scholarly journals Total sleep deprivation alters cardiovascular reactivity to acute stressors in humans

2012 ◽  
Vol 113 (6) ◽  
pp. 903-908 ◽  
Author(s):  
Huan Yang ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Joseph P. DellaValla ◽  
Jason R. Carter
Keyword(s):  
Sex Differences ◽  
Sleep Deprivation ◽  
Cardiovascular Reactivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Epidemiological Studies ◽  
Total Sleep Deprivation ◽  
Increased Risk ◽  
Forearm Vascular Conductance

Exaggerated cardiovascular reactivity to mental stress (MS) and cold pressor test (CPT) has been linked to increased risk of cardiovascular disease. Recent epidemiological studies identify sleep deprivation as an important risk factor for hypertension, yet the relations between sleep deprivation and cardiovascular reactivity remain equivocal. We hypothesized that 24-h total sleep deprivation (TSD) would augment cardiovascular reactivity to MS and CPT and blunt the MS-induced forearm vasodilation. Because the associations between TSD and hypertension appear to be stronger in women, a secondary aim was to probe for sex differences. Mean arterial pressure (MAP), heart rate (HR), and muscle sympathetic nerve activity (MSNA) were recorded during MS and CPT in 28 young, healthy subjects (14 men and 14 women) after normal sleep (NS) and 24-h TSD (randomized, crossover design). Forearm vascular conductance (FVC) was recorded during MS. MAP, FVC, and MSNA ( n = 10) responses to MS were not different between NS and TSD (condition × time, P > 0.05). Likewise, MAP and MSNA ( n = 6) responses to CPT were not different between NS and TSD (condition × time, P > 0.05). In contrast, increases in HR during both MS and CPT were augmented after TSD (condition × time, P ≤ 0.05), and these augmented HR responses persisted during both recoveries. When analyzed for sex differences, cardiovascular reactivity to MS and CPT was not different between sexes (condition × time × sex, P > 0.05). We conclude that TSD does not significantly alter MAP, MSNA, or forearm vascular responses to MS and CPT. The augmented tachycardia responses during and after both acute stressors provide new insight regarding the emerging links among sleep deprivation, stress, and cardiovascular risk.

scholarly journals Role of the ovarian cycle on neural cardiovascular control in sleep-deprived women

2015 ◽  
Vol 118 (4) ◽  
pp. 419-426
Author(s):  
Huan Yang ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Jason R. Carter
Keyword(s):  
Cardiovascular Reactivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Premenopausal Women ◽  
Cold Pressor ◽  
Ovarian Cycle ◽  
Resting Blood Pressure ◽  
Forearm Vascular Conductance ◽  
Resting Muscle

The midluteal (ML) phase of the ovarian cycle is often sympathoexcitatory compared with the early follicular (EF) phase. We recently reported that 24-h total sleep deprivation (TSD) augmented cardiovascular reactivity in both men and women, but that sex differences existed in resting muscle sympathetic nerve activity (MSNA) responses to TSD. In the present study, we hypothesized increased resting MSNA and augmented cardiovascular reactivity to acute laboratory stressors during the ML phase in sleep-deprived women. Heart rate (HR), mean arterial pressure (MAP), forearm vascular conductance (FVC), and MSNA were measured in 14 eumenorrheic women (age, 20 ± 1 yr) during 10 min supine rest, 5 min mental stress (MS) trial, and 2 min cold pressor test (CPT) trial. Subjects were tested twice after TSD: once during EF phase and once during ML phase (randomized, crossover design). Estradiol (29 ± 2 vs. 63 ± 8 pg/ml, P = 0.001) and progesterone (1.6 ± 0.2 vs. 4.4 ± 0.7 ng/ml, P = 0.002) were elevated during the ML phase. Resting supine MAP (75 ± 2 vs. 72 ± 1 mmHg, P = 0.042) was lower during the ML phase. In contrast, resting supine HR, MSNA, and FVC were not significantly different between EF and ML phases. MAP, HR and FVC reactivity to MS were not statistically different between the EF and ML phases. Similarly, MAP and HR reactivity to CPT were not different between the ovarian phases. Contrary to our original hypothesis, the ML phase was not associated with sympathoexcitation or exaggerated cardiovascular reactivity in sleep-deprived premenopausal women. However, our data reveal elevated resting blood pressure during the EF phase in sleep-deprived women.

scholarly journals Sex differences in the modulation of vasomotor sympathetic outflow during static handgrip exercise in healthy young humans

