scholarly journals Effect of acute hyperlipidemia on autonomic and cardiovascular control in humans

2007 ◽  
Vol 103 (1) ◽  
pp. 162-169 ◽  
Author(s):  
Kevin D. Monahan ◽  
Damian J. Dyckman ◽  
Chester A. Ray
Keyword(s):  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Controlled Study ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Control Subjects ◽  
Sympathetic Regulation ◽  
Circulatory Control ◽  
Double Blinded ◽  
Cardiac Period

Blood lipids may detrimentally affect autonomic and circulatory control. We tested the hypotheses that acute elevations in free fatty acids and triglycerides (acute hyperlipidemia) impair baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA: sympathetic BRS), increase MSNA at rest, and augment physiological responses to exercise. Eighteen young adults were examined in this randomized, double-blinded, and placebo-controlled study. BRS was determined using the modified Oxford technique before (pre) and 60 min (post) after initiating infusion of Intralipid (0.8 ml·m−2·min−1) and heparin (1,000 U/h) (experimental; n = 12) to induce acute hyperlipidemia, or saline (0.8 ml·m−2·min−1) and heparin (1,000 U/h) (control; n = 6). Responses to isometric handgrip to fatigue (IHG) were also determined. Blood pressure increased more ( P < 0.05) in experimental than control subjects during the infusion. MSNA at rest (14 ± 2 vs. 11 ± 1 bursts/min), cardiovagal (19.8 ± 1.8 vs. 19.1 ± 2.4 ms/mmHg pre and post, respectively) and sympathetic BRS (−5.5 ± 0.6 vs. −5.2 ± 0.4 au·beat−1·mmHg−1), and the neural and cardiovascular responses to IHG were unchanged by acute hyperlipidemia (pre vs. post) in experimental subjects. Similarly, MSNA at rest (10 ± 2 vs. 12 ± 2 bursts/min), cardiovagal (22.1 ± 4.0 vs. 21.0 ± 4.6 ms/mmHg) and sympathetic BRS (−5.8 ± 0.5 vs. −5.5 ± 0.5 au·beat−1·mmHg−1), and the neural and cardiovascular responses to IHG were unchanged by the infusion in control subjects. These data do not provide experimental support for the concept that acute hyperlipidemia impairs reflex cardiovagal or sympathetic regulation in humans.

Aldosterone impairs baroreflex sensitivity in healthy adults

2007 ◽  
Vol 292 (1) ◽  
pp. H190-H197 ◽  
Author(s):  
Kevin D. Monahan ◽  
Urs A. Leuenberger ◽  
Chester A. Ray
Keyword(s):  
Baroreflex Sensitivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Cardiovascular Responses ◽  
Control Group ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Bolus Infusion ◽  
Baroreflex Function

Animal studies suggest that acute and chronic aldosterone administration impairs baroreceptor/baroreflex responses. We tested the hypothesis that aldosterone impairs baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA, sympathetic BRS) in humans. Twenty-six young (25 ± 1 yr old, mean ± SE) adults were examined in this study. BRS was determined by using the modified Oxford technique (bolus infusion of nitroprusside, followed 60 s later by bolus infusion of phenylephrine) in triplicate before (Pre) and 30-min after (Post) beginning aldosterone (experimental, 12 pmol·kg−1·min−1; n = 10 subjects) or saline infusion (control; n = 10). BRS was quantified from the R-R interval-systolic blood pressure (BP) (cardiovagal BRS) and MSNA-diastolic BP (sympathetic BRS) relations. Aldosterone infusion increased serum aldosterone levels approximately fourfold ( P < 0.05) and decreased ( P < 0.05) cardiovagal (19.0 ± 2.3 vs. 15.6 ± 1.7 ms/mmHg Pre and Post, respectively) and sympathetic BRS [−4.4 ± 0.4 vs. −3.0 ± 0.4 arbitrary units (AU)·beat−1·mmHg−1]. In contrast, neither cardiovagal (19.3 ± 3.3 vs. 20.2 ± 3.3 ms/mmHg) nor sympathetic BRS (−3.8 ± 0.5 vs. −3.6 ± 0.5 AU·beat−1·mmHg−1) were altered (Pre vs. Post) in the control group. BP, heart rate, and MSNA at rest were similar in experimental and control subjects before and after the intervention. Additionally, neural and cardiovascular responses to a cold pressor test and isometric handgrip to fatigue were unaffected by aldosterone infusion ( n = 6 subjects). These data provide direct experimental support for the concept that aldosterone impairs baroreflex function (cardiovagal and sympathetic BRS) in humans. Therefore, aldosterone may be an important determinant/modulator of baroreflex function in humans.

