Maximal rowing has an acute effect on the blood-gas barrier in elite athletes (original) (raw)

Airway Cell Composition at Rest and after an All-out Test in Competitive Rowers

Medicine & Science in Sports & Exercise, 2004

Purposes: This study was designed to assess: a) whether rowing affects airway cell composition, and b) the possible relationship between the degree of ventilation during exercise and airway cells. Subjects and Methods: In nine young, nonasthmatic competitive rowers (mean age Ϯ SD: 16.2 Ϯ 1.0 yr), induced sputum samples were obtained at rest and shortly after an all-out rowing test over 1000 m (mean duration: 200 Ϯ 14 s), during which ventilatory and metabolic variables were recorded breath-by-breath (Cosmed K4b, Italy). Results: At rest, induced sputum showed prevalence of neutrophils (60%) over macrophages (40%); after exercise, total cell and bronchial epithelial cell (BEC) counts tended to increase. In the last minute of exercise, mean V E was 158.0 Ϯ 41.5 L•min Ϫ1 , and V O 2 •kg Ϫ1 62 Ϯ 11 mL•min Ϫ1. Exercise V E correlated directly with postexercise total cell (Spearman : 0.75, P Ͻ 0.05) and macrophage (: 0.82, P Ͻ 0.05) counts. A similar trend was observed for exercise V E and changes in BEC counts from baseline to postexercise (: 0.64, P ϭ 0.11). Exercise V E did not correlate with airway neutrophil counts at rest or after exercise. Expression of adhesion molecules by airway neutrophils, macrophages, and eosinophils decreased after the all-out test. Conclusion: Similar to endurance athletes, nonasthmatic competitive rowers showed increased neutrophils in induced sputum compared with values found in sedentary subjects. The trend toward increased BEC postexercise possibly reflected the effects of high airflows on airway epithelium. Airway macrophages postexercise were highest in rowers showing the most intense exercise hyperpnea, suggesting early involvement of these cells during exercise. However, the low expression of adhesion molecules by all airway cell types suggests that intense short-lived exercise may be associated with a blunted response of airway cells in nonasthmatic well-trained rowers.

Pulmonary gas exchange and breathing pattern during and after exercise in highly trained athletes

1993

Highly trained athletes (HT) have been found to show arterial hypoxaemia during strenuous exercise. A lack of compensatory hyperpnoea and/or a limitation of pulmonary diffusion by pulmonary interstitial oedema have been suggested as causes, but the exact role of each is not clear. It is known, however, that interstitial pulmonary oedema may result in rapid shallow breathing (RSB). The purpose of this study was therefore twofold: firstly, to determine the exact role of a lack of compensatory hyperpnoea versus a widened in ideal alveolar minus arterial oxygen partial pressure difference [P A(i)-aO2] in the decrease in partial pressure of oxygen in arterial blood (P aO2) and, secondly, to detect RSB during recovery in HT. Untrained subjects (UT) and HT performed exhausting incremental exercise. During rest, exercise testing, and recovery, breathing pattern, respiratory gas exchange, and arterial blood gases were measured. The P A(i)-aO2 and the difference in tidal volume (V T) between exercise and recovery for the same level of ventilation, normalized to vital capacity of the subject [ΔV T(%VC)], were then calculated. A large positive ΔV T (%VC) was considered to be the sign of RSB. HT showed a marked hypoxaemia (F=11.6, P F= 3.51, P P P A(i)-aO2 and oxygen consumption was the same for the two groups. The widening P A(i)-aO2 persisted throughout recovery for both HT and UT. The RSB was observed in HT during recovery. These results would suggest that the lack of compensatory hyperpnoea in HT during submaximal exercise was the major factor in the decrease in P aO2. The RSB and the widening P A(i)-aO2 during recovery would suggest that interstitial pulmonary oedema was involved during the strenuous exercise in the case of HT. Lastly, the wide P A(i)-aO2 observed in UT during recovery would suggest that an increase in extravascular pulmonary water may also have been involved for these subjects, although to a lesser extent.

Effects of Endurance Training Intensity on Pulmonary Diffusing Capacity at Rest and after Maximal Aerobic Exercise in Young Athletes

International Journal of Environmental Research and Public Health, 2021

This study compared the effects of varying aerobic training programs on pulmonary diffusing capacity (TLCO), pulmonary diffusing capacity for nitric oxide (TLNO), lung capillary blood volume (Vc) and alveolar–capillary membrane diffusing capacity (DM) of gases at rest and just after maximal exercise in young athletes. Sixteen healthy young runners (16–18 years) were randomly assigned to an intense endurance training program (IET, n = 8) or to a moderate endurance training program (MET, n = 8). The training volume was similar in IET and MET but with different work intensities, and each lasted for 8 weeks. Participants performed a maximal graded cycle bicycle ergometer test to measure maximal oxygen consumption (VO2max) and maximal aerobic power (MAP) before and after the training programs. Moreover, TLCO, TLNO and Vc were measured during a single breath maneuver. After eight weeks of training, all pulmonary parameters with the exception of alveolar volume (VA) and inspiratory volume ...

