scholarly journals H2-receptor-mediated vasodilation contributes to postexercise hypotension

2006 ◽  
Vol 100 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Jennifer L. McCord ◽  
Julie M. Beasley ◽  
John R. Halliwill
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Potential Contribution ◽  
Vascular Conductance ◽  
Men And Women ◽  
Femoral Blood Flow ◽  
Postexercise Hypotension ◽  
Femoral Blood ◽  
Randomized Control ◽  
Automated Auscultation

The early (∼30 min) postexercise hypotension response after a session of aerobic exercise is due in part to H1-receptor-mediated vasodilation. The purpose of this study was to determine the potential contribution of H2-receptor-mediated vasodilation to postexercise hypotension. We studied 10 healthy normotensive men and women (ages 23.7 ± 3.4 yr) before and through 90 min after a 60-min bout of cycling at 60% peak O2 uptake on randomized control and H2-receptor antagonist days (300 mg oral ranitidine). Arterial pressure (automated auscultation), cardiac output (acetylene washin) and femoral blood flow (Doppler ultrasound) were measured. Vascular conductance was calculated as flow/mean arterial pressure. Sixty minutes postexercise on the control day, femoral (Δ62.3 ± 15.6%, where Δ is change; P < 0.01) and systemic (Δ13.8 ± 5.3%; P = 0.01) vascular conductances were increased, whereas mean arterial pressure was reduced (Δ−6.7 ± 1.1 mmHg; P < 0.01). Conversely, 60 min postexercise with ranitidine, femoral (Δ9.4 ± 9.2%; P = 0.34) and systemic (Δ−2.8 ± 4.8%; P = 0.35) vascular conductances were not elevated and mean arterial pressure was not reduced (Δ−2.2 ± 1.3 mmHg; P = 0.12). Furthermore, postexercise femoral and systemic vascular conductances were lower ( P < 0.05) and mean arterial pressure was higher ( P = 0.01) on the ranitidine day compared with control. Ingestion of ranitidine markedly reduces vasodilation after exercise and blunts postexercise hypotension, suggesting H2-receptor-mediated vasodilation contributes to postexercise hypotension.

Postexercise hypotension is not explained by a prostaglandin-dependent peripheral vasodilation

2005 ◽  
Vol 98 (2) ◽  
pp. 447-453 ◽  
Author(s):  
Jennifer M. Lockwood ◽  
Mollie P. Pricher ◽  
Brad W. Wilkins ◽  
Lacy A. Holowatz ◽  
John R. Halliwill
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Potential Contribution ◽  
Vascular Conductance ◽  
Cyclooxygenase Inhibition ◽  
Peripheral Vasodilation ◽  
Arterial Blood ◽  
Single Bout ◽  
Oral Ibuprofen ◽  
Postexercise Hypotension

In normally active individuals, postexercise hypotension after a single bout of aerobic exercise occurs due to an unexplained peripheral vasodilation. Prostaglandin production has been suggested to contribute to the increases in blood flow during and after exercise; however, its potential contribution to postexercise hypotension has not been assessed. The purpose of this study was to determine the potential contribution of a prostaglandin-dependent vasodilation to changes in systemic vascular conductance underlying postexercise hypotension; this was done by inhibiting production of prostaglandins with the cyclooxygenase inhibitor ibuprofen. We studied 11 healthy normotensive men (aged 23.7 ± 4.2 yr) before and during the 90 min after a 60-min bout of cycling at 60% peak O2 uptake on a control and a cyclooxygenase inhibition day (randomized). Subjects received 10 mg/kg of oral ibuprofen on the cyclooxygenase inhibition day. On both study days, arterial blood pressure (automated auscultation) and cardiac output (acetylene uptake) were measured, and systemic vascular conductance was calculated. Inhibition of cyclooxygenase had no effect on baseline values of mean arterial pressure or systemic vascular conductance ( P > 0.2). After exercise on both days, mean arterial pressure was reduced (−2.2 ± 1.0 mmHg change with the control condition and −3.8 ± 1.5 mmHg change with the ibuprofen condition, both P < 0.05 vs. preexercise) and systemic vascular conductance was increased (5.2 ± 5.0% change with the control condition and 8.7 ± 4.1% change with the ibuprofen condition, both P < 0.05 vs. preexercise). There were no differences between study days ( P > 0.6). These data suggest that prostaglandin-dependent vasodilation does not contribute to the increased systemic vascular conductance underlying postexercise hypotension.

