Within the Point presented by Dr. Hopkins (2) several case studies, which have little to do with the debate, are presented as “evidence” of the development of pulmonary edema during heavy sea-level exercise. Anecdotal reports of pulmonary edema induced by emotional stress, sexual intercourse, and exercise at high altitude are all distractions from the central question. Moreover, left ventricular diastolic dysfunction is likely causative in these instances (8) and they represent an entirely different physiological scenario than that of the healthy athlete performing near-maximal exercise at sea level.
We disagree with the assertion that the rapid infusion of 20 ml/kg of normal saline into resting humans can be used as supporting evidence for exercise-induced interstitial edema (4). Rather, it produces a nonphysiological situation (i.e., volume overload by ∼1.5 liters), which results in airflow obstruction and changes to airway responsiveness that are not commensurate with the typical exercise response seen in the population being discussed in this debate.
Our colleague (2) and others (5) argue that the persistence of V̇A/Q̇ inequality during recovery from heavy exercise supports the idea of an exercise-induced increase in extravascular lung water. Specifically, the logic is that interstitial edema compresses the small airways and blood vessels resulting in a mismatch of V̇A/Q̇. However, this is not direct evidence of edema and should not be interpreted as such. As clearly stated within the concluding statements of the original manuscript by Schaffartzik et al. (5): “It [persistent V̇A/Q̇ mismatch owing to pulmonary interstitial edema] is of course not proof of the hypothesis.” We agree. Alternative explanations for V̇A/Q̇ heterogeneity include changes in airway resistance and increases in dead-space ventilation (6, 7). Moreover, increased V̇A/Q̇ heterogeneity with sustained heavy exercise does not result in a change in MRI-derived lung density measures 20 min following exercise (1). The multiple inert-gas elimination technique for determining V̇A/Q̇ has never been directly validated (3) which makes definitive statements about the development of exercise-induced edema difficult. Furthermore, regional estimates of where the edema (i.e., peribronchial and perivascular “cuffing”) occurs based on V̇A/Q̇ heterogeneity measures in humans are speculative. It appears that the indirect methods offer only cause for speculation on the presence of pulmonary edema while direct measurements via CT or MRI consistently fail to demonstrate changes in lung density.
Accumulation of scattered anecdotal reports and circumstantial evidence is not proof of interstitial edema. In our view, the hypothesis continues to await experimental support.
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