Mid Sweden University

Water immersion methods, such as cold water immersion and contrast water therapy are popular recovery interventions after athletic training and competition. Nevertheless, post-exercise cold water immersion may actually inhibit hypertrophic signalling pathways and muscle adaptation to training (1). It is has been commonly assumed that the mechanism of impaired training adaptation is mediated by blunted inflammatory responses to muscle-damaging exercise, although this assumption has been questioned by recent data (2). A weakness of previous studies is omission of active recovery in water immersion interventions, which would arguably be utilised in addition to water immersion by athletic populations. The aim of this study was to compare the influence of three water immersion methods, performed after active recovery, on inflammatory responses to muscle-damaging exercise. Nine male participants (age 20-35 y) performed an intensive exercise protocol, consisting of maximal jumps and sprinting, on four occasions. After each trial, participants completed one of four recovery protocols in a randomised, crossover design (ACT, active recovery only, 10 min cycling; heart rate 120-140 b/min; CWI, active recovery followed by 10 min cold water immersion, 10°C; TWI, active recovery followed by 10 min temperate water immersion, 24°C and CWT, active recovery followed by contrast water therapy, 10 min alternating 10°C and 38°C in 1 min cycles). The study was conducted in accordance with the Declaration of Helsinki and approved by the local ethical review board. Venous blood samples were collected pre-exercise and 5 min, 60 min, 24 h, 48 h and 96 h post-exercise, then analysed for myocyte chemoattractant protein 1 (MCP-1) and creatine kinase (CK) using ELISA and high-sensitivity C-reactive protein (hs-CRP) using a chemiluminescence assay. Two-way repeated measures ANOVA was used to compare biomarker concentrations between groups over time. There were no differences in biomarker concentrations during exercise and recovery between groups across the six time points, however main effects of time were present for all three markers (MCP-1: F(2.32, 18.56) = 23.1, p < 0.0001; CK: F(2.059, 16.47) = 8.74, p = 0.002; hs-CRP: F(1.07, 8.57 = 13.8, p = 0.005). Tukey’s post-hoc analysis of simple time effects revealed increases in MCP-1 at post-5 min versus pre in all groups except CWT. In TWI and CWI, MCP-1 was still elevated above pre at 60 min post-exercise. hs-CRP peaked at 24 h post-exercise in all groups. CK was elevated at post-60 versus pre in all groups and at post-24 except in CWT. Our findings suggest that use of cold or thermoneutral water immersion in combination with active recovery may slightly prolong the immediate post-exercise elevation in MCP-1 but have minimal overall effect on markers of inflammation and muscle damage.

Purpose: The aim of this study was to compare the efficacy of three water immersion interventions performed after active recovery compared to active recovery only on the resolution of inflammation and markers of muscle damage post-exercise. Methods: Nine physically active men (n = 9; age 20‒35 years) performed an intensive loading protocol, including maximal jumps and sprinting on four occasions. After each trial, one of three recovery interventions (10 min duration) was used in a random order: cold-water immersion (CWI, 10 °C), thermoneutral water immersion (TWI, 24 °C), contrast water therapy (CWT, alternately 10 °C and 38 °C). All of these methods were performed after an active recovery (10 min bicycle ergometer), and were compared to active recovery only (ACT). 5 min, 1, 24, 48, and 96 h after exercise bouts, immune response and recovery were assessed through leukocyte subsets, monocyte chemoattractant protein-1, myoglobin and high-sensitivity C-reactive protein concentrations. Results: Significant changes in all blood markers occurred at post-loading (p < 0.05), but there were no significant differences observed in the recovery between methods. However, retrospective analysis revealed significant trial-order effects for myoglobin and neutrophils (p < 0.01). Only lymphocytes displayed satisfactory reliability in the exercise response, with intraclass correlation coefficient > 0.5. Conclusions: The recovery methods did not affect the resolution of inflammatory and immune responses after high-intensity sprinting and jumping exercise. It is notable that the biomarker responses were variable within individuals. Thus, the lack of differences between recovery methods may have been influenced by the reliability of exercise-induced biomarker responses. 

Purpose 

The aim of this study was to investigate within-cycle differences in nocturnal heart rate (HR) and heart rate variability (HRV) in naturally menstruating women (NM) and women using combined hormonal contraceptives (CU) or progestin-only hormonal contraceptives (PU).

Methods 

Physically active participants were recruited into three groups: NM (n = 19), CU (n = 11), and PU (n = 12). Participants’ HR and HRV (with Bodyguard 2 HRV monitor), and blood hormones were monitored during one menstrual cycle (MC) (NM-group) or for 4 weeks (CU and PU-groups). Estradiol, progesterone, and luteinizing hormone were analyzed from fasting blood samples collected four times in the NM (M1 = bleeding, M2 = follicular phase, M3 = ovulation, and M4 = luteal phase) and PU groups (M1 = lowest E2; M2 = M1 + 7 days; M3 = M1 + 14 days; M4 = M1 + 21 days) and twice in the CU group (active and inactive pill phases). After every blood sample, nightly HR and HRV were recorded and examined as an average from two nights.

Results 

Hormonal concentrations differed (p < 0.05) between MC phases in the NM- and PU-groups, but not (p ≥ 0.116) between the active and inactive phases in the CU-group. In the NM- and PU-groups, some of the HRV values were higher, while in the NM-group, HR was lower during M2 compared to M3 (p < 0.049) and M4 (p < 0.035). In the CU-group, HRV values (p = 0.014-0.038) were higher, and HR was lower (p = 0.038) in the inactive phase compared to the first week of the active phase.

Conclusions 

The MC and hormonal cycle phases influence autonomic nervous system balance, which is reflected in measurements of nocturnal HR and HRV. This should be considered when monitoring recovery in physically active individuals.

: The aim of this study was to investigate effects of a single infrared sauna (IRS) session on postexercise recovery of neuromuscular performance, autonomic nervous system function, subjective sleep quality, and muscle soreness. Male basketball players (n = 16) performed two trials consisting of a complex resistance exercise protocol (maximal strength with plyometrics), followed by either 20 min passive recovery (PAS) or IRS (temperature 43±5°C), in a randomized crossover design, with trials separated by one week. Recovery of neuromuscular performance was assessed using 20 m maximal sprint, maximal countermovement-jump (CMJ), and isometric leg press tests, performed 14 hours after exercise. Heart rate (HR), heart rate variability (HRV), sleep diary, muscle soreness, and indirect muscle damage markers were measured pre and post exercise. The decrease in CMJ performance from pre- to post-exercise was attenuated after IRS compared to PAS (p < 0.01). The IRS session resulted in higher HR and lower root mean square of successive differences between normal heartbeats (RMSSD), and high and low frequency power, compared to PAS (p < 0.002). Post-exercise night-time HR and HRV did not differ following IRS vs. PAS. Muscle soreness was less severe, and perceived recovery was higher after IRS compared to PAS (p < 0.01). Post-exercise IRS attenuated the drop in explosive performance and decreased subjective muscle soreness after resistance training, which may enhance mood, readiness, and physical performance of an athlete. A single IRS session had no detrimental effects on recovery of the autonomic nervous system.

INTRODUCTION:Subjective sleep quality may decrease during menstruation, although the duration and composition of sleep remains relatively stable across the menstrual cycle (MC) (1). Recording heart rate variability (HRV) is a tool to monitor the autonomic nervous system and recovery of the body. Meta-analytical data has not revealed significant changes in HRV from the early follicular phase (menses) to the mid-follicular phase (2). However, reduced HRV-values were observed during menses compared to follicular phase in women with pain during menses (dysmenorrhea) (3). Only a few studies have examined effects of the MC on nocturnal HRV. The aim of this study was to investigate how menses and associated pain affects nocturnal HRV and subjective sleep quality.METHODS:Participants included 14 healthy, physically active women, who did not use hormonal contraception. During one MC, participants completed a diary of sleep, MC and related symptoms. HRV was registered every night (Bodyguard 2, Firstbeat Technologies Ltd., Finland). HRV-data (RMSSD and LF/HF-ratio) were analyzed for two nights after a blood sample and over a four-hour period beginning 30 min after bedtime. Only the menses (M) and mid-follicular phases (FP) are used in this study. Blood samples (estradiol, E2, and progesterone, P4) were collected during M (day 2-3 of the MC) and FP (day 7-10) to ensure normal hormonal function associated with the MC (4).RESULTS:E2 was higher (p=0.012) during FP (267±150 pmol/L) compared to M (143±88 pmol/L), but P4 remained stable (p=0.103). Mean heart rate (HRmean) was higher during M (54±8 beats/min) compared to FP (52±7 beats/min, p=0.022). However, HRV-variables did not differ between M and FP (RMSSD: 76.7±34.5 to 77.3±27.0 ms, p=0.872; LF/HF: 1.416±1.380 to 1.273±0.769, p=0.826). Subjectively-assessed sleep quality remained unchanged between M and FP (p=0.349). The change in RMSSD and HRmean between M and FP did not differ (RMSSD: p=0.728; HRmean: p=0.149) between participants with and without menstrual pains.CONCLUSION:Menses has no effect on nocturnal HRV and subjective sleep quality of physically active women, though the higher nocturnal HRmean during M may indicate decreased recovery during menses.

REFERENCES:1. Driver, H.S., Werth, E., et al. The Menstrual Cycle Effects on Sleep. Sleep Med Clin 2008, 3:1–11.2. Schmalenberger, K.M., Eisenlohr-Moul, T.M., et al. A Systematic Review and Meta-Analysis of Within-Person Changes in Cardiac Vagal Activity across the Menstrual Cycle: Implications for Female Health and Future Studies. J Clin Med 2019, 8:1946.3. Jayamala, A.K., Preethi, B.L., et al. Comparative Analysis of Heart Rate Variability During Different Phases of Menstrual Cycle in Eumenorrhea & Dysmenorrhea Subjects. Exp Clin Physiol Biochem 2017, 1.4. Elliot-Sale, K.J., Minahan, C.L., et al. Methodological Considerations for Studies in Sport and Exercise Science with Women as Participants: A Working Guide for Standards of Practice for Research on Women. Sports Med 2021, 51:843–861.

