Changes in pulmonary diffusing capacity and closing volume after running a marathon

Miles, D. S.; Doerr, Christopher E.; Schonfeld, Steven A.; Sinks, David E.; Gotshall, Robert W.

doi:10.1016/0034-5687(83)90090-7

Cited by 71 publications

(66 citation statements)

References 18 publications

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“…Furthermore, heterogeneous ventilation may reflect airway compression by interstitial edema secondary to the increased alveolar epithelial permeability. The decreases in the membrane component of the lung diffusion capacity in the hours after exercise have been interpreted as transient interstitial edema (27,31,37,40). However, other studies using chest radiography (13) or computed tomography and magnetic resonance imaging (29) have failed to provide visual evidence of such edema.…”

Section: Discussionmentioning

confidence: 99%

Maximal rowing has an acute effect on the blood-gas barrier in elite athletes

Hanel

Law²,

Mortensen³

2003

Journal of Applied Physiology

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Hanel, Birgitte, Ian Law, and Jann Mortensen. Maximal rowing has an acute effect on the blood-gas barrier in elite athletes. J Appl Physiol 95: 1076-1082, 2003. First published April 25, 2003 10.1152/japplphysiol.00082.2002The purpose of the study was to evaluate the effects of maximal exercise on the integrity of the alveolar epithelial membrane using the clearance rate of aerosolized 99m Tclabeled diethylenetriaminepentaacetic acid as an index for the permeability of the lung blood-gas barrier. Ten elite rowers (24.3 Ϯ 4.6 yr of age) completed two 20-min pulmonary clearance measurements immediately after and 2 h after 6 min of all-out rowing (initial and late, respectively). All subjects participated in resting control measurements on a separate day. For each 20-min measurement, lung clearance was calculated for 0-7 and 10-20 min. Furthermore, scintigrams were processed from the initial and late measurements of diethylenetriaminepentaacetic acid clearance. Compared with control levels, the pulmonary clearance measurement after rowing was increased from 1.2 Ϯ 0.5 to 2.4 Ϯ 1.0%/min (SD) at 0-7 min (P Ͻ 0.01) and from 0.8 Ϯ 0.3 to 1.5 Ϯ 0.4%/min at 10-20 min (P Ͻ 0.0005), returning to resting levels within 2 h. In 6 of 10 subjects, ventilation distribution on the lung scintigrams was inhomogeneous at the initial measurement. The study demonstrates an acute increased pulmonary clearance after maximal rowing. The ventilation defects identified on the lung scintigrams may represent transient interstitial edema secondary to increased blood-gas barrier permeability induced by mechanical stress. lung function; oarsmen; ventilation defects THERE IS EVIDENCE TO SUGGEST that the integrity of the lung blood-gas barrier (BGB) in elite athletes is altered after short-term maximal exercise (19). The finding of red blood cells and protein in the fluid of bronchoalveolar lavage suggests that this effect may be caused by mechanical stress on the alveolar capillary membrane. In contrast, sustained submaximal exercise [77% of maximal O 2 uptake (V O 2 max )] in elite athletes did not elicit the same ultrastructural changes (18). Hence, only extreme levels of exercise in elite athletes may disrupt the integrity of the BGB, with possibly secondary development of interstitial edema. During maximal exercise, the BGB is subjected to conflicting requirements. A thin barrier is most optimal for efficient gas exchange by diffusion, whereas a strong barrier is needed to withstand the increased pulmonary capillary pressure and the longitudinal tension in the alveolar wall associated with lung inflation (42). If any injury should occur, it may cause these layers to become leaky, thereby increasing permeability.A very sensitive method to evaluate the BGB permeability is measurement of the pulmonary clearance rate using 99m

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Section: Discussionmentioning

confidence: 99%

Maximal rowing has an acute effect on the blood-gas barrier in elite athletes

Hanel

Law²,

Mortensen³

2003

Journal of Applied Physiology

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“…Using echocardiography, impaired left ventricu lar performance evidenced by a decrease in the ratio between systolic blood pressure and end-diastolic diam eter and a decreased end-diastolic and a slightly in creased end-systolic dimension have been reported fol lowing an uninterrupted competitive 24-hour run [4], Also, changes in pulmonary parameters that may reflect a subclinical lung oedema after maximal exercise have been reported [5][6][7][8].…”

