 0.017), day 7 (138 ± 42 cmH2O, p = 0.035), and day 10 (130 ± 41 cmH2O, p = 0.008). There was no change in pre-marathon MEP across days 1, 4, 7, or 10 (p > 0.05). Pre-marathon forced vital capacity was significantly diminished at day 4 (4.74 ± 1.09 versus 4.56 ± 1.09 L, p = 0.035), remaining below baseline at day 7 (p = 0.045) and day 10 (p = 0.015). There were no changes in FEV1, FEV1/FVC, PEF, MIP, or respiratory perceptions during the course of the challenge (p > 0.05). In the 15-day post-challenge period, 5/9 (56%) runners reported symptoms of URTI, relative to 1/9 (11%) pre-challenge. CONCLUSIONS: Single-stage marathon provokes acute expiratory muscle fatigue which may have implications for health and/or performance, but 10 consecutive days of marathon running does not elicit cumulative (chronic) changes in respiratory function or perceptions of dyspnea. These data allude to the robustness of the healthy respiratory system.

Effect of cadence on locomotor-respiratory coupling during upper-body exercise.

INTRODUCTION: Asynchronous arm-cranking performed at high cadences elicits greater cardiorespiratory responses compared to low cadences. This has been attributed to increased postural demand and locomotor-respiratory coupling (LRC), and yet, this has not been empirically tested. This study aimed to assess the effects of cadence on cardiorespiratory responses and LRC during upper-body exercise. METHODS: Eight recreationally-active men performed arm-cranking exercise at moderate and severe intensities that were separated by 10 min of rest. At each intensity, participants exercised for 4 min at each of three cadences (50, 70, and 90 rev min-1) in a random order, with 4 min rest-periods applied in-between cadences. Exercise measures included LRC via whole- and half-integer ratios, cardiorespiratory function, perceptions of effort (RPE and dyspnoea), and diaphragm EMG using an oesophageal catheter. RESULTS: The prevalence of LRC during moderate exercise was highest at 70 vs. 50 rev min-1 (27 ± 10 vs. 13 ± 9%, p = 0.000) and during severe exercise at 90 vs. 50 rev min-1 (24 ± 7 vs. 18 ± 5%, p = 0.034), with a shorter inspiratory time and higher mean inspiratory flow (p < 0.05) at higher cadences. During moderate exercise, [Formula: see text] and f C were higher at 90 rev min-1 (p < 0.05) relative to 70 and 50 rev min-1 ([Formula: see text] 1.19 ± 0.25 vs. 1.05 ± 0.21 vs. 0.97 ± 0.24 L min-1; f C 116 ± 11 vs. 101 ± 13 vs. 101 ± 12 b min-1), with concomitantly elevated dyspnoea. There were no discernible cadence-mediated effects on diaphragm EMG. CONCLUSION: Participants engage in LRC to a greater extent at moderate-high cadences which, in turn, increase respiratory airflow. Cadence rate should be carefully considered when designing aerobic training programmes involving the upper-limbs.

Sex differences in ultramarathon performance in races with comparable numbers of males and females.

There is a prominent sex-based difference in athletic performance such that males outperform females by 7%-14% in races from 100 m to marathon. In ultramarathons, the difference is often much smaller, leading to speculation that females are "built" for the sport. However, data are confounded by the low number of female participants; just 10%-30% in any given race. This study compared data from two ultramarathons where males and females competed in comparable numbers. There were 116 and 146 starters in the 50 mile and 100 mile races, respectively (52% female). Finish times were compared using t tests or Mann-Whitney U tests, a Chi-squared test of independence examined the relationship between sex and ranking, and multivariable linear regressions examined relationships between sex, age, and finish time. There were 96 finishers in the 50 mile race (46% female) and 91 finishers in the 100 mile race (45% female). The median finish time for 50 miles was 12.64 ± 2.11 h with no difference between sexes (1.2%, p = 0.441). However, the top-10 males finished the race ∼85 min faster than the top-10 females (13.8%, p = 0.045). The mean finish time for 100 miles was 31.58 ± 3.36 h with no difference between sexes (3.2%, p = 0.132) and no difference between the top-10 males and top-10 females (4.4%, p = 0.150). Linear and multivariable regression models using sex and age were unable to predict overall finish time in either race. In conclusion, the sex-based performance discrepancy shrinks to 1%-3% in ultramarathons when males and females compete in comparable numbers. Top-performing males still retain a considerable advantage over shorter distances.

