scholarly journals Resistance training increases basal limb blood flow and vascular conductance in aging humans

2006 ◽  
Vol 101 (5) ◽  
pp. 1351-1355 ◽  
Author(s):  
Maria M. Anton ◽  
Miriam Y. Cortez-Cooper ◽  
Allison E. DeVan ◽  
Daria B. Neidre ◽  
Jill N. Cook ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Strength Training ◽  
Whole Body ◽  
Control Group ◽  
Limb Blood Flow ◽  
Vascular Conductance ◽  
Femoral Blood Flow ◽  
Femoral Blood

Age-related reductions in basal limb blood flow and vascular conductance are associated with the metabolic syndrome, functional impairments, and osteoporosis. We tested the hypothesis that a strength training program would increase basal femoral blood flow in aging adults. Twenty-six sedentary but healthy middle-aged and older subjects were randomly assigned to either a whole body strength training intervention group (52 ± 2 yr, 3 men, 10 women) who underwent three supervised resistance training sessions per week for 13 wk or a control group (53 ± 2 yr, 4 men, 9 women) who participated in a supervised stretching program. At baseline, there were no significant differences in blood pressure, cardiac output, basal femoral blood flow (via Doppler ultrasound), vascular conductance, and vascular resistance between the two groups. The strength training group increased maximal strength in all the major muscle groups tested ( P < 0.05). Whole body lean body mass increased ( P < 0.05) with strength training, but leg fat-free mass did not. Basal femoral blood flow and vascular conductance increased by 55–60% after strength training (both P < 0.05). No such changes were observed in the control group. In both groups, there were no significant changes in brachial blood pressure, plasma endothelin-1 and angiotensin II concentrations, femoral artery wall thickness, cardiac output, and systemic vascular resistance. Our results indicate that short-term strength training increases basal femoral blood flow and vascular conductance in healthy middle-aged and older adults.

Postexercise Hemodynamics in Patients With Type 2 Diabetes: Effect of Exercise Intensity and Duration

2017 ◽  
Vol 6 (1) ◽  
pp. 1-8
Author(s):  
Thomas K. Pellinger ◽  
Catherine B. Pearce ◽  
Grant H. Simmons ◽  
Jack L. Snitzer
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Blood Flow ◽  
Systolic Blood Pressure ◽  
Vascular Function ◽  
Muscle Blood Flow ◽  
Vascular Conductance ◽  
Femoral Blood Flow ◽  
Femoral Blood

Background: For individuals with type 2 diabetes (T2D), the hemodynamic response to regular exercise is critical for regulating blood glucose, protecting vascular function, and reducing cardiovascular disease risk, but the hemodynamic responses to differing doses of acute exercise in T2D are unclear. We aimed to compare postexercise (PE) hemodynamics in patients with T2D in response to 4 doses of dynamic exercise. Methods: Eight subjects with well-controlled T2D (42–64 years old.; hemoglobin A1c: 6.6% ± 0.9%) participated in 4 study days, during which they exercised on a cycle ergometer at 4 different combinations of exercise duration and intensity: 30 min at 40% V˙O2peak (30@40), 30 min at 60% V˙O2peak (30@60), 60 min at 40% V˙O2peak (60@40), and 60 min at 60% V˙O2peak (60@60). Heart rate, arterial pressure, and femoral blood flow (Doppler ultrasound) were measured pre-exercise and every 15 min through 120 min PE. Femoral vascular conductance was calculated as flow/pressure. Results: Compared with pre-exercise baseline, femoral blood flow and femoral vascular conductance were higher through at least 105 min of recovery in all conditions (all P &lt; .05), except for the 30@40 trial. Compared with the pre-exercise measures, systolic blood pressure was lower through at least 75 min of recovery in all conditions (all P &lt; .05), except for the 30@40 trial. Conclusion: These results suggest that exercise must be at least moderate in intensity or prolonged in duration (&gt;30 min) to promote sustained PE elevations in skeletal muscle blood flow and reductions in systolic blood pressure in patients with T2D.

