Sourcing UK COVID-19 News: An Analysis of Sourcing Patterns of 15 UK News Outlets Reporting on COVID-19 Across Facebook, Twitter, and Instagram.

How a health emergency is defined and presented through the news media matters for public understanding and health outcomes. Previous studies have endeavored to identify the patterns of news sourcing in crisis coverage, specifically the interplay between political sources and health expert sources, but yielded inconclusive results. This study analyses the types and roles of actors (those entities mentioned in a story) and sources cited in news coverage of COVID-19 by surveying social media posts published by 15 UK news outlets coverage across Facebook, Twitter, and Instagram between 1 January to December 31 2020. Overall, the findings show the prominence of political sources in UK news and that the most frequently named sources were representatives of the UK government. Moreover, when stories involved political actors, they were more likely to be given a voice as a source. This demonstrates how COVID-19 was a generalized crisis for the UK, which cascaded beyond health and into other economic, social, and cultural domains. The data show some variations in sourcing patterns between the different social media platforms. The analysis suggests that this may reflect the conventions of presenting news on each platform, with some tending toward the model of consensus by prioritizing political and government sources, and others contributing to a sphere of legitimate controversy by giving voice to a wider range of sources. This is distinctive and opens up the possibility for further research on how journalists adapt stories for social media and the consequences for public health communication.

Development of lung diffusion to adulthood following extremely preterm birth.

BACKGROUND: Gas exchange in extremely preterm (EP) infants must take place in fetal lungs. Childhood lung diffusing capacity of the lung for carbon monoxide (D LCO) is reduced; however, longitudinal development has not been investigated. We describe the growth of D LCO and its subcomponents to adulthood in EP compared with term-born subjects. METHODS: Two area-based cohorts born at gestational age ≤28 weeks or birthweight ≤1000 g in 1982-1985 (n=48) and 1991-1992 (n=35) were examined twice, at ages 18 and 25 years and 10 and 18 years, respectively, and compared with matched term-born controls. Single-breath D LCO was measured at two oxygen pressures, with subcomponents (membrane diffusion (D M) and pulmonary capillary blood volume (V C)) calculated using the Roughton-Forster equation. RESULTS: Age-, sex- and height-standardised transfer coefficients for carbon monoxide (K CO) and D LCO were reduced in EP compared with term-born subjects, and remained so during puberty and early adulthood (p-values for all time-points and both cohorts ≤0.04), whereas alveolar volume (V A) was similar. Development occurred in parallel to term-born controls, with no signs of pubertal catch-up growth nor decline at age 25 years (p-values for lack of parallelism within cohorts 0.99, 0.65, 0.71, 0.94 and 0.44 for z-D LCO, z-V A, z-K CO, D M and V C, respectively). Split by membrane and blood volume components, findings were less clear; however, membrane diffusion seemed most affected. CONCLUSIONS: Pulmonary diffusing capacity was reduced in EP compared with term-born subjects, and development from childhood to adulthood tracked in parallel to term-born subjects, with no signs of catch-up growth nor decline at age 25 years.

Nitric oxide in exhaled gas and tetrahydrobiopterin in plasma after exposure to hyperoxia.

The fraction of nitric oxide in exhaled gas (FENO) is decreased after exposure to hyperoxia in vivo, although the mechanisms for this decrease is not clear. A key co-factor for nitric oxide synthase (NOS), tetrahydrobiopterin (BH4), has been shown to be oxidized in vitro when exposed to hyperoxia. We hypothesized that the decrease of FENO is due to decreased enzymatic generation of NO due to oxidation of BH4. The present study was performed to investigate the relationship between levels of FENO and plasma BH4 following hyperoxic exposure in humans. Two groups of healthy subjects were exposed to 100% oxygen for 90 minutes. FENO was measured before and 10 minutes (n = 13) or 60 minutes (n = 14) after the exposure. Blood samples were collected at the same time points for quantification of biopterin levels (BH4, BH2 and B) using LC-MS/MS. Each subject was his or her own control, breathing air for 90 minutes on a separate day. Hyperoxia resulted in a 28.6 % decrease in FENO 10 minutes after exposure (p < 0.001), confirming previous findings. Moreover, hyperoxia also caused a 14.2% decrease in plasma BH4 (p = 0.012). No significant differences were observed in the group measured 60 minutes after exposure. No significant correlation was found between the changes in FENO and BH4 after the hyperoxic exposure (r = 0.052, p = 0.795), this might be due to the recovery of BH4 being faster than the recovery of FENO.

