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The acute effects of volume infusion on mechanisms and severity of exercise-induced arterial hypoxemia Zavorsky, Gerald Stanley

Abstract

Incomplete recruitment of pulmonary capillaries could shorten right-to-left ventricular red cell pulmonary transit time (PTT) and explain exercise-induced arterial hypoxemia (EIAH). Volume expansion could dilate and/or recruit pulmonary capillaries, lengthen PTT and improve gas exchange (reduce EIAH). The purpose of this study was to determine whether acute volume expansion using pentastarch changed EIAH and PTT during severe exercise. Twelve male endurance athletes ( VO[sub 2max] = 69.6 ± 7.4 ml • kg⁻¹ • min⁻¹; weight = 74.8 ± 6.0 kg; height = 180.6 ± 7.0 cm) performed 6.5 minutes constant, near-maximal cycling exercise (~92% VO[sub 2max]) on two different days. Seven subjects were classified as having EIAH [minimal arterial PO₂ ( PaO₂) during exercise < 90 mm Hg and/or alveolar-arterial oxygen pressure difference (AaDO₂) during the last 2.5 minutes of exercise > 25 mm Hg]. Pentastarch [(500 mL, 10%), Infusion condition, I] or placebo [(60 mL normal saline), non-infusion condition, N] were infused prior to exercise in a randomized, double-blind fashion. Arterial blood gases, pulmonary transit time, multigated acquisition technique (MUGA)-derived cardiac output (Q̇), and oxygen consumption (VO₂) were measured during exercise. Pentastarch increased plasma volume significantly (+460 ± 422 ml; P = 0.002; n = 12). PTT was measured during the third minute of exercise by first-pass radionuclide cardiography using centroid and deconvolution analysis, while cardiac output (Q) was measured via a count-based ratio method from MUGA technique. PaO₂ (N = 89.5 ± 9.0; I = 90.7 ± 7.7 mm Hg), AaDO₂ (N = 21.8 ± 6.1; I = 22.7 ± 6.8 mm Hg), and arterial oxyhemoglobin saturation [(%SaO₂) , N = 93.9 ± 2.4; I = 93.8 ± 1.6%] at minute three of exercise did not differ between conditions (P > 0.05; n = 12). PTT minute three of exercise was significantly greater in the infusion than non-infusion conditions [I = 2.75 ± 0.32 seconds; N = 2.45 ± 0.21 seconds (P = 0.002)]. Pulmonary blood volume was also greater in the infusion than non-infusion conditions [I = 1.35 ± 0.21; N = 1.22 ± 0.13 liters (P = 0.015)]. VO₂ (N = 4.56 ± 0.54; I = 4.57 ± 0.56 L • min⁻¹) and Q (N = 30.6 + 4.2; I = 30.2 + 3.9 L • min⁻¹) did not differ between conditions. PTT at minute three of exercise was not correlated with PaO₂, AaDO₂, or %SaO₂ in subjects with or without EIAH. However, PTT was correlated with cardiac index (r² = 0.22, P = 0.03) and pre-exercising white blood cell count in the circulating pool (r² = 0.31; P = 0.009) when combining data from both noninfusion and infusion conditions. We conclude that volume expansion does not change EIAH despite increasing PTT, and suggest that PTT (and thus perhaps pulmonary capillary transit time) is not a significant mechanism of EIAH. These results also provide evidence against a morphological limit in pulmonary capillary blood volume capacity during severe exercise.

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