Vasodilation contributes to the rapid hyperemia with rhythmic contractions in humans

1998 ◽  
Vol 76 (4) ◽  
pp. 418-427 ◽  
Author(s):  
J K Shoemaker ◽  
M E Tschakovsky ◽  
R L Hughson

The hypothesis that the rapid increases in blood flow at the exercise onsetare exclusively due to the mechanical effects of the muscle pump was tested in six volunteersduring dynamic handgrip exercise. While supine, each subject completed a series of eightdifferent exercise tests in which brachial artery blood pressure (BP) was altered by25–30 mmHg (1 mmHg = 133.3 Pa) by positioning the arm above or below the heart.Two different weights, corresponding to 4.9 and 9.7% of maximal voluntary isometriccontraction, were raised and lowered at two different contraction rate schedules (1s:1s and 2s:2swork–rest) each with a 50% duty cycle. Beat-by-beat measures of mean blood velocity (MBV)(pulsed Doppler) were obtained at rest and for 5 min following step increases in work ratewith emphasis on the first 24 s. MBV was increased 50–100% above rest following the firstcontraction in both arm positions (p < 0.05). The increase in MBV from rest was greaterin the below position compared with above, and this effect was observed following the first andsubsequent contractions (p < 0.05). However, the positional effect on the increase inMBV could not be explained entirely by the ~40% greater BP in this position. Also, the greaterworkload resulted in greater increases in MBV as early as the first contraction, compared withthe light workload (p < 0.05) despite similar reductions in forearm volume followingsingle contractions. MBV was greater with faster contraction rate tests by 8 s of exercise. Itwas concluded that microvascular vasodilation must act in concert with a reduction in venouspressure to increase forearm blood flow within the initial 2–4 s of exercise.Key words: Doppler, mean blood velocity, arterial diameter,handgrip exercise, perfusion pressure.

2001 ◽  
Vol 91 (5) ◽  
pp. 2359-2365 ◽  
Author(s):  
Amit Anand ◽  
Stacia Remsburg-Sailor ◽  
Sandrine H. Launois ◽  
J. Woodrow Weiss

The mechanisms by which obstructive apneas produce intermittent surges in arterial pressure remain poorly defined. To determine whether termination of obstructive apneas produce peripheral vasoconstriction, we assessed forearm blood flow during and after obstructive events in sleeping patients experiencing spontaneous upper airway obstructions. In all subjects, heart rate was monitored with an electrocardiogram and blood pressure was monitored continuously with digital plethysmography. In 10 patients ( protocol 1), we used forearm plethysmography to assess forearm blood flow, from which we calculated forearm vascular resistance by performing venous occlusions during and after obstructive episodes. In an additional four subjects, we used simultaneous Doppler and B-mode images of the brachial artery to measure blood velocity and arterial diameter, from which we calculated brachial flow continuously during spontaneous apneas ( protocol 2). In protocol 1, forearm vascular resistance increased 71% after apnea termination (29.3 ± 15.4 to 49.8 ± 26.5 resistance units, P < 0.05) with all patients showing an increase in resistance. In protocol 2, brachial resistance increased at apnea termination in all subjects (219.8 ± 22.2 to 358.3 ± 46.1 mmHg · l−1 · min; P = 0.01). We conclude that termination of obstructive apneas is associated with peripheral vasoconstriction.


1964 ◽  
Vol 19 (1) ◽  
pp. 142-146 ◽  
Author(s):  
Adrian Corcondilas ◽  
Gabriel T. Koroxenidis ◽  
John T. Shepherd

With the use of a strain-gauge plethysmograph, the effect of a brief (0.3 sec) contraction of the forearm muscles on forearm blood flow has been studied in eight healthy adults. An increase in flow due to dilatation of the muscle vessels could be detected within a second after the completion of the contraction. This increase was proportional to the strength of the contraction. The blood flow was maximal immediately and decreased rapidly. A second contraction of the same magnitude made during the period of increased flow caused an additional increase in flow. The maximal increase in flow caused by a strong brief contraction was only about 25% of that recorded after strong repeated rhythmic contractions or a sustained contraction. Cervical sympathectomy did not change these findings, indicating the local nature of the response. Since breathing oxygen failed to reduce the dilatation for a given strength of contraction, it is unlikely that oxygen lack was the stimulus for vasodilatation. The oxygen saturation of blood that drained the muscles could not be determined accurately immediately after contraction because at this time, muscle venous blood was contaminated by venous blood from the skin. exercise-induced vasodilatation; local mechanism of vasodilatation; venous O2 saturation during muscle contraction; brachial arterial pressure during vasodilatation; speed of muscle vasodilatation Submitted on May 8, 1963


2001 ◽  
Vol 26 (1) ◽  
pp. 34-43 ◽  
Author(s):  
Jason D. Allen ◽  
Michael Welsch ◽  
Nikki Aucoin ◽  
Robert Wood ◽  
Matt Lee ◽  
...  

