Hyperoxic exercise attenuates post-exercise vasodilatation independent of reduced NO (New et al, 2008) but coincident with a diminished bioavailability of atrial natriuretic peptide (New et al, 2009). The present study investigated the influence of adrenaline (AD) and nor-adrenaline (NA) on post-exercise haemodynamics. 9 males, mean arterial pressure (MAP) = 106 ± 5 mmHg (50 ± 10 yr), not on medication, were studied 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. Left ventricular haemodynamics were assessed via echocardiography and systemic vascular resistance (SVR)/vascular conductance determined by the quotient of MAP/Q and Q/MAP, 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 corrected for plasma volume shifts. AD and NA were determined via reverse-phase high-performance liquid chromatograpy using electrochemical detection. Data were analysed with a two-way repeated measures ANOVA and post-hoc Bonferroni-corrected paired samples T-tests. Hyperoxic exercise blunted post-exercise haemodynamics by attenuating the reductions (from normoxic baseline) in SVR (21 ± 20.7 vs. 38 ± 19.3 %, 11 ± 8.2 vs. 19 ± 5.5 % and 11 ± 8.9 vs. 15 ± 9.6%, P<0.05 vs. normoxic exercise at post, P1 and P2 respectively) and MAP (3 ± 4 [elevation] vs. 0.5 ± 5 mmHg, 3 ± 3 vs. 6 ± 4 mmHg, 3 ± 3 vs. 4 ± 3 mmHg, P<0.05 vs. normoxic exercise at post, P1 and P2 respectively) (Paired samples T-tests). AD and NA concentrations were invariant between conditions P>0.05, Paired samples T-tests; Table 1). These results indicate that an augmented adrenergic response is not a principle governor of the attenuated vasodilatation. Whether changes in alpha- or beta-receptor sensitivity play a role requires further investigation, although, it appears that the deleterious influence of hyperoxia on post-exercise haemodynamics has non-adrenergic origins.
University College Dublin (2009) Proc Physiol Soc 15, PC34
Poster Communications: Regulation of Post-Exercise Haemodynamics Following Hyperoxia in Man: Role of Adrenergic Vasoconstriction
K. J. New1, B. Davies5, J. Hooper3, C. Templeton4, G. Ellis4, D. M. Bailey2,5
1. Exercise Physiology, Swansea Metropolitan University, Swansea, United Kingdom. 2. Neurovascular Laboratory, University of Glamorgan, Pontypridd, United Kingdom. 3. Clinical Biochemistry, Royal Brompton Hospital, London, United Kingdom. 4. Cardiology, Royal Glamorgan Hospital, Llantrisant, United Kingdom. 5. Health and Exercise Science, University of Glamorgan, Pontypridd, United Kingdom.
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Table 1. Systemic Venous Concentration of AD and NA<#13> FIO2, fraction of inspired oxygen. Values are mean &#177; S.D.; two-way repeated measures ANOVA. n=9 for each group.
Where applicable, experiments conform with Society ethical requirements.