scholarly journals Exercise-induced vasodilation is associated with menopause stage in healthy middle-aged women

2012 ◽  
Vol 37 (3) ◽  
pp. 418-424 ◽  
Author(s):  
David J. Moore ◽  
Joaquin U. Gonzales ◽  
Steven H. Tucker ◽  
Steriani Elavsky ◽  
David N. Proctor
Keyword(s):  
Ldl Cholesterol ◽  
Middle Aged ◽  
Vascular Conductance ◽  
Femoral Blood Flow ◽  
Perimenopausal Women ◽  
Vascular Responsiveness ◽  
Leg Exercise ◽  
Exercise Hemodynamics ◽  
Femoral Blood ◽  
Exercise Induced

Leg exercise hemodynamics during single-leg knee extensions were compared among healthy groups of early perimenopausal (n = 15), late perimenopausal (n = 12), and early postmenopausal (n = 11) women. Femoral blood flow (FBF) and vascular conductance (FVC) at rest and during very light work rates (0 and 5 W) were similar among all three menopause stage groups. Vascular responses at 10 W (FBF) and 20 W (FBF and FVC) were significantly higher (P < 0.05) in early perimenopausal compared with late perimenopausal women. At 15 and 25 W, FBF and FVC were similar between late perimenopausal and early postmenopausal groups but higher (P < 0.05) in early perimenopausal women as compared with the other two menopausal groups. In the combined sample of all three menopause stage groups, follicle-stimulating hormone was significantly correlated with vascular conductance during submaximal (15 W) exercise (R = –0.56, P < 0.001), even after adjustment for age, fitness, LDL cholesterol, and abdominal fat (R = –0.46, P = 0.005). Collectively, these findings suggest that in middle-aged women, there is an association between menopause stage and leg vascular responsiveness during exercise.

Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

2005 ◽  
Vol 98 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
Jay T. Williams ◽  
Mollie P. Pricher ◽  
John R. Halliwill
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Causal Link ◽  
Skeletal Muscle Blood Flow ◽  
Leg Blood Flow ◽  
Postexercise Hypotension

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20–31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery V̇o2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, V̇o2 was increased by 11 ± 2%, leg blood flow was increased by 51 ± 18%, leg vascular conductance was increased by 56 ± 19%, and mean arterial pressure was decreased by 2.2 ± 1.0 mmHg (all P < 0.05 vs. preexercise). At the end of the protocol, V̇o2 remained elevated by 4 ± 2% ( P < 0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.

Effects of the menstrual cycle and sex on postexercise hemodynamics

2007 ◽  
Vol 292 (3) ◽  
pp. R1260-R1270 ◽  
Author(s):  
Brenna M. Lynn ◽  
Jennifer L. McCord ◽  
John R. Halliwill
Keyword(s):  
Menstrual Cycle ◽  
Arterial Pressure ◽  
Cardiovascular Regulation ◽  
Endogenous Hormones ◽  
Menstrual Phase ◽  
Percent Reduction ◽  
Vascular Conductance ◽  
Men And Women ◽  
Factors Associated ◽  
Menstruating Women

