Respiratory health of elite athletes – preventing airway injury: a critical review

Elite athletes, particularly those engaged in endurance sports and those exposed chronically to airborne pollutants/irritants or allergens, are at increased risk for upper and lower airway dysfunction. Airway epithelial injury may be caused by dehydration and physical stress applied to the airways during severe exercise hyperpnoea and/or by inhalation of noxious agents. This is thought to initiate an inflammatory cascade/repair process that, ultimately, could lead to airway hyperresponsiveness (AHR) and asthma in susceptible athletes. The authors review the evidence relating to prevention or reduction of the risk of AHR/asthma development. Appropriate measures should be implemented when athletes exercise strenuously in an attempt to attenuate the dehydration stress and reduce the exposure to noxious airborne agents. Environmental interventions are the most important. Non-pharmacological strategies can assist, but currently, pharmacological measures have not been demonstrated to be effective. Whether early prevention of airway injury in elite athletes can prevent or reduce progression to AHR/asthma remains to be established

Physiological comparison of intensity-controlled, isocaloric intermittent and continuous exercise.

International audienceVO2 fluctuations are argued to be an important mechanism underpinning chronic adaptations following interval training. We compared the effect of exercise modality, continuous vs. intermittent realized at a same intensity, on electrical muscular activity, muscular oxygenation and on whole body oxygen uptake. Twelve participants (24 ± 5 years; VO2peak: 43 ± 6 mL· min·kg) performed (i) an incremental test to exhaustion to determine peak work rate (WR); two randomized isocaloric exercises at 70%WRpeak; (ii) 1 bout of 30 min; (iii) 30 bouts of 1 min work intercepted with 1 min passive recovery. For electromyography, only the CON exercise showed change for the vastus lateralis root-mean-square (+6.4 ± 5.1%, P < .01, 95%CI 3.2, 8.3) and mean power frequency (-5.2 ± 4.8, P < .01, 95%CI -8.2, -3.5). Metabolic fluctuations (i.e. Oxygen Fluctuation Index and HHb Fluctuation Index) were higher in the intermittent modality, while post-exercise blood lactate concentrations (4.80 ± 1.50 vs. 2.32 ± 1.21 mM, respectively, for the CON and INT, P < .01, 95%CI 1.72, 3.12) and the time spent over 90% of VO2 target (1644 ± 152 vs. 356 ± 301 sec, respectively, for the CON and INT, P < .01, 95%CI 1130, 1446) were higher in the continuous modality. In conclusion, despite a similar energy expenditure and intensity, intermittent and continuous exercises showed two very different physiological responses. The intermittent modality would lead to a larger recruitment of fast twitch fibres that are less mitochondria-equipped and therefore may be more likely respondent to mitochondrial adaptations. In addition, this modality induces greater metabolic variations, a stimulus who could lead to mitochondrial development

Effect of work: rest cycle duration on VO2 fluctuations during intermittent exercise

International audienceThe succession of on-transient phases that induce a repetition of metabolic changes is a possible mechanism responsible for the greater response to intermittent training (IT). The objective of this study was to quantify [Formula: see text] fluctuations during intermittent exercise characterised by the same work:rest ratio, but different durations and identify which duration leads to the greatest fluctuations. Ten participants (24 ± 5 years; [Formula: see text]: 42 ± 7 mL·min ·kg ) performed (1) an incremental test to exhaustion to determine peak work rate (WR) and oxygen uptake ([Formula: see text]), (2), and three 1 h intermittent exercises alternating work period at 70% WR with passive recovery period of different 1:1 work:recovery duty cycles (30 s:30 s, 60 s:60 s, 120 s:120 s). [Formula: see text] response analysis revealed differences in the fluctuations across the intermittent conditions despite an identical total energy expenditure. The sum of the cycle's nadir-to-peak [Formula: see text] differences (ΣΔ[Formula: see text]) and the oxygen fluctuation index (OFI) were both greater in the 60 s:60 s condition (ΣΔ[Formula: see text]: +38% ± 13% and +19% ± 18% vs. 120 s:120 s and 30 s:30 s, P < 0.05; OFI: +41% ± 29% and +67% ± 62% vs. 120 s:120 s and 30:30 s, P < 0.05). [Formula: see text] fluctuation analysis was successful in identifying the intermittent condition associated with the greatest disturbances: the 60 s:60 s duty cycle induces more [Formula: see text] fluctuations. The present findings also demonstrate that the selection of the duty cycle duration for submaximal intermittent exercise (70% of WR) prescription is of interest to produce high [Formula: see text] fluctuations

Exploiting Local Facilities for Post-Pulmonary Rehabilitation Maintenance Programs in Fibrotic Idiopathic Interstitial Pneumonia Patients: A Pilot Study

International audienc

Exercise-induced metabolic fluctuations influence AMPK, p38-MAPK and CaMKII phosphorylation in human skeletal muscle.

