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Dishman challenged kinesiologists to seek a compromise between “the ideal physiological prescription and a manageable behavioral prescription.” High-intensity interval training (HIIT) is the first exercise modality that has been claimed to meet this challenge, combining substantial benefits for fitness and health with pleasure and enjoyment. If true, these claims may revolutionize the science and practice of exercise. In this paper, four claims are critically appraised: (a) HIIT lowers the risk of mortality more than moderate-intensity continuous exercise, (b) HIIT doubles endurance performance after only 15 min of training over 2 weeks, (c) 1 min of HIIT is equivalent to 45 min of moderate-intensity continuous exercise, and (d) HIIT is more pleasant and enjoyable than moderate-intensity continuous exercise. The evidence for these claims appears questionable. Kinesiology should heed the principle endorsed by Hume, Laplace, and Sagan, namely that extraordinary claims should be supported by commensurate evidence.

Increasing transparency and openness in science is an ongoing endeavor, one that has stimulated self-reflection and reform in many fields. However, kinesiology and its related disciplines are among those exhibiting an “ostrich effect” and a reluctance to acknowledge their methodological shortcomings. Notwithstanding several high-profile cases of scientific misconduct, scholars in the field are frequently engaged in questionable research practices (QRPs) such as biased experimental designs, inappropriate statistics, and dishonest/inexplicit reporting. To advance their careers, researchers are also “gaming the system” by manipulating citation metrics and publishing in predatory and/or pay-to-publish journals that lack robust peer review. The consequences of QRPs in the discipline may be profound: from increasing the false positivity rate to eroding public trust in the very institutions tasked with informing public health policy. But what are the incentives underpinning misconduct and QRPs? And what are the solutions? This narrative review is a consciousness raiser that explores (a) the manifestations of QRPs in kinesiology; (b) the excessive publication pressures, funding pressures, and performance incentives that are likely responsible; and (c) possible solutions for reform.

Nicholas B Tiller,1 April Kinninger,2 Asghar Abbasi,1 Richard Casaburi,1 Harry B Rossiter,1 Matthew J Budoff,2 Alessandra Adami3 1Institute of Respiratory Medicine and Exercise Physiology, Division of Respiratory and Critical Care Physiology and Medicine, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA; 2Division of Cardiology, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA; 3Department of Kinesiology, University of Rhode Island, Kingston, RI, USACorrespondence: Harry B Rossiter, Institute of Respiratory Medicine and Exercise Physiology, Division of Respiratory and Critical Care Physiology and Medicine, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, 1124 W. Carson Street, CDCRC Building, Torrance, CA, 90502, USA, Tel +1 310-222-8200, Email hrossiter@lundquist.orgIntroduction: 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 (β, − 0.05; p = 0.013), driven primarily by D-PPAC difficulty score (β, − 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.Keywords: coronary artery calcium, COPD, muscle, oxidative capacity, physical activity, respiratory

IntroductionSeveral 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.MethodsTwenty-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.ResultsGET 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.ConclusionsIn 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.

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.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).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).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.

The full text is free to read and use for the duration of the Covid-19 pandemic at :https://europepmc.org/abstract/MED/36917254. Articles labelled 'free to read and use' are included in the open access subset. They are still protected by copyright, but are made available under a Creative Commons license, or similar, that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all the articles. Data availability: The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request. 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. No funding was received to develop this manuscript. Nicholas B. Tiller is funded by a postdoctoral fellowship from the Tobacco-Related Disease Research Program (TRDRP; award no. T31FT1692). Camilla R. Illidi is funded by an Accelerate postdoctoral fellowship from the Mathematics of Information Technology and Complex System (MITACS award no. IT28775).

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.

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).

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-minute 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 one minute 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 to 1.01)], but higher CI-6MWT was associated with lower rate of severe ARE [0.95 (0.92 to 0.99)]. Higher HRR was associated with a lower rate of both any ARE [0.97 (0.95 to 0.99)] and severe ARE [0.95 (0.92 to 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.

