LETTER TO THE EDITOR: Does cardiac output determine leg blood-flow?

1986 ◽  
Vol 6 (1) ◽  
pp. 109-109
Author(s):  
K. Aukland
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Leg Blood Flow ◽  
Letter To The Editor

scholarly journals Reduced submaximal leg blood flow after high-intensity aerobic training

2001 ◽  
Vol 91 (6) ◽  
pp. 2619-2627 ◽  
Author(s):  
David N. Proctor ◽  
Jordan D. Miller ◽  
Niki M. Dietz ◽  
Christopher T. Minson ◽  
Michael J. Joyner
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Power Output ◽  
High Intensity ◽  
Aerobic Training ◽  
Muscle Blood Flow ◽  
Splanchnic Blood Flow ◽  
Active Muscle ◽  
Leg Blood Flow ◽  
Power Outputs

This study evaluated the hypothesis that active muscle blood flow is lower during exercise at a given submaximal power output after aerobic conditioning as a result of unchanged cardiac output and blunted splanchnic vasoconstriction. Eight untrained subjects (4 men, 4 women, 23–31 yr) performed high-intensity aerobic training for 9–12 wk. Leg blood flow (femoral vein thermodilution), splanchnic blood flow (indocyanine green clearance), cardiac output (acetylene rebreathing), whole body O2 uptake (V˙o 2), and arterial-venous blood gases were measured before and after training at identical submaximal power outputs (70 and 140 W; upright 2-leg cycling). Training increased ( P < 0.05) peak V˙o 2(12–36%) but did not significantly change submaximalV˙o 2 or cardiac output. Leg blood flow during both submaximal power outputs averaged 18% lower after training ( P = 0.001; n = 7), but these reductions were not correlated with changes in splanchnic vasoconstriction. Submaximal leg V˙o 2 was also lower after training. These findings support the hypothesis that aerobic training reduces active muscle blood flow at a given submaximal power output. However, changes in leg and splanchnic blood flow resulting from high-intensity training may not be causally linked.

Leg crossing with muscle tensing, a physical counter-manoeuvre to prevent syncope, enhances leg blood flow

2007 ◽  
Vol 112 (3) ◽  
pp. 193-201 ◽  
Author(s):  
Jan T. Groothuis ◽  
Nynke van Dijk ◽  
Walter ter Woerds ◽  
Wouter Wieling ◽  
Maria T. E. Hopman
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Orthostatic Intolerance ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Vascular Conductance ◽  
Leg Blood Flow ◽  
Head Up Tilt

In patients with orthostatic intolerance, the mechanisms to maintain BP (blood pressure) fail. A physical counter-manoeuvre to postpone or even prevent orthostatic intolerance in these patients is leg crossing combined with muscle tensing. Although the central haemodynamic effects of physical counter-manoeuvres are well documented, not much is known about the peripheral haemodynamic events. Therefore the purpose of the present study was to examine the peripheral haemodynamic effects of leg crossing combined with muscle tensing during 70° head-up tilt. Healthy subjects (n=13) were monitored for 10 min in the supine position followed by 10 min in 70° head-up tilt and, finally, for 2 min of leg crossing with muscle tensing in 70° head-up tilt. MAP (mean arterial BP), heart rate, stroke volume, cardiac output and total peripheral resistance were measured continuously by Portapres. Leg blood flow was measured using Doppler ultrasound. Leg vascular conductance was calculated as leg blood flow/MAP. A significant increase in MAP (13 mmHg), stroke volume (27%) and cardiac output (18%), a significant decrease in heart rate (−5 beats/min) and no change in total peripheral resistance during the physical counter-manoeuvre were observed when compared with baseline 70° head-up tilt. A significant increase in leg blood flow (325 ml/min) and leg vascular conductance (2.9 arbitrary units) were seen during the physical counter-manoeuvre when compared with baseline 70° head-up tilt. In conclusion, the present study indicates that the physical counter-manoeuvre of leg crossing combined with muscle tensing clearly enhances leg blood flow and, at the same time, elevates MAP.