Effect of Ultra-Marathon Trail Running at Sea Level and Altitude on Alveolar-Capillary Function and Lung Diffusion.

INTRODUCTION: Endurance exercise at altitude can increase cardiac output and pulmonary vascular pressure to levels that may exceed the stress-tolerability of the alveolar-capillary unit. This study examined the effect of ultra-marathon trail racing at different altitudes (ranging from <1000 m to between 1500 - 2700 m) on alveolar-capillary recruitment and lung diffusion. METHODS: Cardiac and lung function were examined before and after an ultra-marathon in 67 runners (age:41 ± 9y, BMI:23 ± 2 kg/m2, 10 females), and following 12-24 h of recovery in a subset (n = 27). Cardiac biomarkers (cTnI & BNP) were assessed from whole blood, while lung fluid accumulation (comet tails), stroke volume (SV) and cardiac output (Q) were quantified via echocardiography. Lung diffusing capacity for carbon monoxide (DLco) and its components, alveolar membrane conductance (Dm) and capillary blood volume (Vc), were determined via a single-breath method at rest and during three stages of submaximal semi-recumbent cycling (20, 30, & 40 W). RESULTS: Average race time was 25 ± 12 h. From pre- to post-race, there was an increase in cardiac biomarkers (cTnI: 0.04 ± .02 vs 0.13 ± .03 ng/ml; BNP: 20 ± 2 vs 112 ± 21 pg/ml, p < 0.01) and lung comet tails (2 ± 1 vs 7 ± 6, p < 0.01), a decrease in resting and exercise SV (76 ± 2 vs 69 ± 2 ml; 40 W: 93 ± 2 vs 88 ± 2 ml, p < 0.01), and an elevation in Q at rest (4.1 ± 0.1 vs 4.6 ± 0.2 l/min, p < 0.01; 40 W: 7.3 ± 0.2 vs 7.4 ± 0.3 l/min, p = 0.899). Resting DLco and Vc decreased after the race (p < 0.01), while Dm was unchanged (p = 0.465); however, during the three stages of exercise DLco, Vc and Dm were all reduced from pre- to post-race (40 W: 36.3 ± 0.9 vs 33.0 ± 0.8 mL/min/mmHg; 83 ± 3 vs 73 ± 2 mL; 186 ± 6 vs 170 ± 7 mL/min/mmHg, respectively, p < 0.01). When corrected for alveolar volume and Q, DLco decreased from pre- to post-race (p < 0.01), and changes in DLco were similar for all ultra-marathon events (p > 0.05). CONCLUSIONS: Competing in an ultra-marathon leads to a transient increase in cardiac injury biomarkers, mild lung-fluid accumulation, and impairments in lung diffusion. Reductions in DLco are predominantly caused by a reduced Vc and possible pulmonary capillary de-recruitment at rest. However, impairments in alveolar-capillary recruitment and Dm both contribute to a fall in exertional DLco following an ultra-marathon. Perturbations in lung diffusion were evident across a range of event distances and varying environmental exposures.

Exercise-induced increases in "liver function tests" in a healthy adult male: Is there a knowledge gap in primary care?

