Abstract

PurposeWe determined whether well-acclimatized humans have a reserve to recruit pulmonary capillaries in response to exercise at high altitude.MethodsAt sea level, lung diffusing capacity for carbon monoxide (DLCO), alveolar-capillary membrane conductance (DmCO), and pulmonary capillary blood volume (Vc) were measured at rest before maximal oxygen consumption (dot{V}{text{O}}_{2hbox{max} }) was determined in seven adults. Then, DLCO, DmCO and Vc were measured pre- and post-exhaustive incremental exercise at 5150 m after ~40 days of acclimatization.ResultsImmediately after exercise at high altitude, there was an increase in group mean DmCO (14 ± 10 %, P = 0.040) with no pre- to post-exercise change in group mean DLCO (46.9 ± 5.8 vs. 50.6 ± 9.6 ml/min/mmHg, P = 0.213) or Vc (151 ± 28 vs. 158 ± 37 ml, P = 0.693). There was, however, a ~20 % increase in DLCO from pre- to post-exercise at high altitude (51.2 ± 0.2 vs. 61.1 ± 0.2 ml/min/mmHg) with a concomitant increase in DmCO (123 ± 2 vs. 156 ± 4 ml/min/mmHg) and Vc (157 ± 3 vs. 180 ± 8 ml) in 2 of the 7 participants. There was a significant positive relationship between the decrease in dot{V}{text{O}}_{2hbox{max} } from sea level to high altitude and the change in DLCO and lung diffusing capacity for nitric oxide (DLNO) from rest to end-exercise at high altitude.ConclusionThese data suggest that recruitment of the pulmonary capillaries in response to exercise at high altitude is limited in most well-acclimatized humans but that any such a reserve may be associated with better exercise capacity.

Highlights

  • We reasoned that individuals with a reserve to recruit and/or distend the pulmonary capillaries in response to exercise at high altitude would exhibit a large pre- to post-exercise increase in DLCO, DLNO, DmCO and Vc

  • It is well known that exposure to airway hypoxia and/ or high altitude elicits recruitment of the pulmonary capillaries due to an increase pulmonary perfusion pressure secondary to hypoxic pulmonary vasoconstriction (Brimioulle et al 1996; de Bisschop et al 2012; Taylor et al 2011). We theorized that this underlying hypoxia-mediated recruitment and distension of the pulmonary capillaries may limit or encroach upon an individual’s reserve to further expand the pulmonary capillary network in response to exercise at high altitude, and that any such limitation would be a source of diminished exercise capacity in this environment via an impairment in the increase in alveolar-capillary surface area for effective gas exchange and a heightened exercise-induced increase in pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR)

  • We found that only 2 of the 7 well acclimated healthy humans studied maintained a reserve to further recruit and distend the pulmonary capillaries in response to exercise at high altitude, as evidenced by a substantial pre- to immediately post-exercise increase in DLCO (~20 %), DmCO (~28 %) and Vc (~15 %) (Fig. 1)

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Summary

Introduction

The elevation in cardiac output and pulmonary perfusion pressure during exercise cause a marked expansion of the highly compliant pulmonary capillaryEur J Appl Physiol (2016) 116:427–437 network (La Gerche et al 2010; Lalande et al 2012; Stokes et al 1981; Tamhane et al 2001; Taylor et al 2014). We considered it possible that exposure to hypobaric hypoxia may elicit maximal, or near maximal, recruitment and distension of the pulmonary vasculature such that no reserve remains for further expansion of the pulmonary capillaries in response to exercise at high altitude Any such limitation in pulmonary capillary recruitment and distension during exercise at high altitude would likely be associated with an inability to adequately increase gas exchange surface area along with an excessive rise in PAP and PVR relative to the metabolic demand of exercise, which in turn would be expected to significantly impair exercise capacity (La Gerche et al 2010; Lalande et al 2012; Naeije et al 2010; Pavelescu et al 2013)

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