The purpose of this study was to investigate the resistance to breathing (RES) in heat and moisture exchanging devices (HME) intended for use during physical activity in the cold. RES was investigated for seventeen HMEs, including different types of filters. In addition, the influence of headwind on RES was tested using four representative HMEs. HMEs were mounted to the face of an artificial head manufactured from ABS plastic. The HMEs were connected to a mechanical lung simulator, which delivered standardised inspiratory and expiratory air flow rates ((Formula presented.), L/s). The delta pressure (Δp, Pa) between ambient air and the air inside the HME was measured, whereupon RES was calculated. The results showed significant (p < 0.05) differences in RES between HMEs from different manufacturers, while the difference was smaller, and in some cases not significant (p > 0.05), between different models/filters within the same brand. The results also showed that RES was highly influenced by different ventilations and headwind conditions. RES increased with increased (Formula presented.) and, when a headwind was introduced, RES decreased during inspiration and increased during expiration. Calculations showed that the oxygen and energy cost for breathing through an HME was very small for most of the tested models. The effect of HME dead space on pulmonary gas fractions depends on the tidal volume. At large tidal volumes and ventilations, the effect of HMEs on pulmonary gas fractions becomes relatively small. 

Introduction: Every March, dogsled drivers (mushers) compete in a 1569-km race across Alaska, involving physical exertion, mental exertion, and sleep deprivation for up to 2 wk. These factors may increase mushers’ vulnerability to illness, making them a relevant study population for acute infection risk factors. Specifically, the influence of psychological factors on illness risk during prolonged physical exertion has rarely been investigated. The aim of this study was to examine the relationship between psychological characteristics, sleep deprivation, and illness incidence in Iditarod mushers. Methods: Fourteen mushers completed 4 psychological instruments to assess state and trait anxiety, resilience and perceived stress, and self-reported upper respiratory symptoms (URS) in the month before the race. Mushers self-reported sleep duration and URS during the race. Results: State and trait anxiety, resilience, and perceived stress did not differ between mushers with and without pre- and in-race URS (P>0.05). However, all mushers who reported in-race URS had reported URS ≤9 d before the race, and the onset of symptoms during the race typically occurred shortly after a rest period. Sleep duration was higher in mushers who reported in-race URS, both before (4.9±0.3 h, P=0.016) and during illness (5.9±1.3 h, P=0.006), vs mushers without in-race URS (3.4±0.8 h). Conclusions: This study highlights recent illness, rest periods, and greater sleep requirements as potential risk factors for URS onset during a multiday endurance challenge, whereas psychological factors were not associated with URS.

Purpose: To examine the effects of intensity and duration of exercise stress on induction of in vivo immunity in humans using experimental contact hypersensitivity (CHS) with the novel antigen diphenylcyclopropenone (DPCP).Methods: Sixty-four healthy males completed either 30 min running at 60% V˙O2peak (30MI), 30 min running at 80% V˙O2peak (30HI), 120 min running at 60% V˙O2peak (120MI), or seated rest (CON). Twenty min later, the subjects received a sensitizing dose of DPCP; and 4 wk later, the strength of immune reactivity was quantified by measuring the cutaneous responses to a low dose-series challenge with DPCP on the upper inner arm. Circulating epinephrine, norepinephrine and cortisol were measured before, after, and 1 h after exercise or CON. Next, to understand better whether the decrease in CHS response on 120MI was due to local inflammatory or T-cell-mediated processes, in a crossover design, 11 healthy males performed 120MI and CON, and cutaneous responses to a dose series of the irritant, croton oil (CO), were assessed on the upper inner arm.Results: Immune induction by DPCP was impaired by 120MI (skinfold thickness -67% vs CON; P < 0.05). However, immune induction was unaffected by 30MI and 30HI despite elevated circulating catecholamines (30HI vs pre: P < 0.01) and greater circulating cortisol post 30HI (vs CON; P < 0.01). There was no effect of 120MI on skin irritant responses to CO.Conclusions: Prolonged moderate-intensity exercise, but not short-lasting high- or short-lasting moderate-intensity exercise, decreases the induction of in vivo immunity. No effect of prolonged moderate-intensity exercise on the skin's response to irritant challenge points toward a suppression of cell-mediated immunity in the observed decrease in CHS. Diphenylcyclopropenone provides an attractive tool to assess the effect of exercise on in vivo immunity.

Bakgrund Ansträngningsutlöst bronkkonstriktion (EIB) innebär en övergående luftvägsobstruktion i samband med ansträngning och definieras som en minskning med ≥ 10% av den forcerade utandningen under första sekunden (FEV1). EIB är vanligt bland elitskidåkare. Referenstestet för diagnostik är torrluftsprovokation men ansträngningstest (ECT) i fält anses ha högre representativitet och sensitivitet men är svårt att standardisera. ECT i köldkammare kombinerar en idrottspecifik provokation med en standardiserad miljö men har aldrig använts för att undersöka förekomsten av EIB bland vinteridrottare. Målet med studien var att kartlägga prevalensen av EIB hos elitskidåkare med hjälp av ECT i kyla. Material och metod De 31 deltagarna (16 kvinnor) var ett slumpmässigt urval av de 174 längdskidåkare och skidskyttar från Sveriges riksidrottsgymnasium och nationella idrottsutbildningar som vintern 2022 deltog i en web-enkät om luftvägssymtom, träning och astma. Sex (19%) deltagare hade använt astmamediciner för en läkardiagnostiserad astma de senaste 12 månaderna. ECT i en köldkammare utfördes (8 min löpning i -14,7 °C, Rh 77% på 85% av beräknad maxpuls) med spirometri före och 5-30 minuter efter. Resultat EIB detekterades hos 7 (23%) av deltagarna, 5 av 25 utan astma och 2 av 6 med astma. En deltagare sjönk >15% på FEV1 och hade ingen tidigare känd astma. Kön, ålder, träningstimmar, allergi, FeNO och förekomst av pip/väs från luftvägarna med andnöd de senaste 12 månaderna skiljde sig inte åt mellan deltagarna med och utan EIB. Slutsats ECT i kyla påvisar en hög förekomst av EIB hos unga, friska, svenska elitskidåkare, redan tidigt i karriären och oavsett tidigare känd astma. Att förekomsten av EIB hos skidåkarna med astma inte var högre skulle kunna vara ett resultat av deras antiinflammatoriska astmaläkemedel eller överdiagnostik.

Exposure to a cold climate is associated with an increased morbidity and mortality, but the specific mechanisms are largely unknown. People with cardiopulmonary disease and winter endurance athletes are particularly vulnerable. This study aimed to map multiple domains of airway responses to exercise in subzero temperature in healthy individuals. Thirty-one healthy subjects underwent whole-body exposures for 50 minutes on two occasions in an environmental chamber with intermittent moderate-intensity exercise in +10 °C and -10 °C. Lung function, plasma/urine CC16 , and symptoms were investigated before and after exposures. Compared to baseline, exercise in -10 °C decreased FEV1 (p=0.002), FEV1/FVC (p&lt;0.001), and increased R20Hz (p=0.016), with no differences between exposures. Reactance increased after +10 °C (p=0.005), which differed (p=0.042) from a blunted response after exercise in -10 °C. Plasma CC16 increased significantly within exposures, without differences between exposures. Exercise in -10 °C elicited more intense symptoms from the upper airways, compared to +10 °C. Symptoms from the lower airways were few and mild.  Short-duration moderate-intensity exercise in -10 °C induces mild symptoms from the lower airways, no lung function decrements or enhanced leakage of biomarkers of airway epithelial injury, and no peripheral bronchodilatation, compared to exercise in +10 °C. 

Purpose Exposure to cold air may harm the airways. It is unclear to what extent heavy exercise adds to the cold-induced effects on peripheral airways, airway epithelium, and systemic immunity among healthy individuals. We investigated acute effects of heavy exercise in sub-zero temperatures on the healthy airways. Methods Twenty-nine healthy individuals underwent whole body exposures to cold air in an environmental chamber at - 15 degrees C for 50 min on two occasions; a 35-min exercise protocol consisting of a 5-min warm-up followed by 2 x 15 min of running at 85% of VO(2)max vs. 50 min at rest. Lung function was measured by impulse oscillometry (IOS) and spirometry before and immediately after exposures. CC16 in plasma and urine, and cytokines in plasma were measured before and 60 min after exposures. Symptoms were surveyed pre-, during and post-trials. Results FEV1 decreased after rest (- 0.10 +/- 0.03 L, p < 0.001) and after exercise (- 0.06 +/- 0.02 L, p = 0.012), with no difference between trials. Exercise in - 15 degrees C induced greater increases in lung reactance (X5; p = 0.023), plasma CC16 (p < 0.001) as well as plasma IL-8 (p < 0.001), compared to rest. Exercise induced more intense symptoms from the lower airways, whereas rest gave rise to more general symptoms. Conclusion Heavy exercise during cold air exposure at - 15 degrees C induced signs of an airway constriction to a similar extent as rest in the same environment. However, biochemical signs of airway epithelial stress, cytokine responses, and symptoms from the lower airways were more pronounced after the exercise trial.

Humans react to cold with various symptoms. Previous studies enquiring about symptoms during cold exposure have for the most part been population based studies using questionnaries and have focused on a narrow spectrum of symptoms. The purpose of this study was to study the effect of cold air and physical exercise on a wide range of symptoms in healthy individuals.