Factors associated with the menstrual cycle, such as the endogenous hormones estrogen and progesterone, have dramatic effects on cardiovascular regulation. It is unknown how this affects postexercise hemodynamics. Therefore, we examined the effects of the menstrual cycle and sex on postexercise hemodynamics. We studied 14 normally menstruating women [24.0 (4.2) yr; SD] and 14 men [22.5 (3.5) yr] before and through 90 min after cycling at 60% V̇o2 peak for 60 min. Women were studied during their early follicular, ovulatory, and mid-luteal phases; men were studied once. In men and women during all phases studied, mean arterial pressure was decreased after exercise throughout 60 min ( P < 0.001) postexercise and returned to preexercise values at 90 min ( P = 0.089) postexercise. Systemic vascular conductance was increased following exercise in both sexes throughout 60 min ( P = 0.005) postexercise and tended to be elevated at 90 min postexercise ( P = 0.052), and femoral vascular conductance was increased following exercise throughout 90 min ( P < 0.001) postexercise. Menstrual phase and sex had no effect on the percent reduction in arterial pressure ( P = 0.360), the percent rise in systemic vascular conductance ( P = 0.573), and the percent rise in femoral vascular conductance ( P = 0.828) from before to after exercise, nor did the pattern of these responses differ across recovery with phase or sex. This suggests that postexercise hemodynamics are largely unaffected by sex or factors associated with the menstrual cycle.

scholarly journals Sex differences in leg vasodilation during graded knee extensor exercise in young adults

2007 ◽  
Vol 103 (5) ◽  
pp. 1583-1591 ◽  
Author(s):  
Beth A. Parker ◽  
Sandra L. Smithmyer ◽  
Justin A. Pelberg ◽  
Aaron D. Mishkin ◽  
Michael D. Herr ◽  
...  
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Knee Extensor ◽  
Activity Levels ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Vasodilatory Response ◽  
Femoral Blood Flow ◽  
Femoral Blood ◽  
Response To Exercise

Limb vascular conductance responses to pharmacological and nonexercise vasodilator stimuli are generally augmented in women compared with men. In the present investigation, we tested the hypothesis that exercise-induced vasodilator responses are also greater in women than men. Sixteen women and 15 men (20–30 yr) with similar fitness and activity levels performed graded quadriceps exercise (supine, single-leg knee extensions, 40 contractions/min) to maximal exertion. Active limb hemodynamics (left common femoral artery diameter and volumetric blood flow), heart rate (ECG), and beat-to-beat mean arterial blood pressure (MAP; radial artery tonometry) were measured during each 3-min workload (4.8 and 8 W/stage for women and men, respectively). The hyperemic response to exercise (slope of femoral blood flow vs. workload) was greater ( P < 0.01) in women as was femoral blood flow at workloads >15 W. The leg vasodilatory response to exercise (slope of calculated femoral vascular conductance vs. absolute workload) was also greater in women than in men ( P < 0.01) because of the sex difference in hyperemia and the women's lower MAP (∼10–15 mmHg) at all workloads ( P < 0.05). The femoral artery dilated to a significantly greater extent in the women (∼0.5 mm) than in the men (∼0.1 mm) across all submaximal workloads. At maximal exertion, femoral vascular conductance was lower in the men (men, 18.0 ± 0.6 ml·min−1·mmHg−1; women, 22.6 ± 1.4 ml·min−1·mmHg−1; P < 0.01). Collectively, these findings suggest that the vasodilatory response to dynamic leg exercise is greater in young women vs. men.

Oxidative stress contributes to chronic leg vasoconstriction in estrogen-deficient postmenopausal women

2007 ◽  
Vol 102 (3) ◽  
pp. 890-895 ◽  
Author(s):  
Kerrie L. Moreau ◽  
Ashley R. DePaulis ◽  
Kathleen M. Gavin ◽  
Douglas R. Seals
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Ascorbic Acid ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Postmenopausal Women ◽  
Oxidized Ldl ◽  
Duplex Ultrasound ◽  
Vascular Conductance ◽  
Leg Blood Flow