Effect of morphine on sympathetic nerve activity in humans

2002 ◽  
Vol 93 (5) ◽  
pp. 1764-1769 ◽  
Author(s):  
Jason R. Carter ◽  
Charity L. Sauder ◽  
Chester A. Ray
Keyword(s):  
Opioid Receptor ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Cardiovascular Responses ◽  
Endogenous Opioids ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Trial Drug

There are conflicting reports for the role of endogenous opioids on sympathetic and cardiovascular responses to exercise in humans. A number of studies have utilized naloxone (an opioid-receptor antagonist) to investigate the effect of opioids during exercise. In the present study, we examined the effect of morphine (an opioid-receptor agonist) on sympathetic and cardiovascular responses at rest and during isometric handgrip (IHG). Eleven subjects performed 2 min of IHG (30% maximum) followed by 2 min of postexercise muscle ischemia (PEMI) before and after systemic infusion of morphine (0.075 mg/kg loading dose + 1 mg/h maintenance) or placebo (saline) in double-blinded experiments on separate days. Morphine increased resting muscle sympathetic nerve activity (MSNA; 17 ± 2 to 22 ± 2 bursts/min; P < 0.01) and increased mean arterial pressure (MAP; 87 ± 2 to 91 ± 2 mmHg; P < 0.02), but it decreased heart rate (HR; 61 ± 4 to 59 ± 3; P < 0.01). However, IHG elicited similar increases for MSNA, MAP, and HR between the control and morphine trial (drug × exercise interaction = not significant). Moreover, responses to PEMI were not different. Placebo had no effect on resting, IHG, and PEMI responses. We conclude that morphine modulates cardiovascular and sympathetic responses at rest but not during isometric exercise.

Baroreflex control of muscle sympathetic nerve activity in postural orthostatic tachycardia syndrome

2005 ◽  
Vol 289 (3) ◽  
pp. H1226-H1233 ◽  
Author(s):  
N. Muenter Swift ◽  
N. Charkoudian ◽  
R. M. Dotson ◽  
G. A. Suarez ◽  
P. A. Low
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Valsalva Maneuver ◽  
Muscle Sympathetic Nerve Activity ◽  
Vasoactive Drug ◽  
Postural Orthostatic Tachycardia Syndrome ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Control Subjects ◽  
Healthy Control

Postural orthostatic tachycardia syndrome (POTS) is characterized by excessive tachycardia during orthostasis. To test the hypothesis that patients with POTS have decreased sympathetic neural responses to baroreflex stimuli, we measured heart rate (HR) and muscle sympathetic nerve activity (MSNA) responses to three baroreflex stimuli including vasoactive drug boluses (modified Oxford technique), Valsalva maneuver, and head-up tilt (HUT) in POTS patients and healthy control subjects. The MSNA response to the Valsalva maneuver was significantly greater in the POTS group (controls, 26 ± 7 vs. POTS, 48 ± 6% of baseline MSNA/mmHg; P = 0.03). POTS patients also had an exaggerated MSNA response to 30° HUT (controls, 123 ± 24 vs. POTS, 208 ± 30% of baseline MSNA; P = 0.03) and tended to have an exaggerated response to 45° HUT (controls, 137 ± 27 vs. POTS, 248 ± 58% of baseline MSNA; P = 0.10). Sympathetic baroreflex sensitivity calculated during administration of the vasoactive drug boluses also tended to be greater in the POTS patients; however, this did not reach statistical significance ( P = 0.15). Baseline MSNA values during supine rest were not different between the groups (controls, 23 ± 4 vs. POTS, 16 ± 5 bursts/100 heartbeats; P = 0.30); however, resting HR was significantly higher in the POTS group (controls, 58 ± 3 vs. POTS, 82 ± 4 beats/min; P = 0.0001). Our results suggest that POTS patients have exaggerated MSNA responses to baroreflex challenges compared with healthy control subjects, although resting supine MSNA values did not differ between the groups.

scholarly journals Whole body heat stress attenuates the pressure response to muscle metaboreceptor stimulation in humans