Circulatory effects of moderately and severely increased intracranial pressure in the dog

1972 ◽  
Vol 36 (6) ◽  
pp. 721-727 ◽  
Author(s):  
Norberto C. Gonzalez ◽  
John Overman ◽  
John A. Maxwell
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Peripheral Resistance ◽  
Arterial Blood ◽  
Femoral Blood Flow ◽  
Femoral Blood

✓ Anesthetized dogs were subjected to elevated intracranial pressure (ICP) of 60 and 100 mm Hg. At 60 mm Hg, decreases in heart rate and arterial blood pressure were observed associated with an increase in femoral blood flow that suggested vasodilation in the somatic areas. Cardiac output showed little change. Subsequent elevation of ICP to 100 mm Hg was followed by an increase in arterial blood pressure; cardiac output increased, and femoral flow increased still further. Since resistance to flow did not change, the hypertension was thought to be due to an increase in flow rather than peripheral resistance. An increase in heart rate was associated with the elevation in cardiac output; the fact that femoral blood flow increased proportionately more than cardiac output suggested a redistribution of blood flow. The changes in peripheral blood flow and in cardiac output were associated with a decrease in the arteriovenous oxygen (A–VO2) difference. No signs of tissue hypoxia were observed; specifically there was no significant change in the lactate-to-pyruvate ratio; the changes in A–VO2 difference were correlated with changes in flow and the product of the two variables, namely, oxygen consumption, remained unchanged. The data show that experimental elevation of ICP restricted to moderate levels is followed by hemodynamic changes suggesting peripheral vasodilation, and that when an increase in blood pressure then occurs, it is due to an increase in blood flow despite the decrease in peripheral resistance.

scholarly journals Human muscle length-dependent changes in blood flow

2012 ◽  
Vol 112 (4) ◽  
pp. 560-565 ◽  
Author(s):  
John McDaniel ◽  
Stephen J. Ives ◽  
Russell S. Richardson
Keyword(s):  
Blood Flow ◽  
Knee Joint ◽  
Joint Angle ◽  
Muscle Blood Flow ◽  
Muscle Length ◽  
Limb Blood Flow ◽  
Knee Joint Angle ◽  
Femoral Blood Flow ◽  
Femoral Blood ◽  
Cyclic Changes

Although a multitude of factors that influence skeletal muscle blood flow have been extensively investigated, the influence of muscle length on limb blood flow has received little attention. Thus the purpose of this investigation was to determine if cyclic changes in muscle length influence resting blood flow. Nine healthy men (28 ± 4 yr of age) underwent a passive knee extension protocol during which the subjects' knee joint was passively extended and flexed through 100–180° knee joint angle at a rate of 1 cycle per 30 s. Femoral blood flow, cardiac output (CO), heart rate (HR), stroke volume (SV), and mean arterial pressure (MAP) were continuously recorded during the entire protocol. These measurements revealed that slow passive changes in knee joint angle did not have a significant influence on HR, SV, MAP, or CO; however, net femoral blood flow demonstrated a curvilinear increase with knee joint angle ( r2 = 0.98) such that blood flow increased by ∼90% (125 ml/min) across the 80° range of motion. This net change in blood flow was due to a constant antegrade blood flow across knee joint angle and negative relationship between retrograde blood flow and knee joint angle ( r2 = 0.98). Thus, despite the absence of central hemodynamic changes and local metabolic factors, blood flow to the leg was altered by changes in muscle length. Therefore, when designing research protocols, researchers need to be cognizant of the fact that joint angle, and ultimately muscle length, influence limb blood flow.

scholarly journals Systemic and regional hemodynamic response to activation of the exercise pressor reflex in patients with peripheral artery disease

2020 ◽  
Vol 318 (4) ◽  
pp. H916-H924 ◽  
Author(s):  
Danielle Jin-Kwang Kim ◽  
Marcos Kuroki ◽  
Jian Cui ◽  
Zhaohui Gao ◽  
J. Carter Luck ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Peripheral Artery Disease ◽  
Plantar Flexion ◽  
Peripheral Artery ◽  
Exercise Pressor Reflex ◽  
Femoral Blood Flow ◽  
Femoral Blood ◽  
Pressor Reflex ◽  
Artery Disease