A routine clinical assessment in a 39-year-old male revealed liver function tests at 1.4-2.3 times the normal limit. He was asymptomatic, had no personal/family history of liver disease, and did not drink or use recreational drugs. He was in good physical condition and engaged in regular running and resistance exercise. Negative workup included tests for hepatitis A, B, and C, M-proteins, and antimitochondrial antibodies. Abdominal ultrasound was unremarkable. The patient was referred to a gastroenterologist who ordered repeat liver function tests (LFTs) and a liver biopsy. Before his follow-up assessment the patient abstained from exercise for seven days, after which all LFTs had normalized. The abnormal liver panel was thus likely due to exercise-induced muscle damage and/or changes in hepatocyte membrane permeability. Importantly, the diagnostic pathway did not include any assessment of muscle biomarkers (e.g., creatine kinase) or the patient's exercise training habits. This case highlights a knowledge gap in primary care regarding the possible causes of LFT abnormalities in young adults.

Lung function responses to cold water ingestion: A randomised controlled crossover trial.

This study tested the hypothesis that cold water ingestion would reduce lung function and thereby confound its measurement in a way that is mediated by both temperature and volume. In a randomised crossover trial, 10 healthy adults performed spirometry before and 5, 10, 15, and 30-minutes after consuming one-of-four drinks: 500 mL or 1000 mL refrigerated water (∼2 °C); identical water volumes at ambient temperature (∼18 °C). Ingesting 1000 mL cold water significantly reduced forced vital capacity (FVC) for at least 10 min (mean difference =0.28 L, p < 0.05, d=1.19) and forced expiratory volume in 1 s (FEV1) for at least 15 min (0.20-0.30 L, p < 0.05, d=1.01). Ingesting 500 mL cold water reduced FEV1 for 5 min (0.09 L, p < 0.05, d=1.05). Room-temperature water had no influence on lung function. To avoid confounding the measurement of lung function, we conclude that individuals should avoid drinking cold water, especially in large volumes, immediately prior to a given test.

Baseless Claims and Pseudoscience in Health and Wellness: A Call to Action for the Sports, Exercise, and Nutrition-Science Community.

The global health and wellness industry has an estimated value of US$4 trillion. Profits derive from heath club memberships, exercise classes, diets, supplements, alternative 'therapies', and thousands of other products and services that are purported to improve health, recovery, and/or sports performance. The industry has expanded at an alarming rate, far outstripping the capacity of federal bodies to regulate the market and protect consumer interests. As a result, many products are sold on baseless or exaggerated claims, feigned scientific legitimacy, and questionable evidence of safety and efficacy. This article is a consciousness raiser. Herein, the implications of the mismatch between extraordinary health and performance claims and the unextraordinary scientific evidence are discussed. Specifically, we explore how pseudoscience and so-called 'quick fix' interventions undermine initiatives aimed at evoking long-term behavior change, impede the ongoing pursuit of sports performance, and lead to serious downstream consequences for clinical practice. Moreover, pseudoscience in health and wellness, if left unchecked and unchallenged, may have profound implications for the reputation of exercise science as a discipline. This is a call to action to unify exercise scientists around the world to more proactively challenge baseless claims and pseudoscience in the commercial health and wellness industry. Furthermore, we must shoulder the burden of ensuring that the next generation of exercise scientists are sufficiently skilled to distinguish science from pseudoscience, and information from mis- and disinformation. Better population health, sports performance, and the very reputation of the discipline may depend on it.

Extraordinary Claims in the Literature on High-Intensity Interval Training (HIIT): I. Bonafide Scientific Revolution or a Looming Crisis of Replication and Credibility?

The literature on high-intensity interval training (HIIT) contains claims that, if true, could revolutionize the science and practice of exercise. This critical analysis examines two varieties of claims: (i) HIIT is effective in improving various indices of fitness and health, and (ii) HIIT is as effective as more time-consuming moderate-intensity continuous exercise. Using data from two recent systematic reviews as working examples, we show that studies in both categories exhibit considerable weaknesses when judged through the prism of fundamental statistical principles. Predominantly, small-to-medium effects are investigated in severely underpowered studies, thus greatly increasing the risk of both type I and type II errors of statistical inference. Studies in the first category combine the volatility of estimates associated with small samples with numerous dependent variables analyzed without consideration of the inflation of the type I error rate. Studies in the second category inappropriately use the p > 0.05 criterion from small studies to support claims of 'similar' or 'comparable' effects. It is concluded that the situation in the HIIT literature is reminiscent of the research climate that led to the replication crisis in psychology. As in psychology, this could be an opportunity to reform statistical practices in exercise science.

