Prevalence Of Eih Depends On Temperature Corrections Applied But Is Without Effect On Vo2 Peak.

Abstract

Exercise-induced hypoxemia (EIH) is reported to occur in ∼50% of trained athletes, with much evidence suggesting a reduction in maximal aerobic power. While PaO2 is normally measured at 37°C and must be corrected for any exercise-induced hyperthermia, more than half of previous studies have failed to do so, or have used rectal temperature, which is an unreliable index. Hence the true prevalence of the phenomenon is uncertain. Importantly, none has examined the effects of any hypoxemia on the arterial oxygen content (CaO2) of blood being delivered to exercising muscle. PURPOSE: To determine the effect of correcting PaO2 values for temperatures measured simultaneously in the rectum, arterial blood, the oesophagus and exercising muscle on CaO2 and the prevalence of EIH during incremental treadmill exercise to exhaustion. METHODS: A group of 23 trained males (age 26±5 yrs; VO2peak 65.2±1.6 mL·kg-1·min-1) performed incremental treadmill exercise to VO2 peak while arterial blood samples were taken every 2 min and CaO2 and PaO2, measured at 37°C, corrected for simultaneous measurements of rectal, arterial blood, oesophageal and exercising muscle temperatures. Prevalence of EIH in each case was determined using the commonly accepted definition of DPaO2 across exercise ≥ 10 mmHg. RESULTS: When uncorrected for ambient temperature DPaO2 was -20.8 ± 5.0 mmHg (mean ± SD) giving an EIH prevalence of 96% and CaO2 fell significantly. When corrected for rectal temperature DPaO2 was -14.7 ± 7.8 mmHg and prevalence 73%; corrected for blood temperature DPaO2 was - 7.7 ± 6.5 mmHg and prevalence 35%; corrected for oesophageal temperature DPaO2 was -8.1 ± 7.7 mmHg and prevalence 48%; corrected for active muscle temperature DPaO2 was +8.2 ± 7.8 mmHg and prevalence 0%. There were no significant changes in CaO2 when rectal, blood, oesophageal and muscle temperature corrections were applied. Unsurprisingly there were no correlations between DPaO2 and VO2 peak. CONCLUSIONS: While there was a significant DPaO2 at the site of oxygen loading (oesophageal/pulmonary artery) with an EIH prevalence of 48% this fell to zero at the site of oxygen unloading (active muscle). Site specific corrections for ambient temperature indicated that any hypoxemia is without effect on muscle oxygen delivery and hence maximal aerobic power.