Arterial blood pressure and forearm vascular conductance responses to sustained and rhythmic isometric exercise and arterial occlusion in trained rock climbers and untrained sedentary subjects

1997 ◽  
Vol 76 (2) ◽  
pp. 174-180 ◽  
Author(s):  
Richard A. Ferguson ◽  
Margaret D. Brown
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Isometric Exercise ◽  
Arterial Occlusion ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Forearm Vascular Conductance ◽  
Sedentary Subjects

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

scholarly journals Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans

2013 ◽  
Vol 304 (5) ◽  
pp. H759-H766 ◽  
Author(s):  
Seth T. Fairfax ◽  
Jaume Padilla ◽  
Lauro C. Vianna ◽  
Michael J. Davis ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Burst Size ◽  
Muscle Sympathetic Nerve Activity ◽  
Common Femoral Artery ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Arterial Blood

Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, −2.9 ± 1.1%; and multiple bursts, −11.0 ± 1.4%; both, P < 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (+3.1 ± 0.5%; P < 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.

scholarly journals Cardiac and vasomotor components of the carotid baroreflex control of arterial blood pressure during isometric exercise in humans

2006 ◽  
Vol 572 (3) ◽  
pp. 869-880 ◽  
Author(s):  
James P. Fisher ◽  
Shigehiko Ogoh ◽  
Ellen A. Dawson ◽  
Paul J. Fadel ◽  
Niels H. Secher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Isometric Exercise ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Exercise In Humans

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia

1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Plasma Catecholamines ◽  
Central Blood Volume ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

Muscle chemoreflex causes renal vascular constriction

1996 ◽  
Vol 270 (3) ◽  
pp. H951-H956 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
J. E. Sulentic ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Vascular Conductance ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Significant Difference ◽  
Renal Vascular ◽  
Muscle Chemoreflex ◽  
Renal Sympathetic

The purpose of this study was to investigate the effects of the muscle chemoreflex on vascular conductance in innervated and denervated kidneys. During each experiment, six dogs ran at 10 km/h for 8-16 min, and the muscle chemoreflex was stimulated by reducing hindlimb blood flow (HLBF) (0%-74%) at 4-min intervals. Small reductions in HLBF did not cause changes in arterial blood pressure or renal vascular conductance. However, further reductions of HLBF caused increases in arterial blood pressure and decreases in renal vascular conductance. Decreases in renal vascular conductance occurred in the denervated kidneys when the HLBF was reduced below 1,500 +/- 215 ml/min and occurred in the innervated kidneys when HLBF was reduced below 1,402 +/- 161 ml/min. There was not a significant difference between the reductions in HLBF required to cause a decrease in vascular conductance in the innervated and denervated kidneys. These results demonstrate that reductions in HLBF cause decreases in renal vascular conductance, which are not dependent on renal sympathetic nerve activity.

Sympathoadrenal-circulatory regulation during sustained isometric exercise in young and older men

1991 ◽  
Vol 261 (5) ◽  
pp. R1061-R1069 ◽  
Author(s):  
J. A. Taylor ◽  
G. A. Hand ◽  
D. G. Johnson ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Isometric Exercise ◽  
Older Men ◽  
Electromyographic Activity ◽  
Isometric Handgrip ◽  
Significant Group ◽  
Arterial Blood ◽  
Older Subjects

The aim of this study was to test the hypothesis that the arterial blood pressure, vasoconstrictor, and sympathoadrenal adjustments to sustained submaximal isometric exercise become augmented with advancing age in humans. Fourteen young (26 +/- 1 yr) and 14 older (66 +/- 1 yr) healthy males performed isometric handgrip exercise at 30% of maximal voluntary force until exhaustion (inability to maintain target force). Maximal handgrip force was quite similar in the young and older subjects (402 +/- 20 vs. 392 +/- 20 N, respectively). The two groups did not differ significantly on any variable at rest. During sustained handgrip to exhaustion, peak levels of both perceived exertion and contracting forearm electromyographic activity were similar in the young and older men, suggesting equivalent voluntary efforts. Exercise time was not different in the two groups (315 +/- 27 s in young vs. 339 +/- 17 s in older men). Throughout exercise the increases in arterial blood pressure were very similar in the young and older subjects. Heart rate increased less (P less than 0.05), but stroke volume (impedance cardiography) tended to decrease less (not significant) in the older men; thus the increases in cardiac output were not different in the two groups. During the latter portion of exercise, systemic vascular resistance tended to increase in both the young and older men, with no significant group differences. The blood flow responses in the whole calf (venous occlusion plethysmography) and the calf skin (laser-Doppler velocimetry) were similar in the young and older subjects, as were the corresponding increases in vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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