Patients with peripheral artery disease (PAD) have an accentuated exercise pressor reflex (EPR) during exercise of the affected limb. The underlying hemodynamic changes responsible for this, and its effect on blood flow to the exercising extremity, are unclear. We tested the hypothesis that the exaggerated EPR in PAD is mediated by an increase in total peripheral resistance (TPR), which augments redistribution of blood flow to the exercising limb. Twelve patients with PAD and 12 age- and sex-matched subjects without PAD performed dynamic plantar flexion (PF) using the most symptomatic leg at progressive workloads of 2–12 kg (increased by 1 kg/min until onset of fatigue). We measured heart rate, beat-by-beat blood pressure, femoral blood flow velocity (FBV), and muscle oxygen saturation ([Formula: see text]) continuously during the exercise. Femoral blood flow (FBF) was calculated from FBV and baseline femoral artery diameter. Stroke volume (SV), cardiac output (CO), and TPR were derived from the blood pressure tracings. Mean arterial blood pressure and TPR were significantly augmented in PAD compared with control during PF. FBF increased during exercise to an equal extent in both groups. However, [Formula: see text] of the exercising limb remained significantly lower in PAD compared with control. We conclude that the exaggerated pressor response in PAD is mediated by an abnormal TPR response, which augments redistribution of blood flow to the exercising extremity, leading to an equal rise in FBF compared with controls. However, this increase in FBF is not sufficient to normalize the SmO2 response during exercise in patients with PAD. NEW & NOTEWORTHY In this study, peripheral artery disease (PAD) patients and healthy control subjects performed graded, dynamic plantar flexion exercise. Data from this study suggest that previously reported exaggerated exercise pressor reflex in patients with PAD is driven by greater vasoconstriction in nonexercising vascular territories which also results in a redistribution of blood flow to the exercising extremity. However, this rise in femoral blood flow does not fully correct the oxygen deficit due to changes in other mechanisms that require further investigation.

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.

Peripheral vasodilatation induced by a vasopressin analogue with selective V2-agonism in dogs

1989 ◽  
Vol 256 (6) ◽  
pp. H1621-H1626 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Hemodynamic Effects ◽  
Femoral Blood Flow ◽  
Peripheral Vasodilatation ◽  
Femoral Blood

The selective V2-agonist 4-valine-8-D-arginine vasopressin (VDAVP) increases cardiac output and heart rate and decreases total peripheral resistance in dogs. The mechanism of these hemodynamic effects was examined in the present studies. When infused into the left coronary artery of six conscious dogs for 1 h, VDAVP (10 ng.kg-1.min-1) increased cardiac output and decreased total peripheral resistance more than when given intravenously in the same animals. Administration of VDAVP into the carotid circulation elicited effects that did not differ significantly from those after intravenous infusion at the same rate in six conscious dogs. After destruction of the central nervous system in five dogs anesthetized with pentobarbital, VDAVP failed to increase cardiac output and heart rate but lowered mean arterial pressure and total peripheral resistance. Finally, infusion of VDAVP into the femoral artery of six anesthetized dogs increased femoral blood flow at rates of 1, 5, and 10 ng.kg-1.min-1, whereas none of these rates increased femoral blood flow when given intravenously. Thus the hemodynamic effects of VDAVP appear to result primarily from a peripheral vasodilatory action, with possible contribution from a positive inotropic effect. We found no evidence that central effects of VDAVP were importantly involved in its cardiovascular action.

Integrative control of the skeletal muscle microcirculation in the maintenance of arterial pressure during exercise

2004 ◽  
Vol 97 (3) ◽  
pp. 1112-1118 ◽  
Author(s):  
Michael D. Delp ◽  
Donal S. O'Leary
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Dynamic Exercise ◽  
Whole Body ◽  
Control Mechanisms ◽  
Vascular Control ◽  
Vascular Conductance ◽  
Body Dynamic

Skeletal muscle blood flow and vascular conductance are influenced by numerous factors that can be divided into two general categories: central cardiovascular control mechanisms and local vascular control mechanisms. Central cardiovascular control mechanisms are thought to be designed primarily for the maintenance of arterial pressure and central cardiovascular homeostasis, whereas local vascular control mechanisms are thought to be designed primarily for the maintenance of muscle homeostasis. To support the high metabolic rates that can be generated during muscle contraction, skeletal muscle has a tremendous capacity to vasodilate and increase oxygen and nutrient delivery. During whole body dynamic exercise at maximal oxygen consumption (V̇o2 max), the skeletal muscle receives 85–90% of cardiac output. Yet despite receiving such a large fraction of cardiac output during high-intensity exercise, a vasodilator reserve remains with the potential to produce further elevations in skeletal muscle vascular conductance and blood flow. However, because maximal cardiac output is reached during exercise at V̇o2 max, further elevations in muscle vascular conductance would produce a fall in arterial pressure. Therefore, limits on muscle perfusion must be imposed during whole body exercise to prevent such drops in pressure. Effective arterial pressure control in response to a potentially hypotensive challenge during high-intensity exercise occurs primarily through reflex-mediated increases in sympathetic nerve activity, which are capable of modulating vasomotor tone of the skeletal muscle resistance vasculature. Thus skeletal muscle vascular conductance and perfusion are primarily mediated by local factors at rest and during exercise, but other centrally mediated control systems are superimposed on the dominant local control mechanisms to provide an integrated regulation of both arterial pressure and skeletal muscle vascular conductance and perfusion during whole body dynamic exercise.

