scholarly journals GABAergic contribution to the muscle mechanoreflex-mediated heart rate responses at the onset of exercise in humans

2018 ◽  
Vol 314 (4) ◽  
pp. H716-H723 ◽  
Author(s):  
André L. Teixeira ◽  
Plinio S. Ramos ◽  
Milena Samora ◽  
Jeann L. Sabino-Carvalho ◽  
Djalma R. Ricardo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Vastus Lateralis ◽  
Arterial Blood ◽  
Exercise Onset ◽  
Muscle Mechanoreceptor ◽  
Muscle Mechanoreflex ◽  
First Time ◽  
Exercise In Humans

Previous studies have indicated that central GABAergic mechanisms are involved in the heart rate (HR) responses at the onset of exercise. On the basis of previous research that showed similar increases in HR during passive and active cycling, we reasoned that the GABAergic mechanisms involved in the HR responses at the exercise onset are primarily mediated by muscle mechanoreceptor afferents. Therefore, in this study, we sought to determine whether central GABA mechanisms are involved in the muscle mechanoreflex-mediated HR responses at the onset of exercise in humans. Twenty-eight healthy subjects (14 men and 14 women) aged between 18 and 35 yr randomly performed three bouts of 5-s passive and active cycling under placebo and after oral administration of diazepam (10 mg), a benzodiazepine that produces an enhancement in GABAA activity. Beat-to-beat HR (electrocardiography) and arterial blood pressure (finger photopletysmography) were continuously measured. Electromyography of the vastus lateralis was obtained to confirm no electrical activity during passive trials. HR increased from rest under placebo and further increased after administration of diazepam in both passive (change: 12 ± 1 vs. 17 ± 1 beats/min, P < 0.01) and active (change: 14 ± 1 vs. 18 ± 1 beats/min, P < 0.01) cycling. Arterial blood pressure increased from rest similarly during all conditions ( P > 0.05). Importantly, no sex-related differences were found in any variables during experiments. These findings demonstrate, for the first time, that the GABAergic mechanisms significantly contribute to the muscle mechanoreflex-mediated HR responses at the onset of exercise in humans. NEW & NOTEWORTHY We found that passive and voluntary cycling evokes similar increases in heart rate and that these responses were enhanced after diazepam administration, a benzodiazepine that enhances GABAA activity. These findings suggest that the GABAergic system may contribute to the muscle mechanoreflex-mediated vagal withdrawal at the onset of exercise in humans.

Rapid blunting of sympathetic vasoconstriction in the human forearm at the onset of exercise

2003 ◽  
Vol 94 (5) ◽  
pp. 1785-1792 ◽  
Author(s):  
M. E. Tschakovsky ◽  
R. L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Lower Body Negative Pressure ◽  
Rapid Onset ◽  
Arterial Blood ◽  
Sympathetic Vasoconstriction ◽  
Exercise Onset ◽  
Forearm Vascular Conductance ◽  
Forearm Exercise

The purpose of this study was to test the hypothesis that sympathetic vasoconstriction is rapidly blunted at the onset of forearm exercise. Nine healthy subjects performed 5 min of moderate dynamic forearm handgrip exercise during −60 mmHg lower body negative pressure (LBNP) vs. without (control). Beat-by-beat forearm blood flow (Doppler ultrasound), arterial blood pressure (finger photoplethysmograph), and heart rate were collected. LBNP elevated resting heart rate by ∼45%. Mean arterial blood pressure was not significantly changed ( P = 0.196), but diastolic blood pressure was elevated by ∼10% and pulse pressure was reduced by ∼20%. At rest, there was a 30% reduction in forearm vascular conductance (FVC) during LBNP ( P = 0.004). The initial rapid increase in FVC with exercise onset reached a plateau between 10 and 20 s of 126.6 ± 4.1 ml · min−1 · 100 mmHg−1 in control vs. only 101.6 ± 4.1 ml · min−1 · 100 mmHg−1 in LBNP (main effect of condition, P = 0.003). This difference was quickly abolished during the second, slower phase of adaptation in forearm vascular tone to steady state. These data are consistent with a rapid onset of functional sympatholysis, in which local substances released with the onset of muscle contractions impair sympathetic neural vasoconstrictor effectiveness.