A total of 31 healthy subjects were experimentally exposed to +10 °C and -10 °C in an environmental chamber for one hour, on two separate occasions. During each exposure, subjects performed an intermittent moderate-intensity running protocol between 62-78% of maximal oxygen consumption (VO2 max). At five timepoints, before, during and after the exposures, subjects were asked about 18 symptoms and their intensity. The Borg CR10 scale was used to rate the intensity from 0 to 11, where 0 meant "none" and 11 meant "maximal". The sum of all five Borg CR10-scores were added together to form a single score for each exposure. Paired Wilcoxon signed-rank test was used for analysis. Data are presented as medians.

Symptoms of cough, eye irritation, physical discomfort, and cold extremities were present only at -10 °C. Compared to exercise in +10 °C, exercise in -10 °C induced significantly higher summed symptom scores for eye irritation 2.0 vs 0.5 (p=0.011), rhinitis 12.0 vs 8.0 (p=0.000), nasal irritation 3.5 vs 0.5 (p=0.001), cold face 7.0 vs 1.0 (p=0.000), physical discomfort 6.5 vs 0.0 (p=0.000), and cold extremities 10.0 vs 0.5 (p=0.000).

In healthy subjects, moderate-intensity exercise in -10 °C can induce and enhance the intensity of a wide range of symptoms. Symptoms of the lower airways were infrequent and mild.

Bakgrund: Exponering för kyla leder till ökad sjuklighet och dödlighet i befolkningen. Tidigare studier av symptom i samband med köldexponering har mestadels varit befolkningsbaserade enkätstudier fokuserade på ett smalt symptomspektrum. Syftet meddenna studie var att undersöka effekten av kyla och fysisk aktivitet på ett brett spektrumav symptom hos friska individer.Material och metod: Trettioen friska försökspersoner exponerades i en köldkammare för +10 °C och -10 °C under en timme, vid två separata tillfällen. Under varje exponeringsprang försökspersonerna intermittent på 62-78% av maximal syreupptagningsförmåga. Vid fem tillfällen, före, under och efter exponeringarna, frågades försökspersonerna om 18 symptom och dessas intensitet. Borgs CR10 skala användes för att skatta intensitetenfrån 0 till 11, där 0 betydde ”inget alls” och 11 betydde ”maximalt”. Maximalt Borg-värdeför varje symptom under exponeringarna jämfördes med värdena innan exponeringarna. Summan av alla fem Borg CR10-värdena jämfördes mellan de två exponeringarna. PairedWilcoxon signed-rank test användes för analyser. Data presenteras som medianvärden.Resultat: En signifikant stegring av symptomen hosta, ögonirritation, fysiskt obehag ochkalla extremiteter förekom endast vid -10 °C. I jämförelse med fysisk aktivitet i +10 °C, gav fysisk aktivitet i -10 °C upphov till signifikant högre summerade värden för ögonirritation 2,0 jfr 0,5 (p=0,011), rinit 12,0 jfr 8,0 (p=0,000), irritation i näsan 3,5 jfr 0,5 (p=0,001), kyla i ansiktet 7,0 jfr 1,0 (p=0,000), fysiskt obehag 6,5 jfr 0,0 (p=0,000), och kalla extremiteter 10,0 jfr 0,5 (p=0,000).Slutsats: Hos friska individer kan fysisk aktivitet på måttlig intensitet i -10 °C ge upphovtill och öka intensiteten av ett brett spektrum av symptom. Symptom från de nedre luftvägarna var milda och inte frekventa vid de aktuella exponeringarna.

INTRODUCTION: During or shortly after strenuous exercise, some individuals may exhibit exercise-induced bronchoconstriction (EIB) (1). Training in sub-zero temperatures, where the inspired air is cold and dry, can exacerbate the physiological stimuli that give rise to EIB and accentuate lung injury (2). To date, little is known about the training factors, such as duration and modality of exercise that result in airway damage in cold environments. Here, we aimed to examine the influence of exercise duration in cold on lung function and EIB incidence among healthy individuals.

METHODS: Eighteen healthy, non-asthmatic, physically active volunteers (males/females: 14/4, age: 29.4 ± 5.9 years old, maximal oxygen consumption [V̇O2max]: 61.3 ± 8.7 ml/kg/min) who had never competed at the elite level, completed two moderate-intensity (60% V̇O2max) climate chamber running trials at -15 ºC lasting for 30 and 90 min in a randomized cross-over design. Impulse oscillometry (IOS) was conducted before, 12, and 50 min post-trials to assess resistance at 5 and 20 Hz as well as reactance at 5Hz. Forced expiratory volume in 1s (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio were measured via dynamic spirometry before, 15, and 55 min after the trials. Two-way repeated measures ANOVAs were performed to determine the impact of trial and time on the percentage change of IOS and spirometry variables.

RESULTS: There were no significant effects of trial (30 min vs 90 min trial), time (pre-trial vs post-trial time points), or interaction effects for any spirometry or IOS variable. None of the participants exhibited EIB, defined as a ≥10% reduction in FEV1, at any time point (15 min after exercise: +0.37 ±1.95% for the 30 min trial and -0.25 ± 3.47% for the 90 min trial; 55 min after exercise: +0.85 ± 2.32% for the 30 min trial and +0.15 ± 3.97% for the 90 min trial).

CONCLUSION: The acute lung function responses to exercise did not differ between the 30- and 90-min trials. Additionally, moderate-intensity exercise at -15 ºC did not lead to lung function decrements or onset of EIB in healthy individuals who train regularly outdoors.

References1. Anderson, S., & Kippelen, P. (2010). Stimulus and mechanisms of exercise-induced bronchoconstriction. Breathe, 7(1), 25-33.2. Stensrud, T., Berntsen, S., & Carlsen, K. (2007). Exercise capacity and exercise-induced bronchoconstriction (EIB) in a cold environment. Respiratory Medicine, 101(7), 1529-1536.

Background: Strenuous exercise in sub-zero environments may cause airway injury and exerciseinduced bronchoconstriction (EIB) (1). Atopic disposition is a risk factor for EIB development (2). However, it is currently unknown whether atopic disposition influences the acute respiratory responses to exercise in a sub-zero climate. Aim: To examine whether the respiratory responses to short- and long-duration exercise at -15⁰C differ between atopic and non-atopic subjects. Methods: Eighteen non-asthmatic, endurance-trained volunteers (males/females: 14/4, age: 29.4 ± 5.9 years old, maximal oxygen consumption (V̇O2max): 61.3 ± 8.7 ml/kg/min) were screened for atopy via the Allergy Questionnaire for Athletes (3) and completed two moderate-intensity (60% V̇O2max) environmental chamber running trials at -15⁰C lasting for 30 and 90 min in a randomized cross-over design. The study was conducted in accordance with the Declaration of Helsinki and was approved by the Swedish Ethical Review Authority. Dynamic spirometry (4) was performed at baseline and 15 and 55 min post-exercise to measure forced expiratory volume in 1 sec (FEV1). Venous blood samples collected pre-exercise and 10 and 65 min post-exercise were analysed for serum Clara cell secretory protein (CC16) using an enzyme-linked immunosorbent assay. A respiratory questionnaire (5) was administered before, immediately after and 20 min after exercise to examine the proportion of affirmative responses (‘YES’) to the occurrence of four symptoms (cough, wheezing, chest tightness and hypersecretion of mucus) associated with lower airways. To examine 2- and 3-way interaction effects on the relative change in FEV1 from baseline as well as the CC16 concentration, a 3-factor repeated measures ANOVA and a linear mixed-effects model were employed, respectively. A twoproportion z-test was performed to compare the symptom frequency between the two groups. Analyses entailing multiple comparisons were adjusted with the Benjamini-Hochberg method. Results: Atopy was identified in 10 subjects (56%, 7/3: men/women). There were no significant interaction effects for FEV1 or CC16 concentration (group x trial, FEV1: p = 0.35, CC16: p = 0.50; group x time, FEV1: p = 0.10, CC16: 0.10; group x trial x time, FEV1: p = 0.39, CC16: p = 0.51). Nevertheless, immediately after the 90-min trial, the onset of airway symptoms was significantly more frequent in atopic volunteers than their non-atopic peers (22.5% vs 0%, p < 0.01) with no intergroup differences observed 20 min post-trial. Atopic status did not affect the occurrence of the lower airway symptoms immediately after (10% in atopic vs 0% in non-atopic, p = 0.08) or 20 min after (5% in atopic vs 0% in non-atopic, p = 0.19) the 30-min trial. Conclusion: Atopy is not a major risk for bronchoconstriction when moderate-intensity exercise of either short or long duration is performed in a sub-zero climate by non-asthmatic subjects. Although the extent of bronchial epithelial damage did not differ between the two groups, atopic disposition may transiently elicit more lower airway symptoms after prolonged exercise. Reference 1 :- Hanstock, H.G.; Ainegren, M.; Stenfors, N. "Exercise in Sub-zero Temperatures and Airway Health: Implications for Athletes With Special Focus on Heat-and-Moisture-Exchanging Breathing Devices." Frontiers in Sports and Active Living. 2020, 2: 34. Reference 2 :- Bauza, D.; Silveyra, P. ‘’Asthma, atopy, and exercise: Sex differences in exerciseinduced bronchoconstriction.’’ Experimental Biology and Medicine. 2021, 246, 1400-1409 Reference 3 :- Bonini, M.; Braido, F.; Rasi, G.; Bonini, S.; Baiardini, I.; Del Giacco, S.; Gramiccioni, C.; Manara, M.; Tagliapietra, G.; Scardigno, A.; Sargentini, V.; Brozzi, M. "AQUA : Allergy Questionnaire 67 for Athletes. Development and Validation." Medicine and Science in Sports and Exercise. 2009, 41, 1034-1041 Reference 4 :- Graham, B. L., Steenbruggen, I., Miller, M. R., Barjaktarevic, I. Z., Cooper, B. G., Hall, G. L., Hallstrand, T. S., Kaminsky, D. A., McCarthy, K., McCormack, M. C., Oropez, C. E., Rosenfeld, M., Stanojevic, S., & Swanney, M. P. Standardization of Spirometry 2019 Update. An Official American Thoracic Society and European Respiratory Society Technical Statement. Am J Respir Crit Care Med. 2019; 200: E70–88 Reference 5 :- Kennedy, M.D.; Faulhaber, M. "Respiratory Function and Symptoms Post Cold Air Exercise in Female High and Low Ventilation Sport Athletes." Allergy, Asthma & Immunology Research. 2018, 10, 43-51. PC21 Influence of aerobic training on exercise capacity and mitoch