This study compared forearm vasoreactivity in 15 Type 1 diabetic subjects with 15 healthy controls. The groups were matched for age, exercise capacity, and the absence of other cardiovascular risk factors. Vasoreactivity was measured using strain gauge plethysmography, at rest, after arterial occlusion (OCC), and following OCC coupled with handgrip exercise (ROCC). Forearm blood flows were significantly elevated between conditions 2.58 ± 0.37 ml/100mltissue at rest to 26.80 ± 6.56 after OCC and 32.80 ± 8.26ml/100mltissue following ROCC in Type 1 diabetic subjects. There were no differences in forearm blood flow between groups for any of the conditions. These data indicate the degree of forearm blood flow is directly related to the intensity of the vasodilatory stimulus. However, our study did not reveal evidence of impaired vasodilatory capacity in Type 1 diabetic subjects compared to controls in the absence of other risk factors. Key words: IDDM, vascular function, exercise, fitness, and reactive hyperemia


1988 ◽  
Vol 75 (6) ◽  
pp. 615-619 ◽  
Author(s):  
Jacques Lenders ◽  
Harry Houben ◽  
Rudolf Van Valderen ◽  
Jacques Willemsen ◽  
Theo Thien

1. To determine the reproducibility of a mental arithmetic stress test and a handgrip exercise test, we studied the responses of blood pressure, heart rate, forearm blood flow and plasma catecholamines on two occasions, with an interval of at least 1 week, in 24 normotensive and 22 hypertensive subjects. 2. The se of a single observation of the percentage changes of blood pressure ranged from 3.9 to 9.3% in normotensive subjects and from 3.9 to 7.4% in hypertensive subjects in both tests. For heart rate, these values were 4.9–12.3% in the normotensive subjects and 4.8–5.7% in the hypertensive subjects. However, there was a wide individual scatter of these haemodynamic responses during both tests. The forearm blood flow, only measured during mental arithmetic, had an se of a single observation of 33.7%. 3. In 10 normotensive subjects the se of a single observation of the change in plasma noradrenaline was 0.16 nmol/l during handgrip exercise and 0.09 nmol/l during mental arithmetic. The corresponding values for plasma adrenaline were 0.04 and 0.05 nmol/l. 4. In conclusion, although both tests showed a rather low se of a single observation for the blood pressure and heart rate responses in normo- and hyper-tensive subjects, there was a considerable individual variability. If related to the mean forearm blood flow responses, the se of a single observation of the forearm blood flow response was of similar magnitude. The limited intra-individual reproducibility of both tests should be borne in mind when interpreting pharmacological intervention studies or studies evaluating sympathoadrenal reactivity in cardiovascular disorders.


1984 ◽  
Vol 57 (6) ◽  
pp. 1688-1695 ◽  
Author(s):  
S. M. Fortney ◽  
C. B. Wenger ◽  
J. R. Bove ◽  
E. R. Nadel

To study the effect of hyperosmolality on thermoregulatory responses, five men [average maximal O2 consumption (VO2 max) = 48 ml X kg-1 X min-1] cycled at 65-75% VO2max for up to 30 min in a 30 degrees C, 40% relative humidity environment under three conditions. First, control tests (C) were performed where preexercise plasma volume (PV) and osmolality (Osm) averaged 3,800 ml and 282 mosmol X kg-1, respectively. Second, exercise tests (D) were performed following dehydration induced by fluid restriction and mild exercise (30% VO2max) in hot (40 degrees C) ambient conditions. Each subject then rested in cool surroundings 1 h before performing the exercise test. Preexercise PV and Osm averaged 3,606 ml and 293 mosmol X kg-1, respectively. Third, exercise tests (I) were performed following dehydration, but during the 1-h rest interval, 3% saline was infused so that PV was restored to 3,826 ml and Osm averaged 294 mosmol X kg-1 prior to exercise. During D, esophageal temperatures (Tes) were significantly higher than C, an avg 0.56 degrees C after 20 min exercise due to a 0.22 degrees C increase in Tes threshold for vasodilation, a 39% reduction in slope of the forearm blood flow (BF)-Tes relationship, a 32% average reduction in maximal exercise BF, and a 0.22 degrees C increase in Tes sweating threshold. During I, responses were similar to D, except the BF-Tes slope and the maximum BF were not significantly different from C. Thus hyperosmolality modifies thermoregulation by elevating thresholds for both vasodilation and sweating even without decreases in PV.