Hyperoxia lowers sympathetic activity at rest but not during exercise in humans

1991 ◽  
Vol 260 (5) ◽  
pp. R873-R878 ◽  
Author(s):  
D. R. Seals ◽  
D. G. Johnson ◽  
R. F. Fregosi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Total Activity ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Exercise In Humans

The primary aim of this study was to determine the influence of systemic hyperoxia on sympathetic nervous system behavior at rest and during submaximal exercise in humans. In seven healthy subjects (aged 19-31 yr) we measured postganglionic sympathetic nerve activity to skeletal muscle (MSNA) in the leg, antecubital venous norepinephrine concentrations, heart rate, and arterial blood pressure during normoxic rest (control) followed by 3- to 4-min periods of either hyperoxic (100% O2 breathing) rest, normoxic exercise (rhythmic handgrips at 50% of maximum force), or hyperoxic exercise. During exercise, isocapnia was maintained by adding CO2 to the inspirate as necessary. At rest, hyperoxia lowered MSNA burst frequency (12-42%) and total activity (6-42%) in all subjects; the average reductions were 25 and 23%, respectively (P less than 0.05 vs. control). Heart rate also decreased during hyperoxia (6 +/- 1 beats/min, P less than 0.05), but arterial blood pressure was not affected. During hyperoxic compared with normoxic exercise, there were no differences in the magnitudes of the increases in MSNA burst frequency or total activity, plasma norepinephrine concentrations, or mean arterial blood pressure. In contrast, the increase in heart rate during hyperoxic exercise (13 +/- 2 beats/min) was less than the increase during normoxic exercise (20 +/- 2 beats/min; P less than 0.05). We conclude that, in healthy humans, systemic hyperoxia 1) lowers efferent sympathetic nerve activity to skeletal muscle under resting conditions without altering venous norepinephrine concentrations and 2) has no obvious modulatory effect on the nonactive muscle sympathetic nerve adjustments to rhythmic exercise.

Trigeminal Depressor Response during Percutaneous Microcompression of the Trigeminal Ganglion for Trigeminal Neuralgia

Neurosurgery ◽  
1988 ◽  
Vol 23 (6) ◽  
pp. 745-748 ◽  
Author(s):  
Jeffrey A. Brown ◽  
Mark C. Preul
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Trigeminal Neuralgia ◽  
Arterial Blood Pressure ◽  
Trigeminal Ganglion ◽  
Depressor Response ◽  
Arterial Blood ◽  
First Time ◽  
Transient Bradycardia ◽  
Intravenous Atropine

Abstract Percutaneous microcompression of the trigeminal ganglion for trigeminal neuralgia was performed 23 times on 21 patients. Significant abrupt drops in heart rate and blood pressure (P &lt; 0.0002) occurred when the needle entered the foramen ovale or upon balloon advancement or inflation. In 16 of 23 (70%) procedures, the heart rate fell abruptly to 60 or less, by a mean of 38%. Mean arterial blood pressure decreased transiently by 31% during 12 of 23 (55%) procedures. Our findings of transient bradycardia and hypotension upon mechanical stimulation or compression of the mandibular nerve or trigeminal ganglion show for the first time the presence of a trigeminal depressor response in humans. We recommend that heart rate and arterial blood pressure be monitored continuously during percutaneous microcompression of the trigeminal ganglion. Intravenous atropine should be available for immediate use, and an external pacemaker should be fitted preoperatively.

scholarly journals Estimating coupling directions in the cardiorespiratory system using recurrence properties

2013 ◽  
Vol 371 (1997) ◽  
pp. 20110624 ◽  
Author(s):  
Norbert Marwan ◽  
Yong Zou ◽  
Niels Wessel ◽  
Maik Riedl ◽  
Jürgen Kurths
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Conditional Probabilities ◽  
Recurrence Plots ◽  
Cardiorespiratory System ◽  
Arterial Blood ◽  
The Mean ◽  
First Time

The asymmetry of coupling between complex systems can be studied by conditional probabilities of recurrence, which can be estimated by joint recurrence plots. This approach is applied for the first time on experimental data: time series of the human cardiorespiratory system in order to investigate the couplings between heart rate, mean arterial blood pressure and respiration. We find that the respiratory system couples towards the heart rate, and the heart rate towards the mean arterial blood pressure. However, our analysis could not detect a clear coupling direction between the mean arterial blood pressure and respiration.

Compression Stocking Length Effects on Arterial Blood Pressure and Heart Rate Following Head-Up Tilt in Healthy Volunteers

2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Volunteers ◽  
Arterial Blood Pressure ◽  
Compression Stocking ◽  
Arterial Blood ◽  
Head Up Tilt ◽  
Length Effects

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

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