Critical Power and Respiratory Compensation Point Are Not Equivalent in Patients with COPD.

INTRODUCTION: Several studies report that pulmonary oxygen uptake (V̇O 2 ) at the respiratory compensation point (RCP) is equivalent to the V̇O 2 at critical power (CP), suggesting that the variables can be used interchangeably to demarcate the threshold between heavy and severe intensity domains. However, if RCP is a valid surrogate for CP, their values should correspond even when assessed in patients with chronic obstructive pulmonary disease (COPD) in whom the "normal" mechanisms linking CP and RCP are impeded. The aim of this study was to compare V̇O 2 at CP with V̇O 2 at RCP in patients with COPD. METHODS: Twenty-two COPD patients (14 male/8 female; forced expiratory volume in 1 s, 46% ± 17% pred) performed ramp-incremental cycle ergometry to intolerance (5-10 W·min -1 ) for the determination of gas exchange threshold (GET) and RCP. CP was calculated from the asymptote of the hyperbolic power-duration relationship from 3-5 constant-power exercise tests to intolerance. CP was validated with a 20-min constant-power ride. RESULTS: GET was identified in 20 of 22 patients at a V̇O 2 of 0.93 ± 0.18 L·min -1 (75% ± 13% V̇O 2peak ), whereas RCP was identified in just 3 of 22 patients at a V̇O 2 of 1.40 ± 0.39 L·min -1 (85% ± 2% V̇O 2peak ). All patients completed constant-power trials with no difference in peak physiological responses relative to ramp-incremental exercise ( P > 0.05). CP was 46 ± 22 W, which elicited a V̇O 2 of 1.04 ± 0.29 L·min -1 (90% ± 9% V̇O 2peak ) during the validation ride. The difference in V̇O 2 at 15 and 20 min of the validation ride was 0.00 ± 0.04 L, which was not different from a hypothesized mean of 0 ( P = 0.856), thereby indicating a V̇O 2 steady state. CONCLUSIONS: In COPD patients, who present with cardiopulmonary and/or respiratory-mechanical dysfunction, CP can be determined in the absence of RCP. Accordingly, CP and RCP are not equivalent in this group.

Potential Long-Term Health Problems Associated with Ultra-Endurance Running: A Narrative Review.

It is well established that physical activity reduces all-cause mortality and can prolong life. Ultra-endurance running (UER) is an extreme sport that is becoming increasingly popular, and comprises running races above marathon distance, exceeding 6 h, and/or running fixed distances on multiple days. Serious acute adverse events are rare, but there is mounting evidence that UER may lead to long-term health problems. The purpose of this review is to present the current state of knowledge regarding the potential long-term health problems derived from UER, specifically potential maladaptation in key organ systems, including cardiovascular, respiratory, musculoskeletal, renal, immunological, gastrointestinal, neurological, and integumentary systems. Special consideration is given to youth, masters, and female athletes, all of whom may be more susceptible to certain long-term health issues. We present directions for future research into the pathophysiological mechanisms that underpin athlete susceptibility to long-term issues. Although all body systems can be affected by UER, one of the clearest effects of endurance exercise is on the cardiovascular system, including right ventricular dysfunction and potential increased risk of arrhythmias and hypertension. There is also evidence that rare cases of acute renal injury in UER could lead to progressive renal scarring and chronic kidney disease. There are limited data specific to female athletes, who may be at greater risk of certain UER-related health issues due to interactions between energy availability and sex-hormone concentrations. Indeed, failure to consider sex differences in the design of female-specific UER training programs may have a negative impact on athlete longevity. It is hoped that this review will inform risk stratification and stimulate further research about UER and the implications for long-term health.

