Strength training reduces arterial blood pressure but not sympathetic neural activity in young normotensive subjects

2003 ◽  
Vol 94 (6) ◽  
pp. 2212-2216 ◽  
Author(s):  
Jason R. Carter ◽  
Chester A. Ray ◽  
Emily M. Downs ◽  
William H. Cooke
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Resistance Training ◽  
Exercise Training ◽  
Resistance Exercise ◽  
Arterial Blood Pressure ◽  
Whole Body ◽  
Arterial Blood ◽  
Blood Pressures ◽  
Body Resistance

The effects of resistance training on arterial blood pressure and muscle sympathetic nerve activity (MSNA) at rest have not been established. Although endurance training is commonly recommended to lower arterial blood pressure, it is not known whether similar adaptations occur with resistance training. Therefore, we tested the hypothesis that whole body resistance training reduces arterial blood pressure at rest, with concomitant reductions in MSNA. Twelve young [21 ± 0.3 (SE) yr] subjects underwent a program of whole body resistance training 3 days/wk for 8 wk. Resting arterial blood pressure ( n = 12; automated sphygmomanometer) and MSNA ( n = 8; peroneal nerve microneurography) were measured during a 5-min period of supine rest before and after exercise training. Thirteen additional young (21 ± 0.8 yr) subjects served as controls. Resistance training significantly increased one-repetition maximum values in all trained muscle groups ( P < 0.001), and it significantly decreased systolic (130 ± 3 to 121 ± 2 mmHg; P = 0.01), diastolic (69 ± 3 to 61 ± 2 mmHg; P = 0.04), and mean (89 ± 2 to 81 ± 2 mmHg; P = 0.01) arterial blood pressures at rest. Resistance training did not affect MSNA or heart rate. Arterial blood pressures and MSNA were unchanged, but heart rate increased after 8 wk of relative inactivity for subjects in the control group (61 ± 2 to 67 ± 3 beats/min; P = 0.01). These results indicate that whole body resistance exercise training might decrease the risk for development of cardiovascular disease by lowering arterial blood pressure but that reductions of pressure are not coupled to resistance exercise-induced decreases of sympathetic tone.

Measurement Of Bradykinin-Induced Venous Dilation By Ultrasound And Correlation With Heart Rate, Arterial And Venous Pressure And Endothelial Damage

1981 ◽  
Author(s):  
G J Stewart ◽  
R G Schaub ◽  
R E Cartee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Carotid Arteries ◽  
Jugular Vein ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Endothelial Damage ◽  
Whole Body ◽  
Arterial Blood

This study was done to correlate known cardiovascular responses to bradykinin (increased heart rate, lowered arterial blood pressure) with recently demonstrated endothelial damage and proposed venous dilation. Healthy dogs of mixed breed were used. Blood pressures and heart rate were monitored and recorded on a Narco physiograph. The diameter of a jugular vein was monitored with an ADR ultrasound machine using a 10 MHz probe with linear array of crystals and recorded on polaroid prints. Jugular veins and carotid arteries were removed and prepared for scanning electron microscopy after removal of blood and partial in situ fixation by whole body perfusion. The response of arterial pressure was dose dependent with no change at 6 ug/min, variable drop at 12 ug/min and 22-40% drop at 60 ug/min and above. Venous pressure increased in 1 dog but was unchanged in 4 others. The increase of heart rate paralled the drop in arterial blood pressure. The diameter of a jugular vein increased in 3 of 3 monitored dogs by 25, 33, 50% of baseline diameter (average increase 36%) with high (300 ug/min) bradykinin. Endothelial damage (microtears) occurred around 70-80% of branches, at some valves and on the main vessel occassionally. The tears were infiltrated with leukocytes and some red cells and platelets indicating that tearing occurred while blood was still circulating, i.e. before dissection for removal of vessels. Carotid arteries showed no tears. Dilation of arteries would be limited by their elastic layers (missing in veins). These observations show that venous dilation and endothelial tearing around side branches are part of the cardiovascular response to blood born bradykinin. They also show that venous dilation can be measured by ultrasound.

Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans

2002 ◽  
Vol 283 (5) ◽  
pp. R1221-R1226 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Whole Body ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
The Relationship

To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ∼0.5°C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [ΔMAP 8.4 ± 1.2 mmHg; ΔTPR 0.96 ± 0.85 peripheral resistance units (PRU)] compared with normothermia (ΔMAP 15.4 ± 1.4 mmHg, ΔTPR 7.13 ± 1.18 PRU; all P < 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.

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

scholarly journals Resistance Training Controls Arterial Blood Pressure in Rats with L-NAME- Induced Hypertension

2013 ◽  
Author(s):  
Ayslan Jorge Santos de Araujo ◽  
Anne Carolline Veríssimo dos Santos ◽  
Karine dos Santos Souza ◽  
Marlúcia Bastos Aires ◽  
Valter Joviniano Santana-Filho ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistance Training ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Induced Hypertension

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.

scholarly journals Heat stress alters hemodynamic responses during the Valsalva maneuver

2010 ◽  
Vol 108 (6) ◽  
pp. 1591-1594 ◽  
Author(s):  
Scott L. Davis ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Phase Ii ◽  
Valsalva Maneuver ◽  
Late Phase ◽  
Thermal Conditions ◽  
Whole Body ◽  
Hemodynamic Responses ◽  
Arterial Blood

The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ∼0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (ΔMAP) relative to pre-Valsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = −20 ± 8 mmHg; IIb = −13 ± 7 mmHg) compared with normothermia (IIa = −1 ± 15 mmHg; IIb = 3 ± 13 mmHg). ΔMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase IIb during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia ( P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.

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