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Arterial hypoxemia and performance during intense exercise Koskolou, Maria D.

Abstract

A substantial decrease in percent arterial hemoglobin saturation (%SaC₂) has been observed in some highly aerobically trained athletes during intense exercise [≥ 90% of maximal oxygen uptake (V0₂[formula omitted]) or oxygen uptake (VO₂) ≥ 3.5 1‧minˉ¹] at sea level, and a reduction in %Sa0₂ has been associated with impaired performance. In order to explore the level of hypoxemia which is sufficient to impair maximal performance, 7 well-trained male cyclists (V0₂[formula omitted] ≥ 60 ml‧kgˉ¹‧minˉ¹ or V0₂[formula omitted] ≥ 5 1‧minˉ¹) who did not develop exercise-induced hypoxemia performed a 5-min performance cycle test to exhaustion at maximal intensity as controlled by the subject, under three experimental conditions: normoxemia (%SaO₂ > 94%), and artificially induced mild (%SaO₂ = 87±1%) and moderate (%SaO₂ = 90±1%) hypoxemia. %SaO₂ was continuously measured using an ear oximeter. In the two hypoxemic conditions, pure N₂ was added to the inspired air throughout the performance test according to the oximeter readings so as to achieve the desired hypoxemic level averaged over the 5-min period. Performance was evaluated as the total work output (Worktot) performed in the 5-min cycle test. Heart rate and ventilatory parameters were measured continuously during the test. ANOVA for repeated measures was used to compare differences in the results among the three experimental conditions. Performance progressively decreased with decreasing %SaO₂ (mean Worktot = 107.40 kJ, 104.07 kJ, and 102.52 kJ, under normoxemia, mild, and moderate hypoxemia, respectively), but only performance in the moderate hypoxemia condition was significantly different than normoxemia (p = 0.0216). Mean heart rate (HR) was similar in the three experimental conditions (p = 0.9536). Similarly, mean VO₂ was not significantly different among conditions (p = 0.1751). However, end-tidal partial pressure of CO₂ (PETCO₂) was significantly lower (p = 0.0053) during moderate hypoxemia compared with normoxemia, and VE/VCO₂ was significantly higher (p = 0.0052) in both hypoxemic conditions when compared with normoxemia, indicating hyperventilation possibly compensating for increasing metabolic acidosis during hypoxemia. It is concluded that maximal performance capacity is significantly impaired in highly trained cyclists working under an arterial oxyhemoglobin saturation level of 87% but not under a milder desaturation level of 90%. Since VO₂ was not different among the experimental conditions, the reduction in maximal performance capacity is possibly related to a worsening of the metabolic acidosis elicited by hypoxemia.

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