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.

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.

Stabilising function of the human diaphragm in response to involuntary augmented breaths induced with or without lower-limb movements.

NEW FINDINGS: What is the central question of this study? Is the stabilising function of the diaphragm altered differentially in response to involuntary augmented breaths induced with or without lower-limb movements? What is the main finding and its importance? At equivalent levels of ventilation, the diaphragm generated higher passive pressure but moved significantly less during incremental cycle ergometry compared with progressive hypercapnia. Diaphragm excursion velocity and power output did not differ between the two tasks. These findings imply that the power output of the diaphragm during stabilising tasks involving the lower limbs may be preserved via coordinated changes in contractile shortening. ABSTRACT: Activity of key respiratory muscles, such as the diaphragm, must balance the demands of ventilation with the maintenance of stable posture. Our aim was to test whether the stabilising function of the diaphragm would be altered differentially in response to involuntary augmented breaths induced with or without lower-limb movements. Ten healthy volunteers (age 21 (2) years; mean (SD)) performed progressive CO2 -rebreathe (5% CO2 , 95% O2 ) followed 20 min later by incremental cycle exercise (15-30 W/min), both in a semi-recumbent position. Ventilatory indices, intrathoracic pressures and ultrasonographic measures of diaphragm shortening were assessed before, during and after each task. From rest to iso-time, inspiratory tidal volume and minute ventilation increased two- to threefold. At equivalent levels of tidal volume and minute ventilation, mean inspiratory transdiaphragmatic pressure ( P ¯ di ${\bar P_{{\rm{di}}}}$ ) was consistently higher during exercise compared with CO2 -rebreathe due to larger increases in gastric pressure and the passive component of P ¯ di ${\bar P_{{\rm{di}}}}$ (i.e., mechanical output due to static contractions), and yet diaphragm excursion was consistently lower. This lower excursion during exercise was accompanied by a reduction in excursion time with no difference in the active component of P ¯ di ${\bar P_{{\rm{di}}}}$ . Consequently, the rates of increase in excursion velocity (excursion/time) and power output (active P ¯ di ${\bar P_{{\rm{di}}}}$ × velocity) did not differ between the two tasks. In conclusion, the power output of the human diaphragm during dynamic lower-limb exercise appears to be preserved via coordinated changes in contractile shortening. The findings may have significance in settings where the ventilatory and stabilising functions of the diaphragm must be balanced (e.g., rehabilitation).

Does Cold-Water Endurance Swimming Affect Pulmonary Function in Healthy Adults?

The acute effects of cold-water endurance swimming on the respiratory system have received little attention. We investigated pulmonary responses to cold-water endurance swimming in healthy recreational triathletes. Pulmonary function, alveolar diffusing capacity (DLCO), fractional exhaled nitric oxide (FENO) and arterial oxygen saturation by pulse oximetry (SpO2) were assessed in 19 healthy adults one hour before and 2.5 h after a cold-water (mean ± SD, 10 ± 0.9 °C) swim trial (62 ± 27 min). In addition, 12 out of the 19 participants measured pulmonary function, forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) 3, 10, 20 and 45 min post-swim by maximal expiratory flow volume loops and DLCO by the single breath technique. FVC and FEV1 were significantly reduced 3 min post-swim (p = 0.02) (p = 0.04), respectively, and five of 12 participants (42%) experienced exercise-induced bronchoconstriction (EIB), defined as a ≥ 10% drop in FEV1. No significant changes were observed in pulmonary function 2.5 h post-swim. However, mean FENO and DLCO were significantly reduced by 7.1% and 8.1% (p = 0.01) and (p < 0.001), respectively, 2.5 h post-swim, accompanied by a 2.5% drop (p < 0.001) in SpO2. The absolute change in DLCO correlated significantly with the absolute decline in core temperature (r = 0.52; p = 0.02). Conclusion: Cold-water endurance swimming may affect the lungs in healthy recreational triathletes lasting up to 2.5 h post-swim. Some individuals appear to be more susceptible to pulmonary impairments than others, although these mechanisms need to be studied further.

