EFFECTS OF ISOMETRIC EXERCISE AND COLD PRESSOR TEST ON BLOOD PRESSURE, BLOOD FLOW, AND HEART RATE.

1995 ◽  
Vol 27 (Supplement) ◽  
pp. S185
Author(s):  
B. M. Bacik ◽  
R. L Wiley ◽  
R. H. Cox
1981 ◽  
Vol 61 (s7) ◽  
pp. 161s-164s ◽  
Author(s):  
P. Bolli ◽  
F. W. Amann ◽  
L. Hulthén ◽  
W. Kiowski ◽  
F. R. Bühler

1. Stressful sympathetic stimulation (cold pressor test) was applied to 18 patients with essential hypertension and 15 normotensive subjects. Intra-arterial blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during the cold pressor test; tests were repeated after regional postsynaptic α1-adrenoceptor blockade with prazosin. 2. Under basal conditions mean blood pressure (P < 0.001), heart rate (P < 0.01), forearm blood flow (P < 0.001) as well as adrenaline concentration (P < 0.01), but not noradrenaline, was higher in patients with essential hypertension. 3. During the cold pressor test, mean blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations increased and forearm flow decreased (all P < 0.001). 4. Stress-stimulated plasma adrenaline was higher in essential hypertensive patients than in normotensive subjects (P < 0.01). In the former the stress-induced increase in plasma adrenaline correlated with the increase in mean blood pressure (r = 0.514; P < 0.05). 5. Prazosin increased forearm blood flow more in essential hypertension (P < 0.001). This increase correlated with the resting plasma adrenaline in the hypertensive (r = 0.710; P < 0.001), but not in normotensive, subjects. 6. When the cold pressor test was repeated during postsynaptic α1-adrenoceptor blockade forearm blood flow did not decrease; instead it increased further in both groups (P < 0.05). 7. Thus in essential hypertension elevated plasma adrenaline concentration reflects sympathetic overactivity as also expressed by enhanced α-adrenoceptor-mediated vasoconstriction.


1985 ◽  
Vol 69 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Gianfranco Parati ◽  
Guido Pomidossi ◽  
Agustin Ramirez ◽  
Bruno Cesana ◽  
Giuseppe Mancia

1. In man evaluation of neural cardiovascular regulation makes use of a variety of tests which address the excitatory and reflex inhibitory neural influences that control circulation. Because interpretation of these tests is largely based on the magnitude of the elicited haemodynamic responses, their reproducibility in any given subject is critical. 2. In 39 subjects with continuous blood pressure (intra-arterial catheter) and heart rate monitoring we measured (i) the blood pressure and heart rate rises during hand-grip and cold-pressor test, (ii) the heart rate changes occurring during baroreceptor stimulation and deactivation by injection of phenylephrine and trinitroglycerine, and (iii) the heart rate and blood pressure changes occurring with alteration in carotid baroreceptor activity by a neck chamber. Each test was carefully standardized and performed at 30 min intervals for a total of six times in each subject. 3. The results showed that the responses to any test were clearly different from one another and that this occurred in all subjects studied. For the group as a whole the average response variability (coefficient of variation) ranged from 10.2% for the blood pressure response to carotid baroreceptor stimulation to 44.2% for the heart rate response to cold-pressor test. The variability of the responses was not related to basal blood pressure or heart rate, nor to the temporal sequence of the test performance. 4. Thus tests employed for studying neural cardiovascular control in man produce responses whose reproducibility is limited. This phenomenon may make it more difficult to define the response magnitude typical of each subject, as well as its comparison in different conditions and diseases.


1993 ◽  
Vol 3 (5) ◽  
pp. 303-310 ◽  
Author(s):  
Frank Weise ◽  
Dominique Laude ◽  
Arlette Girard ◽  
Philippe Zitoun ◽  
Jean-Philippe Siché ◽  
...  