Background Strenuous endurance exercise in sub-zero temperatures can cause airway damage that may lead to EIB. Prolonged exercise can also elicit greater immune perturbations than short-duration exercise. However, the influence of exercise duration on lung function and systemic immunity in sub-zero temperatures has not been established. Additionally, it is currently unknown whether atopic disposition, which is risk factor for EIB, influences respiratory responses in a sub-zero climate. The aim of this study was to compare respiratory and systemic immune responses to two cold air running trials of short and long duration, as well as to examine whether the responses differed between atopic and non-atopic subjects. Methods Eighteen healthy, endurance-trained subjects (males/females: 14/4; age: 29.4 +/- 5.9 years old; BMI: 23.1 +/- 1.7; atopic/non-atopic: 10/8) completed two moderate-intensity climate chamber running trials at - 15 degrees C, lasting 30 and 90 min, in a randomized, cross-over design. Lung function (spirometry and impulse oscillometry), serum CC16, respiratory symptoms, and blood leukocyte counts were examined before and after the trials. Results Lung function was not significantly affected by exercise or exercise duration. CC16 concentration increased after both trials (p = 0.027), but the response did not differ between trials. Respiratory symptom intensity was similar after each trial. There was a greater increase in neutrophils (p < 0.001), and a decrease in eosinophils (p < 0.001) after the 90-min bout. The 90-min protocol increased X5 compared to the 30-min protocol only in atopic subjects (p = 0.015) while atopy increased lower airway symptoms immediately after the 90-min session (p = 0.004). Conclusions Our results suggest that a 90-min bout of moderate-intensity exercise at - 15 degrees C does not cause substantial lung function decrements, airway epithelial damage or respiratory symptoms compared to 30 min running in the same environment, despite a heightened redistribution of white blood cells. However, exercise at - 15 degrees C may cause airway injury and evoke respiratory symptoms, even at moderate intensity. Atopic status may lead to greater peripheral bronchodilation and higher frequency of respiratory symptoms after long-duration exercise in cold. Trial registration: 01/02/2022 ISRCTN13977758. This trial was retrospectively registered upon submission to satisfy journal guidelines. The authors had not initially registered the study, as the intervention was considered to be a controlled simulation of exercise in a naturally occurring environment (i.e. sub-zero air) for healthy volunteers.

The prevalence of asthma is high in winter endurance athletes with onset typically occurring during adolescence; later than classical asthma. It is well accepted that cold and dry air is involved in the pathogenesis, but nevertheless there remain gaps in current understanding of how cold air influences the immunological profile of the airways. This in part limits our ability to make recommendations about which environmental conditions are harmful to healthy athletes and at which temperatures training or racing should be modified or cancelled. Several studies have collectively demonstrated lymphocytic and neutrophilic inflammation in winter athletes with and without bronchial hyperresponsiveness (BHR), as well as a pro-inflammatory cytokine profile and damage-associated molecular patterns. Lymphocyte infiltration to bronchial tissues may increase during the winter competition season. Eosinophilic inflammation may distinguish between winter athletes with and without BHR. Single bouts of exercise in sub-zero temperatures increase biomarkers of airway damage such as serum Clara cell protein 16 to a greater extent than in warm, humid conditions. It remains to be investigated whether prolonged, steady-state or short, high-intensity exercise in sub-zero climates is more damaging to the airways. Moreover, the effect of protective devices such as heat-exchanger masks on airway immune responses warrants investigation.

Since early studies investigated the influence of exercise on salivary secretory IgA(SIgA) in the 1980s, there has been demand for non-invasive biomarkers capableof monitoring the immune response to exercise, training and stress, and provideinsight into whether such stressors may influence susceptibility to URTI. In spiteof >30 years of research and ~200 original articles investigating a multitude ofcandidate markers, this tool remains elusive. Transmission of URTIs has beendemonstrated via the nasal and ocular mucosae, so maintainence of a strong‘first line of defence’ at mucosal surfaces is likely important for host defence. Tearfluid has been recently highlighted as a non-invasive medium for assessment ofhydration status (through determination of tear osmolarity) and blood glucoseconcentrations (via glucose-sensing contact lenses). Prompted by the searchfor viable non-invasive immune biomarkers, this thesis set out to explore thepotential of tear SIgA to assess immune status. First, in a prospective monitoringstudy, we demonstrated that tear SIgA secretion falls ~50% during the weekbefore experiencing upper respiratory symptoms (URS), with a 30% reductionin tear SIgA secretion conferring a six-fold increased chance of experiencing URSin the following week. Next, we undertook three studies to explore the influenceof everyday stressors on tear SIgA secretion. Both a two-hour bout of moderateintensityexercise and two-minutes of acute psychological stress caused animmediate ~50% decrease in tear SIgA concentration. The observations fromthe first study suggest that these reductions are of sufficient magnitude totemporarily compromise host defence, in line with the ‘open window’ theory.Dehydration, on the other hand, did not influence tear SIgA secretion. Thesestudies provide the first experimental evidence that tear SIgA has potentialas a non-invasive marker of mucosal immune competence that is sensitive toeveryday stressors and has utility to assess common cold risk.

Asthma and exercise-induced bronchoconstriction (EIB) are common in high-level athletes and especially prevalent in cross-country ski athletes. In a recent online questionnaire distributed to high level Swedish cross-country skiers, 29% of adolescent athletes (age 15-19) and 35% of senior athletes self-reported physician-diagnosed asthma. Cross-country skiing has been identified as an independent risk factor for development of EIB and it has been hypothesized that a combination of the cold and dry climate, high ventilation rates, training frequency and duration may contribute to airway inflammation and trigger bronchoconstriction during or shortly after exercise. Alongside pharmacological management, there may be strategies that athletes and coaches can utilise to manage asthma or EIB. Several studies suggest that warm up routines containing short bouts of high-intensity exercise may offer protection against subsequent EIB, termed a ‘refractory period’. In cross-country skiers, refractoriness was observed in around a third of athletes in a small cohort. Other athletes may display a gradual, progressive EIB; whether these athletes also respond to high-intensity warm-up warrants further investigation. Heat-exchanger masks have been shown to reduce the severity of EIB substantially in athletes with mild to severe EIB in cold conditions (-15°C to -25°C). It is recommended that athletes with asthma/EIB explore the efficacy of high-intensity warm-up regimes on airway responses and utilise heat exchanger masks, especially on the coldest days.

Asthma is highly prevalent among winter endurance athletes. This “occupational disease” of cross-country skiers, among others, was acknowledged during the 1990s, with the pathogenesis attributed to repeated and prolonged exposure to cold, dry air combined with high rates of ventilation during exercise. Nevertheless, more than 25 years later, the prevalence of asthma among Scandinavian cross-country skiers is unchanged, and prevention remains a primary concern for sports physicians. Heat-and-moisture-exchanging breathing devices (HMEs) prevent exercise-induced bronchoconstriction in subjects with pre-existing disease and may have potential as a preventative intervention for healthy athletes undertaking training and competition in winter endurance sports. Herein we firstly provide an overview of the influence of temperature and humidity on airway health and the implications for athletes training and competing in sub-zero temperatures. We thereafter describe the properties and effects of HMEs, identify gaps in current understanding, and suggest avenues for future research.

Transmission of upper respiratory tract infections (URTI) has been demonstrated at the ocular surface (Bischoff et al., 2011). Thus, the immunological profile of the tear fluid likely plays an important role in host defence against URTI, and moreover provides a non-invasive medium for assessment of immune status. We recently demonstrated that tear secretory IgA (SIgA) has potential as a biomarker of URTI risk (Hanstock et al., 2016). It is likely that several other antimicrobial proteins abundant in tears such as lactoferrin (Lf) and lysozyme (Lys) contribute to host defence at the ocular surface (McDermott, 2013).

 PURPOSE: To explore the potential of tear Lf and Lys to evaluate risk of subsequent URTI independently and in combination with tear SIgA data from the same subjects presented in Hanstock et al., (2016).

 METHODS: Forty healthy, physically active subjects were recruited during the common-cold season. Subjects reported upper respiratory symptoms (URS) daily and provided weekly tear samples for 4 weeks. If URS were reported for ≥ 48h, subjects provided a nasopharyngeal swab for identification of common-cold pathogens using RT-PCR and a tear sample. Following an episode of URS, subjects reported daily URS until they had been symptom-free for 4 weeks at which time a ‘Recovery’ tear sample was collected. Tear Lf and Lys concentration was determined using ELISA.

