Overconsumption of sugar-sweetened beverages has been implicated in the pathogenesis of CVD. The objective of the present study was to elucidate acute haemodynamic and microcirculatory responses to the ingestion of sugary drinks made from sucrose, glucose or fructose at concentrations similar to those often found in commercial soft drinks. In a randomised cross-over study design, twelve young healthy human subjects (seven men) ingested 500 ml tap water in which was dissolved 60 g of either sucrose, glucose or fructose, or an amount of fructose equivalent to that present in sucrose (i.e. 30 g fructose). Continuous cardiovascular monitoring was performed for 30 min before and at 60 min after ingestion of sugary drinks, and measurements included beat-to-beat blood pressure (BP) and impedance cardiography. Additionally, microvascular endothelial function testing was performed after iontophoresis of acetylcholine and sodium nitroprusside using laser Doppler flowmetry. Ingestion of fructose (60 or 30 g) increased diastolic and mean BP to a greater extent than the ingestion of 60 g of either glucose or sucrose (P< 0·05). Ingestion of sucrose and glucose increased cardiac output (CO; P< 0·05), index of contractility (P< 0·05) and stroke volume (P< 0·05), but reduced total peripheral resistance (TPR; P< 0·05), which contrasts with the tendency of fructose (60 and 30 g) to increase resistance. Microvascular endothelial function did not differ in response to the ingestion of various sugary drinks. In conclusion, ingestion of fructose, but not sucrose, increases BP in healthy human subjects. Although sucrose comprises glucose and fructose, its changes in TPR and CO are more related to glucose than to fructose.

We examined whether responder type groups reflecting patterns of hemodynamic reactivity might also differ in recovery responses. Cardiac output (CO), total peripheral resistance (TPR), systolic and diastolic blood pressure, heart rate, and Heather index were assessed at rest and during speech and cold pressor tasks in young adults. Participants (n = 152) were classified as myocardial, vascular, or mixed-mild responders based on CO and TPR responses to speech presentation. Vascular responders exhibited slower CO and TPR speech recovery than the myocardial and/or mixed-mild groups. Responder type differences in reactivity showed limited task-generalizability. The sustained vascular response pattern of the vascular group is consistent with that seen in hypertension. In light of associations of heightened TPR with markers of disease risk, this suggests potentially negative health implications for vascular responders.

The present study examined the hemodynamics underlying blood pressure elevations for evidence of a shift in the control of blood pressure during prolonged mental stress. Mean arterial pressure (MAP), cardiac output (CO), and total peripheral resistance (TPR) were measured at rest, during a 28-min mental arithmetic stress task, and during recovery, in 30 young healthy men and women. The stress task elicited a sustained increase in MAP: CO rose during the first half of the task but returned to baseline levels during the last quarter of the task, whereas TPR increased as the task progressed. When participants' hemodynamic reactions were classified as cardiac, vascular, or neither, there were more cardiac reactors early relative to late in the task, whereas there were more vascular reactors late relative to early. Thus, the sustained pressor response was initially supported mainly by cardiac mechanisms but subsequently by predominantly vascular mechanisms.

This study investigated the influences of both perceived control and physical effort on cardiovascular reactivity. Undergraduates (N = 32) played a video game task interrupted by aversive noise. Perceived control of the noise was manipulated by instructions indicating the presence or absence of a contingency between performance and noise presentations. Physical effort was manipulated by controlling the physical force required to perform the task. There was a significant main effect of control on systolic blood pressure (SBP) and total peripheral resistance (TPR), with both increasing more during low than high control conditions. The results suggest that high perceived control over aversive noise in an effortful task reduces SBP and TPR reactivity relative to low perceived control. The results are consistent with the idea that control buffers the reactivity associated with task performance under aversive conditions.

Previous studies demonstrated distinct cardiovascular patterns associated with threat and challenge appraisals for groups of participants. We extend these results by assessing whether appraisals continue to be associated with these cardiovascular response patterns within an individual as appraisals change. Participants completed four verbal mental arithmetic tasks for which they made appraisals before and after each task. Cardiac reactivity and total peripheral resistance (TPR) were calculated for the first and last minutes of each task, and the number of responses and percent correct were measured for each task. In line with our prediction, pretask appraisals were related to some task-related cardiac responses across the four tasks. In addition, task-related cardiovascular reactivity and behaviors both influenced appraisals following the task. Our findings suggest that an idiographic analysis of appraisals, cardiovascular physiology, and task-related behaviors provides a richer understanding of the appraisal process and reveals sex differences deserving further assessment.

A quantitative, theory-driven model of hemodynamics was developed, relating reactivity in blood pressure to orthogonal dimensions of “hemodynamic profile” and “compensation deficit,” which were derived from the (multiplicative) interaction of cardiac output and total peripheral resistance. A Finapres 2300e was used to estimate blood pressure, cardiac output, and total peripheral resistance in 100 healthy men and women during mental arithmetic and cold pressor tasks on two occasions. Results were consistent with model predictions. As predicted, cardiac output and peripheral resistance reactions were curvilinearly related, and blood pressure reactivity was strongly related to compensation deficit (r = .76–.89). Conversely, the orthogonally defined hemodynamic profile remained independent of blood pressure reactivity (r = .11 or less). The data show that the present model overcomes several difficulties and inconsistencies in previous attempts to obtain an independent measure of hemodynamic profile. The new model could help to elucidate sources of cardiovascular pathogenesis not suggested from the study of blood pressure reactivity alone.