Hyperoxia and lack of ascorbic acid deplete tetrahydrobiopterin without affecting NO generation in endothelial cells.

Nitric oxide (NO) may protect against gas bubble formation and risk of decompression sickness. We have previously shown that the crucial co-factor tetrahydrobiopterin (BH4) is oxidized in a dose-dependent manner when exposed to hyperoxia similar to diving conditions but with minor effects on the NO production by nitric oxide synthase. By manipulating the intracellular redox state, we further investigated the relationship between BH4 levels and production of NO in human endothelial cells (HUVECs). HUVECs were cultured with and without ascorbic acid (AA) and the glutathione (GSH) synthesis inhibitor buthionine sulfoximine, prior to hyperoxic exposure. The levels of biopterins and GSH were determined in cell lysates while the production of NO was determined in intact cells. Omitting AA resulted in a 91% decrease in BH4 levels (0.49 ± 0.08 to 0.04 ± 0.01 pmol/106 cells, p⟨0.001) at 20 kPa oxygen (O2), and 88% decrease (0.24 ± 0.03 to 0.03 ± 0.01 pmol/106 cells, p=0.01) after exposure to 60 kPa O2. The NO generation was decreased by 23% (74.5 ± 2.2 to 57.3 ± 5.6 pmol/min/mg protein, p⟨0.001) at 20 kPa O2, but no significant change was observed at 60 kPa O2. GSH depletion had no effects on the NO generation. No correlation was found between NO generation and the corresponding intracellular BH4 concentration (p=0.675, r=-0.055) or the BH4 to BH2 ratio (p=0.983, r=0.003), determined across 18 in vitro experiments. Decreased BH4 in HUVECs, due to hyperoxia or lack of ascorbic acid, does not imply corresponding decreases in NO generation.

Decrease of tetrahydrobiopterin and NO generation in endothelial cells exposed to simulated diving.

Purpose: Nitric oxide (NO) has been shown to protect against bubble formation and the risk of decompression sickness. We hypothesize that oxidation of tetrahydrobiopterin (BH4) leads to a decreased production of NO during simulated diving. Methods: Human umbilical vein endothelial cells (HUVEC) were exposed to hyperoxia or simulated diving for 24 hours. The levels of biopterins (BH4, BH2 and B) were determined by LC-MS/MS, and the production of NO by monitoring the conversion of L-arginine to L-citrulline. Results: Exposure to hyperoxia decreased BH4 in a dose-dependent manner; by 48 ± 15% following exposure to 40 kPa O2 (P⟨0.001 vs. control at 20 kPa O2), and 70 ± 16% following exposure to 60 kPa O2. Exposure to 40 kPa O2 decreased NO production by 25 ± 9%, but there was no further decrease when increasing oxygen exposure to 60 kPa (25 ± 10%). No additional effects of simulated diving were observed, indicating no additive or synergistic effects of hyperbaria and hyperoxia on the BH4 level or NO generation. Conclusion: NO generation in intact human endothelial cells was decreased by simulated diving, as well as by hyperoxic exposure, while BH4 levels seem to be affected only by hyperoxia. Hence, the results suggest that BH4 is not the sole determinant of NO generation in HUVEC.

Lung hyperinflation and functional exercise capacity in patients with COPD - a three-year longitudinal study.