Physical Activity, Muscle Oxidative Capacity, and Coronary Artery Calcium in Smokers with and without COPD.

Introduction: Severe chronic obstructive pulmonary disease (COPD) is partly characterized by diminished skeletal muscle oxidative capacity and concurrent dyslipidemia. It is unknown whether such metabolic derangements increase the risk of cardiovascular disease. This study explored associations among physical activity (PA), muscle oxidative capacity, and coronary artery calcium (CAC) in COPDGene participants. Methods: Data from current and former smokers with COPD (n = 75) and normal spirometry (n = 70) were retrospectively analyzed. Physical activity was measured for seven days using triaxial accelerometry (steps/day and vector magnitude units [VMU]) along with the aggregate of self-reported PA amount and PA difficulty using the PROactive D-PPAC instrument. Muscle oxidative capacity (k) was assessed via near-infrared spectroscopy, and CAC was assessed via chest computerized tomography. Results: Relative to controls, COPD patients exhibited higher CAC (median [IQR], 31 [0-431] vs 264 [40-799] HU; p = 0.003), lower k (mean ± SD = 1.66 ± 0.48 vs 1.25 ± 0.37 min-1; p < 0.001), and lower D-PPAC total score (65.2 ± 9.9 vs 58.8 ± 13.2; p = 0.003). Multivariate analysis-adjusting for age, sex, race, diabetes, disease severity, hyperlipidemia, smoking status, and hypertension-revealed a significant negative association between CAC and D-PPAC total score (ß, -0.05; p = 0.013), driven primarily by D-PPAC difficulty score (ß, -0.03; p = 0.026). A 1 unit increase in D-PPAC total score was associated with a 5% lower CAC (p = 0.013). There was no association between CAC and either k, steps/day, VMU, or D-PPAC amount. Conclusion: Patients with COPD and concomitantly elevated CAC exhibit greater perceptions of difficulty when performing daily activities. This may have implications for exercise adherence and risk of overall physical decline.

Sex-Specific Physiological Responses to Ultramarathon.

PURPOSE: Despite a growing body of literature on the physiological responses to ultramarathon, there is a paucity of data in females. This study assessed the female physiological response to ultramarathon and compared the frequency of perturbations to a group of race- and time-matched males. METHODS: Data were collected from 53 contestants of an ultramarathon trail race at the Ultra-Trail du Mont-Blanc (UTMB®) in 2018/19. Before and within 2 h of the finish, participants underwent physiological assessments, including blood sampling for biomarkers (creatine kinase-MB isoenzyme [CK-MB], cardiac troponin I [cTnI], brain natriuretic peptide [BNP], and creatinine [Cr]), pulmonary function testing (spirometry, exhaled NO, diffusing capacities, and mouth pressures), and transthoracic ultrasound (lung comet tails, cardiac function). Data from eight female finishers (age = 36.6 ± 6.9 yr; finish time = 30:57 ± 11:36 h:min) were compared with a group of eight time-matched males (age = 40.3 ± 8.3 yr; finish time = 30:46 ± 10:32 h:min). RESULTS: Females exhibited significant pre- to postrace increases in BNP (25.8 ± 14.6 vs 140.9 ± 102.7 pg·mL -1 ; P = 0.007) and CK-MB (3.3 ± 2.4 vs 74.6 ± 49.6 IU·L -1 ; P = 0.005), whereas males exhibited significant pre- to postrace increases in BNP (26.6 ± 17.5 vs 96.4 ± 51.9 pg·mL -1 ; P = 0.002), CK-MB (7.2 ± 3.9 vs 108.8 ± 37.4 IU·L -1 ; P = 0.002), and Cr (1.06 ± 0.19 vs 1.23 ± 0.24 mg·dL -1 ; P = 0.028). Lung function declined in both groups, but males exhibited additional reductions in lung diffusing capacities (DL CO = 34.4 ± 5.7 vs 29.2 ± 6.9 mL⋅min -1 ⋅mm Hg -1 , P = 0.004; DL NO = 179.1 ± 26.2 vs 152.8 ± 33.4 mL⋅min -1 ⋅mm Hg -1 , P = 0.002) and pulmonary capillary blood volumes (77.4 ± 16.7 vs 57.3 ± 16.1 mL; P = 0.002). Males, but not females, exhibited evidence of mild postrace pulmonary edema. Pooled effect sizes for within-group pre- to postrace changes, for all variables, were generally larger in males versus females ( d = 0.86 vs 0.63). CONCLUSIONS: Ultramarathon negatively affects a range of physiological functions but generally evokes more frequent perturbations, with larger effect sizes, in males compared to females with similar race performances.