 RESULTS: Eleven students reported episodes of URS; nine returned positive virology tests for human rhinovirus (URTI). Twenty-two students remained symptom-free during the monitoring period (Healthy) and seven were excluded due to non-compliance. Tear Lys concentration (Lys-C) and secretion rate (Lys-SR) were lower in URTI vs. Healthy (p<0.01 and p<0.05 respectively) but there was no difference in Lf-C and Lf-SR. The potential of Lf and Lys to assess URS risk was determined by comparing Lf and Lys the week before URS with Recovery samples. Tear Lf-C, Lf-SR and Lys-C were not altered before URS, whereas Lys-SR tended to be reduced in the week before URS (p<0.1). A binary logistic regression incorporating tear flow rate, Lys-C, Lf-C and SIgA-C as predictors was able to correctly identify subjects at risk of URS in the next week with 70% accuracy (95% CI: 54 – 85%) but only 27% sensitivity.

 CONCLUSION: Although tear Lys was decreased during URTI, the new model including tear Lys and Lf was not able to improve upon the utility of tear SIgA alone to assess URS risk in this small cohort. Larger datasets will be required to evaluate and optimise model performance for models based on tear SIgA, possibly in combination with other biomarkers, to predict URTI.

Tear secretory immunoglobulin-A (SIgA) is a putative biomarker of common-cold risk with potential utility in non-invasive diagnostics. As SIgA secretion at the ocular surface is under strong autonomic control, we investigated the relationship between HR reactivity and tear SIgA responses to novel experiential stress. Thirty-two healthy participants undertook a 60-second zip-line ride to evoke acute stress and a seated-rest control trial in a randomised-crossover design. We recorded heart rate (HR) continuously and collected unstimulated tear samples 5-min-pre-, 2-min-post- and 20-min-post-stress/control. Stress increased HR and state anxiety whereas tear SIgA concentration decreased 44% post-stress vs. control. Higher peak HR values during stress uniquely explained 21% of the variance in tear SIgA reactivity to stress (p < .01); high HR reactors displayed greater decreases in tear SIgA concentration. We conclude that physiological arousal increases immune reactivity to acute stress and highlight tear SIgA as a minimally-invasive, physiologically relevant biomarker of immune reactivity.

Tears have attracted interest as a minimally-invasive biological fluid from which to assess biomarkers. Lactoferrin (Lf) and lysozyme (Lys) are abundant in the tear fluid and have antimicrobial properties. Since the eye is a portal for infection transmission, assessment of immune status at the ocular surface may be clinically relevant. Therefore, the aim of this series of studies was to investigate the tear fluid antimicrobial proteins (AMPs) Lf and Lys as biomarkers of mucosal immune status. To be considered biomarkers of interest, we would expect tear AMPs to respond to stressors known to perturb immunity but be robust to confounding variables, and to be lower in participants with heightened risk or incidence of illness. We investigated the relationship between tear AMPs and upper respiratory tract infection (URTI; study 1) as well as the response of tear AMPs to prolonged treadmill exercise (study 2) and dehydration (study 3). Study 1 was a prospective cohort study conducted during the common cold season whereas studies 2 and 3 used repeated-measures crossover designs. In study 1, tear Lys concentration (C) as well as tear AMP secretion rates (SRs) were lower in individuals who reported pathogen-confirmed URTI (n = 9) throughout the observation period than in healthy, pathogen-free controls (n = 17; Lys-C, P = 0.002, d = 0.85; Lys-SR, P < 0.001, d = 1.00; Lf-SR, P = 0.018, d = 0.66). Tear AMP secretion rates were also lower in contact lens wearers. In study 2, tear AMP SRs were 42–49% lower at 30 min−1 h post-exercise vs. pre-exercise (P < 0.001, d = 0.80–0.93). Finally, in study 3, tear AMPs were not influenced by dehydration, although tear AMP concentrations (but not secretion rates) displayed diurnal variation. We conclude that Lf and Lys have potential as biomarkers of mucosal immune competence; in particular, whether these markers are lower in infection-prone individuals warrants further investigation.

Training in cold climates is an established risk factor for development of exercise-induced bronchoconstriction and asthma. Inhalation of large volumes of cold and dry air challenges the airways’ capacity to condition inspired air, leading to acute airway injury, and over time, bronchial hyperresponsiveness. We lack evidence-informed guidelines regarding ‘safe’ thresholds for exercise in cold climates, i.e., temperatures (as well as exercise intensities/durations) that do not substantially increase the risk for healthy individuals to develop asthma. This study aimed to investigate the effect of temperature on systemic asthma- and exercise-associated cytokine responses to moderate-intensity exercise among healthy individuals. 31 healthy participants provided written, informed consent to participate in this randomised, crossover trial. On separate days, participants completed a 5 min warm up followed by 30 min running exercise (62-78% VO2peak) in a climate chamber at 10 or -10°C. Blood samples were taken pre and 1 h post-exercise and analysed for 10 cytokines (GM-CSF, IL-10, IL-13, IL-17E, IL-1β, IL-4, IL-5, IL-6, IL-8 and TNF-α) using multiplex ELISA. Values below the lower limit of detection for the assay were excluded. Data from 21 participants were analysed using two-way repeated measures ANOVA. IL-6 and IL-8 increased post-exercise (IL-6: log2 fold change: 0.47±0.67, p=0.001; IL-8: log2 fold change: 0.16±0.27, p=0.001). There were no differences in the response magnitude of any cytokine to exercise in -10 versus 10°C. We conclude that exposure to -10°C does not exacerbate inflammatory responses to moderate-intensity exercise, including for cytokines associated with exercise-induced asthma.FootnotesCite this article as ERJ Open Research 2022; 8: Suppl. 8, 214.This article was presented at the 2022 ERS Lung Science Conference, in session “Poster Session 2”.This is an ERS Lung Science Conference abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).

Every year, the European Respiratory Society (ERS) organises the Lung Science Conference (LSC), in Estoril, to discuss basic and translational science. The topic of the 20th LSC was “Mucosal immunology of the lung: balancing protective immunity and chronic inflammation”. This was the first time that the LSC was organised as a hybrid congress with both in person and online attendance. In addition to an outstanding scientific programme, the LSC provides excellent opportunities for career development and inclusion of early career members (ECMs). All scientific and poster sessions are chaired by an ECM who is paired with a senior faculty to allow ECMs to become acquainted with session chairing, and there is a session organised by the Early Career Member Committee (ECMC) dedicated to career development. Moreover, travel bursaries are made available to abstract authors, and all bursary recipients and first-time attendees are invited to take part in a mentorship lunch. In this article, we provide the names of the ECM awardees and describe the scientific highlights of the LSC 2022 for those who could not attend.

High-intensity interval training (HIT) encompasses a wide range of training prescriptions where up to nine variables can be manipulated (Buchheit and Laursen, 2013, Sports Medicine, 43(5), 313–338). Four weeks of HIT with longer intervals and accumulated work durations (AWD) has been shown to elicit greater improvements in peak oxygen consumption (V O 2peak ) despite more modest physiological, hormonal and perceptual responses (Sylta et al., 2017, Medicine & Science in Sports & Exercise, 49(6), 1137–1146). However, immunological responses to different HIT pre- scriptions have rarely been investigated. The purpose of this study was to compare the cumulative effects of a four-week HIT intervention, performed either as short or long intervals with the same AWD, on V O 2peak , the immunological biomarker salivary secretory IgA (s-IgA) and upper respiratory illness (URI) incidence. In addition, we explored the influence of HIT on serum cortisol, testosterone, 25(OH)D and ferritin as biomarkers related to immune competence. Following local ethics committee approval, twenty-five well-trained male cyclists and triath- letes provided written consent to take part and were randomised to one of three HIT groups (Long Intervals [LI]: 4 × 8min; Short Intervals 1 [SI1]: 4×[12 × 40/20s]; Short Intervals 2 [SI2]: 4×[8 ×40/20s]). Participants per- formed three cycling HIT sessions per week for four weeks at maximal session effort (“isoeffort”) intensity, supplemented with ad libitumlow-intensity training. Participants recorded upper respiratory symptoms (URS) daily using the Jackson Common Cold Scale; episodes of URI were identified retrospectively. V O 2peak as well as rested saliva and blood biomarkers were analysed before and after the training period. Fourteen of twenty-five participants reported an episode of URI (LI: 4/8, SI1: 4/8, SI2: 6/9) but there were no differences in URI incidence, severity or duration between groups. Following the train- ing intervention, we observed a moderate increase in V O 2peak across the cohort (mean± SD: 4.75 ± 0.42 to 4.86 ± 0.43 L· min−1 ,Cohen’s d= 0.65, 90% confidence intervals: [0.16, 1.13]) but the change in V O 2peak was not different between groups. Serum cortisol displayed a moderate increase (367 ± 98 to 415 ± 108 nmol· L −1 ,d=0.60 [0.12, 1.08]) and 25(OH)D a large decrease (79.2 ± 17.1 to 70.4 ± 17.6 nmol· L −1 ,d= -0.87 [−1.36,−0.37]) from pre- to post-training, but there were no differences in the magnitude of the responses between groups. Four weeks’HIT did not influence s-IgA secretion rate, serum testosterone or ferritin. We conclude that four weeks’ AWD-matched HIT performed as short- or long-intervals at isoeffort intensity does not differentially influence ill- ness incidence, immunological responses to training nor other immune-related biomarkers. This observation can be viewed as a positive finding for training planning, since it could allow coaches some flexibility in constructing AWD-matched isoeffort HIT sessions to achieve performance goals, without concern about detrimental effects on athletes’ immune status.