2016 ◽  
Vol 121 (5) ◽  
pp. 1178-1186 ◽  
Author(s):  
Jian Cui ◽  
Cheryl Blaha ◽  
Lawrence I. Sinoway
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Whole Body ◽  
Isometric Handgrip ◽  
Whole Body Heat Stress ◽  
Body Heat

The effects of whole body heat stress on sympathetic and cardiovascular responses to stimulation of muscle metaboreceptors and mechanoreceptors remains unclear. We examined the muscle sympathetic nerve activity (MSNA), blood pressure, and heart rate in 14 young healthy subjects during fatiguing isometric handgrip exercise, postexercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed under normothermic and whole body heat stress (increase internal temperature ~0.6°C via a heating suit) conditions. Heat stress increased the resting MSNA and heart rate. Heat stress did not alter the mean blood pressure (MAP), heart rate, and MSNA responses (i.e., changes) to fatiguing exercise. During PECO, whole body heat stress accentuated the heart rate response [change (Δ) of 5.8 ± 1.5 to Δ10.0 ± 2.1 beats/min, P = 0.03], did not alter the MSNA response (Δ16.4 ± 2.8 to Δ17.3 ± 3.8 bursts/min, P = 0.74), and lowered the MAP response (Δ20 ± 2 to Δ12 ± 1 mmHg, P < 0.001). Under normothermic conditions, passive stretch during PECO evoked significant increases in MAP and MSNA (both P < 0.001). Of note, heat stress prevented the MAP and MSNA responses to stretch during PECO (both P > 0.05). These data suggest that whole body heat stress attenuates the pressor response due to metaboreceptor stimulation, and the sympathetic nerve response due to mechanoreceptor stimulation.

Isometric handgrip training reduces arterial pressure at rest without changes in sympathetic nerve activity

2000 ◽  
Vol 279 (1) ◽  
pp. H245-H249 ◽  
Author(s):  
Chester A. Ray ◽  
Dario I. Carrasco
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Voluntary Contraction ◽  
Isometric Handgrip ◽  
Nerve Activity ◽  
Muscle Ischemia

The purpose of this study was to determine whether isometric handgrip (IHG) training reduces arterial pressure and whether reductions in muscle sympathetic nerve activity (MSNA) mediate this drop in arterial pressure. Normotensive subjects were assigned to training ( n = 9), sham training ( n = 7), or control ( n = 8) groups. The training protocol consisted of four 3-min bouts of IHG exercise at 30% of maximal voluntary contraction (MVC) separated by 5-min rest periods. Training was performed four times per week for 5 wk. Subjects' resting arterial pressure and heart rate were measured three times on 3 consecutive days before and after training, with resting MSNA (peroneal nerve) recorded on the third day. Additionally, subjects performed IHG exercise at 30% of MVC to fatigue followed by muscle ischemia. In the trained group, resting diastolic (67 ± 1 to 62 ± 1 mmHg) and mean arterial pressure (86 ± 1 to 82 ± 1 mmHg) significantly decreased, whereas systolic arterial pressure (116 ± 3 to 113 ± 2 mmHg), heart rate (67 ± 4 to 66 ± 4 beats/min), and MSNA (14 ± 2 to 15 ± 2 bursts/min) did not significantly change following training. MSNA and cardiovascular responses to exercise and postexercise muscle ischemia were unchanged by training. There were no significant changes in any variables for the sham training and control groups. The results indicate that IHG training is an effective nonpharmacological intervention in lowering arterial pressure.

Endurance exercise training is associated with elevated basal sympathetic nerve activity in healthy older humans

1994 ◽  
Vol 77 (3) ◽  
pp. 1366-1374 ◽  
Author(s):  
A. V. Ng ◽  
R. Callister ◽  
D. G. Johnson ◽  
D. R. Seals
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Acute Stress ◽  
Muscle Sympathetic Nerve Activity ◽  
Cold Pressor Test ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Control Subjects

