Pulmonary perfusion heterogeneity is increased by sustained, heavy exercise in humans

Abstract

Exercise presents a considerable stress to the pulmonary system and ventilation-perfusion (Va/Q) heterogeneity increases with exercise, affecting the efficiency of gas exchange. In particular, prolonged heavy exercise and maximal exercise are known to increase Va/Q heterogeneity and these changes persist into recovery. We hypothesized that the spatial heterogeneity of pulmonary perfusion would be similarly elevated after prolonged exercise. To test this, athletic subjects (n = 6, Vo(2max) = 61 ml. kg(-1).min(-1)) with exercising Va/Q heterogeneity previously characterized by the multiple inert gas elimination technique (MIGET), performed 45 min of cycle exercise at approximately 70% Vo(2max). MRI arterial spin labeling measures of pulmonary perfusion were acquired pre- and postexercise (at 20, 40, 60 min post) to quantify the spatial distribution in isogravitational (coronal) and gravitationally dependent (sagittal) planes. Regional proton density measurements allowed perfusion to be normalized for density and quantified in milliliters per minute per gram. Mean lung density did not change significantly in either plane after exercise (P = 0.19). Density-normalized perfusion increased in the sagittal plane postexercise (P =or <0.01) but heterogeneity did not (all P >or= 0.18), likely because of perfusion redistribution and vascular recruitment. Density-normalized perfusion was unchanged in the coronal plane postexercise (P = 0.66), however, perfusion heterogeneity was significantly increased as measured by the relative dispersion [RD, pre 0.62(0.07), post 0.82(0.21), P < 0.0001] and geometric standard deviation [GSD, pre 1.74(0.14), post 2.30(0.56), P < 0.005]. These changes in heterogeneity were related to the exercise-induced changes of the log standard deviation of the ventilation distribution, an MIGET index of Va/Q heterogeneity (RD R(2) = 0.68, P < 0.05, GSD, R(2) = 0.55, P = 0.09). These data are consistent with but not proof of interstitial pulmonary edema as the mechanism underlying exercise-induced increases in both spatial perfusion heterogeneity and Va/Q heterogeneity.

Early subclinical increase in pulmonary water content in athletes performing sustained heavy exercise at sea level: ultrasound lung comet-tail evidence

“…Conversely, we observed acute postrace decline in vital capacity and airflow rates at midand low lung volumes. These results suggest functional changes at the level of small airways, which are compressed in the presence of interstitial pulmonary edema and/or local bronchial-bronchiolar mucosal inflammation (4,48), so far causing increasing ventilation-perfusion heterogeneity (5). Moreover, we found a correlation between the intensity of the anti-inflammatory response (IL-10 and IL-1ra) and MVV at stress, suggesting a protective anti-inflammatory cascade in well-trained athletes, as hypothesized previously (30,33).…”

Maximal Exercise Does Not Increase Ventilation Heterogeneity In Healthy, Trained Adults

“…In support of this, magnetic resonance imaging (MRI) derived perfusion heterogeneity has been demonstrated to increase following prolonged exercise in healthy trained subjects (Burnham et al 2009). In contrast, whether ventilation heterogeneity increases with exercise remains speculative (Hopkins 2006;Burnham et al 2009). …”

“…Nevertheless, potential causes for this include subtle anatomical factors that limit the capacity of airways or pulmonary vessels to cope with increased flow, changes in airway or vascular tone, airway secretions, and/or mild interstitial pulmonary edema (Podolsky et al 1996;Dempsey and Wagner 1999;McKenzie et al 2005;Hopkins 2006;Zavorsky et al 2006a;Burnham et al 2009). These postulated mechanisms may give rise to changes in ventilation and/or perfusion heterogeneity (Wagner 1992).…”

Lung injury related to extreme environments

“…The importance of mild oedema in reducing exercise capacity has been questioned [43]. 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].…”

“…Recent studies have shown that mean PAP-flow relationships vary from 0.5 to 3 mmHg?L -1 ?min -1 , a six-fold variation associated with PAP .40 mmHg during high-intensity dynamic exercise at cardiac outputs .25-30 L?min -1 in some athletes [65]. Normal but steep PAP-flow relationships may limit exercise capacity through excessive afterloading of the right ventricle [44]. However, redistribution of blood flow occurs [64] and pulmonary capillary pressures may still be high enough to cause capillary stress failure in highly motivated athletes.…”