International audienceDuring transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). On two separate occasions, nine men performed a continuous (30-min) and an intermittent exercise (30 × 1-min intervals separated by 1-min of recovery) at 70% of V˙O2peak. Skeletal muscle biopsies from the vastus lateralis were taken at rest and at +0 h and +3 h after each exercise. Metabolic fluctuations that correspond to exercise-induced variation in metabolic rates were determined by analysis of VO2 responses. During intermittent exercise metabolic fluctuations were 2.8-fold higher despite identical total work done to continuous exercise (317 ± 41 vs. 312 ± 56 kJ after intermittent and continuous exercise, respectively). Increased phosphorylation of AMP-activated protein kinase (AMPK) (~2.9-fold, P < 0.01), calcium/calmodulin-dependent protein kinase II (CaMKII) (~2.7-fold, P < 0.01) and p38-mitogen-activated protein kinase (MAPK) (~4.2-fold, P < 0.01) occurred immediately in both exercises and to a greater extent after the intermittent exercise (condition x time interaction, P < 0.05). A single bout of intermittent exercise induces a greater activation of these signaling pathways regulating PGC-1α when compared to a single bout of continuous exercise of matched work and intensity. Chronic adaptations to exercise on mitochondria biogenesis are yet to be investigated

Cerebral oxygenation during hyperoxia-induced increase in exercise tolerance for untrained men.

International audienceThis study aimed to investigate the involvement of cerebral oxygenation in limitation of maximal exercise. We hypothesized that O2 supplementation improves physical performance in relation to its effect on cerebral oxygenation during exercise. Eight untrained men (age 27 ± 6 years; VO2 max 45 ± 8 ml min(-1) kg(-1)) performed two randomized exhaustive ramp exercises on a cycle ergometer (1 W/3 s) under normoxia and hyperoxia (FIO2 = 0.3). Cerebral (ΔCOx) and muscular (ΔMOx) oxygenation responses to exercise were monitored using near-infrared spectroscopy. Power outputs corresponding to maximal exercise intensity, to threshold of ΔCOx decline (ThCOx) and to the respiratory compensation point (RCP) were determined. Power output (W max = 302 ± 20 vs. 319 ± 28 W) and arterial O2 saturation estimated by pulse oximetry (SpO2 = 95.7 ± 0.9 vs. 97.0 ± 0.5 %) at maximal exercise were increased by hyperoxia (P < 0.05). However, the ΔMOx response during exercise was not significantly modified with hyperoxia. RCP (259 ± 17 vs. 281 ± 25 W) and ThCOx (259 ± 23 vs. 288 ± 30 W) were, however, improved (P < 0.05) with hyperoxia and the ThCOx shift was related to the W max improvement with hyperoxia (r = 0.71, P < 0.05). The relationship between the change in cerebral oxygenation response to exercise and the performance improvement with hyperoxia supports that cerebral oxygenation is limiting the exercise performance in healthy young subjects

Prevalence and characteristics of asthma in the aquatic disciplines

Background Despite the health benefits of swimming as a form of exercise, evidence exists that both the swimming pool environment and endurance exercise are etiologic factors in the development of asthma. The prevalence of asthma in swimmers is high compared with that in participants in other Olympic sport disciplines. There are no publications comparing the prevalence of asthma in the 5 aquatic disciplines. Objective The purpose of this study is to examine and compare the prevalence of asthma in the aquatic disciplines and in contrast with other Olympic sports. Methods Therapeutic Use Exemptions containing objective evidence of athlete asthma/airway hyperresponsiveness (AHR) were collected for all aquatic athletes participating in swimming, diving, synchronized swimming, water polo, and open water swimming for major events during the time period from 2004-2009. The prevalence of asthma/AHR in the aquatic disciplines was analyzed for statistical significance (with 95% CIs) and also compared with that in other Olympic sports. Results Swimming had the highest prevalence of asthma/AHR in comparison with the other aquatic disciplines. The endurance aquatic disciplines have a higher prevalence of asthma/AHR than the aquatic nonendurance disciplines. Asthma/AHR is more common in Oceania, Europe, and North America than in Asia, Africa, and South America. In comparison with other Olympic sports, swimming, synchronized swimming, and open water swimming were among the top 5 sports for asthma/AHR prevalence. Conclusion Asthma/AHR in the endurance aquatic disciplines is common at the elite level and has a varied geographic distribution. Findings from this study demonstrate the need for development of aquatic discipline-specific prevention, screening, and treatment regimens. © 2015 American Academy of Allergy, Asthma & Immunology

