Abstract
PURPOSE: Using an acute bout of dynamic exercise the present study sought to determine the role of a redox-mediated regulation of post-exercise hemodynamics in men.
METHODS: Nine pre-hypertensive males, MAP = 106 ? 5 mmHg not on medication, were studied following 30-minutes of cycle exercise at 70% maximal oxygen consumption. The subjects were followed post-exercise for 2-hours. Left ventricular hemodynamics were assessed via echocardiography and systemic vascular resistance (SVR)/vascular conductance (SVC) determined by the quotient of MABP/ and /MABP, respectively. Peripheral venous blood was sampled from an antecubital vein pre-, immediately post-, 1-hour post- (P1) and 2-hours post- (P2) exercise and metabolite concentrations were corrected for plasma volume shifts. Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH). Lipid soluble antioxidant levels were measured using HPLC, whilst Ascorbic acid was assayed by fluorimetry. RESULTS: Hyperoxic exercise blunted post-exercise hemodynamics by significantly attenuating the reductions (from normoxic baseline) 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 in ascorbic acid concentration by P2 (Pandlt;0.05).
METHODS: Nine pre-hypertensive males, MAP = 106 ? 5 mmHg not on medication, were studied following 30-minutes of cycle exercise at 70% maximal oxygen consumption. The subjects were followed post-exercise for 2-hours. Left ventricular hemodynamics were assessed via echocardiography and systemic vascular resistance (SVR)/vascular conductance (SVC) determined by the quotient of MABP/ and /MABP, respectively. Peripheral venous blood was sampled from an antecubital vein pre-, immediately post-, 1-hour post- (P1) and 2-hours post- (P2) exercise and metabolite concentrations were corrected for plasma volume shifts. Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH). Lipid soluble antioxidant levels were measured using HPLC, whilst Ascorbic acid was assayed by fluorimetry. RESULTS: Hyperoxic exercise blunted post-exercise hemodynamics by significantly attenuating the reductions (from normoxic baseline) 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 in ascorbic acid concentration by P2 (Pandlt;0.05).
| Original language | English |
|---|---|
| Title of host publication | N/A |
| Publication status | Published - 1 Jun 2010 |
| Event | American College of Sports Medicine, Baltimore - Baltimore, USA Duration: 1 Jun 2010 → 1 Jun 2010 |
Conference
| Conference | American College of Sports Medicine, Baltimore |
|---|---|
| Period | 1/06/10 → 1/06/10 |
Keywords
- oxidative stress
- post-exercise haemodynamics
- oxygen tension