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Prevalence of exercise-induced arterial hyposemia in female asthmatic athletes Lynn, Brenna Meaghan

Abstract

It has been suggested that habitual exercise training may cause mechanically or chemically mediated endothelial dysfunction during heavy exercise, which may lead to exercise-induced arterial hypoxemia. Cellular adhesion molecules E- and P-selectin have been used as direct markers of endothelial injury. Elevated plasma levels of these inflammatory mediators along with IL-6 have been present in acute lung injury and also after intense exercise. To determine whether asthmatic female athletes have higher incidence of exercise-induced arterial hypoxemia (EIAH) and higher plasma levels of soluble P-selectin and IL-6 when compared to controls, 16 female asthmatics (age = 26.4 ± 5.7 yrs; ht = 165.7 ± 7.6 cm; wt = 61.7 ± 10.9 kg; VO[sub 2max]= 46.8 ± 8.0 mL•kg⁻¹•min⁻¹, range 29.3 to 57.3 mL•kg⁻¹•min⁻¹) and 16 female non-asthmatic athletes (age = 26.2 ± 4.2 yrs; ht = 167.2 ± 6.8 cm; wt = 57.5 ± 6.0 kg; VO[sub 2max]= 51.9 ± 8.2 mL•kg⁻¹•min⁻¹, range 40.0 to 67.9 mL•kg⁻¹•min⁻¹) were tested during the mid-follicular phase of their menstrual cycle. Subjects completed an incremental maximal treadmill test on the first day of testing. Exercise-induced arterial hypoxemia (%SaO₂ ≤ 93%) was seen in 7 of the 16 asthmatics and 8 of the 16 control subjects. On day 2 during the run to exhaustion test, 6 of 16 asthmatics decreased %SaO₂ to less than 93%, whereas 9 of the 16 controls developed EIAH. The data failed to show significance (p >0.05) in %SaO₂ between groups on Day 1 (p = 0.74) and Day 2 (p = 0.93). There was a significant decrease in saturation over time for both groups (p = 0.00 and p = 0.00). P-selectin and IL-6 were . measured on Day 2 by enzyme immunoassay before and after the treadmill run to exhaution test. With exercise, there was a significant change over time for both Pselectin (p = 0.00) and IL-6 (p = 0.00). No significant group by time interaction was seen in pre-post concentration of P-selectin (p = 0.37) or IL-6 (p = 0.43). There was however a significant difference in pre-post concentration of IL-6 (p = 0.04) between those controls that displayed EIAH and those that did not develop EIAH. No significance was seen in asthmatics with respect to IL-6 and EIAH. Plasma concentrations of soluble Pselectin (p = 0.94) and IL-6 (p = 0.27) were not significantly different between groups. No statistical significance was apparent in P-selectin and hypoxemia between groups. The incidence of EIAH in an asthmatic population is not significantly higher in asthmatics when compared to controls. The increased levels in plasma P-selectin and IL- 6 after intense exercise may represent endothelial dysfunction. However, increased plasma level of P-selectin and IL-6 were seen in both groups and therefore cannot support the hypothesis that asthmatics show increased levels of inflammatory markers due to lung damage from chronic-recurrent high stresses of breathing during exercise training.

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