scholarly journals Cardiovascular control during whole body exercise

2016 ◽  
Vol 121 (2) ◽  
pp. 376-390 ◽  
Author(s):  
Stefanos Volianitis ◽  
Niels H. Secher
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Muscle Group ◽  
Whole Body ◽  
Muscle Groups ◽  
Exercise Muscle

It has been considered whether during whole body exercise the increase in cardiac output is large enough to support skeletal muscle blood flow. This review addresses four lines of evidence for a flow limitation to skeletal muscles during whole body exercise. First, even though during exercise the blood flow achieved by the arms is lower than that achieved by the legs (∼160 vs. ∼385 ml·min−1·100 g−1), the muscle mass that can be perfused with such flow is limited by the capacity to increase cardiac output (42 l/min, highest recorded value). Secondly, activation of the exercise pressor reflex during fatiguing work with one muscle group limits flow to other muscle groups. Another line of evidence comes from evaluation of regional blood flow during exercise where there is a discrepancy between flow to a muscle group when it is working exclusively and when it works together with other muscles. Finally, regulation of peripheral resistance by sympathetic vasoconstriction in active muscles by the arterial baroreflex is critical for blood pressure regulation during exercise. Together, these findings indicate that during whole body exercise muscle blood flow is subordinate to the control of blood pressure.

Regional blood flow and vascular resistance during hypothermia in dog

1961 ◽  
Vol 201 (3) ◽  
pp. 485-491 ◽  
Author(s):  
Bjorn Westin ◽  
N. Sehgal ◽  
N. S. Assali
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sine Wave ◽  
Blood Flows ◽  
Femoral Blood Flow ◽  
Regional Vascular Resistance ◽  
Femoral Blood ◽  
Carotid Flow

Changes in regional blood flow and regional vascular resistance during hypothermia in dogs with intact or abolished shivering mechanisms were measured with sine-wave electromagnetic flowmeters. In animals with shivering intact, cooling produced a fall in renal and carotid blood flows, despite a rise or no change in cardiac output. The fall was caused by an increase in renal and carotid vascular resistances. Femoral blood flow increased because of a decrease in vascular resistance. In animals with shivering abolished, cooling evoked a fall in the cardiac output and in renal and femoral blood flows, due to an increase in the vascular resistance. Upon rewarming, femoral flow immediately rose to values far above control. Carotid flow increased during cooling because of a decline in carotid resistance. Such a decline might have been related to the elevated blood Pco2 observed in the nonshivering animals.

The role of aortic chemoreceptors during severe CO hypoxia

1985 ◽  
Vol 63 (5) ◽  
pp. 509-514 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cardiac Output ◽  
Whole Body ◽  
Limb Blood Flow ◽  
Intact Group ◽  
Anesthetized Dogs ◽  
Dialysis Method

The importance of aortic chemoreceptors in the circulatory responses to severe carbon monoxide (CO) hypoxia was studied in anesthetized dogs. The aortic chemoreceptors were surgically denervated in eight dogs prior to the induction of CO hypoxia, with nine other dogs serving as intact controls. Values for both whole body and hindlimb blood flow, vascular resistance, and O2 uptake were determined prior to and at 30 min of CO hypoxia in the two groups. Arterial O2 content was reduced 65% using an in situ dialysis method to produce CO hypoxia. At 30 min of hypoxia, cardiac output increased but limb blood flow remained at prehypoxic levels in both groups. This indicated that aortic chemoreceptor input was not necessary for the increase in cardiac output during severe CO hypoxia, nor for the diversion of this increased flow to nonmuscle tissues. Limb O2 uptake decreased during CO hypoxia in the aortic-denervated group but remained at prehypoxic levels in the intact group. The lower resting values for limb blood flow in the aortic-denervated animals required a greater level of O2 extraction to maintain resting O2 uptake. When CO hypoxia was superimposed upon this compensation, an O2 supply limitation occurred because the limb failed to vasodilate even as maximal levels for O2 extraction were approached.

Sign in / Sign up

Export Citation Format

Share Document