Chronotropic index during 6-minute walk and acute respiratory events in COPDGene.

BACKGROUND: Lower heart rate (HR) increases during exercise and slower HR recovery (HRR) after exercise are markers of worse autonomic function that may be associated with risk of acute respiratory events (ARE). METHODS: Data from 6-min walk testing (6MWT) in COPDGene were used to calculate the chronotropic index (CI) [(HR immediately post 6MWT - resting HR)/((220 - age) - resting HR)] and HRR at 1 min after 6MWT completion. We used zero-inflated negative binomial regression to test associations of CI and HRR with rates of any ARE (requiring steroids and/or antibiotics) and severe ARE (requiring emergency department visit or hospitalization), among all participants and in spirometry subgroups (normal, chronic obstructive pulmonary disease [COPD], and preserved ratio with impaired spirometry). RESULTS: Among 4,484 participants, mean follow-up time was 4.1 years, and 1,966 had COPD. Among all participants, CI-6MWT was not associated with rate of any ARE [adjusted incidence rate ratio (aIRR) 0.98 (0.95-1.01)], but higher CI-6MWT was associated with lower rate of severe ARE [0.95 (0.92-0.99)]. Higher HRR was associated with a lower rate of both any ARE [0.97 (0.95-0.99)] and severe ARE [0.95 (0.92-0.98)]. Results were similar in the COPD spirometry subgroup. CONCLUSION: Heart rate measures derived from 6MWT tests may have utility in predicting risk of acute respiratory events and COPD exacerbations.

Cardiorespiratory demands of competitive rock climbing.

Rock climbing has become a mainstream sport, contested on the Olympic stage. The work/rest pattern of bouldering is unique among disciplines, and little is known about its physiological demands. This study characterised the cardiorespiratory responses to simulated competition. Eleven elite boulderers (7 male) volunteered to participate (age = 23.3 ± 4.5 years; mass = 68.2 ± 9.7 kg; stature = 1.73 ± 0.06 m; body fat = 10.4% ± 5%). Subjects completed incremental treadmill running to determine maximal capacities. On a separate day, they undertook a simulated Olympic-style climbing competition comprising 5 boulder problems, each separated by 5 min of rest. Pulmonary ventilation, gas exchange, and heart rate were assessed throughout. Total climbing time was 18.9 ± 2.7 min. Bouldering elicited a peak oxygen uptake of 35.8 ± 7.3 mL·kg-1·min-1 (∼75% of treadmill maximum) and a peak heart rate of 162 ± 14 beats·min-1 (∼88% of maximum). Subjects spent 22.9% ± 8.6% of climbing time above the gas exchange threshold. At exercise cessation, there was an abrupt and significant increase in tidal volume (1.4 ± 0.4 vs. 1.8 ± 0.4 L; p = 0.006, d = 0.83) despite unchanged minute ventilation. Cardiorespiratory parameters returned to baseline within 4 min of the rest period. In conclusion, competitive bouldering elicits substantial cardiorespiratory demand and evidence of tidal volume constraint. Further studies are warranted to explore the effect of cardiorespiratory training on climbing performance. Novelty: Competitive bouldering evokes a high fraction of maximal oxygen uptake and prolonged periods above the gas exchange threshold. Climbing appears to impose a constraint on tidal volume expansion. Cardiorespiratory indices in elite climbers return to baseline within 2-4 min.