Dongxing Zhao,1,2 Asghar Abbasi,1 Richard Casaburi,1 Alessandra Adami,3 Nicholas B Tiller,1 Wei Yuan,1,4 Christopher Yee,5 Nicholas G Jendzjowsky,1 David M MacDonald,6,7 Ken M Kunisaki,6,7 William W Stringer,1 Janos Porszasz,1 Barry J Make,8 Russell P Bowler,8 Harry B Rossiter1 On behalf of the COPDGene Investigators1Rehabilitation Clinical Trials Center, Division of Respiratory and Critical Care Physiology and Medicine, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, CA, USA; 2State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510120, People’s Republic of China; 3Department of Kinesiology, University of Rhode Island, Kingston, RI, USA; 4Respiratory Medicine Department, Beijing Friendship Hospital Affiliated of Capital Medical University, Beijing, 100050, People’s Republic of China; 5MemorialCare Long Beach Medical Center, Long Beach, CA, USA; 6Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, University of Minnesota, Minneapolis, MN, USA; 7Minneapolis VA Health Care System, Minneapolis, MN, USA; 8National Jewish Health, Denver, CO, USACorrespondence: Harry B Rossiter Email hrossiter@ucla.eduBackground: Slow heart rate recovery (HRR) after exercise is associated with autonomic dysfunction and increased mortality. What HRR criterion at 1-minute after a 6-minute walk test (6MWT) best defines pulmonary impairment?.Study Design and Methods: A total of 5008 phase 2 COPDGene (NCT00608764) participants with smoking history were included. A total of 2127 had COPD and, of these, 385 were followed-up 5-years later. Lung surgery, transplant, bronchiectasis, atrial fibrillation, heart failure and pacemakers were exclusionary. HR was measured from pulse oximetry at end-walk and after 1-min seated recovery. A receiver operator characteristic (ROC) identified optimal HRR cut-off. Generalized linear regression determined HRR association with spirometry, chest CT, symptoms and exacerbations.Results: HRR after 6MWT (bt/min) was categorized in quintiles: ≤ 5 (23.0% of participants), 6– 10 (20.7%), 11– 15 (18.9%), 16– 22 (18.5%) and ≥ 23 (18.9%). Compared to HRR≤ 5, HRR≥ 11 was associated with (p< 0.001): lower pre-walk HR and 1-min post HR; greater end-walk HR; greater 6MWD; greater FEV1%pred; lower airway wall area and wall thickness. HRR was positively associated with FEV1%pred and negatively associated with airway wall thickness. An optimal HRR ≤ 10 bt/min yielded an area under the ROC curve of 0.62 (95% CI 0.58– 0.66) for identifying FEV1< 30%pred. HRR≥ 11 bt/min was the lowest HRR associated with consistently less impairment in 6MWT, spirometry and CT variables. In COPD, HRR≤ 10 bt/min was associated with (p< 0.001): ≥ 2 exacerbations in the previous year (OR=1.76[1.33– 2.34]); CAT≥ 10 (OR=1.42[1.18– 1.71]); mMRC≥ 2 (OR=1.42[1.19– 1.69]); GOLD 4 (OR=1.98[1.44– 2.73]) and GOLD D (OR=1.51[1.18– 1.95]). HRR≤ 10 bt/min was predicted COPD exacerbations at 5-year follow-up (RR=1.83[1.07– 3.12], P=0.027).Conclusion: HRR≤ 10 bt/min after 6MWT in COPD is associated with more severe expiratory flow limitation, airway wall thickening, worse dyspnoea and quality of life, and future exacerbations, suggesting that an abnormal HRR≤ 10 bt/min after a 6MWT may be used in a comprehensive assessment in COPD for risk of severity, symptoms and future exacerbations.Keywords: autonomic dysfunction, chest computed tomography, COPD exacerbation, exercise, spirometry

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 (V˙E, 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

Ultra-endurance has been defined as any exercise bout that exceeds 6 h. A number of exceptional, record-breaking performances by female athletes in ultra-endurance sport have roused speculation that they might be predisposed to success in such events. Indeed, while the male-to-female performance gap in traditional endurance sport (e.g., marathon) remains at ~ 10%, the disparity in ultra-endurance competition has been reported as low as 4% despite the markedly lower number of female participants. Moreover, females generally outperform males in extreme-distance swimming. The issue is complex, however, with many sports-specific considerations and caveats. This review summarizes the sex-based differences in physiological functions and draws attention to those which likely determine success in extreme exercise endeavors. The aim is to provide a balanced discussion of the female versus male predisposition to ultra-endurance sport. Herein, we discuss sex-based differences in muscle morphology and fatigability, respiratory-neuromechanical function, substrate utilization, oxygen utilization, gastrointestinal structure and function, and hormonal control. The literature indicates that while females exhibit numerous phenotypes that would be expected to confer an advantage in ultra-endurance competition (e.g., greater fatigue resistance, greater substrate efficiency, and lower energetic demands), they also exhibit several characteristics that unequivocally impinge on performance (e.g., lower O2-carrying capacity, increased prevalence of GI distress, and sex-hormone effects on cellular function/injury risk). Crucially, the advantageous traits may only manifest as ergogenic in the extreme endurance events which, paradoxically, are those that females less often contest. The title question should be revisited in the coming years, when/if the number of female participants increases.