Intensive training periods may negatively influence immune function, but the immunological consequences of specific high-intensity training (HIT) prescriptions are not well defined. Purpose: This study explored whether three different HIT prescriptions influence multiple health-related biomarkers and whether biomarker responses to HIT were associated with upper respiratory illness (URI) risk. Methods: Twenty-five male cyclists and triathleteswere randomised to three HIT groups and completed twelve HIT sessions over four weeks. Peak oxygen consumption (V̇O2peak) was determined using an incremental cycling protocol, while resting serum biomarkers (cortisol, testosterone, 25(OH)D and ferritin), salivary immunoglobulin-A (s-IgA) and energy availability (EA) were assessed before and after the training intervention. Participants self-reported upper respiratory symptoms during the interventionand episodes of URI were identified retrospectively. Results: Fourteen athletes reported URIs, but there were no differences in incidence, duration or severity between groups. Increased risk of URI was associated with higher s-IgA secretion rates (odds ratio=0.90, 90% CI:0.83-0.97). Lower pre-intervention cortisol and higher EA predicted a 4% increase in URI duration. Participants with higher V̇O2peak reported higher total symptom scores (incidence rate ratio=1.07, 90% CI:1.01-1.13). Conclusions: Although multiple biomarkers wereweakly associated with risk of URI, the direction of associations between s-IgA, cortisol, EA and URI risk were inverse to previous observations and physiological rationale. There was a cluster of URIs within the first week of the training intervention, but no samples were collected at this time-point. Future studies should incorporate more frequent sample time-points, especially around the onset of new training regimes, and include athletes with suspected or known nutritional deficiencies.

Intensified training periods may increase incidence of upper respiratory illness (URI) in athletes (Meeusen et al., 2013,Medicine and Science in Sports and Exercise, 45(1), 186–205). Many physiological and nutritional risk factors have beenassociated with increased risk of URI (Bermon et al., 2017, Exercise Immunology Review, 23, 8–50), including reductionsin salivary IgA (sIgA), elevated cortisol, vitamin D insufficiency, iron deficiency and low energy availability (EA). However, few studies have explored the relative importance of each of thesehealth-related biomarkers in a multivariate model. Our aimwas therefore to investigate the relationship between multiplebiological risk factors for illness and incidence, duration andseverity of URIs that present during intensified training. 3815Twenty-five well-trained male cyclists and triathletes (age 30 ± 9 y, VO2peak 64 ± mL· kg−1· min−1) performed one ofthree different high-intensity interval training (HIT) programmes for three sessions per week over four weeks in November-December. The study received local ethical approval and participants provided written, informed consentto participate. Participants performed each HIT session at “isoeffort” intensity and sessions were matched for total accumulated work duration. Participants logged upper respiratorysymptoms (URS) daily using the Jackson Common Cold Scale; episodes of URI were identified retrospectively using the followinga priori criteria: weekly symptom score > 14 or selfreportedcommon cold for > 2 consecutive days (Jacksonet al., 1958, American Medical Association Archives of Internal Medicine, 101, 267–278). Before commencing the training period, VO2peak was determined using an incremental maximal cycling protocol and participants provided rested, fasted blood and saliva samples prior to the training period foranalysis of plasma 25(OH)D, ferritin, cortisol, testosterone and sIgA secretion rate. EA was calculated based on a 3-day registration of energy intake and expenditure relative to fat-free mass measured in a rested, fasted state using indirect calorimetry (Torstveit et al., 2018 February, International Journal of Sport Nutrition and Exercise Metabolism, 1–28). We used a zero-inflated negative binomial model to investigate the relationship between baseline VO2peak, health-related biomarkers and URI incidence/duration/global URS severity. Fourteen athletes(56%) reported an episode of URI during the four-week monitoring period. Higher sIgA was associated with reduced risk of URI (odds ratio = 0.90, 90% confidence interval (CI): [0.83,0.97]). Lower plasma cortisol (P = 0.02) and higher EA (P = 0.02) were associated with longer URI duration; holding cortisol constant, the incidence risk ratio (IRR) for a one-unit increase in EA was 1.04 (90% CI: [1.01, 1.07]). Participants with higher VO2peak reported higher total symptom scores during the intervention period (P = 0.03, IRR = 1.07, 90% CI: [1.01,1.13]). Several health-related biomarkers and physiological parameters may therefore be associated with risk and severityof URI, including sIgA, cortisol, EA and VO2peak.

INTRODUCTION: Winter endurance athletes such as cross-country skiers have an increased prevalence of asthma (Eriksson et al., 2018, Scand J Med Sci Sport). Heat-and-moisture exchangers (HMEs) such as masks and mouthpieces with a filter to facilitate warming and humidification of inspired air may protect the airways from injury during exercise in cold, dry climates. However, if there is evidence of impaired exercise capacity, athletes will likely avoid using such devices. The aim of this study was to investigate the influence of an HME mask (AirTrim Sport, Vapro AB, Västerås, Sweden) on heart rate (HR), breathing rate (BR), muscle oxygenation (SmO2) and perceived exertion at fixed submaximal workloads. METHODS: 23 active, healthy participants without asthma aged 31 ± 8 years (15 men, 8 women) performed a familiarisation test followed by two experimental trials with and without HME in a randomised, crossover design. All tests were performed at a 4% gradient on a motorised treadmill and consisted of a submaximal incremental warm-up followed by a maximal, self-paced 4-min running time trial (TT). During the familiarisation test, participants wore a portable oxygen uptake system (Metamax 3B, Cortex Biophysik, Leipzig, Germany) with the TT used to derive VO2peak. Submaximal VO2 was interpolated to derive speeds estimated to elicit 65, 70, 75 and 90% of VO2peak. In two subsequent trials performed in a climate chamber at -15 degrees Celsius, participants ran for 5 min at speeds equivalent to 65, 70 and 75% VO2peak, 3 min at 90% and 12 min at 65% VO2peak. HR and BR were monitored via a chest harness (LifeMonitor, Equivital, Cambridge, UK); mean SmO2 from the right and left quadriceps was derived using near infra-red sensors (MOXY, Fortiori Design, Hutchinson MN, USA). Data were summarised as 1 min epochs, taken from 90 to 30 s before the end of each stage. Borg 6-20 rating of perceived exertion (RPE) was reported 1 min before the end of each stage. Data were analysed using repeated-measures ANOVA and linear mixed models. The study was approved by the regional ethical review board and conducted according to the Declaration of Helsinki. RESULTS: HR was 2.5 beats/min higher during the HME trial (95% CI: 0.3 - 4.6, p=.03). In the male participants only, SmO2 was lower during the HME trial than control (-2.3%, 95% CI: -0.1 - -4.5, p=.04). The female participants reported higher RPE (0.65 AU) during the HME trial (p=.009). There was no difference in BR between the HME and control trials. CONCLUSION: Despite potentially small increases in dead space and resistance to breathing, an HME did not affect BR during submaximal exercise in -15 degrees C. However, higher HR during exercise with an HME, as well as lower SmO2 in the male participants and higher RPE in the female participants, indicates slightly higher physiological stress during steady-state exercise with an HME. It would therefore be relevant to investigate whether an HME affects maximal exercise capacity in sub-zero temperatures.

Background Heavy endurance training in sub-zero environments increases risk of exercise-induced asthma. Heat-and-moisture exchangers (HME) can prevent exercise-induced bronchoconstriction but it is not known whether they protect against inflammatory responses to exercise in healthy individuals.

Objective To investigate whether use of an HME during exercise in a sub-zero environment affects post-exercise inflammatory responses.

Design Investigator-blind randomised crossover trial.

Setting Environmental chamber at -15°C.

Participants 23 healthy, trained participants aged 18–53 (15 male, 8 female, VO2peak 57±6 and 50±4 mL/kg/min; mean±SD).

Interventions Two experimental trials with and without HME, consisting of 30-min moderate-intensity running followed by a 4-min maximal running time-trial. Plasma samples were obtained pre- and 1h-post-exercise and analysed for a panel of 10 cytokines using a multiplex immunoassay.

Main Outcome Measurements Plasma cytokine concentrations (GM-CSF, IL-1β, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, IL-17E/25, TNF-α). Data were log-transformed then analysed using two-way repeated-measures ANOVA; one participant was an extreme outlier and excluded.

Results Five cytokines (GM-CSF, IL-1β, IL-4, IL-13, IL-17E/25) returned <20% concentrations within detection limits and were excluded from further analysis. The other cytokines returned >85% samples in range. IL-6, IL-8 and IL-10 increased after exercise (IL-6: F=36, p≤0.0001; IL-8: F=39, p≤0.0001; IL-10: F(1,21)=8.9, p=0.0072). There was a trend towards a greater post-exercise increase in IL-10 with HME (HME: median 0.062 (range -0.203–1.053) pg/mL; no-HME: 0.047 (-0.079–0.50) pg/mL; F=3.0, p=0.096). There were no significant interactions for other cytokines.

Conclusions Use of an HME during exercise in a sub-zero environment did not affect systemic pro- and anti-inflammatory cytokine responses to exercise. Local inflammatory markers in the lungs may be relevant to investigate in future studies.

Purpose: Research has not convincingly demonstrated the utility of saliva secretory Immunoglobulin-A (SIgA) as a biomarker of upper-respiratory-tract-infection (URTI) risk and disagreement exists about the influence of heavy exercise ('open-window-theory') and dehydration on saliva SIgA. Prompted by the search for viable alternatives, we compared the utility of tear and saliva SIgA to predict URTI prospectively (study-one) and assessed the influence of exercise (study-two) and dehydration (study-three) using a repeated-measures-crossover design.Methods: In study-one, forty subjects were recruited during the common-cold season. Subjects provided tear and saliva samples weekly and recorded upper-respiratory-symptoms (URS) daily for 3-weeks. RT-PCR confirmed common-cold pathogens in 9 of 11 subjects reporting URS (82%). Predictive utility of tear and saliva SIgA was explored by comparing healthy samples with those collected the week pre-URS. In study-two, thirteen subjects performed a 2-hour run at 65% VO2peak. In study-three, thirteen subjects performed exercise-heat-stress to 3% body-mass-loss followed by overnight fluid restriction.Results: Tear SIgA concentration and secretion rate were 48% and 51% lower respectively during URTI and 34% and 46% lower the week pre-URS (P<0.05) but saliva SIgA remained unchanged. URS risk the following week increased 9-fold (95% CI: 1.7 to 48) when tear SIgA secretion rate <5.5 μg[BULLET OPERATOR]min and 6-fold (95% CI: 1.2 to 29) when tear SIgA secretion rate decreased >30%. Tear SIgA secretion rate >5.5 μg[BULLET OPERATOR]min or no decrease >30% predicted subjects free of URS in >80% of cases. Tear SIgA concentration decreased post-exercise (-57%: P<0.05) in line with the 'open-window-theory' but was unaffected by dehydration. Saliva flow rate decreased and saliva SIgA concentration increased post-exercise and during dehydration (P<0.05).Conclusion: Tear SIgA has utility as a non-invasive biomarker of mucosal immunity and common-cold risk.