BACKGROUND: Lung hyperinflation contributes to dyspnea, morbidity and mortality in chronic obstructive pulmonary disease (COPD). The inspiratory-to-total lung capacity (IC/TLC) ratio is a measure of lung hyperinflation and is associated with exercise intolerance. However, knowledge of its effect on longitudinal change in the 6-min walk distance (6MWD) in patients with COPD is scarce. We aimed to study whether the IC/TLC ratio predicts longitudinal change in 6MWD in patients with COPD. METHODS: This prospective cohort study included 389 patients aged 40-75 years with clinically stable COPD in Global Initiative for Chronic Obstructive Lung Disease stages II-IV. The 6MWD was measured at baseline, and after one and 3 years. We performed generalized estimating equation regression analyses to examine predictors for longitudinal change in 6MWD. Predictors at baseline were: IC/TLC ratio, age, gender, pack years, fat mass index (FMI), fat-free mass index (FFMI), number of exacerbations within 12 months prior to inclusion, Charlson index for comorbidities, forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and light and hard self-reported physical activity. RESULTS: Reduced IC/TLC ratio (p < 0.001) was a statistically significant predictor for decline in 6MWD. With a 0.1-unit decrease in baseline IC/TLC ratio, the annual decline in 6MWD was 12.7 m (p < 0.001). Study participants with an IC/TLC ratio in the upper quartiles maintained their 6MWD from baseline to year 3, while it was significantly reduced for the patients with an IC/TLC ratio in the lower quartiles. Absence of light and hard physical activity, increased age and FMI, decreased FEV1 and FVC, more frequent exacerbations and higher Charlson comorbidity index were also predictors for lower 6MWD at any given time, but did not predict higher rate of decline over the timespan of the study. CONCLUSION: Our findings demonstrated that patients with less lung hyperinflation at baseline maintained their functional exercise capacity during the follow-up period, and that it was significantly reduced for patients with increased lung hyperinflation.

Peak oxygen uptake and breathing pattern in COPD patients--a four-year longitudinal study.

BACKGROUND: Activities of daily living in patients with chronic obstructive pulmonary disease (COPD) are limited by exertional dyspnea and reduced exercise capacity. The aims of the study were to examine longitudinal changes in peak oxygen uptake (V̇O2peak), peak minute ventilation (V̇Epeak) and breathing pattern over four years in a group of COPD patients, and to examine potential explanatory variables of change. METHODS: This longitudinal study included 63 COPD patients, aged 44-75 years, with a mean forced expiratory volume in one second (FEV1) at baseline of 51 % of predicted (SD = 14). The patients performed two cardiopulmonary exercise tests (CPETs) on treadmill 4.5 years apart. The relationship between changes in V̇O2peak and V̇Epeak and possible explanatory variables, including dynamic lung volumes and inspiratory capacity (IC), were analysed by multivariate linear regression analysis. The breathing pattern in terms of the relationship between minute ventilation (V̇E) and tidal volume (VT) was described by a quadratic equation, VT = a + b∙V̇E + c∙V̇E (2), for each test. The VTmax was calculated from the individual quadratic relationships, and was the point where the first derivative of the quadratic equation was zero. The mean changes in the curve parameters (CPET2 minus CPET1) and VTmax were analysed by bivariate and multivariate linear regression analyses with age, sex, height, changes in weight, lung function, IC and inspiratory reserve volume as possible explanatory variables. RESULTS: Significant reductions in V̇O2peak (p < 0.001) and V̇Epeak (p < 0.001) were related to a decrease in resting IC and in FEV1. Persistent smoking contributed to the reduction in V̇O2peak. The breathing pattern changed towards a lower VT at a given V̇E and was related to the reduction in FEV1. CONCLUSION: Increasing static hyperinflation and increasing airway obstruction were related to a reduction in exercise capacity. The breathing pattern changed towards more shallow breathing, and was related to increasing airway obstruction.

Myopic Shift during Hyperbaric Oxygenation Attributed to Lens Index Changes.

PURPOSE: To examine ocular lens parameters and structural changes to elucidate mechanisms underlying the myopic shift and cataract-related changes that occur in some patients during hyperbaric oxygen (HBO) therapy. METHODS: Scheimpflug images (Nidek EAS-1000) of the crystalline lens, measurements of scattered light, objective refraction, keratometry, tonometry, and axial length of the eye were obtained after the first day of HBO therapy and repeated when patients had completed 19 days of the treatment. RESULTS: Significant reduction in mean (± SD) optical density was found in the lens nucleus, -2.8 (± 4.3) units (p = 0.009) and -2.2 (± 4.1) units (p = 0.027) within circular and oval areas, respectively. Significant decrease in mean (± SD) backward scattered light was measured, -0.4 (± 0.8) units (p = 0.022). Mean (± SD) myopic shift was -0.58 (± 0.39) diopters (p < 0.001), whereas cortical optical density, forward scattered light, lenticular parameters, keratometry, tonometry, anterior chamber depth, and axial length of the eye appeared unchanged. CONCLUSIONS: Transient myopic shift reported in patients during HBO therapy is attributed to changes in the refractive index of the lens. No changes in lens curvatures or thickness were found after treatment.

Posterior segment changes of the eye during hyperbaric oxygen therapy.

