S Ogoh1, M K Dalsgaard, N H Secher, P B Raven. 1. Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA. sogoh@hsc.unt.edu
Abstract
AIMS: Cardiac failure and ischaemic heart disease patients receive standard of care cardiac beta(1)-adrenergic blockade medication. Such medication reduces cardiac output and cerebral blood flow. It is unknown whether the beta(1)-adrenergic blockade-induced reduction of cardiac output in the presence of an exercise-induced reduction in cardiac-arterial baroreflex gain affects cerebral blood flow variability. This study evaluated the influence of cardiac output variability on beat-to-beat middle cerebral arterymean blood velocity (MCA V(mean)) during exercise with and without cardiac beta(1)-adrenergic blockade. METHODS:Eight men (22 +/- 1 years; mean +/- SE) performed 15 min bouts of moderate (105 +/- 11 W) and heavy (162 +/- 8 W) intensity cycling before and after cardio-selective beta(1)-adrenergic blockade (0.15 mg kg(-1) metoprolol). The relationship between changes in cardiac output or mean arterial pressure (MAP) and MCA V(mean) as well as cardiac-arterial baroreflex gain were evaluated using transfer function analysis. RESULTS: Both exercise intensities decreased the low frequency (LF) transfer function gain between cardiac output and MCA V(mean) (P < 0.05) with no significant influence of beta(1)-blockade. In contrast, the LF transfer function gain between MAP and MCA V(mean) remained stable also with no significant influence of metoprolol (P > 0.05). The LF transfer function gain between MAP and HR, an index of cardiac-arterial baroreflex gain, decreased from rest to heavy exercise with and without beta(1)-blockade (P < 0.05). CONCLUSION: These findings suggest that the exercise intensity related reduction in cardiac-arterial baroreflex function at its operating point does not influence the dynamic control of MCA V(mean), even when the ability of exercise-induced increase in cardiac output is reduced by cardiac beta(1)-adrenergic blockade.
RCT Entities:
AIMS: Cardiac failure and ischaemic heart diseasepatients receive standard of care cardiac beta(1)-adrenergic blockade medication. Such medication reduces cardiac output and cerebral blood flow. It is unknown whether the beta(1)-adrenergic blockade-induced reduction of cardiac output in the presence of an exercise-induced reduction in cardiac-arterial baroreflex gain affects cerebral blood flow variability. This study evaluated the influence of cardiac output variability on beat-to-beat middle cerebral artery mean blood velocity (MCA V(mean)) during exercise with and without cardiac beta(1)-adrenergic blockade. METHODS: Eight men (22 +/- 1 years; mean +/- SE) performed 15 min bouts of moderate (105 +/- 11 W) and heavy (162 +/- 8 W) intensity cycling before and after cardio-selective beta(1)-adrenergic blockade (0.15 mg kg(-1) metoprolol). The relationship between changes in cardiac output or mean arterial pressure (MAP) and MCA V(mean) as well as cardiac-arterial baroreflex gain were evaluated using transfer function analysis. RESULTS: Both exercise intensities decreased the low frequency (LF) transfer function gain between cardiac output and MCA V(mean) (P < 0.05) with no significant influence of beta(1)-blockade. In contrast, the LF transfer function gain between MAP and MCA V(mean) remained stable also with no significant influence of metoprolol (P > 0.05). The LF transfer function gain between MAP and HR, an index of cardiac-arterial baroreflex gain, decreased from rest to heavy exercise with and without beta(1)-blockade (P < 0.05). CONCLUSION: These findings suggest that the exercise intensity related reduction in cardiac-arterial baroreflex function at its operating point does not influence the dynamic control of MCA V(mean), even when the ability of exercise-induced increase in cardiac output is reduced by cardiac beta(1)-adrenergic blockade.