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).

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).

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.

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.