Physical exertion was once crucial for survival because energy (food) was derived predominantly from hunting and foraging; this, in turn, shaped the genome of modern man. In contemporary society, human genes and human lives are incongruent; physical activity is no longer a prerequisite for securing calories, our jobs are largely sedentary, and scarcely is a predominance of leisure time devoted to structured exercise. Reducing sedentary time and following a structured exercise regimen has been shown, unequivocally, to improve long-term weight management and reduce the risk of noncommunicable diseases. Nevertheless, many are not meeting the most conservative of physical activity guidelines. This chapter begins by distinguishing among the terms of physical activity, exercise, and sport before overviewing the principal physiological benefits of regular exercise. There is a discussion of the juxtaposition between the benefits of regular exercise and the pathophysiological consequences of extreme exercise behavior. Finally, there is an overview of the genetically-inherited traits that mediate the physiological adaptation to exercise training and other molecular mechanisms that likely underpin exercise and performance.

Ultra-endurance has been defined as any exercise bout that exceeds 6 h. A number of exceptional, record-breaking performances by female athletes in ultra-endurance sport have roused speculation that they might be predisposed to success in such events. Indeed, while the male-to-female performance gap in traditional endurance sport (e.g., marathon) remains at ~ 10%, the disparity in ultra-endurance competition has been reported as low as 4% despite the markedly lower number of female participants. Moreover, females generally outperform males in extreme-distance swimming. The issue is complex, however, with many sports-specific considerations and caveats. This review summarizes the sex-based differences in physiological functions and draws attention to those which likely determine success in extreme exercise endeavors. The aim is to provide a balanced discussion of the female versus male predisposition to ultra-endurance sport. Herein, we discuss sex-based differences in muscle morphology and fatigability, respiratory-neuromechanical function, substrate utilization, oxygen utilization, gastrointestinal structure and function, and hormonal control. The literature indicates that while females exhibit numerous phenotypes that would be expected to confer an advantage in ultra-endurance competition (e.g., greater fatigue resistance, greater substrate efficiency, and lower energetic demands), they also exhibit several characteristics that unequivocally impinge on performance (e.g., lower O

Drinking cold water evokes decreases in spirometric indices of lung function. We studied whether this could be explained by changes in exhaled-breath temperature (EBT), airflow dynamics, and spirometer measurement sensitivity.\ud \ud Methods\ud In a randomized/crossover design, 10 healthy adults consumed 1000 mL refrigerated water (2.1 ± 0.64 °C) or water at room temperature (19.4 ± 0.5 °C), with EBT assessed at baseline and at 5, 10, 15 and 30-min post-ingestion. The influence of EBT on pneumotachograph measurement characteristics was modelled using computational fluid dynamics (CFD).\ud \ud Results\ud At 5-min post-ingestion, EBT was lower (p < 0.001) following the ingestion of cold water versus water at room-temperature (31.7 ± 1.1 vs. 33.0 ± 0.9 °C), and remained lower until 30-min post-ingestion. At a flow of 8 L s―1, a decrease in EBT of 2.1 °C (as observed following cold-water ingestion) was modelled to underpredict lung volume by 0.7%.\ud \ud Conclusions\ud Cold water reduces EBT below baseline but effects pneumotachograph measurements only negligibly. Therefore, decreased lung function following cold-water ingestion likely has a physiological explanation which warrants further study.

