VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema

Abstract

Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25–75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore, higher pulmonary vascular pressures in such subjects.

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

“…In the present study, the pulmonary clearance measurement started 9 min after termination of a 6-min all-out exercise in elite rowers able to produce very high pulmonary capillary pressures. We found that the pulmonary clearance was still increased at 10-20 min and normalized after 2 h. This suggests that resolution of the ventilation inhomogeneity begins ϳ30 min after exercise, in agreement with the study of Schaffartzik et al (35). Two subjects still had small defects on the lung scintigrams 2 h after exercise, despite a normalized pulmonary clearance, indicating defects, which require more time to recovery.…”

“…We found nonuniform ventilation distribution in the lungs, indicating constriction of the airways immediately after exercise, as shown by the study of Schaffartzik et al (35), who found ventilation-perfusion inequality in the early recovery from heavy exercise. The lack of increased bronchial responsiveness excludes asthmatic disease.…”

Ventilation-perfusion inequality during normoxic and hypoxic exercise in the emu

“…Various mechanisms of the increase in V /Q inequality have been proposed, including 1) a reduced common dead space-to-tidal volume ratio and therefore reduced admixture of the expired air, unmasking existing V /Q heterogeneity present at rest (27); 2) nonuniform pulmonary vasoconstriction and increased pulmonary arterial pressure (4); 3) interstitial edema (22,23); or 4) ventilatory time-constant inequality (27). None of these mechanisms have been investigated in exercising birds; however, the rather nonelastic structure of the avian lung may reduce the importance of those mechanisms relying on pressure changes in the pulmonary tissue and/or microenvironment.…”

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake

“…While several subsequent studies in endurance athletes have reported a signi®cant fall in arterial oxyhaemoglobin saturation (S a O 2 ) with exercise intensities at or close to maximal oxygen uptake ( O 2max ; Williams et al 1986;Powers et al 1992;Harms and Stager 1995) the mechanism of EIH remains uncertain. Several hypotheses have been suggested including intra-and extra-pulmonary shunts (Dempsey et al 1984;Powers et al 1992), inadequate hyperventilation (Dempsey et al 1984;Powers et al 1984;Miyachi and Tabata 1992;Harms and Stager 1995;Turcotte et al 1997; Gavin et al 1998), an oxygen diusion limitation based on low pulmonary capillary blood transit time or interstitial oedema (Dempsey et al 1982;Wagner et al 1986;Schaartzik et al 1992) and ventilation-perfusion inequalities (Torre-Bueno et al 1985;Hammond et al 1986;Wagner et al 1986;Schaartzik et al 1992;Hopkins and McKenzie 1993;Hopkins et al 1994).…”