Background and Aims: Winter endurance athletes have a high prevalence of exercise-induced bronchoconstriction (EIB) and asthma, probably due to repeated and prolonged inhalation of cold and dry air. Heat- and moisture-exchanging devices (HME) warm and humidify inhaled air and prevent EIB. The aim of this study was to share cross-country skiers and biathletes' experiences of training and competition in low temperatures, views on temperature limits, usage of HME, and consequences of cold exposure on their health. Methods: Eleven Swedish World Championship or Olympic medalists in cross-country skiing and biathlon were interviewed and transcripts were analyzed using qualitative content analysis. Results: Participants described how cold temperatures predominantly affected the airways, face, and extremities. During training, extreme cold was managed by choosing warmer clothing, modification of planned sessions, use of HME, delaying training, or changing location. In competition, participants described limited possibility for such choices and would prefer adjustment of existing rules (i.e., more conservative temperature limits), especially since they understood elite skiing in low temperatures to present an occupational hazard to their health. Participants had at times used HMEs during training in cold environments but described mixed motives for their use—that HMEs warm and humidify cold inhaled air but introduce additional resistance to breathing and can cause problems due to mucus and ice build-up. Skiers also perceived that they had become more sensitive to cold during the latter part of their careers. Conclusions: The present study gives a unique insight into the “cold” reality of being an elite athlete in skiing and biathlon. Cold exposure results in negative health consequences that are preventable, which means that rules must be followed, and organizers should acknowledge responsibility in protecting athletes from occupational hazards. Development of evidence-based guidelines for protection of athletes' respiratory health should be a focus for future translational research. 

BACKGROUND: This study used metabolic phenotyping to explore the responses of highly-trained cross-country skiers to a standardized exercise test, which was part of the athletes' routine testing, and determine whether metabolic phenotyping could discriminate specific physiological, performance, and illness characteristics.

METHODS: Twenty-three highly-trained cross-country skiers (10 women and 13 men) participated in this study. Capillary whole-blood samples were collected before (at rest) and 2.5 min after (post-exercise) a roller-ski treadmill test consisting of 5-6 × 4-min submaximal stages followed by a self-paced time trial (~ 3 min) and analyzed using mass spectrometry. Performance level was defined by International Ski Federation distance and sprint rankings. Illness data were collected prospectively for 33 weeks using the Oslo Sports Trauma Research Center Questionnaire on Health Problems. Orthogonal partial least squares-discriminant analyses (OPLS-DA) followed by enrichment analyses were used to identify metabolic phenotypes of athlete groups with specific physiological, performance, and illness characteristics.

RESULTS: Blood metabolite phenotypes were significantly different after the standardized exercise test compared to rest for metabolites involved in energy, purine, and nucleotide metabolism (all OPLS-DA p < 0.001). Acute changes in the metabolic phenotype from rest to post-exercise could discriminate athletes with: (1) higher vs. lower peak blood lactate concentrations; (2) superior vs. inferior performance levels in sprint skiing, and (3) ≥ 2 vs. ≤ 1 self-reported illness episodes in the 33-week study period (all p < 0.05). The most important metabolites contributing to the distinction of groups according to (1) post-exercise blood lactate concentrations, (2) sprint performance, and (3) illness frequency were: (1) inosine, hypoxanthine, and deoxycholic acid, (2) sorbitol, adenosine monophosphate, and 2-hydroxyleuroylcarnitine, and (3) glucose-6-phosphate, squalene, and deoxycholic acid, respectively.

CONCLUSION: Metabolic phenotyping discriminated between athlete groups with higher vs. lower post-exercise blood lactate concentrations, superior vs. inferior sprint skiing performance, and more vs. less self-reported illnesses. While the biological relevance of the identified biomarkers requires validation in future research, metabolic phenotyping shows promise as a tool for routine monitoring of highly-trained endurance athletes.

Although high and simulated altitude training has become an increasingly popular training method, no study has investigated the influence of acute hypoxic exposure on balance in team-sport athletes. Therefore, the purpose of this study was to investigate whether acute exposure to normobaric hypoxia is detrimental to balance performance in highly-trained basketball players. Nine elite and nine sub-elite male basketball players participated in a randomized, single-blinded, cross-over study. Subjects performed repeated trials of a single-leg balance test (SLBT) in an altitude chamber in normoxia (NOR; approximately sea level) with FiO2 20.9% and PiO2 ranging from 146.7 to 150.4 mmHg and in normobaric hypoxia (HYP; ~3,800 m above sea level) with FiO2 13.0% and PiO2 ranging from 90.9 to 94.6 mmHg. The SLBT was performed three times: 15 min after entering the environmental chamber in NOR or HYP, then two times more interspersed by 3-min rest. Peripheral oxygen saturation (SpO2) and heart rate (HR) were recorded at four time points: after the initial 15-min rest inside the chamber and immediately after each SLBT. Across the cohort, the balance performance was 7.1% better during NOR than HYP (P < 0.01, η2pηp2 = 0.58). However, the performance of the elite group was not impaired by HYP, whereas the sub-elite group performed worse in the HYP condition on both legs (DL: P = 0.02, d = 1.23; NDL: P = 0.01, d = 1.43). SpO2 was lower in HYP than NOR (P < 0.001, η2pηp2 = 0.99) with a significant decline over time during HYP. HR was higher in HYP than NOR (P = 0.04, η2pηp2 = 0.25) with a significant increase over time. Acute exposure to normobaric hypoxia detrimentally affected the balance performance in sub-elite but not elite basketball players.

Background: Exposure to cold air is associated with increased morbidity and mortality in the general population. It is difficult to study the effects of whole-body exposure to cold air under controlled conditions in real life. Objectives: The aim of this study was to (1) explore and describe the experience of symptoms in humans during experimental and controlled exposures to cold air, by using controlled environmental chamber exposures and qualitative methodology, and to (2) categorise the symptoms. Method: The study used a randomised, double blind design, in which 34 subjects undertook rest and moderate-intensity exercise in an environmental chamber set to two or three different temperatures (0, −10, and −17°C) on separate occasions. During the chamber exposures, subjects were interviewed. Qualitative content analysis was selected as the method of analysis. Findings: Subjects reported 50 distinct symptoms during the exposures. The symptoms were grouped into ten sub-categories and two major categories; airway versus whole-body symptoms. Conclusion: We have identified a broad range of symptoms in humans undertaking rest and moderate-intensity exercise at sub-zero temperatures. The symptoms and their categories may well be used to more extensively and quantitatively map cold-induced morbidity.

The International Olympic Committee's (IOC) consensus statement on 'methods for recording and reporting of epidemiological data on injury and illness in sport' recommended standardising methods to advance data collection and reporting consistency. However, additional aspects need to be considered when these methods are applied to specific sports settings. Therefore, we have developed a snow sports-specific extension of the IOC statement to promote the harmonisation of injury and illness registration methods among athletes of all levels and categories in the different disciplines governed by the International Ski and Snowboard Federation (FIS), which is also applicable to other related snow sports such as biathlon, ski mountaineering, and to some extent, para snow sports. The panel was selected with the aim of representing as many different areas of expertise/backgrounds, perspectives and diversity as possible, and all members were assigned to thematic subgroups based on their profiles. After panel formation, all members were provided with an initial draft of this extension, which was used as a basis for discussion of aspects specific to the discipline, application context, level and sex within their snow sports subgroup topic. The outcomes were then aligned with the IOC's existing consensus recommendations and incorporated into a preliminary manuscript draft. The final version of this snow sports-specific extension was developed and approved in two iterative rounds of manuscript revisions by all consensus panel members and a final meeting to clarify open discussion points. This snow sports-specific extension of the IOC statement is intended to guide researchers, international and national sports governing bodies, and other entities recording and reporting epidemiological data in snow sports to help standardise data from different sources for comparison and future research.

Heat‐ and moisture exchanging breathing devices (HME) humidify and heat inhaled air and prevent exercise‐induced bronchoconstriction. HMEs have potential as primary preventers against airway damage and asthma induced by exercise in sub‐zero temperatures. HME usage among athletes has not been previously investigated.

This study surveyed the usage of and attitudes towards HMEs among elite skiers.

We invited all 347 students from Swedish National Elite Sports Schools in cross‐country skiing and biathlon to participate in a web‐survey. The response rate was 55%, 53% were women, 30% had asthma, and 87% were cross‐country skiers. Their mean (range) age was 17 (15‐19) years.

HMEs were used often or occasionally by 71% of respondents, while. 68% reported respiratory symptoms while training in sub‐zero temperatures. The most common temperature threshold for using HMEs was −15 °C. Almost all participants believed that HMEs prevent airway problems induced by training in cold. The participants were motivated, and confident in succeeding, to increase their HME usage during exercise in −10 °C or colder, if recommended.

Swedish adolescent skiers commonly use HMEs and have positive attitudes towards increased HME usage. HMEs may constitute a simple and effective prevention strategy against airway symptoms and asthma among winter endurance athletes.