We tested the hypothesis that endurance training is associated with altered basal levels of muscle sympathetic nerve activity (MSNA) and responses to acute stress in healthy older adults. MSNA (peroneal microneurography) and plasma norepinephrine (NE) concentrations were measured during supine rest, a cold pressor test, and isometric handgrip (40% maximal voluntary force to exhaustion) in 16 older masters endurance athletes [10 men, 6 women; 66 +/- 1 (SE) yr] and 15 healthy normotensive untrained control subjects (9 men, 6 women; 65 +/- 1 yr). The athletes had higher levels of estimated daily energy expenditure and maximal oxygen uptake and lower levels of resting heart rate and body fat than the control subjects (all P < 0.05). MSNA during supine rest was elevated in the athletes whether expressed as burst frequency (43 +/- 2 vs. 32 +/- 3 bursts/min, respectively; P < 0.05) or burst incidence (75 +/- 4 vs. 52 +/- 5 bursts/100 heartbeats, respectively; P < 0.01). These whole group differences were due primarily to markedly higher levels of MSNA in the athletic vs. untrained women (48 +/- 4 vs. 25 +/- 3 bursts/min, 82 +/- 3 vs. 38 +/- 3 bursts/100 heartbeats, respectively, P < 0.001). In contrast, basal plasma NE concentrations were not significantly different in the athletes vs. control subjects. The MSNA and plasma NE responses to acute stress tended to be greater in the athletes. These findings indicate that vigorous regular aerobic exercise is associated with an elevated level of MSNA at rest and a tendency for an enhanced response to acute stress in healthy normotensive older humans.

Alteration of baroreflex control of forearm vascular resistance by dietary fatty acids

1990 ◽  
Vol 259 (6) ◽  
pp. R1164-R1171 ◽  
Author(s):  
D. E. Mills ◽  
M. Mah ◽  
R. P. Ward ◽  
B. L. Morris ◽  
J. S. Floras
Keyword(s):  
Fish Oil ◽  
Vascular Resistance ◽  
Cold Pressor Test ◽  
Cardiovascular Responses ◽  
Dietary Fatty Acids ◽  
Borage Oil ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Forearm Vascular Resistance

The effects of dietary safflower (control, n = 10), borage (n = 9), and fish oil (n = 10), as sources of linoleic, gamma-linolenic, and eicosapentaenoic acid, respectively, at a dose of 4.5 ml/day for 4 wk, on cardiovascular responses to lower body negative pressure (LBNP) were studied in normotensive humans in a randomized, double-blind design. Pre- and postsupplementation, subjects were exposed to 5 min of -10 and -40 mmHg LBNP. Blood pressure (BP), heart rate (HR), forearm blood flow (FBF), forearm vascular resistance (FVR), and plasma norepinephrine (PNE) were measured at each level. Subjects were then exposed to a cold-pressor test, isometric handgrip, and forearm ischemia. At pretest, LBNP reduced BP and FBF and increased HR and FVR in all groups. After diets, the PNE and vasoconstrictor responses to -40 mmHg LBNP, as well as the reflex vasodilation on its cessation, were significantly augmented by borage oil. No diet differences were observed in the HR responses to LBNP or in the responses to the other tasks, with the exception that fish oil increased FBF after forearm ischemia. These data indicate that borage oil augments the arterial baroreflex control of vascular resistance. The vasodilatory effects of fish oil may be mediated via local mechanisms.

Moderate whole-body heating attenuates the exercise pressor reflex responses in older humans

2021 ◽  
Author(s):  
Jian Cui ◽  
Zhaohui Gao ◽  
Cheryl Blaha ◽  
J. Carter Luck ◽  
Kristen Brandt ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Whole Body ◽  
Isometric Handgrip ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Isometric Handgrip Exercise ◽  
Fatiguing Exercise

Prior reports show that whole-body heat stress attenuates the pressor response to exercise in young healthy subjects. The effects of moderate whole-body heating (WBH, e.g. increase in internal temperature Tcore ~0.4-0.5 °C) or limb heating on sympathetic and cardiovascular responses to exercise in older healthy humans remains unclear. We examined the muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR) in 14 older (62 ± 2 yrs) healthy subjects during fatiguing isometric handgrip exercise and post exercise circulatory occlusion (PECO). The protocol was performed under normothermic, moderate WBH and local limb (i.e. forearm) heating conditions during 3 visits. During the mild WBH stage (increase in Tcore <0.3 °C), HR increased, whereas BP and MSNA decreased from baseline. Under the moderate WBH condition (increase in Tcore ~0.4 °C), BP decreased, HR increased, while MSNA was unchanged from baseline. Compared with the normothermic trial, the absolute MAP during fatiguing exercise and PECO were lower during the WBH trial. Moreover, MSNA and MAP responses (i.e. changes) to fatiguing exercise were also less than those seen during the normothermic trial. Limb heating induced a similar increase in forearm muscle temperature with that seen in the WBH trial (~0.7-1.5 °C). Limb heating did not alter resting MAP, HR or MSNA. The MSNA and hemodynamic responses to exercise in limb heating trial were not different from those in the normothermic trial. These data suggest that moderate WBH attenuates MSNA and BP responses to exercise in older healthy humans.