PURPOSE: To examine central retinal thickness, retinal and vitreo-retinal structures, and ocular blood flow during a standard protocol of hyperbaric oxygen (HBO2) therapy. METHODS: Retinal thickness and color scans of the vitreo-retinal structures were obtained before and after 19 days of HBO2 therapy in 15 patients by optical coherence tomography (OCT). Pulsatile ocular blood flow was measured by ocular blood flow tonometry. Ocular refraction and axial length of the eye were monitored for control. RESULTS: Significant reduction was found in mean retinal thickness, -1.7 ± 1.6 µm (range -3.9 to 1.1 µm) (p < 0.001) in nine subfields within the 6-mm-diameter circle around the central macula. An insignificant decrease in pulsatile ocular blood flow of -19.0 ± 148.8 µl/minute was measured. No morphological changes were seen in retinal and vitreo-retinal structures. A mean myopic shift of -0.62 ± 0.39 D (p < 0.001) developed while axial length of the eye remained unchanged. CONCLUSIONS: A small decrease in central retinal thickness was seen during the study period, but the changes were not correlated to the myopic shift. No significant changes in vitreo-retinal structures or ocular pulsatile blood flow occurred.

Pulmonary gas transfer in children and adolescents born extremely preterm.

In extremely preterm-born infants, gas exchange takes place in developmentally fetal lungs, disturbing normal acinar growth and differentiation, potentially with long term negative consequences for lung function. The aim was to compare alveolar function in children and adolescents born extremely preterm and at term by measuring diffusing capacity of the lung for carbon monoxide (DLCO). Since this procedure may be challenging for subjects with shortcomings often seen after extremely preterm birth, we also assessed the reproducibility of the method. DLCO and DLCO adjusted for lung volume (KCO) were measured twice within 2 weeks in two population-based cohorts born at gestational age ≤28 weeks or with birth weight ≤1000 g, aged 10.6 years (n = 35) and 17.7 years (n = 46), and in 81 term-born controls individually matched for sex, age and place of birth. Reproducibility of DLCO measurements was in the same range for preterm and term-born children and young adults, and coefficients of variation were below 10% for all subgroups. KCO was significantly reduced with 7.9% and 7.2% for the oldest and youngest preterm birth cohorts, respectively. Reproducibility of DLCO in children and young adults born extremely preterm was adequate. DLCO and KCO were modestly reduced, supporting recent reports suggesting continuing alveolar growth throughout childhood.

Exhaled nitric oxide and lung function after moderate normobaric hyperoxic exposure.

INTRODUCTION: Pulmonary oxygen toxicity is associated with inflammatory responses in the airways and alveoli. The purpose of this study was to investigate whether the changes in exhaled nitric oxide (FE(NO)) after exposure to normobaric hyperoxia (NBO), 100% oxygen (O2) at 1 atmosphere absolute (atm abs) for 90 minutes, are associated with changes in lung function. METHODS: Eighteen healthy non-smoking subjects were exposed to NBO breathing 100% oxygen and to breathing ambient air, both for 90 minutes on separate days and in random order. Dynamic and static lung volumes, maximal expiratory flow rates, distribution of ventilation including closing volume and slope of phase III of the nitrogen washout curve (delta N2), diffusion capacity (D(L)CO) and FE(NO) were measured before and after the exposures. RESULTS: The mean reduction in FE(NO) was 20% (SD = 20) after the NBO exposure (p < 0.001). Static and dynamic lung volumes, maximal expiratory flow rates, DLCO and distribution of ventilation were unchanged. No association was found between the changes in the lung function variables and the change in FE(NO). DISCUSSION: Unchanged indices of distribution of ventilation and maximal expiratory flow rates indicate no small airways' dysfunction, and unchanged DLCO suggests preserved gas transfer in the lung despite a significant reduction in FE(NO). FE(NO) might be an index of oxygen exposure, but further studies over a wide range of oxygen exposures are necessary to establish the role of FE(NO) as a marker of pulmonary oxygen toxicity.

Quantitative computed tomography measures of emphysema and airway wall thickness are related to respiratory symptoms.