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confidence: 99%

Left Ventricular Performance during Exercise and in the Recovery Period following Extensive Exercise in Athletes

Rasmussen¹,

Lund²,

Jensen³

et al. 1991

Am J Noninvas Cardiol

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Left ventricular performance was studied in 9 well-trained athletes at rest, during maximal exercise, and during the recovery period following exercise. All athletes showed an expected response to maximal bicycle exercise in the supine position. During the recovery period signs of impaired diastolic as well as systolic performance were noted. Abnormal filling characteristics and relatively increased duration of systole at the expense of diastole prevailed 25 min after exercise was stopped, reflecting a decrease in left ventricular diastolic distensibility and a compromised contractility. These findings were paralleled by signs of myocardial oxygen debt/increased oxygen consumption during the recovery period. At the last recovery recording (25 min after exercise), the athletes had a ventricular function which showed some resemblance to the characteristics of left ventricles with concentric hypertrophy. The study suggests that the athletes succumbed to myocardial oxygen debt up to 25 min after maximal exercise.

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“…Experimental studies demonstrate evidence of heterogeneous lung perfusion following prolonged exercise [44]. There is evidence that hyponatraemia, which particularly occurs in marathon running, contributes to pulmonary oedema [45][46][47][48][49][50][51][52][53]. This occurs especially in marathon runners who ingest excess water while racing.…”

Section: Exercise-induced Pulmonary Oedemamentioning

confidence: 99%

Lung injury related to extreme environments

Adir

Bové

2014

Eur Respir Rev

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@ERSpublications Lung injury is a well understood and preventable consequence of water immersion while swimming and diving http://ow.ly/AOdvgAs extreme sports become more popular, related respiratory injury may compromise the athlete's performance and result in morbidity and even mortality. In this article we will discuss different lung injuries in relation to performing different activities in an extreme environment. Hydrostatic lung injuriesThe evolution of fish to amphibians, reptiles to endothermic birds and mammals has been accompanied by a progressively thinner pulmonary blood gas barrier, to accommodate the constraint of increased oxygen uptake and carbon dioxide output [1]. Accordingly, pulmonary circulation has evolved as a separate high flow-low pressure system. In humans, mean pulmonary artery pressures (PAP) are 8-20 mmHg, pulmonary wedge pressures are 5-14 mmHg and pulmonary capillary pressures are 8-12 mmHg [2]. A low-pressure regimen preserves the integrity of an alveolar capillary membrane only 0.3 mm thick. However, this structure is vulnerable to increased pressures during strenuous exercise or environmental hypoxic exposure as a cause of stress failure of the pulmonary capillaries and accumulation of extravascular lung water [3]. Reports of lung injury related to extremes of exercise and variations in ambient pressure and altitude confirm this vulnerability. The resulting lung injury takes the form of noncardiogenic pulmonary oedema.The occurrence of noncardiogenic pulmonary oedema and pulmonary haemorrhage has been described in relation to a variety of disorders related to auto-and exogenous immunological reactions, infections and certain inhalants. However, numerous reports of lung injury manifesting as pulmonary oedema with associated haemorrhage have been described more recently in relation to immersion underwater, swimming, extreme exercise and exposure to altitude. In addition, pulmonary oedema resulting from negative intra-alveolar pressure has been described in the anaesthesia literature and may play a role in exercise-and immersion-induced pulmonary oedema. Haemodynamically induced pulmonary oedemaA single mechanism responsible for production of noncardiogenic pulmonary oedema related to immersion, altitude and exercise has not been identified. However, a combination of haemodynamically related factors, alterations in capillary integrity, increased blood volume and increased cardiac output may all contribute to the syndrome. WEST et al.[4] described exercise-induced pulmonary haemorrhage in race For editorial comments see page 401.

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Changes in pulmonary diffusing capacity and closing volume after running a marathon

Cited by 71 publications

References 18 publications

Maximal rowing has an acute effect on the blood-gas barrier in elite athletes

Maximal rowing has an acute effect on the blood-gas barrier in elite athletes

Left Ventricular Performance during Exercise and in the Recovery Period following Extensive Exercise in Athletes

Lung injury related to extreme environments

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