| Summary: | Demonstration of a greater elevation in the (ideal) alveolar/arterial oxygen difference in
habitually active female subjects with exercise-induced arterial hypoxemia, at equivalent
submaximal levels of oxygen uptake compared to inactive controls, suggests functional or
structural compromise of the blood-gas interface may occur with chronic-recurrent
intensive exercise. Mechanical and/or chemically mediated pulmonary endothelial
dysfunction during heavy exercise may alter vascular tone and permeability, leading to
interstitial edema and accentuation of ventilation-perfusion mismatch and/or diffusion
limitation. Elevated plasma levels of soluble endothelial cell adhesion molecules E- and Pselectin
have been demonstrated in acute lung injury and have been used as indirect
markers of endothelial activation or injury. Therefore, plasma levels of these selectins
were measured by enzyme immunoassay in fourteen habitually active, eumenorrheic
female subjects (mean±SD: age = 28.9±5.51; VO₂[sub peak] = 49.4±8.2 ml.kg⁻¹.min⁻¹, range 32.3
to 63.7 ml.kg⁻¹.min⁻¹; TLC = 5.41±0.68 L, 101±9.3% predicted) before and after an
incremental maximal exercise test during the follicular phase of their menstrual cycle
(cycle day = 6.2±1.2, serum progesterone = 80+100 pmol.L⁻¹). Arterial partial pressure of
oxygen (PaO₂) was measured and corrected for esophageal temperature, arterial
oxyhemoglobin saturation (%Sa0₂) was calculated from blood gas variables and
measured with pulse oximetry, and the (ideal) alveolar/arterial oxygen gradient was
calculated from the ideal gas equation. Pulmonary gas exchange efficiency was
maintained at peak exercise in ten subjects, while decrements in arterial partial pressure of
oxygen during exercise of greater than 1.3 kilopascals (10 mmHg) were seen in three of
the remaining four subjects. One subject displayed a minimal %Sa0₂ of 94% and was
included in the mild hypoxemia group. Maximum likelihood ANOVA procedures, used on
account of missing data, showed significant differences between groups averaged over
time for Pa0₂ (p<0.01) and %Sa02 (p=0.04), while the group by time interaction for the
(ideal) A-aD0₂ approached significance (p=0.07). Averaged over time, changes in
alveolar P0₂ , arterial PC0₂ , pH and temperature were not significantly different between
groups. Plasma concentrations of soluble E-selectin were not significantly different before
or after exercise (p=0.16), but plasma concentrations of P-selectin rose significantly (mean
increase ± SD; 21.5±24.8 ngmL'1, p=0.007). No significant group by time interaction was
noted in pre-post exercise concentrations of either E-selectin (p=0.74) or P-selectin
(p=0.42) between subjects who demonstrated normal gas exchange and subjects who
displayed mild to moderate exercise-induced gas exchange impairment. The correlation
between absolute (ngmL⁻¹) and relative (%) change in soluble E- and P-selectin, and
VO₂[sub peak], maximal A-aD0₂ and PaC0₂ was not significant, nor was the correlation between
minimal exercise Pa02 and either absolute (r=0.16, p=0.61) or relative (r=0.18, p=0.57)
change in soluble E-selectin. However, absolute change in plasma concentration of
soluble P-selectin was significantly correlated with minimal Pa0₂ (r=-0.60, p=0.04), while
the correlation between the relative change in P-selectin and minimal Pa0₂ approached
significance (r=-0.46, p=0.14). The increase in plasma P-selectin induced by heavy
exercise may represent platelet and/or endothelial activation. Correlation with impairment
of arterial oxygenation is compatible with the hypothesis that pulmonary endothelial
dysfunction may occur during intense exercise in some habitually active female subjects. === Education, Faculty of === Kinesiology, School of === Graduate
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