2011 ◽  
Vol 301 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
Sara S. Jarvis ◽  
Tiffany B. VanGundy ◽  
M. Melyn Galbreath ◽  
Shigeki Shibata ◽  
Kazunobu Okazaki ◽  
...  
Keyword(s):  
Sex Differences ◽  
Neural Control ◽  
Fiber Type ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Static Exercise ◽  
Burst Frequency ◽  
Efferent Pathway

Sex differences in sympathetic neural control during static exercise in humans are few and the findings are inconsistent. We hypothesized women would have an attenuated vasomotor sympathetic response to static exercise, which would be further reduced during the high sex hormone [midluteal (ML)] vs. the low hormone phase [early follicular (EF)]. We measured heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) in 11 women and 10 men during a cold pressor test (CPT) and static handgrip to fatigue with 2 min of postexercise circulatory arrest (PECA). HR increased during handgrip, reached its peak at fatigue, and was comparable between sexes. BP increased during handgrip and PECA where men had larger increases from baseline. Mean ± SD MSNA burst frequency (BF) during handgrip and PECA was lower in women (EF, P < 0.05), as was ΔMSNA-BF smaller (main effect, both P < 0.01). ΔTotal activity was higher in men at fatigue (EF: 632 ± 418 vs. ML: 598 ± 342 vs. men: 1,025 ± 416 a.u./min, P < 0.001 for EF and ML vs. men) and during PECA (EF: 354 ± 321 vs. ML: 341 ± 199 vs. men: 599 ± 327 a.u./min, P < 0.05 for EF and ML vs. men). During CPT, HR and MSNA responses were similar between sexes and hormone phases, confirming that central integration and the sympathetic efferent pathway was comparable between the sexes and across hormone phases. Women demonstrated a blunted metaboreflex, unaffected by sex hormones, which may be due to differences in muscle mass or fiber type and, therefore, metabolic stimulation of group IV afferents.

scholarly journals Total sleep deprivation and pain perception during cold noxious stimuli in humans

2016 ◽  
Vol 13 (1) ◽  
pp. 12-16 ◽  
Author(s):  
Robert A. Larson ◽  
Jason R. Carter
Keyword(s):  
Sex Differences ◽  
Sleep Deprivation ◽  
Pain Perception ◽  
Productivity Loss ◽  
Cold Pressor Test ◽  
Sleep Loss ◽  
Pain Response ◽  
Men And Women ◽  
Total Sleep Deprivation ◽  
Perceived Pain

AbstractBackground and aimsA substantial portion of the population suffers from chronic pain leading to significant health care costs and lost productivity. Loss of sleep duration and quality are widely reported in patients suffering from a variety of acute orchronicpain conditions. Conversely, sleep loss has been known to elevate pain perception; thus a potential bi-directional relationship exists between sleep deprivation and pain. To date, the majority of studies examining the relationship between experimentally induced pain and sleep loss have focused on the measurement of pain threshold. Additionally, despite evidence of sex differences in ratings of perceived pain, previous studies examining pain following sleep loss have not probed for sex differences. We examined the effects of 24-h total sleep deprivation (TSD) on perceived pain during a 2-min cold pressor test (CPT). We hypothesized that TSD would augment perceived pain and that women would demonstrate an elevated pain response compared to men.MethodsTesting was carried out in 14 men and 13 women. All subjects reported to be nonsmokers with no history of cardiovascular disease, autonomic dysfunction, asthma, or diabetes. All female subjects were free of oral contraceptive use, and were tested during the early follicular phase of the menstrual cycle. Trial order was randomized and testing sessions (Normal sleep (NS) and TSD) were separated by approximately one month. Subjects immersed their left hand, up to the wrist, in an ice water bath (∼1° C), and perceived pain was recorded every 15 s from a modified Borg scale (6–20 arbitrary units a.u.).ResultsPerceived pain responses during CPT were augmented following TSD (Δ 1.2 a.u.; time × condition, p < 0.05). The augmented pain response following TSD was noted when perceived pain was expressed as mean (NS Δ 7.0 ± 0.5 vs. TSD Δ 8.2 ± 0.5 a.u.; p < 0.05) or peak (NS Δ 8.9 ± 0.6 vs. TSD Δ 10.2 ± 0.5 a.u.; p < 0.05) perceived pain. The effects of TSD on perceived pain were similar in both men and women (condition × time × sex, p > 0.05).Conclusions and implicationsWe conclude that TSD significantly augments perceived pain during CPT, but this response was not sex dependent. These findings support emerging evidence that adequate sleep represents a relevant, and cost effective, preventative/therapeutic strategy to reduce self-perceived pain in both men and women.

