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

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.

1993 ◽  
Vol 264 (2) ◽  
pp. R262-R267
Author(s):  
J. Michalicek ◽  
G. Campbell

Mean arterial blood pressure (P(a)) and heart rate (HR) were studied in normal conscious cane toads (Bufo marinus) or in autonomically blocked animals treated variously with bretylium, atropine, phentolamine, and propranolol. Partial or total autonomic blockade had no effect on resting values of the variables tested, with the exception that atropine treatment of bretylium-treated toads caused an increase of heart rate by 5.3 +/- 1.3 beats/min. In graded hemorrhage, aliquots of blood (1.68 ml/100 g body wt) were removed at 60-min intervals. There was extensive plasma recruitment, and blood could be removed up to 10.08 ml/100 g without inducing cardiovascular shock. Each hemorrhage caused an initial transient decrease in P(a) and increase in HR followed by recovery toward prehemorrhage values. Repeated hemorrhage caused a progressive rise in basal HR and fall in basal P(a). The effects of drug treatments suggest that transient increases in HR may be caused by the release of adrenal catecholamines. In addition, hemorrhage may increase sympathetic tone so that basal HR becomes elevated, which, together with sympathetic vasoconstriction, limits the progressive fall of basal P(a).


2002 ◽  
Vol 92 (2) ◽  
pp. 651-656 ◽  
Author(s):  
Chester A. Ray ◽  
Kevin D. Monahan

The purpose of the present study was to determine sympathetic vascular transduction in young normotensive black and white adults. We hypothesized that blacks would demonstrate augmented transduction of muscle sympathetic nerve activity (MSNA) into vascular resistance. To test this hypothesis, MSNA, forearm blood flow, heart rate, and arterial blood pressure were measured during lower body negative pressure (LBNP). At rest, no differences existed in arterial blood pressure, heart rate, forearm blood flow, and forearm vascular resistance (FVR). Likewise, LBNP elicited comparable responses of these variables for blacks and whites. Baseline MSNA did not differ between blacks and whites, but whites demonstrated greater increases during LBNP (28 ± 7 vs. 55 ± 18%, 81 ± 21 vs. 137 ± 42%, 174 ± 81 vs. 556 ± 98% for −5, −15, and −40 mmHg LBNP, respectively; P < 0.001). Consistent with smaller increases in MSNA but similar FVR responses during LBNP, blacks demonstrated greater sympathetic vascular transduction (%FVR/%MSNA) than whites (0.95 ± 0.07 vs. 0.82 ± 0.07 U; 0.82 ± 0.11 vs. 0.64 ± 0.09 U; 0.95 ± 0.37 vs. 0.35 ± 0.09 U; P < 0.01). In summary, young whites demonstrate greater increases in MSNA during baroreceptor unloading than age-matched normotensive blacks. However, more importantly, for a given increase in MSNA, blacks demonstrate greater forearm vasoconstriction than whites. This finding may contribute to augmented blood pressure reactivity in blacks.


2018 ◽  
Vol 314 (4) ◽  
pp. H716-H723 ◽  
Author(s):  
André L. Teixeira ◽  
Plinio S. Ramos ◽  
Milena Samora ◽  
Jeann L. Sabino-Carvalho ◽  
Djalma R. Ricardo ◽  
...  

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.


2014 ◽  
Vol 63 (6) ◽  
pp. 435-438 ◽  
Author(s):  
Kunihiko Tanaka ◽  
Shiori Tokumiya ◽  
Yumiko Ishihara ◽  
Yumiko Kohira ◽  
Tetsuro Katafuchi

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  

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.


2020 ◽  
Author(s):  
Bharti Bhandari ◽  
Manisha Mavai ◽  
Yogendra Raj Singh ◽  
Bharati Mehta ◽  
Omlata Bhagat

A single episode of breath-holding (BH) is known to elevate the blood pressure, and regular breathing exercise lowers the blood pressure. This prompted us to investigate how a series of BH epochs would affect the cardiovascular system. To observe arterial blood pressure (ABP) and heart rate (HR) changes associated with a series of “BH epochs” following maximum inspiration and maximum expiration and find the underlying mechanisms for the change by autonomic activity. Thirty-five healthy young adults were instructed to hold their breath repetitively, for 5 minutes, in two patterns, one following maximum inspiration and other following maximum expiration. ABP and ECG (for Heart Rate Variability) were continuously recorded at rest and during both the maneuvers. Capillary blood gases (BG) were zanalyzed at baseline and at the breakpoint of the last epoch of BH. ABP rose significantly at the breakpoint during both the maneuvers. No change in HR was observed. There was significant fall in PO2 from 94.7 (4.1) mmHg at baseline to 79.1 (9.0) mmHg during inspiratory and 76.90 (12.1) mmHg during expiratory BH. Similarly, SPO2 decreased from 96.3 (1.9) % at baseline to 95.4 (1.5) % and 94.5 (2.7) % during inspiratory and expiratory BH, respectively. Rise in PCO2 from 39.5(3.1) mmHg at baseline to 42.9 (2.7) mmHg and 42.1 (2.8) mmHg during inspiratory and expiratory BH respectively was observed. There was no significant correlation between blood gases and arterial blood pressure. Among HRV parameters, a significant decrease in SDNN, RMSSD, HFnu, total power and SD1/SD2 and the significant increase in LFnu, LF/HF and SD2 were observed during both BH patterns. Rhythmic BH patterns affect the cardiovascular system in similar way as a single episode of BH. Sympathetic overactivity could be the postulated mechanism for the same. © 2019 Tehran University of Medical Sciences. All rights reserved. Acta Med Iran 2019;57(8):492-498.


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