Effect of nutritive and non-nutritive sweeteners on hemodynamic responses to acute stress: a randomized crossover trial in healthy women

Abstract Background The mechanisms by which chronic stress increases the risk of non-communicable diseases remain poorly understood. On one hand, chronic stress may increase systemic vascular resistance (SVR) and blood pressure, which may lead to blood vessels injury and altered myocardial perfusion. On the other hand, chronic stress may promote the overconsumption of sugar-containing foods and favor obesity. There is indeed evidence that sweet foods are preferentially consumed to alleviate stress responses. The effects of nutritive and non-nutritive sweeteners (NNS) on hemodynamic stress responses remain however largely unknown. Objective/design This study aimed at comparing the effects of sucrose-containing and NNS-containing drinks, as compared to unsweetened water, on hemodynamic responses to acute stress in twelve healthy female subjects. Acute stress responses were elicited by a 30-min mental stress (5-min Stroop’s test alternated with 5-min mental arithmetic) and a 3-min cold pressure test (CPT), each preceded by a resting baseline period. Hemodynamic stress responses were investigated by the repeated measurement of mean arterial pressure and the continuous monitoring of cardiac output by thoracic electrical bioimpedance measurement. SVR was selected as a primary outcome because it is a sensitive measure of hemodynamic responses to acute stress procedures. Results With all three drinks, SVR were not changed with mental stress (P = 0.437), but were increased with CPT (P = 0.045). Both mental stress and CPT increased mean arterial pressure and heart rate (all P < 0.001). Cardiac output increased with mental stress (P < 0.001) and remained unchanged with CPT (P = 0.252). No significant differences in hemodynamic responses were observed between water, sucrose and NNS (stress × condition, all P > 0.05). Conclusions These results demonstrate that sucrose and NNS do not alter hemodynamic responses to two different standardized acute stress protocols.

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Effects of mental stress on autonomic cardiac modulation during weightlessness

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00865.2009 ◽

2010 ◽

Vol 298 (1) ◽

pp. H202-H209 ◽

Cited By ~ 14

Author(s):

André E. Aubert ◽

Bart Verheyden ◽

Constantin d′Ydewalle ◽

Frank Beckers ◽

Omer Van den Bergh

Keyword(s):

Heart Rate ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

High Frequency ◽

Mental Stress ◽

Mental Arithmetic ◽

Low Frequency ◽

Arithmetic Task ◽

Mental Arithmetic Task ◽

Normalized Units

Sustained weightlessness affects all body functions, among these also cardiac autonomic control mechanisms. How this may influence neural response to central stimulation by a mental arithmetic task remains an open question. The hypothesis was tested that microgravity alters cardiovascular neural response to standardized cognitive load stimuli. Beat-to-beat heart rate, brachial blood pressure, and respiratory frequency were collected in five astronauts, taking part in three different short-duration (10 to 11 days) space missions to the International Space Station. Data recording was performed in supine position 1 mo before launch; at days 5 or 8 in space; and on days 1, 4, and 25 after landing. Heart rate variability (HRV) parameters were obtained in the frequency domain. Measurements were performed in the control condition for 10 min and during a 5-min mental arithmetic stress task, consisting of deducting 17 from a four-digit number, read by a colleague, and orally announcing the result. Our results show that over all sessions (pre-, in-, and postflight), mental stress induced an average increase in mean heart rate (Δ7 ± 1 beats/min; P = 0.03) and mean arterial pressure (Δ7 ± 1 mmHg; P = 0.006). A sympathetic excitation during mental stress was shown from HRV parameters: increase of low frequency expressed in normalized units (Δ8.3 ± 1.4; P = 0.004) and low frequency/high frequency (Δ1.6 ± 0.3; P = 0.001) and decrease of high frequency expressed in normalized units (Δ8.9 ± 1.4; P = 0.004). The total power was not influenced by mental stress. No effect of spaceflight was found on baseline heart rate, mean arterial pressure, and HRV parameters. No differences in response to mental stress were found between pre-, in-, and postflight. Our findings confirm that a mental arithmetic task in astronauts elicits sympathovagal shifts toward enhanced sympathetic modulation and reduced vagal modulation. However, these responses are not changed in space during microgravity or after spaceflight.

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Melatonin attenuates the skin sympathetic nerve response to mental stress

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00470.2013 ◽

2013 ◽

Vol 305 (9) ◽

pp. H1382-H1386 ◽

Cited By ~ 14

Author(s):