Inhibitory effect of atrial natriuretic factor on sympathetic ganglionic neurotransmission in humans

1995 ◽  
Vol 269 (2) ◽  
pp. R406-R412 ◽  
Author(s):  
J. S. Floras
Keyword(s):  
Atrial Natriuretic Factor ◽  
Muscle Sympathetic Nerve Activity ◽  
Acetylcholinesterase Inhibitor ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Inhibitory Effect ◽  
Double Blind Study ◽  
Double Blind ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

I have previously documented an inhibitory effect of atrial natriuretic factor (ANF) on postganglionic muscle sympathetic nerve activity (MSNA) in normal subjects that was consistent with either a central or ganglionic sympathoinhibitory action. To test the latter hypothesis, I examined, in seven young normotensive men, the effect of saline (as vehicle) and ANF (50 micrograms, then 50 ng.kg-1.min-1), given on 2 separate days according to a random double-blind study design, on blood pressure, heart rate, and MSNA before and after ganglionic neurotransmission was stimulated with edrophonium (ED; 12 mg iv), a rapidly reversible acetylcholinesterase inhibitor without central nervous system effects, and during subsequent augmentation of central sympathetic outflow by a cold pressor test (CPT). In five of these subjects, the protocol was replicated during nitroprusside infusion (0.4 micrograms.kg-1.min-1). ED increased MSNA during vehicle (P < 0.005) and nitroprusside (P < 0.003) but not during ANF infusion. The sympathoneural response to the combined stimuli of ED and CPT was also attenuated by ANF compared with either saline or nitroprusside infusions. Conclusions were that 1) postganglionic MSNA is increased by ED, 2) this facilitative effect of ED is attenuated by ANF, and 3) modulation of ganglionic neurotransmission is one mechanism for the relative sympatho-inhibition observed when ANF is infused at this dose.

scholarly journals Abnormal sympathetic neural recruitment patterns and hemodynamic responses to cold pressor test in women with posttraumatic stress disorder

2020 ◽  
Vol 318 (5) ◽  
pp. H1198-H1207 ◽  
Author(s):  
Jeung-Ki Yoo ◽  
Mark B. Badrov ◽  
Mu Huang ◽  
Ryan A. Bain ◽  
Raymond P. Dorn ◽  
...  
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Pressor Test ◽  
Activity Burst ◽  
Circulatory Control

The novel findings of the present study are that women with posttraumatic stress disorder (PTSD) have an augmented pressor response to the sympathoexcitatory stimulus of a cold pressor test (CPT) compared with healthy control subjects. Although integrated muscle sympathetic nerve activity burst responses were not significantly different between groups, total sympathetic action potential discharge in response to the CPT was markedly elevated in women with PTSD exhibiting increased firing of low-threshold axons as well as the recruitment of latent subpopulations of larger-sized axons that are otherwise silent at baseline. Aberrant autonomic circulatory control in response to sympathoexcitatory stimulus may in part explain the propensity toward developing hypertension and cardiovascular disease in this population.

scholarly journals Effects of the cold pressor test on muscle sympathetic nerve activity in humans.

Hypertension ◽  
1987 ◽  
Vol 9 (5) ◽  
pp. 429-436 ◽  
Author(s):  
R G Victor ◽  
W N Leimbach ◽  
D R Seals ◽  
B G Wallin ◽  
A L Mark
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Nerve Activity ◽  
Pressor Test

scholarly journals Sympathetic neural responses to 24-hour sleep deprivation in humans: sex differences

2012 ◽  
Vol 302 (10) ◽  
pp. H1991-H1997 ◽  
Author(s):  
Jason R. Carter ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Joseph P. DellaValla ◽  
Huan Yang
Keyword(s):  
Sex Differences ◽  
Sleep Deprivation ◽  
Muscle Sympathetic Nerve Activity ◽  
Operating Point ◽  
Neural Responses ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Baroreflex Function ◽  
Normal Sleep ◽  
Spontaneous Fluctuations

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA ( r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.

EXERCISE AND FAMILIAL HYPERTENSION ON CARDIOVASCULAR REACTIVITY TO THE COLD PRESSOR TEST IN AFRICAN AMERICANS

2002 ◽  
Vol 34 (5) ◽  
pp. S112
Author(s):  
V Bond ◽  
P Vaccaro ◽  
R Blakely ◽  
D Williams ◽  
T O. Obisesan ◽  
...  
Keyword(s):  
African Americans ◽  
Cardiovascular Reactivity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Pressor Test
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