RATIONALE: There is limited knowledge about the relationship between respiratory symptoms and quantitative high-resolution computed tomography measures of emphysema and airway wall thickness. OBJECTIVES: To describe the ability of these measures of emphysema and airway wall thickness to predict respiratory symptoms in subjects with and without chronic obstructive pulmonary disease (COPD). METHODS: We included 463 subjects with chronic obstructive pulmonary disease (COPD) (65% men) and 488 subjects without COPD (53% men). All subjects were current or ex-smokers older than 40 years. They underwent spirometry and high-resolution computed tomography examination, and completed an American Thoracic Society questionnaire on respiratory symptoms. MEASUREMENTS AND MAIN RESULTS: Median (25th percentile, 75th percentile) percent low-attenuation areas less than -950 Hounsfield units (%LAA) was 7.0 (2.2, 17.8) in subjects with COPD and 0.5 (0.2, 1.3) in subjects without COPD. Mean (SD) standardized airway wall thickness (AWT) at an internal perimeter of 10 mm (AWT-Pi10) was 4.94 (0.33) mm in subjects with COPD and 4.77 (0.29) in subjects without COPD. Both %LAA and AWT-Pi10 were independently and significantly related to the level of dyspnea among subjects with COPD, even after adjustments for percent predicted FEV(1). AWT-Pi10 was significantly related to cough and wheezing in subjects with COPD, and to wheezing in subjects without COPD. Odds ratios (95% confidence intervals) for increased dyspnea in subjects with COPD and in subjects without COPD were 1.9 (1.5-2.3) and 1.9 (0.6-6.6) per 10% increase in %LAA, and 1.07 (1.01-1.14) and 1.11 (0.99-1.24) per 0.1-mm increase in AWT-Pi10, respectively. CONCLUSIONS: Quantitative computed tomography assessment of the lung parenchyma and airways may be used to explain the presence of respiratory symptoms beyond the information offered by spirometry.

Phakic and pseudophakic eyes in patients during hyperbaric oxygen therapy.

PURPOSE: To examine the optical components of phakic and pseudophakic eyes during hyperbaric oxygen (HBO) therapy, and to quantify their relative impact on ocular refractive changes. METHODS: HBO therapy was given to 16 phakic and six pseudophakic patients for 90 min daily at a pressure of 240 kPa, 5 d a week for 20 days. An eye examination was performed on the first day of HBO therapy and repeated when the patients had completed 19 days of the treatment. Refractive error, best-corrected visual acuity, corneal power, radius, thickness and volume, anterior chamber depth, axial length, lens opacity, and intraocular pressure were measured in all patients. Serum glucose, glycosylated hemoglobin, serum electrolytes, and protein were measured in the phakic patients. RESULTS: In the phakic group, a significant myopic shift (≥ -0.50 D) occurred in 26 (81%) single eyes during the treatment. The median myopic shift was -0.63 D (min -0.25 D/max -1.88 D) in the OD, and -0.69 D (min -0.38 D/max -2.25 D) in the OS. No myopic shift appeared in the pseudophakic patients; the median refractive changes were +0.06 D (min -0.13 D/max +0.25 D) in the OD and +0.13 D (min 0.00 D/max +0.25 D) in the OS. Intraocular pressure, serum electrolytes, glucose, and glycosylated hemoglobin remained unchanged. CONCLUSIONS: Myopic shifts occurred in phakic but not in pseudophakic eyes during HBO therapy. The myopic shifts must be attributed to changes in the crystalline lens.

Bronchial nitric oxide flux and alveolar nitric oxide concentration after exposure to hyperoxia.

BACKGROUND: The fraction of nitric oxide in exhaled gas (FE(NO)) is reduced by 30-70% after exposure to partial pressures of oxygen (Po2) of 200-240 kPa for 90 min. The purpose of this study was to partition FE(NO) into its flow-independent alveolar and bronchial components. A reduced bronchial NO flux (JawNO) is associated with induced bronchoconstriction, while increased alveolar NO concentration (C(A)NO) is associated with increased alveolar dead space. METHODS: There were 12 patients undergoing hyperbaric oxygen (HBO) therapy for 90 min at a Po2 of 240 kPa and 20 healthy subjects exposed to normobaric hyperoxia (NBO) breathing 100% oxygen for 90 min who were compared to a control group of 6 subjects breathing ambient air. FE(NO) was measured at flow rates from 30 to 250 ml x s(-1) before and after the exposures and the Högman Märilainen algorithm was used to calculate JawNO and C(A)NO. RESULTS: FE(NO) at an expiratory flow rate of 50 ml x s(-1) was reduced from 17.6 +/- 8.3 to 12.3 +/- 6.3 ppb after HBO exposure and from 17.8 +/- 6.2 to 13.3 +/- 5.2 ppb after NBO exposure. There was a significant reduction in JawNO, but unchanged C(A)NO. There were no changes in the control experiment. DISCUSSION: The reduction in FE(NO) after exposure to normobaric and hyperbaric hyperoxia appears to be predominantly an airway effect. An unchanged and low C(A)NO indicate preserved integrity of the gas exchange units without increased alveolar dead space at rest.