Matthew D. Muller ◽

Charity L. Sauder ◽

Chester A. Ray

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Sympathetic Nerve ◽

Mental Stress ◽

Sympathetic Nerve Activity ◽

Mental Arithmetic ◽

Experimental Testing ◽

Double Blind ◽

Before And After ◽

The Mean

Melatonin attenuates muscle sympathetic nerve responses to sympathoexcitatory stimuli, but it is unknown whether melatonin similarly attenuates reflex changes in skin sympathetic nerve activity (SSNA). In this double-blind, placebo-controlled, crossover study, we tested the hypothesis that melatonin (3 mg) would attenuate the SSNA response to mental stress (mental arithmetic). Twelve healthy subjects underwent experimental testing on two separate days. Three minutes of mental stress occurred before and 45 min after ingestion of melatonin (3 mg) or placebo. Skin temperature was maintained at 34°C. Reflex increases in SSNA (peroneal nerve), mean arterial pressure, and heart rate (HR) to mental stress before and after melatonin were determined. Melatonin lowered HR (pre, 66 ± 3 beats/min; and post, 62 ± 3 beats/min, P = 0.046) and SSNA (pre, 14,282 ± 3,706 arbitrary units; and post, 9,571 ± 2,609 arbitrary units, P = 0.034) at rest. In response to mental stress, SSNA increases were significantly attenuated following melatonin ingestion (second minute, 114 ± 30 vs. 74 ± 14%; and third minute, 111 ± 29 vs. 54 ± 12%, both P < 0.05). The mean arterial pressure increase to mental stress was blunted in the third minute (20 ± 2 vs. 17 ± 2 mmHg, P = 0.032), and the HR increase was blunted in the first minute (33 ± 3 vs. 29 ± 3 beats/min, P = 0.034) after melatonin. In summary, exogenous melatonin attenuates the SSNA response to mental stress.

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Sympathetic neural reactivity to mental stress in offspring of hypertensive parents: 20 years revisited

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00378.2016 ◽

2016 ◽

Vol 311 (2) ◽

pp. H426-H432 ◽

Cited By ~ 12

Author(s):

Ida T. Fonkoue ◽

Min Wang ◽

Jason R. Carter

Keyword(s):

Mean Arterial Pressure ◽

Arterial Pressure ◽

Mental Stress ◽

Sympathetic Nerve Activity ◽

Mental Arithmetic ◽

Muscle Sympathetic Nerve Activity ◽

Baseline Heart Rate ◽

History Of ◽

Family History Of Hypertension ◽

Neural Reactivity

A number of recent studies have highlighted large interindividual variability of muscle sympathetic nerve activity (MSNA) responsiveness to mental stress in humans. The purpose of this study was to examine blood pressure (BP) and MSNA responsiveness to mental stress in a large and generalizable cohort of young adults with and without family history of hypertension (FHH). We hypothesized that subjects with FHH would demonstrate greater sympathoexcitation to mental stress than subjects without FHH. A total of 87 subjects (55 men and 32 women, 18–40 yr of age) from recently published ( n = 45) and ongoing ( n = 42) studies were examined; 57 subjects (19 with FHH and 38 without FHH) had complete MSNA recordings at baseline. Heart rate (HR), BP, and MSNA were recorded during 5 min of supine rest and 5 min of mental stress (mental arithmetic). Resting MSNA and HR were not statistically different between subjects with and without FHH ( P > 0.05), whereas resting mean arterial pressure was higher in subjects with FHH (86 ± 2 vs. 80 ± 1 mmHg, P < 0.05). Mental stress increased MSNA in subjects with FHH (Δ5 ± 1 bursts/min), but not in subjects without FHH [Δ1 ± 1 burst/min, P < 0.01 (time × group)]. Mental stress increased mean arterial pressure (Δ12 ± 1 and Δ10 ± 1 mmHg, P < 0.001) and HR (Δ19 ± 2 and Δ16 ± 2 beats/min, P < 0.001) in subjects with and without FHH, but these increases were not different between groups [ P ≥ 0.05 (time × group)]. MSNA and BP reactivity to mental stress were not correlated in either group. In conclusion, FHH was associated with heightened MSNA reactivity to mental stress, despite a dissociation between MSNA and BP responsiveness.

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Cardiovascular and sympathoadrenal responses to mental stress: influence of beta-blockade

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.6.h1443 ◽

1988 ◽

Vol 255 (6) ◽

pp. H1443-H1451 ◽

Cited By ~ 14

Author(s):

U. Freyschuss ◽

P. Hjemdahl ◽

A. Juhlin-Dannfelt ◽

B. Linde

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Mental Stress ◽

Beta Blockade ◽

Rate Dependent ◽

Before And After ◽

Peripheral Vasodilatation ◽

Arterial Plasma

Cardiovascular, sympathoadrenal, and subjective responses to mental stress induced by a color-word conflict test (CWT) were studied in 30 healthy males before and after intravenous administration of either placebo, beta 1-blockade by metoprolol (0.15 mg/kg), or nonselective beta-blockade by propranolol (0.15 mg/kg). CWT responses were reproducible. Mean arterial pressure increased by 20%. A mainly heart rate-dependent 65% increase in cardiac output (thermodilution) was associated with 25% decreases of both systemic (SVR) and calf vascular (CVR) resistances. Arterial plasma epinephrine (Epi) was doubled, and norepinephrine (NE) increased by 50%. Self-evaluated stress score correlated positively with changes in cardiac output and inversely with changes in SVR during CWT. Both metoprolol and propranolol halved heart rate responses; whereas increases in mean arterial pressure, Epi, and NE were uninfluenced. Metoprolol reduced the increase in stroke volume, and propranolol abolished it. SVR and CVR responses were attenuated by metoprolol and abolished by propranolol. The results suggest that mental stress accelerates the heart through neurogenic mechanisms and that peripheral vasodilatation is achieved through the concerted actions of reduced vasoconstrictor activity and elevated circulating Epi.

