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Time course and mechanisms of hemoconcentration in response to mental stress
Dolf de Boer1, Christopher Ring, Douglas Carroll
1Behavioural Medicine Group, School of Sport and Exercise Sciences, University of Birmingham, B15 2TT Birmingham, UK. dxd033@bham.ac.uk
Hemoconcentration with mental stress exposure may be involved in the triggering of acute cardiovascular events. In the present study, hematocrit was measured repeatedly at baseline, during a 4 min mental stress task and during 20 min of recovery. Blood was sampled every 1-2 min throughout. Blood pressure, heart rate and R-wave to pulse interval, a measure of cardiac contractility, were measured with the same periodicity. The stress task elicited a 1.3% increase in hematocrit, which was sustained with full return to baseline level occurring only after 16 min of recovery. Between-subject correlations between hematocrit and hemodynamic activity were low. Aggregate within-subject coefficients were more impressive; the temporal profile of hematocrit correlated significantly with all hemodynamic variables. Similar within-subject analyses indicated that whereas cardiac contractility was correlated with hematocrit both during stress-related increase and subsequent recovery, blood pressure was related to hematocrit only during the increase. This suggests that stress-induced hemoconcentration may driven by different mechanisms than those which underlie its recovery.
Hemoconcentration with mental stress exposure may be involved in the triggering of acute cardiovascular events. In the present study, hematocrit was measured repeatedly at baseline, during a 4 min mental stress task and during 20 min of recovery. Blood was sampled every 1-2 min throughout. Blood pressure, heart rate and R-wave to pulse interval, a measure of cardiac contractility, were measured with the same periodicity. The stress task elicited a 1.3% increase in hematocrit, which was sustained with full return to baseline level occurring only after 16 min of recovery. Between-subject correlations between hematocrit and hemodynamic activity were low. Aggregate within-subject coefficients were more impressive; the temporal profile of hematocrit correlated significantly with all hemodynamic variables. Similar within-subject analyses indicated that whereas cardiac contractility was correlated with hematocrit both during stress-related increase and subsequent recovery, blood pressure was related to hematocrit only during the increase. This suggests that stress-induced hemoconcentration may driven by different mechanisms than those which underlie its recovery.
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