Risk of misclassification of decompression sickness.

Decompression sickness (DCS) is classified on the basis of which organ system is affected, and neurological DCS is considered more severe than DCS in joints and skin with respect to response to recompression treatment and risk of long-term sequelae. Gas bubble formation interstitially in the tissues or in the circulation is considered to be the mechanism for all types of DCS. Ten patients diagnosed as having DCS in joints or skin, by doctors experienced in diving medicine, underwent clinical examination by a neurologist and had an electroencephalogram. Eight of the ten subjects had findings suggesting central nervous system deficits. The findings indicate that DCS of the central nervous system often accompanies DCS of the joints and skin, and that local skin and joint symptoms may draw attention away from cerebral symptoms. We recommend that all cases with DCS should initially be treated as neurological DCS.

Cerebral diffusion and perfusion deficits in North Sea divers.

BACKGROUND: Diving is associated with a risk of cerebral decompression illness, and the prevalence of neurological symptoms is higher in divers compared with control groups. Microvascular dysfunction due to gas microembolism and exposure to hyperoxia are possible mechanisms, which may result in cerebral diffusion and perfusion deficits. PURPOSE: To investigate if possible functional derangements of the microvasculature and microstructure would be more prevalent among symptomatic divers. MATERIAL AND METHODS: Magnetic resonance imaging (MRI) was performed in 91 former divers and 45 controls. Individual parametric images of apparent diffusion coefficient (ADC), cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) were generated on the basis of diffusion- and perfusion-weighted imaging. To identify regions with statistically significant differences between groups (P < 0.05, corrected for false discovery rate), voxel-wise ANCOVA analysis was performed for each of the four parametric images. RESULTS: Significant regional group differences were found in all four parametric comparisons. Gross regional ADC differences were seen throughout the brain, including large frontal and temporal white-matter regions, the hippocampus, and parts of the cerebellum. Differences in the perfusion maps were localized in fewer and smaller clusters, including parts of the cerebellum, the putamen, and the anterior watershed regions. CONCLUSION: Regional functional abnormalities as measured by diffusion- and perfusion-weighted imaging were identified in the divers, and there was a partial co-localization of the regions identified in the perfusion and the diffusion images. The findings may explain some of the long-term clinical symptoms reported among professional divers.

Correction to: The effect of low dose marine protein hydrolysates on short-term recovery after high intensity performance cycling: a double-blinded crossover study.

The original article [1] contains errors in Tables 1 and 3: Table 1 erroneously mentions use of a treadmill which should instead state 'bicycle', and Table 3 has a minor typesetting mistake.

The effect of low dose marine protein hydrolysates on short-term recovery after high intensity performance cycling: a double-blinded crossover study.