Systemic but not local rehydration restores dehydration-induced changes in pulmonary function in healthy adults.

Water transport and local (airway) hydration are critical for the normal functioning of lungs and airways. Currently, there is uncertainty regarding the effects of systemic dehydration on pulmonary function. Our aims were 1) to clarify the impact of exercise- or fluid restriction-induced dehydration on pulmonary function in healthy adults; and 2) to establish whether systemic or local rehydration can reverse dehydration-induced alterations in pulmonary function. Ten healthy participants performed four experimental trials in a randomized order (2 h exercise in the heat twice and 28 h fluid restriction twice). Pulmonary function was assessed using spirometry and whole body plethysmography in the euhydrated, dehydrated, and rehydrated states. Oral fluid consumption was used for systemic rehydration and nebulized isotonic saline inhalation for local rehydration. Both exercise and fluid restriction induced mild dehydration (2.7 ± 0.7% and 2.5 ± 0.4% body mass loss, respectively; P < 0.001) and elevated plasma osmolality (P < 0.001). Dehydration across all four trials was accompanied by a reduction in forced vital capacity (152 ± 143 mL, P < 0.01) and concomitant increases in residual volume (216 ± 177 mL, P < 0.01) and functional residual capacity (130 ± 144 mL, P < 0.01), with no statistical differences between modes of dehydration. These changes were normalized by fluid consumption but not nebulization. Our results suggest that, in healthy adults: 1) mild systemic dehydration induced by exercise or fluid restriction leads to pulmonary function impairment, primarily localized to small airways; and 2) systemic, but not local, rehydration reverses these potentially deleterious alterations.NEW & NOTEWORTHY This study demonstrates that, in healthy adults, mild systemic dehydration induced by exercise in the heat or a prolonged period of fluid restriction leads to negative alterations in pulmonary function, primarily localized to small airways. Oral rehydration, but not nebulized isotonic saline, is able to restore pulmonary function in dehydrated individuals. Our findings highlight the importance of maintaining an adequate systemic fluid balance to preserve pulmonary function.

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).

Lung function and oxygen saturation after participation in Norseman Xtreme Triathlon.

OBJECTIVES: To examine evidence of exercise-induced bronchoconstriction (EIB) defined as ≥10% reduction in forced expiratory volume in one second (FEV1 ) and exercise-induced arterial hypoxemia (EIAH) defined as ≥4% reduction in oxygen saturation (SpO2 ) from before to after participation in the Norseman Xtreme Triathlon. Secondarily, to assess whether changes in FEV1 and SpO2 are related to respiratory symptoms, training volume, and race time. METHODS: In this quasi-experimental non-controlled study, we included 63 triathletes (50♂/13♀) aged 40.3 (±9.0) years (mean ± SD). Fifty-seven (46♂/11♀) measured lung function and 54 (44♂/10♀) measured SpO2 before the race, 8-10 minutes after the race (post-test 1) and the day after the race (post-test 2). Respiratory symptoms and training volume were recorded with modified AQUA questionnaire. ANOVA for repeated measures was used to detect differences in lung function and SpO2 . Statistical significance was accepted at 0.05 level. RESULTS: Twenty-six participants (46%) presented with EIB at post-test 1 and 16 (28%) at post-test 2. Lung function variables were significantly reduced from baseline to post-test 1 and 2. Thirty-five participants (65%) showed evidence of mild to moderate EIAH. No significant correlations were observed except a weak correlation between maximal reduction in FEV1 and respiratory symptoms (r = 0.35, P = .016). CONCLUSION: Our results demonstrated that 46% of the participants presented with EIB and 65% showed evidence of EIAH after the Norseman Xtreme Triathlon. Changes in FEV1 and SpO2 were not correlated to weekly training hours or race time. We observed a weak correlation between maximal reduction in FEV1 and respiratory symptoms.