Basal whole leg blood flow and vascular conductance are reduced in estrogen-deficient postmenopausal compared with premenopausal women. The underlying mechanisms are unknown, but oxidative stress could be involved. We studied 9 premenopausal [23 ± 1 yr (mean ± SE)] and 20 estrogen-deficient postmenopausal (55 ± 1 yr) healthy women. During baseline control, oxidized low-density lipoprotein (LDL), a marker of oxidative stress, was 50% greater in the postmenopausal women ( P < 0.001). Basal whole leg blood flow (duplex ultrasound of femoral artery) was 34% lower in the postmenopausal women because of a 38% lower leg vascular conductance ( P < 0.0001); mean arterial pressure was not different. Intravenous administration of a supraphysiological dose of the antioxidant ascorbic acid increased leg blood flow by 15% in the postmenopausal women as a result of an increase in leg vascular conductance (both P < 0.001), but it did not affect leg blood flow in premenopausal controls or mean arterial pressure in either group. In the pooled subjects, the changes in leg blood flow and leg vascular conductance with ascorbic acid were related to baseline plasma oxidized LDL ( r = 0.46 and 0.53, P < 0.01) and waist-to-hip ratio and total body fat ( r = 0.41–0.44, all P < 0.05). Our results are consistent with the hypothesis that oxidative stress contributes to chronic leg vasoconstriction and reduced basal whole leg blood flow in estrogen-deficient postmenopausal women. This oxidative stress-related suppression of leg vascular conductance and blood flow may be linked in part to increased total and abdominal adiposity.

scholarly journals Aerobic training and cutaneous vasodilation in young and older men

1999 ◽  
Vol 86 (5) ◽  
pp. 1676-1686 ◽  
Author(s):  
Carla M. Thomas ◽  
Jane M. Pierzga ◽  
W. Larry Kenney
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Aerobic Training ◽  
Older Men ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Forearm Vascular Conductance ◽  
Response To Exercise ◽  
Cutaneous Vascular Conductance

To determine the effect and underlying mechanisms of exercise training and the influence of age on the skin blood flow (SkBF) response to exercise in a hot environment, 22 young (Y; 18–30 yr) and 21 older (O; 61–78 yr) men were assigned to 16 wk of aerobic (A; YA, n = 8; OA, n = 11), resistance (R; YR, n = 7; OR, n = 3), or no training (C; YC, n = 7; OC, n = 7). Before and after treatment, subjects exercised at 60% of maximum oxygen consumption (V˙o 2 max) on a cycle ergometer for 60 min at 36°C. Cutaneous vascular conductance, defined as SkBF divided by mean arterial pressure, was monitored at control (vasoconstriction intact) and bretylium-treated (vasoconstriction blocked) sites on the forearm using laser-Doppler flowmetry. Forearm vascular conductance was calculated as forearm blood flow (venous occlusion plethysmography) divided by mean arterial pressure. Esophageal and skin temperatures were recorded. Only aerobic training (functionally defined a priori as a 5% or greater increase inV˙o 2 max) produced a decrease in the mean body temperature threshold for increasing forearm vascular conductance (36.89 ± 0.08 to 36.63 ± 0.08°C, P < 0.003) and cutaneous vascular conductance (36.91 ± 0.08 to 36.65 ± 0.08°C, P < 0.004). Similar thresholds between control and bretylium-treated sites indicated that the decrease was mediated through the active vasodilator system. This shift was more pronounced in the older men who presented greater training-induced increases in V˙o 2 maxthan did the young men (22 and 9%, respectively). In summary, older men improved their SkBF response to exercise-heat stress through the effect of aerobic training on the cutaneous vasodilator system.

Coronary effects of endothelin-1 during acute hypertension in anaesthetized goats

2002 ◽  
Vol 103 (s2002) ◽  
pp. 376S-379S ◽  
Author(s):  
Nuria FERNÁNDEZ ◽  
María ANGELES MARTÍNEZ ◽  
Angel Luis GARCÍA-VILLALÓN ◽  
Luis MONGE ◽  
Godofredo DIÉGUEZ
Keyword(s):  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Coronary Flow ◽  
Circumflex Coronary Artery ◽  
Aortic Constriction ◽  
Vascular Conductance ◽  
Acute Hypertension ◽  
Endothelin 1 ◽  
Artery Flow