Is airway damage during physical exercise related to airway dehydration? Inputs from a computational model.

In healthy subjects, at low minute ventilation (V̇ E ) during physical exercise, the water content and the temperature of the airways are well regulated. However, with the increase in V̇ E ,the bronchial mucosa becomes dehydrated and epithelial damage occurs. Our goal was to demonstrate the correspondence between the ventilatory threshold inducing epithelial damage, measured experimentally, and the dehydration threshold, estimated numerically. In 16 healthy adults, we assessed epithelial damage before and following a 30-min continuous cycling exercise at 70% of maximal work rate, by measuring the variation pre- to post-exercise of serum club cell protein (cc16/cr). Blood samples were collected at rest, just at the end of the standardized 10-min warm-up, and immediately, 30 min and 60 min post-exercise. V̇ E was measured continuously during exercise. Airway water and heat losses were estimated using a computational model adapted to the experimental conditions and were compared to a literature-based threshold of dehydration. Eleven participants exceeded the threshold for bronchial dehydration during exercise (group A) and 5 did not (group B). Compared to post warm-up, the increase in cc16/cr post-exercise was significant (mean increase ± SEM: 0.48 ± 0.08 ng.l -1 ,i.e. 101 ± 32%, p < 0.001) only in group A but not in group B (mean difference ± SEM: 0.10 ± 0.04 ng.l -1 ,i.e. 13 ± 7 %, p = 0.79). Our findings suggest that the use of a computational model may be helpful to estimate an individual dehydration threshold of the airways that is associated with epithelial damage during physical exercise.info:eu-repo/semantics/publishe

Prevalence of lower airway dysfunction in athletes : a systematic review and meta-analysis by a subgroup of the IOC consensus group on ‘acute respiratory illness in the athlete’

Please read abstract in the article.http://bjsm.bmj.comhj2023Sports Medicin

International Olympic Committee (IOC) consensus statement on acute respiratory illness in athletes part 1 : acute respiratory infections

Acute illnesses affecting the respiratory tract are common and form a significant component of the work of Sport and Exercise Medicine (SEM) clinicians. Acute respiratory illness (ARill) can broadly be classified as non-infective ARill and acute respiratory infections (ARinf). The aim of this consensus is to provide the SEM clinician with an overview and practical clinical approach to ARinf in athletes. The International Olympic Committee (IOC) Medical and Scientific Commission appointed an international consensus group to review ARill (non-infective ARill and ARinf) in athletes. Six subgroups of the IOC Consensus group were initially established to review the following key areas of ARill in athletes: (1) epidemiology/risk factors for ARill, (2) ARinf, (3) non-infective ARill including ARill due to environmental exposure, (4) acute asthma and related conditions, (5) effects of ARill on exercise/sports performance, medical complications/return-to-sport and (6) acute nasal/vocal cord dysfunction presenting as ARill. Several systematic and narrative reviews were conducted by IOC consensus subgroups, and these then formed the basis of sections in the consensus documents. Drafting and internal review of sections were allocated to ‘core’ members of the consensus group, and an advanced draft of the consensus document was discussed during a meeting of the main consensus core group in Lausanne, Switzerland on 11 to 12 October 2021. Final edits were completed after the meeting. This consensus document (part 1) focusses on ARinf, which accounts for the majority of ARill in athletes. The first section of this consensus proposes a set of definitions and classifications of ARinf in athletes to standardise future data collection and reporting. The remainder of the consensus paper examines a wide range of clinical considerations related to ARinf in athletes: epidemiology, risk factors, pathology/pathophysiology, clinical presentation and diagnosis, management, prevention, medical considerations, risks of infection during exercise, effects of infection on exercise/sports performance and return-to-sport guidelines.http://bjsm.bmj.comhj2023Sports Medicin