Introduction: COPD is characterized by inactivity and muscle deconditioning. We recently showed a negative association between muscle oxidative capacity and serum triglyceride concentrations in severe COPD. It is unclear whether these maladaptations contribute to increased cardiometabolic disease risk. Aim. To assess relationships among muscle oxidative capacity, coronary artery calcium (CAC), and hepatic steatosis (liver-to-spleen Hounsfield Unit ratio) in smokers with and without COPD. Methods. Data from 90 COPDGene subjects (GOLD 1/2/3/4=10/12/6/7; 55 smoking controls with normal spirometry) were retrospectively analyzed. CAC and L/S were assessed from chest CT. Muscle oxidative capacity was estimated from the O2 consumption recovery rate constant (k) using near-infrared spectroscopy. Results. k was lower in COPD than controls (1.31±0.44 vs. 1.67±0.45min-1; p 0.05). L/S was greater in COPD (1.45±0.49 vs. 1.31±0.26; p=0.038, d=0.36), and the threshold for fatty liver disease (L/S

Introduction: COPD causes inflammation and alters circulating immune cell populations. In health, exercise mobilizes immune cells and promotes anti-inflammation. Aim: To determine the change in circulating immune cell subtypes in response to exercise in COPD and controls. Methods: Age- and sex-matched ex-smokers with (n=5) and without (n=4) COPD performed a single bout of high-intensity interval exercise (10x 1 min at 120% peak work rate, 2 min recovery). Venous blood was collected at baseline (BSL) and post-exercise (0, 30 and 120 min) to quantify 12 immune cell subtypes using multicolor flow cytometry. Two-way ANOVA (Dunnett’s posthoc) assessed the effects of time x group. Results: Leukocytes were increased (p Conclusion Exercise-induced leukocytosis was not different between COPD and controls. Exercise predominantly altered lymphoid cell fractions in both groups. However, exercise-induced increases in NK and TReg subtypes were absent in COPD. These data suggest that the potentially beneficial effects of exercise on immunosurveilance are attenuated in COPD. Support: TRDRP 28FT-001

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.

This paper assessed the blood pressure, heart rate, and mouth-pressure responses to indoor rock climbing (bouldering) and associated training exercises. Six well-trained male rock climbers (mean ± SD age, 27.7 ± 4.7 yr; stature, 177.7 ± 7.3 cm; mass, 69.8 ± 12.1 kg) completed two boulder problems (6b and 7a+ on the Fontainebleau Scale) and three typical training exercises [maximum voluntary contraction (MVC) isometric pull-up, 80% MVC pull-ups to fatigue, and campus board to fatigue]. Blood pressure and heart rate were measured via an indwelling femoral arterial catheter, and mouth pressure via a mouthpiece manometer. Bouldering evoked a peak systolic pressure of 200 ± 17 mmHg (44 ± 21% increase from baseline), diastolic pressure of 142 ± 26 mmHg (70 ± 32% increase), mean arterial pressure of 163 ± 18 mmHg (56 ± 25% increase), and heart rate of 176 ± 22 beats/min (76 ± 35% increase). The highest systolic pressure was observed during the campus board exercise (218 ± 33 mmHg), although individual values as high as 273/189 mmHg were recorded. Peak mouth pressure during climbing was 31 ± 46 mmHg, and this increased independently of climb difficulty. We concluded that indoor rock climbing and associated exercises evoke a substantial pressor response resulting in high blood pressures that may exceed those observed during other upper-limb resistance exercises. These findings may inform risk stratification for climbers.

Drawing on reflections from a collaborative autoethnography, this article argues that ultramarathon running is defied by a 'dark' ecological sensibility (Morton 2007, 2010, 2016), characterised by moments of pain, disgust, and the macabre. In contrast to existing accounts, we problematise the notion that runners 'use' nature for escape and/or competition, while questioning the aesthetic-causal relationships often evinced within these accounts. With specific reference to the discursive, embodied, spatial and temporal aspects of the sport, we explore the way in which participants begin to appreciate the immense power of nature, while being humbled by the fragile and unstable foundations of human experience. Accordingly this article contributes novel insights into the human-nature complex that seek to move beyond Romantic analyses towards a more sophisticated understanding of the relationships between (nature) sport, people and place.

Objectives Compliant surfaces beneath a casualty diminish the quality of cardiopulmonary resuscitation (CPR) in clinical environments. To examine this issue in a sporting environment, we assessed chest compression quality and rescuer exertion upon compliant sports safety matting. Methods Twenty-seven advanced life support providers volunteered (13 male/14 female; mass = 79.0 ± 12.5 kg; stature = 1.77 ± 0.09 m). Participants performed 5 × 2 min, randomized bouts of continuous chest compressions on a mannequin, upon five surfaces: solid floor; low-compliance matting; low-compliance matting with a backboard; high-compliance matting; high-compliance matting with a backboard. Measures included chest compression depth and rate, percentage of adequate compressions, and rescuer heart rate and perceived exertion. Results Chest compression depth and rate were significantly lower upon high-compliance matting relative to other surfaces (pp Conclusion Providers of CPR should be alerted to the detrimental effects of compliant safety matting in a sporting environment and prepare to alter the targeted compression depth and rescuer rotation intervals accordingly.

