Hyperoxia negatively impacts on post exercise hemodynamic status in the human whereas the effect on coagulation is not clear. 9 males (50 ±10 years) were studied for 2-hours following 30-minutes of cycle exercise at 70% maximal oxygen consumption in hyperoxia (50% O2) and normoxia (21% O2). Subjects were followed post-exercise for 2-hours. Echocardiography assessed cardiac output ( ) determined systemic vascular resistance (SVR) [MAP/ ] and vascular conductance (SVC) [ /MAP]. Blood was sampled from an antecubital vein pre-, immediately post-, 1-hour (P1) and 2-hours post- (P2) exercise and corrected for hemoconcentration/dilution. Plasma was assayed for fibrinogen, international normalized ratio (INR), activated partial thromboplastin time (aPTT), activated partial thromboplastin time ratio (aPTTr), and prothrombin time (PT) by coagulometry. Lipid hydroperoxides (LOOH) were determined spectrophotometrically whilst blood was also assayed for selective antioxidants (HPLC and fluorimetry). Hyperoxic exercise blunted post-exercise hemodynamics by significantly attenuating the reductions in SVR and MAP (Pandlt;0.05). Ascorbic acid was elevated across the hyperoxic exercise trial in comparison to the normoxic condition (Pandlt;0.05) with a selective increase by P2 (Pandlt;0.05). Hyperoxic exercise has a deleterious effect on post-exercise hemodynamics but not hemostasis when corrected for plasma volume change.
|Statws||Cyhoeddwyd - 4 Ebrill 2011|
|Digwyddiad|| Experimental Biology, Washington DC - Washington USA|
Hyd: 4 Ebrill 2011 → 4 Ebrill 2011
|Cynhadledd||Experimental Biology, Washington DC|
|Cyfnod||4/04/11 → 4/04/11|