2007 ◽  
Vol 293 (1) ◽  
pp. H805-H812 ◽  
Author(s):  
Benjamin C. Thompson ◽  
Tanvi Fadia ◽  
Danny M. Pincivero ◽  
Barry W. Scheuermann

Previous studies suggest that women experience less vascular occlusion than men when generating the same relative contractile force. This study examined forearm blood flow (FBF) in women and men during isometric handgrip exercise requiring the same relative force. Thirty-eight subjects [20 women and 18 men, 22.8 ± 0.6 yrs old (means ± SE)] performed low- and moderate-force handgrip exercise on two occasions. Subjects performed five maximum voluntary contractions (MVC) before exercise to determine 20% and 50% MVC target forces. Time to task failure (TTF) was determined when the subject could not maintain force within 5% of the target force. Mean blood velocity was measured in the brachial artery with the use of Doppler ultrasonography. Arterial diameter was measured at rest and used to calculate absolute FBF (FBFa; ml/min) and relative FBF (FBFr; ml·min−1·100 ml−1). Women generated less ( P < 0.05) absolute maximal force (208 ± 10 N) than men (357 ± 17 N). The TTF was longer ( P < 0.05) at 20% MVC for women (349 ± 32 s) than for men (230 ± 23 s), but no difference between the sexes was observed at 50% MVC (women: 69 ± 5 s; men: 71 ± 8 s). FBFa and FBFr increased ( P < 0.05) from rest to TTF in both women and men during 20% and 50% MVC trials. FBFr was greater in women than in men at ≥30% TTF during 50% MVC. At exercise durations ≥60% of TTF, FBFa was lower ( P < 0.05) in women than in men during handgrip at 20% MVC. Despite the longer exercise duration for women at the lower contraction intensity, FBFr was similar between the sexes, suggesting that muscle perfusion is matched to the exercising muscle mass independent of sex.


2005 ◽  
Vol 289 (5) ◽  
pp. R1387-R1391 ◽  
Author(s):  
Hemma Resch ◽  
Claudia Zawinka ◽  
Solveig Lung ◽  
Günther Weigert ◽  
Leopold Schmetterer ◽  
...  

Intravenous administration of histamine causes an increase in choroidal blood flow and retinal vessel diameter in healthy subjects. The mechanism underlying this effect remains to be elucidated. In the present study, we hypothesized that H2 receptor blockade alters hemodynamic effects of histamine in the choroid and retina. Eighteen healthy male nonsmoking volunteers were included in this randomized, double-masked, placebo-controlled two-way crossover study. Histamine (0.32 μg·kg−1·min−1 over 30 min) was infused intravenously in the absence (NaCl as placebo) or presence of the H2 blocker cimetidine (2.3 mg/min over 50 min). Ocular hemodynamic parameters, blood pressure, and intraocular pressure were measured before drug administration, after infusion of cimetidine or placebo, and after coinfusion of histamine. Subfoveal choroidal blood flow and fundus pulsation amplitude were measured with laser-Doppler flowmetry and laser interferometry, respectively. Retinal arterial and venous diameters were measured with a retinal vessel analyzer. Retinal blood velocity was assessed with bidirectional laser-Doppler velocimetry. Histamine increased subfoveal choroidal blood flow (+14 ± 15%, P < 0.001), fundus pulsation amplitude (+11 ± 5%, P < 0.001), retinal venous diameter (+3.0 ± 3.6%, P = 0.002), and retinal arterial diameter (+2.8 ± 4.2%, P < 0.01) but did not change retinal blood velocity. The H2 antagonist cimetidine had no significant effect on ocular hemodynamic parameters. In addition, cimetidine did not modify effects of histamine on choroidal blood flow, fundus pulsation amplitude, retinal venous diameter, and retinal arterial diameter compared with placebo. The present data confirm that histamine increases choroidal blood flow and retinal vessel diameters in healthy subjects. This ocular vasodilator effect of histamine is, however, not altered by administration of an H2 blocker. Whether the increase in blood flow is mediated via H1 receptors or other hitherto unidentified mechanisms remains to be elucidated.


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