BACKGROUND: Knowledge of the effect of marine protein hydrolysate (MPH) supplementation to promote recovery after high intensity performance training is scarce. The aim of this study was to examine the effect of MPH supplementation to whey protein (WP) and carbohydrate (CHO): (CHO-WP-MPH), on short-term recovery following high intensity performance, compared to an isoenergetic and isonitrogenous supplement of WP and CHO: (CHO-WP), in male cyclists. METHODS: This was a double-blinded crossover study divided into three phases. Fourteen healthy men participated. In phase I, an incremental bicycle exercise test was performed for establishment of intensities used in phase II and III. In phase II (9-16 days after phase 1), the participants performed first one high intensity performance cycling session, followed by nutrition supplementation (CHO-WP-MPH or CHO-WP) and 4 hours of recovery, before a subsequent high intensity performance cycling session. Phase III (1 week after phase II), was similar to phase II except for the nutrition supplementation, where the participants received the opposite supplementation compared to phase II. Primary outcome was difference in time to exhaustion between the cycling sessions, after nutrition supplementations containing MPH or without MPH. Secondary outcomes were differences in heart rate (HR), respiratory exchange ratio (RER), blood lactate concentration and glucose. RESULTS: The mean age of the participants was 45.6 years (range 40-58). The maximal oxygen uptake (mean ± SD) measured at baseline was 54.7 ± 4.1 ml∙min- 1∙kg- 1. There were no significant differences between the two nutrition supplementations measured by time to exhaustion at the cycling sessions (meandiff = 0.85 min, p = 0.156, 95% confidence interval (CI), - 0.37, 2.06), HR (meandiff = 0.8 beats pr.min, p = 0.331, 95% CI, - 0.9, 2.5), RER (meandiff = - 0.05, p = 0.361, 95% CI -0.07 - 0.17), blood lactate concentration (meandiff = - 0.24, p = 0.511, 95% CI, - 1.00, 0.53) and glucose (meandiff = 0.23, p = 0.094, 95% CI, - 0.05, 0.51). CONCLUSIONS: A protein supplement with MPH showed no effects on short-term recovery in middle-aged healthy male cyclists compared to a protein supplement without MPH. TRIAL REGISTRATION: The study was registered 02.05.2017 at ClinicalTrials.gov (Protein Supplements to Cyclists, NCT03136133 , https://clinicaltrials.gov/ct2/show/NCT03136133?cond=marine+peptides&rank=1 .

Postexercise reduction in lung diffusion capacity is not attenuated by skin cooling.

Pulmonary diffusion capacity for carbon monoxide (DL(CO)) is reduced by approximately 10% 1-6 h after maximal exercise. The mechanisms may be interstitial alveolar oedema and reduced pulmonary capillary blood volume. It was hypothesized that thermal stress following exercise contributes to the reduction in DL(CO), and that skin cooling would attenuate the postexercise reduction in DL(CO). Cutaneous vascular conductance (CVC), mean surface temperature (MST), rectal temperature and DL(CO) were measured before and 90 min after maximal incremental cycle exercise. Thereafter, the subjects were exposed to cold air without eliciting shivering one day and another day served as control. The measurements were repeated 120 min after exercise. Twelve healthy subjects (six male) aged 20-27 years were studied. DL(CO) was reduced by 7.1% (SD = 6.3%, P = 0.003) and 7.6% (SD = 5.3%, P<0.001) 90 and 120 min after exercise in the control experiment. It was reduced by 5.6% (SD = 5.5%, P = 0.014) 90 min after exercise and remained reduced by 6.1% (SD = 6.1%, P = 0.012) after cooling despite a significant reduction in CVC and in MST from 31.9 (SD = 0.6) degrees C to 27.4 (SD = 1.9) degrees C. We conclude that the postexercise reduction in DL(CO) is present when thermal status is restored after exercise, and that it is not influenced by further skin surface cooling.

Ventilatory Efficiency in Children and Adolescents Born Extremely Preterm.

Purpose: Children and adolescents born extremely preterm (EP) have lower dynamic lung volumes and gas transfer capacity than subjects born at term. Most studies also report lower aerobic capacity. We hypothesized that ventilatory efficiency was poorer and that breathing patterns differed in EP-born compared to term-born individuals. Methods: Two area-based cohorts of participants born with gestational age ≤28 weeks or birth weight ≤1000 g in 1982-85 (n = 46) and 1991-92 (n = 35) were compared with individually matched controls born at term. Mean ages were 18 and 10 years, respectively. The participants performed an incremental treadmill exercise test to peak oxygen uptake with data averaged over 20 s intervals. For each participant, the relationship between exhaled minute ventilation ([Formula: see text]E) and carbon dioxide output ([Formula: see text]CO2) was described by a linear model, and the relationship between tidal volume (VT) and [Formula: see text]E by a quadratic model. Multivariate regression analyses were done with curve parameters as dependent variables, and the categories EP vs. term-born, sex, age, height, weight and forced expiratory volume in 1 s (FEV1) as independent variables. Results: In adjusted analyses, the slope of the [Formula: see text]E-[Formula: see text]CO2 relationship was significantly steeper in the EP than the term-born group, whereas no group difference was observed for the breathing pattern, which was related to FEV1 only. Conclusion: EP-born participants breathed with higher [Formula: see text]E for any given CO2 output, indicating lower ventilatory efficiency, possibly contributing to lower aerobic capacity. The breathing patterns did not differ between the EP and term-born groups when adjusted for FEV1.