Pulmonary system limitations to endurance exercise performance in humans

Experimental Physiology, 2012

Accumulating evidence over the past 25 years depicts the healthy pulmonary system as a limiting factor of whole-body endurance exercise performance. This brief overview emphasizes three respiratory system-related mechanisms which impair O 2 transport to the locomotor musculature [arterial O 2 content (C aO 2) × leg blood flow (Q L)], i.e. the key determinant of an individual's aerobic capacity and ability to resist fatigue. First, the respiratory system often fails to prevent arterial desaturation substantially below resting values and thus compromises C aO 2. Especially susceptible to this threat to convective O 2 transport are well-trained endurance athletes characterized by high metabolic and ventilatory demands and, probably due to anatomical and morphological gender differences, active women. Second, fatiguing respiratory muscle work (W resp) associated with strenuous exercise elicits sympathetically mediated vasoconstriction in limb-muscle vasculature, which compromisesQ L. This impact on limb O 2 transport is independent of fitness level and affects all individuals, but only during sustained, highintensity endurance exercise performed above ∼85% maximal oxygen uptake. Third, excessive fluctuations in intrathoracic pressures accompanying W resp can limit cardiac output and thereforeQ L. Exposure to altitude exacerbates the respiratory system limitations observed at sea level, further reducing C aO 2 and substantially increasing exercise-induced W resp. Taken together, the intact pulmonary system of healthy endurance athletes impairs locomotor muscle O 2 transport during strenuous exercise by failing to ensure optimal arterial oxygenation and compromisingQ L. This respiratory system-related impact exacerbates the exercise-induced development of fatigue and compromises endurance performance.

Diffusion capacity of the lung in young and old endurance athletes

2013

▶ master athletes • ▶ diff usion capacity • ▶ FEV 1 • ▶ transfer coeffi cient Diff usion Capacity of the Lung in Young and Old Endurance Athletes endurance athletes are partly exempt from the age-related decline in lung function. Another factor to consider is the diff usion capacity of the lungs. In sedentary people the diff usion capacity of the lung does not limit exercise capacity. The inability to increase the diff usion capacity with training [ 34 ] may explain why the diff usion capacity 1) can limit performance in faster marathon runners and 2) in young fi t people predicts the maximal oxygen uptake with athletes having a better lung diff usion capacity than non-athletes . The diff usion capacity decreases, however, with age [ 19 , 39 ] and is signifi cantly reduced after exercise [ 8 , 24 , 27 , 43 ] . In fact, particularly at maximal eff ort exercise may cause pulmonary oedema [ 8 , 24 ] and damage the pulmonary blood-gas barrier (BGB) . As a consequence, repeated endurance events over the years may reduce the integrity of the lung and result in a diminished diff usion capacity and cause the exerciseinduced hypoxemia that is more prevalent and occurring at a lower maximal oxygen uptake level in older than younger endurance athletes Abstract

A century of exercise physiology: lung fluid balance during and following exercise

European Journal of Applied Physiology

Purpose This review recalls the principles developed over a century to describe trans-capillary fluid exchanges concerning in particular the lung during exercise, a specific condition where dyspnea is a leading symptom, the question being whether this symptom simply relates to fatigue or also implies some degree of lung edema. Method Data from experimental models of lung edema are recalled aiming to: (1) describe how extravascular lung water is strictly controlled by “safety factors” in physiological conditions, (2) consider how waning of “safety factors” inevitably leads to development of lung edema, (3) correlate data from experimental models with data from exercising humans. Results Exercise is a strong edemagenic condition as the increase in cardiac output leads to lung capillary recruitment, increase in capillary surface for fluid exchange and potential increase in capillary pressure. The physiological low microvascular permeability may be impaired by conditions causing damage ...