Purpose: Cold air exposure is associated with increased respiratory morbidity and mortality. Repeated inhalation of cold and dry air is considered the cause of the high prevalence of asthma among winter endurance athletes. This study assessed whether a heat- and moisture-exchanging breathing device (HME) attenuates airway responses to high-intensity exercise in sub-zero temperatures among healthy subjects. Methods: Using a randomized cross-over design, 23 healthy trained participants performed a 30-min warm-up followed by a 4-min maximal, self-paced running time trial in − 15 °C, with and without HME. Lung function was assessed pre- and immediately post-trials. Club cell protein (CC-16), 8-isoprostane, and cytokine concentrations were measured in plasma and urine pre- and 60 min post trials. Symptoms were assessed prior to, during, and immediately after each trial in the chamber. Results: HME use attenuated the decrease in forced expiratory volume in 1 s (FEV1) post trials (∆FEV1: mean (SD) HME − 0.5 (1.9) % vs. no-HME − 2.7 (2.7) %, p = 0.002). HME also substantially attenuated the median relative increase in plasma-CC16 concentrations (with HME + 27% (interquartile range 9–38) vs no-HME + 121% (55–162), p &lt; 0.001) and reduced airway and general symptom intensity, compared to the trial without HME. No significant changes between trials were detected in urine CC16, 8-isoprostane, or cytokine concentrations. Conclusion: The HME attenuated acute airway responses induced by moderate-to-maximal-intensity exercise in − 15 °C in healthy subjects. Further studies are needed to examine whether this HMEs could constitute primary prevention against asthma in winter endurance athletes. 

Maximal exercise capacity is reduced at altitude or during hypoxia at sea level. It has been suggested that this might reflect increased right ventricular afterload due to hypoxic pulmonary vasoconstriction. We have shown previously that the pulmonary vascular sensitivity to hypoxia is enhanced by sustained isocapnic hypoxia, and inhibited by intravenous iron. In this study, we tested the hypothesis that elevated pulmonary artery pressure contributes to exercise limitation during acute hypoxia. Twelve healthy volunteers performed incremental exercise tests to exhaustion breathing 12% oxygen, before and after sustained (8-h) isocapnic hypoxia at sea level. Intravenous iron sucrose (n = 6) or saline placebo (n = 6) was administered immediately before the sustained hypoxia. In the placebo group, there was a substantial (12.6 ± 1.5 mmHg) rise in systolic pulmonary artery pressure (SPAP) during sustained hypoxia, but no associated fall in maximal exercise capacity breathing 12% oxygen. In the iron group, the rise in SPAP during sustained hypoxia was markedly reduced (3.4 ± 1.0 mmHg). There was a small rise in maximal exercise capacity following sustained hypoxia within the iron group, but no overall effect of iron, compared with saline. These results do not support the hypothesis that elevated SPAP inhibits maximal exercise capacity during acute hypoxia in healthy volunteers.

Purpose: To identify how performance is affected during maximal exercise in sub-zero conditions with the use of a heat-and-moisture-exchanging mask between men and women.

Methods: 23 healthy participants (eight female, 15 male; age 18-53 y) performed two simulated four-minute competition efforts including a graded warm-up at -15℃ in randomized order either with or without mask first. Breathing frequency, heart rate and velocity were measured constantly. Capillary blood samples were collected 2 min pre-and post-maximal test.

Results: There was an overall negative effect of the mask on performance for both sexes (Women: -5 ± 21m; Men: -17 ± 30m,  p = 0.033). Female participants accumulated more blood lactate than men during the effort with mask (9.3 ± 3.1 vs. 7.8 ± 1.4 mmol⋅L-1, p = 0.044 ). Men had an increased breathing frequency in the first 80-s of the time trial with the mask (p < 0.05). Women exhibited more even pacing, whilst men tended towards a negative pacing strategy, this observation was not affected by the mask. There was no change in heart rate between trials in either sex.

Conclusions: Competition performance in both sexes is hindered by wearing a mask in sub-zero conditions. The mechanisms through which this hindrance occurs are different between sexes.

Practical applications: Men and women should consider whether using a mask in short competition efforts is worthwhile for them at -15℃. Future research is required around longer competitions in sub-zero conditions.

INTRODUCTION: Heat-and-moisture exchanging masks (HMEs) are commonly used by athletes experiencing cold-air induced airway obstructions such as exercise-induced asthma to negate symptoms in training and competition. These masks have been demonstrated as an effective intervention at wide ranging intensity levels and duration for preventing airway obstructions (3). A large proportion of cross-country skiers experience asthma symptoms whilst training and competing in cold conditions (1, 2). As large numbers of athletes in cross country skiing and other outdoor winter endurance sports train and compete in cold conditions around the globe, links have been inferred between prolonged cold air inhalation and the development of exercise-induced asthma (2). The aim of this study was to investigate the effect of an HME on the performance (defined as distance completed) of healthy people during a maximal self-paced exercise test. METHODS: Twenty-three healthy, well-trained participants (eight females, 15 males; age 18-53 y) performed two simulated competition efforts at -15 degrees Celsius in randomized order either with or without mask first. The protocol was 5 min each at 65, 70 and 75% of VO2 Max followed by 3 min at 90% VO2 Max and a further 12 min at 65% before a 5 min pause to simulate a competition warm up followed by a 4 min maximal self-paced running test. A t-test was performed to compare performance outcomes. Two-way repeated measures ANOVA was used to examine effects of trial order and gender on performance. Linear regressions were used to investigate relationships between key physiological and biometric data and the effect of the HME on performance. All statistical analyses were performed with R using the jamovi interface. The study was conducted according to the declaration of Helsinki and approved by the regional ethics committee. RESULTS: Participants ran significantly further without HME (Mean: 931m, SD: 106m) than with HME (Mean: 918m, SD: 110m, p=0.039). No significant effect of trial order was observed (p=0.816). Body mass negatively correlated with the magnitude of the effect of the mask on performance; participants with higher body mass had a greater negative effect of the mask (r2 = 0.215, p= 0.026). No relationships were found between the effect of the HME and sex, age, ventilation, absolute or relative VO2peak. CONCLUSION: Our findings suggest that HME usage hinders maximal running performance in healthy subjects to an extent that may be sufficient to alter competition outcomes. Potential effects of sex, body mass and performance level should also be investigated further. References: 1. Larsson, K. et al. (1993), Br Med J, 307(6915), pp. 1326–1329. 2. Eriksson, L. M. et al. (2018), Scand J Med Sci Sport, 28(1), pp. 180–186. doi: 10.1111/sms.12879. 3. Nisar, M. et al. (1992), Thorax, 47(6), p. 446. doi: 10.1136/thx.47.6.446.

Purpose: To investigate whether use of an HME in sub-zero temperatures affects the physiological demands of fixed-intensity submaximal exercise, and whether the effect of the HME differed between sexes.

Methods: Twenty-three healthy, trained participants (15 male, 8 female, VO2peak 57 ± 6 and 50 ± 4 mL·kg-1·min-1; mean ± SD) gave written, informed consent to participate in the study. Participants completed two experimental trials, with and without HME. Each experimental trial consisted of 30-min submaximal treadmill running in -15°C. Muscle oxygenation (SmO2) and relative deoxyhaemoglobin concentration [HHb] were determined using wireless near-infrared spectroscopy sensors placed bilaterally on m. vastus lateralis. Nineteen complete datasets were obtained (12 men and 7 women) and analysed using linear mixed models.

Results: There were significant sex × trial interactions for SmO2 (p=0.007) and [HHb] (p=0.009); in the men only, SmO2 was lower (-3.8%, 95% CI: -1.9–-5.6%) and [HHb] was higher (0.42 AU, 95% CI: 0.2–0.65) from 5 min into the HME trial, whereas in the women there was no difference between trials.

Conclusion: The lower SmO2 and higher [HHb] in the men during fixed-intensity exercise with HME indicates greater O2 extraction at the tissues. Thus, an HME could be interpreted as increasing the physiological demands of exercise in men. We could speculate that airflow limitation from the HME could be exacerbated by higher absolute rates of ventilation resulting in reduced tissue oxygen delivery.

Practical Applications: Our observations could have implications for athletes when deciding whether to use an HME during training and competition.

Purpose: Heat-and-moisture-exchanging devices (HME) are commonly used by endurance athletes during training in sub-zero environments, but their effects on performance are unknown. We investigated the influence of HME usage on running performance at − 15 °C. Methods: Twenty-three healthy adults (15 male, 8 female; age 18–53 years; V˙ O 2peak men 56 ± 7, women 50 ± 4 mL·kg−1·min−1) performed two treadmill exercise tests with and without a mask-style HME in a randomised, crossover design. Participants performed a 30-min submaximal warm-up (SUB), followed by a 4-min maximal, self-paced running time-trial (TT). Heart rate (HR), respiratory frequency (fR), and thoracic area skin temperature (Tsk) were monitored using a chest-strap device; muscle oxygenation (SmO2) and deoxyhaemoglobin concentration ([HHb]) were derived from near-infra-red-spectroscopy sensors on m. vastus lateralis; blood lactate was measured 2 min before and after the TT. Results: HME usage reduced distance covered in the TT by 1.4%, despite similar perceived exertion, HR, fR, and lactate accumulation. The magnitude of the negative effect of the HME on performance was positively associated with body mass (r2 = 0.22). SmO2 and [HHb] were 3.1% lower and 0.35 arb. unit higher, respectively, during the TT with HME, and Tsk was 0.66 °C higher during the HME TT in men. HR (+ 2.7 beats·min−1) and Tsk (+ 0.34 °C) were higher during SUB with HME. In the male participants, SmO2 was 3.8% lower and [HHb] 0.42 arb. unit higher during SUB with HME. Conclusion: Our findings suggest that HME usage impairs maximal running performance and increases the physiological demands of submaximal exercise.