The coronary effects of endothelin-1 (ET-1) during acute hypertension were examined in anesthetized goats, where the left circumflex coronary artery flow was electromagnetically measured and hypertension was induced by constriction of the thoracic aorta. In six non-treated goats, aortic constriction increased arterial pressure (mean arterial pressure = 128±5mmHg) and coronary flow (by 34%) without changing coronary vascular conductance. In this case, ET-1 (0.01–0.3nmol) when injected intracoronarily, decreased coronary vascular conductance, which was similar in hypertension and in normotension. In eight NG-nitro-L-arginine methyl ester-treated goats, aortic constriction increased arterial pressure (mean arterial pressure = 131±5mmHg) and coronary flow (by 26%) and decreased coronary vascular conductance (by 17%). In this case, ET-1 (0.01–0.3nmol) also decreased coronary vascular conductance, which was similar in NG-nitro-L-arginine methyl ester-treated hypertension that observed in normotension. Therefore, acute hypertension attenuates the coronary vasoconstriction caused by ET-1, and this attenuation might be related to mechanisms other than changes in NO release.

The Postexercise Increase in the Threshold for Cutaneous Vasodilation and Sweating is Not Observed With Extended Recovery

2005 ◽  
Vol 30 (1) ◽  
pp. 113-121 ◽  
Author(s):  
Glen P. Kenny ◽  
W. Shane Journeay
Keyword(s):  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
No Reduction ◽  
Treadmill Running ◽  
Whole Body ◽  
Exercise Recovery ◽  
Mean Skin Temperature ◽  
Cutaneous Vasodilation ◽  
Postexercise Hypotension

The following study was conducted to evaluate the hypothesis that an increase in the postexercise onset threshold for cutaneous vasodilation (ThVD) and sweating (ThSW) would not be observed upon the restoration of baseline mean arterial pressure (MAP). Subjects remained either seated resting for 15 min or performed 15 min of treadmill running at 70% [Formula: see text]peak followed by either 20- (short) or 60-min (extended) recovery. At the end of each recovery protocol (20 and 60 min) a water perfusion suit was then used to increase mean skin temperature until ThVD and ThSW was noted. Exercise resulted in an increase in ThVD and ThSW of 0.24 ± 0.03 and 0.24 ± 0.02 °C, respectively, above no-exercise for the short recovery (p < 0.05). No increase was measured for the extended recovery. Postexercise MAP was significantly reduced prior to whole-body warming for the short recovery whereas no reduction was measured for the extended recovery. The increase in ThVD and ThSW, measured during the early stages of recovery, is reversed with the reestablishment of baseline MAP. Key words: postexercise hypotension, exercise recovery, baroreceptors, heat stress

Role of cardiac output in the pressor responses to graded muscle ischemia in man

1978 ◽  
Vol 45 (4) ◽  
pp. 574-580 ◽  
Author(s):  
F. Bonde-Petersen ◽  
L. B. Rowell ◽  
R. G. Murray ◽  
G. G. Blomqvist ◽  
R. White ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Conductance ◽  
Total Occlusion ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Leg Exercise

Ten men repeatedly performed leg exercise (100–150 W) for 7 min with 30-min recovery periods interspersed. Both legs were made ischemic by total occlusion (OCCL), first for 3 min immediately after exercise and second for 30 s before exercise ended and 3 min into recovery. In addition legs were occluded for 3 min at rest (seated). OCCL at rest increased mean arterial pressure (MAP) by 9 Torr but did not affect cardiac output (CO) or heart rate (HR). OCCL at the end of exercise significantly raised MAP and HR above control values during 3-min recovery but CO was unaffected. OCCL 30 s before the end of exercise further increased MAP and HR significantly during recovery; MAP, CO, and HR were significantly increased above control values (CO by 2.1 1-min-1) during the 3rd min of recovery. We conclude that a strong reflex from ischemic legs maintains normal or elevated CO during leg OCCL. Thus CO was too high relative to total vascular conductance so that MAP was elevated.

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