scholarly journals Social technology restriction alters state-anxiety but not autonomic activity in humans

2011 ◽  
Vol 301 (6) ◽  
pp. R1773-R1778 ◽  
Author(s):  
John J. Durocher ◽  
Kelly M. Lufkin ◽  
Michelle E. King ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Young Adults ◽  
Technology Use ◽  
State Anxiety ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Social Technology ◽  
Autonomic Activity ◽  
Isometric Handgrip ◽  
Arterial Blood

Social technology is extensively used by young adults throughout the world, and it has been suggested that interrupting access to this technology induces anxiety. However, the influence of social technology restriction on anxiety and autonomic activity in young adults has not been formally examined. Therefore, we hypothesized that restriction of social technology would increase state-anxiety and alter neural cardiovascular regulation of arterial blood pressure. Twenty-one college students (age 18–23 yr) were examined during two consecutive weeks in which social technology use was normal or restricted (randomized crossover design). Mean arterial pressure (MAP), heart rate, and muscle sympathetic nerve activity (MSNA) were measured at rest and during several classic autonomic stressors, including isometric handgrip, postexercise muscle ischemia, cold pressor test, and mental stress. Tertile analysis revealed that restriction of social technology was associated with increases (12 ± 2 au; range 5 to 21; n = 7), decreases (−6 ± 2 au; range −2 to −11; n = 6), or no change (0 ± 0 au; range −1 to 3; n = 8) in state-anxiety. Social technology restriction did not alter MAP (74 ± 1 vs. 73 ± 1 mmHg), heart rate (62 ± 2 vs. 61 ± 2 beats/min), or MSNA (9 ± 1 vs. 9 ± 1 bursts/min) at rest, and it did not alter neural or cardiovascular responses to acute stressors. In conclusion, social technology restriction appears to have an interindividual influence on anxiety, but not autonomic activity. It remains unclear how repeated bouts, or chronic restriction of social technology, influence long-term psychological and cardiovascular health.

Muscle sympathetic nerve responses to physiological changes in prostaglandin production in humans

2001 ◽  
Vol 90 (2) ◽  
pp. 624-629 ◽  
Author(s):  
Kelly J. Doerzbacher ◽  
Chester A. Ray
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Muscle Sympathetic Nerve Activity ◽  
Exercise Bout ◽  
Cardiovascular Responses ◽  
Isometric Handgrip ◽  
Muscle Ischemia ◽  
Before And After ◽  
Exercise Induced ◽  
Exercise In Humans

Previous studies suggest that prostaglandins may contribute to exercise-induced increases in muscle sympathetic nerve activity (MSNA). To test this hypothesis, MSNA was measured at rest and during exercise before and after oral administration of ketoprofen, a cyclooxygenase inhibitor, or placebo. Twenty-one subjects completed two bouts of graded dynamic and isometric handgrip to fatigue. Each exercise bout was followed by 2 min of postexercise muscle ischemia. The second exercise bouts were performed after 60 min of rest in which 11 subjects were given ketoprofen (300 mg) and 10 subjects received a placebo. Ketoprofen significantly lowered plasma thromboxane B2 in the drug group (from 36 ± 6 to 22 ± 3 pg/ml, P < 0.04), whereas thromboxane B2 in the placebo group increased from 40 ± 5 to 61 ± 9 pg/ml from trial 1 to trial 2 ( P < 0.008). Ketoprofen and placebo did not change sympathetic and cardiovascular responses to dynamic handgrip, isometric handgrip, and postexercise muscle ischemia. There was no relationship between thromboxane B2concentrations and MSNA or arterial pressure responses during both exercise modes. The data indicate that physiological increases or decreases in prostaglandins do not alter exercise-induced increases in MSNA and arterial pressure in humans. These findings suggest that contraction-induced metabolites other than prostaglandins mediate MSNA responses to exercise in humans.

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