Background In this Position Statement, the International Society of Sports Nutrition (ISSN) provides an objective and critical review of the literature pertinent to nutritional considerations for training and racing in single-stage ultra-marathon. Recommendations for Training. i) Ultra-marathon runners should aim to meet the caloric demands of training by following an individualized and periodized strategy, comprising a varied, food-first approach; ii) Athletes should plan and implement their nutrition strategy with sufficient time to permit adaptations that enhance fat oxidative capacity; iii) The evidence overwhelmingly supports the inclusion of a moderate-to-high carbohydrate diet (i.e., ~ 60% of energy intake, 5–8 g·kg− 1·d− 1) to mitigate the negative effects of chronic, training-induced glycogen depletion; iv) Limiting carbohydrate intake before selected low-intensity sessions, and/or moderating daily carbohydrate intake, may enhance mitochondrial function and fat oxidative capacity. Nevertheless, this approach may compromise performance during high-intensity efforts; v) Protein intakes of ~ 1.6 g·kg− 1·d− 1 are necessary to maintain lean mass and support recovery from training, but amounts up to 2.5 g.kg− 1·d− 1 may be warranted during demanding training when calorie requirements are greater; Recommendations for Racing. vi) To attenuate caloric deficits, runners should aim to consume 150–400 Kcal·h− 1 (carbohydrate, 30–50 g·h− 1; protein, 5–10 g·h− 1) from a variety of calorie-dense foods. Consideration must be given to food palatability, individual tolerance, and the increased preference for savory foods in longer races; vii) Fluid volumes of 450–750 mL·h− 1 (~ 150–250 mL every 20 min) are recommended during racing. To minimize the likelihood of hyponatraemia, electrolytes (mainly sodium) may be needed in concentrations greater than that provided by most commercial products (i.e., > 575 mg·L− 1 sodium). Fluid and electrolyte requirements will be elevated when running in hot and/or humid conditions; viii) Evidence supports progressive gut-training and/or low-FODMAP diets (fermentable oligosaccharide, disaccharide, monosaccharide and polyol) to alleviate symptoms of gastrointestinal distress during racing; ix) The evidence in support of ketogenic diets and/or ketone esters to improve ultra-marathon performance is lacking, with further research warranted; x) Evidence supports the strategic use of caffeine to sustain performance in the latter stages of racing, particularly when sleep deprivation may compromise athlete safety.

The physiological demands of marathon and ultra-marathon running are substantial, affecting multiple body systems. There have been several reviews on the physiological contraindications of participation; nevertheless, the respiratory implications have received relatively little attention. This paper provides an up-to-date review of the literature pertaining to acute pulmonary and respiratory muscle responses to marathon and ultra-marathon running. Pulmonary function was most commonly assessed using spirometry, with infrequent use of techniques including single-breath rebreathe and whole-body plethysmography. All studies observed statistically significant post-race reductions in one-or-more metrics of pulmonary function, with or without evidence of airway obstruction. Nevertheless, an independent analysis revealed that post-race values rarely fell below the lower-limit of normal and are unlikely, therefore, to be clinically significant. This highlights the virtue of healthy baseline parameters prior to competition and, although speculative, there may be more potent clinical manifestations in individuals with below-average baseline function, or those with pre-existing respiratory disorders (e.g., asthma). Respiratory muscle fatigue was most commonly assessed indirectly using maximal static mouth-pressure manoeuvres, and respiratory muscle endurance via maximum voluntary ventilation (MVV12). Objective nerve-stimulation data from one study, and others documenting the time-course of recovery, implicate peripheral neuromuscular factors as the mechanism underpinning such fatigue. Evidence of respiratory muscle fatigue was more prevalent following marathon compared to ultra-marathon, and might be a factor of work rate, and thus exercise ventilation, which is tempered during longer races. Potential implications of respiratory muscle fatigue on health and marathon/ultra-marathon performance have been discussed, and include a diminished postural stability that may increase the risk of injury when running on challenging terrain, and possible respiratory muscle fatigue-induced effects on locomotor limb blood flow. This review provides novel insights that might influence marathon/ultra-marathon preparation strategies, as well as inform medical best-practice of personnel supporting such events.

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.\ud \ud 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.\ud \ud 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.\ud \ud 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.