The Effect of Different Training Loads on the Lung Health of Competitive Youth Swimmers

International Journal of Exercise Science, 2018

Airway hyperresponsiveness (AHR), airway inflammation, and respiratory symptoms are common in competitive swimmers, however it is unclear how volume and intensity of training exacerbate these problems. Thus, our purpose was to measure AHR, inflammation, and respiratory symptoms after low, moderate, and high training loads in swimmers. Competitive youth swimmers (n=8) completed nine weeks of training split into three blocks (Low, Moderate, and High intensity). Spirometry at rest and post-bronchial provocation [Eucapnic Voluntary Hyperpnea (EVH)] and Fractional Exhaled Nitric Oxide (FeNO) were completed at the end of each training block. A weekly self-report questionnaire determined respiratory symptoms. Session Rating of Perceived Exertion (sRPE) quantified internal training loads. Internal load was significantly lower after Moderate training (4840 ± 971 AU) than after High training (5852 ± 737 AU) (p = 0.02, d = 1.17). Pre-EVH FEV1 was significantly decreased after Moderate (4.52 ± ...

Respiratory parameters in elite athletes – does sport have an influence?

Revista Portuguesa de Pneumologia (English Edition), 2015

Introduction: Unlike large population studies about cardiovascular components and how they adapt to intensive physical activity, there is less research into the causes of enlargement of the respiratory system in athletes (e.g. vital capacity, maximum flow rates and pulmonary diffusion capacity). The purpose of this research was to study and compare pulmonary function in different types of sports and compare them with controls in order to find out which sports improve lung function the most. Materials and method: Pulmonary functional capacities, vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in one second (FEV1) and maximum voluntary ventilation (MVV) of 493 top athletes belonging to 15 different sports disciplines and of 16 sedentary individuals were studied. Pulmonary function test was performed according to ATS/ERS guidelines. Results: Basketball, water polo players and rowers had statistically higher vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in one second (FEV1) than the healthy sedentary control individuals. Football and volleyball players had lower VC while FVC was higher in the football group compared to controls. Peak expiratory flow was lower in boxing, kayak, rugby, handball, taekwondo and tennis. The maximum voluntary ventilation (MVV) was significantly higher in water polo players and rowers. Boxers had statistically lower MVV than the controls. Players of other sports did not differ from the control group. Pages 6 2 S. Mazic et al.

Chapter 3. Exercise and airway physiology: interactions with immune and allergic responses

European Respiratory Monograph, 2005

Pulmonary ventilation (V9E) increases during exercise to meet metabolic needs . In particular, V9E increases proportionally to the CO 2 produced at muscular level, up to the point where lactic threshold (LT) is achieved. Above LT, V9E increases in excess to the CO 2 produced by the working muscles, because additional CO 2 is generated from the bicarbonate component of lactate isocapnic buffering. At higher work loads, a further increase in V9E occurs with a decrease in CO 2 in order to compensate for metabolic acidosis. In most normal individuals, exercise is terminated well below the maximum ventilation a subject can achieve voluntarily. This may not be the case in pulmonary disorders (either obstructive or restrictive) and in highly trained athletes, who may reach a V9E w200 L?min -1 at high-intensity exercise. The usual ventilatory response to exercise is for V9E to be dominated by an increase in tidal volume (VT) at low-to-moderate work loads, with respiratory frequency increasing only at high levels of exercise. This pattern, however, may vary among subjects and types of exercise, but it is also affected by lung size [2] or airway calibre or both. This chapter will first examine how changes in airway physiology may affect the pattern of the ventilatory response to exercise and performance. Therefore, the effects of exercise on airway calibre and their relationships to airway inflammation will be reviewed.

Pulmonary Mechanics and Gas Exchange during Exercise in Kenyan Distance Runners

Medicine & Science in Sports & Exercise, 2014

Purpose: The purpose of this study was to determine arterial blood gases, the mechanical limits for generating expiratory flow and the work performed by the respiratory muscles during treadmill exercise in Kenyan runners. Methods: Kenyan runners (10 men and 4 women; mean T SD age = 25.2 T 1.3 yr) were instrumented with a radial artery catheter, an esophageal balloon-tipped catheter, and an esophageal temperature probe for the determination of blood gases, the work of breathing and core temperature, respectively. Testing occurred at 1545 m above sea level. Results: There were significant decreases in the arterial partial pressure of O 2 and oxyhemoglobin saturation and a widening of the alveolar-to-arterial difference in O 2 from rest to peak exercise. The mechanical work of breathing increased with increasing minute ventilation and was commensurate with values expected for treadmill running in elite athletes. During heavy exercise, significant expiratory flow limitation was present in half of the subjects while the remaining subjects demonstrated impending flow limitation. Conclusions: Pulmonary system limitations were present in Kenyan runners in the form of exercise-induced arterial hypoxemia, expiratory flow limitation, and high levels of respiratory muscle work. It appears that Kenyan runners do not posses a pulmonary system that confers a physiological advantage.