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Endothelial selectins and pulmonary gas exchange in female aerobic athletes

University of British Columbia

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.

Thesis/Dissertation

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2009-07-10

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http://hdl.handle.net/2429/10649

Human Kinetics

University of British Columbia

UBCV

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