2019 ◽  
Vol 222 ◽  
pp. 102581 ◽  
Author(s):  
Brittney A. Herrington ◽  
Scott F. Thrall ◽  
Leah M. Mann ◽  
Michael M. Tymko ◽  
Trevor A. Day

10.4085/16-20 ◽  
2020 ◽  
Author(s):  
Lentini Matylda ◽  
Scalia Joseph ◽  
Berger Lebel Frédérike ◽  
Touma Fadi ◽  
Jhajj Aneet ◽  
...  

Abstract Context: Athletes are often exposed to pain due to injury and competition. There is preliminary evidence that cardiovascular measures could be an objective measure of pain, but the cardiovascular response can be influenced by psychological factors such as catastrophizing. Objectives: The purpose of our study was to use a painful cold pressor test to measure the relationship between catastrophizing, pain, and cardiovascular variables in athletes. Design: Pre-post test. Setting: We completed all measures in a laboratory setting. Participants: Thirty-six male rugby athletes participated in the study. Main outcome measures: We measured catastrophizing with the Pain Catastrophizing Scale and pain with a Numeric Pain Rating Scale. Cardiovascular measures included heart rate, systolic, and diastolic blood pressure, and heart rate variability. Results: During the cold pressor test, participants experienced a significant increase in pain (0 to 4.1±2.2), systolic blood pressure (126.7±16.5mm Hg to 149.7±23.4mm Hg), diastolic blood pressure (76.9±8.3mm Hg to 91.9±11.5mm Hg) and heart rate variability (from 0.0164ms±0.0121 to 0.0400ms±0.0323) (all p<.001). In addition, there was a significant decrease in heart rate after the cold pressor test (p=0.04). There was a significant correlation between athlete's pain catastrophizing to both pain intensity and change in heart rate during the cold pressor test (p=.017 and p=.003 respectively). A significant linear regression indicated pain and catastrophizing explained 29% of the variance of the change in heart rate (p=.003). Conclusion: Athletes who have catastrophizing thoughts are more likely to experience higher levels of pain and a greater cardiovascular response during a painful stimulus. The change in cardiovascular variables may be a good alternative for an objective measure of pain in athletes in the future.


2005 ◽  
Vol 99 (5) ◽  
pp. 1866-1871 ◽  
Author(s):  
William G. Schrage ◽  
Brad W. Wilkins ◽  
Vicki L. Dean ◽  
John P. Scott ◽  
Nancy K. Henry ◽  
...  

ATP released from circulating erythrocytes is a potential signal regulating muscle blood flow during exercise (exercise hyperemia), and intravascular ATP appears to blunt sympathetic vasoconstriction during exercise. Erythrocytes from patients with cystic fibrosis (CF) do not release ATP. The goal of the present study was to determine whether increases in forearm blood flow during exercise are blunted in CF patients and whether CF patients exhibit greater vasoconstrictor responsiveness during exercise. Nine control subjects and 10 CF patients who were free of other disease complications (∼96% O2 saturation) performed incremental rhythmic forearm exercise at 5, 10, and 15% of maximum handgrip strength for 21 min (7 min at each workload). We used a cold pressor test to evoke sympathetic vasoconstriction under resting conditions and at each exercise workload. As a control, subjects performed a second exercise bout without the cold pressor test. Continuous brachial artery blood velocity was monitored beat-to-beat, and vessel diameter was assessed by Doppler ultrasound. Artery diameter, as well as blood pressure, heart rate, and O2 saturation, was measured at steady-state exercise and at 1 min into the cold pressor stimulus. Blood pressure and heart rate responses to the forearm exercise and each cold pressor test were similar in both groups ( P > 0.05). Contrary to our hypothesis, forearm blood flow ( P = 0.91) and forearm vascular conductance ( P = 0.82) were similar at rest and at each level of exercise between CF patients and controls. Additionally, there was no difference in the degree of sympathetic vasoconstriction between groups at rest and at each level of exercise ( P = 0.22). Our results suggest that ATP released from the deformation of erythrocytes is not an obligatory signal for exercise hyperemia in human skeletal muscle.


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