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Evidence that meal fat content does not impact hemodynamic reactivity to or recovery from repeated mental stress tasks

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2014-0111 ◽

2014 ◽

Vol 39 (11) ◽

pp. 1314-1321

Author(s):

Veronica J. Poitras ◽

David J. Slattery ◽

Brendon J. Gurd ◽

Kyra E. Pyke

Keyword(s):

Stress Responses ◽

Mental Stress ◽

Stress Reactivity ◽

Mental Arithmetic ◽

Peripheral Resistance ◽

Fat Content ◽

Hemodynamic Stress ◽

Hemodynamic Reactivity ◽

The Impact ◽

Fat Meal

The magnitude (reactivity) and duration (recovery) of hemodynamic stress responses are predictive of cardiovascular risk, and fat intake has been shown to enhance hemodynamic reactivity to psychological stress tasks. The objective of this study was to determine the impact of a high-fat meal (HFM) on the magnitude and stability of hemodynamic stress reactivity and recovery. This was assessed by: (i) the peak changes from baseline to during stress for heart rate (HR); mean, systolic, and diastolic blood pressure; cardiac output; and total peripheral resistance; and (ii) the residual arousal in hemodynamic parameters at 2 points post-stress (“early” and “late” recovery). On different days, 10 healthy males (aged 23.2 ± 3.3 years) consumed either a HFM (54 g fat) or low-fat meal (LFM; 0 g fat) (∼1000 calories each), followed by 4 hourly 10-min stress tasks (mental arithmetic and speech tasks). Pre-stress (baseline) parameters did not differ between HFM and LFM conditions (all P > 0.05). Plasma triglycerides were greater following the HFM versus the LFM (P = 0.023). No reactivity or recovery parameters differed between meals (all P > 0.05). Stress reactivity and recovery parameters were stable over the 4 stress tasks (main effects of time, all P > 0.05), with the exception of HR (P < 0.05). Contrary to previous reports, meal fat content did not impact hemodynamic reactivity to laboratory stressors. These data also provide the first evidence that meal fat content does not impact hemodynamic recovery from repeated mental stress tasks.

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Central and peripheral hemodynamic responses to passive limb movement: the role of arousal

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00851.2011 ◽

2012 ◽

Vol 302 (1) ◽

pp. H333-H339 ◽

Cited By ~ 16

Author(s):

Massimo Venturelli ◽

M. Amann ◽

J. McDaniel ◽

J. D. Trinity ◽

A. S. Fjeldstad ◽

...

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Stroke Volume ◽

Visual Feedback ◽

Passive Movement ◽

Afferent Feedback ◽

Hemodynamic Responses

The exact role of arousal in central and peripheral hemodynamic responses to passive limb movement in humans is unclear but has been proposed as a potential contributor. Thus, we used a human model with no lower limb afferent feedback to determine the role of arousal on the hemodynamic response to passive leg movement. In nine people with a spinal cord injury, we compared central and peripheral hemodynamic and ventilatory responses to one-leg passive knee extension with and without visual feedback (M+VF and M-VF, respectively) as well as in a third trial with no movement or visual feedback but the perception of movement (F). Ventilation (V̇e), heart rate, stroke volume, cardiac output, mean arterial pressure, and leg blood flow (LBF) were evaluated during the three protocols. V̇e increased rapidly from baseline in M+VF (55 ± 11%), M-VF (63 ± 13%), and F (48 ± 12%) trials. Central hemodynamics (heart rate, stroke volume, cardiac output, and mean arterial pressure) were unchanged in all trials. LBF increased from baseline by 126 ± 18 ml/min in the M+VF protocol and 109 ± 23 ml/min in the M-VF protocol but was unchanged in the F protocol. Therefore, with the use of model that is devoid of afferent feedback from the legs, the results of this study reveal that, although arousal is invoked by passive movement or the thought of passive movement, as evidenced by the increase in V̇e, there is no central or peripheral hemodynamic impact of this increased neural activity. Additionally, this study revealed that a central hemodynamic response is not an obligatory component of movement-induced LBF.

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Increased cardiac output following occlusion of the descending thoracic aorta in dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1982.243.1.r152 ◽

1982 ◽

Vol 243 (1) ◽

pp. R152-R158 ◽

Cited By ~ 3

Author(s):

J. K. Stene ◽

B. Burns ◽

S. Permutt ◽

P. Caldini ◽

M. Shanoff

Keyword(s):

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Thoracic Aorta ◽

Vascular System ◽

Superior Vena ◽

Vena Cava ◽

Right Atrial ◽

Mean Systemic Pressure ◽

Extracorporeal Bypass

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.

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