Dynamic regulation of leg vasomotor tone in patients with chronic heart failure

1991 ◽  
Vol 71 (3) ◽  
pp. 1070-1075 ◽  
Author(s):  
M. J. Sullivan ◽  
F. R. Cobb
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Work Rate ◽  
Vasomotor Tone ◽  
Leg Blood Flow ◽  
Leg Exercise

We examined the central hemodynamic (n = 5) and leg blood flow (n = 9) responses to one- and two-leg bicycle exercise in nine ambulatory patients with chronic heart failure due to left ventricular systolic dysfunction (ejection fraction 17 +/- 9%). During peak one- vs. two-leg exercise, leg blood flow (thermodilution) tended to be higher (1.99 +/- 0.91 vs. 1.67 +/- 0.91 l/min, P = 0.07), whereas femoral arteriovenous oxygen difference was lower (13.6 +/- 3.1 vs. 15.0 +/- 2.9 ml/dl, P less than 0.01). Comparison of data from exercise stages matched for single-leg work rate during one- vs. two-leg exercise demonstrated that cardiac output was similar while both oxygen consumption and central arteriovenous oxygen differences were lower, indicating relative improvement in the cardiac output response at a given single-leg work rate during one-leg exercise. This was accompanied by higher leg blood flow (1.56 +/- 0.76 vs. 1.83 +/- 0.72 l/min, P = 0.02) and a tendency for leg vascular resistance to be lower (92 +/- 54 vs. 80 +/- 48 Torr.l-1.min, P = 0.08) without any change in blood lactate. These data indicate that, in patients with chronic heart failure, leg vasomotor tone is dynamically regulated, independent of skeletal muscle metabolism, and is not determined solely by intrinsic abnormalities in skeletal muscle vasodilator capacity. Our results suggest that relative improvements in central cardiac function may lead to a reflex release of skeletal muscle vasoconstrictor tone in this disorder.

Leg Blood Flow and Central Circulation at Various Blood Volumes: A Peroperative Study of Nine Patients with Varicose Veins

1977 ◽  
Vol 53 (4) ◽  
pp. 349-354
Author(s):  
B. Brismar ◽  
R. Cronestrand ◽  
L. Jorfeldt ◽  
A. Juhlin-Dannfelt
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Varicose Veins ◽  
Peripheral Circulation ◽  
Right Atrial ◽  
Surgical Trauma ◽  
Aged Patients ◽  
Leg Blood Flow ◽  
Before And After ◽  
Capillary Pressures

1. In a group of nine middle-aged patients undergoing varicose vein surgery, cardiac output, right atrial, pulmonary arterial and capillary pressures, and leg blood flow were measured after induction of general anaesthesia but before operation, and also during operation before and after blood substitution. 2. Under anaesthesia, the mean preoperative blood flows in the superficial and common femoral arteries were 160 ml/min and 280 ml/min respectively. These flows are comparable with those obtained in other studies under similar conditions but lower than values obtained in conscious subjects. During the operation the leg blood flow decreased by 24%. As cardiac output remained unchanged, the fractional leg blood flow fell. After transfusion of 900 ml of blood the leg blood flow doubled. 3. It is concluded that anaesthesia, surgical trauma and variations in blood volume greatly influence the leg blood flow and that an adequate substitution of operative blood loss is of utmost importance to achieve an optimum peripheral circulation.

scholarly journals Central and peripheral contributors to skeletal muscle hyperemia: response to passive limb movement

2010 ◽  
Vol 108 (1) ◽  
pp. 76-84 ◽  
Author(s):  
John McDaniel ◽  
Anette S. Fjeldstad ◽  
Steve Ives ◽  
Melissa Hayman ◽  
Phil Kithas ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Limb Movement ◽  
Leg Blood Flow ◽  
Passive Exercise

The central and peripheral contributions to exercise-induced hyperemia are not well understood. Thus, utilizing a reductionist approach, we determined the sequential peripheral and central responses to passive exercise in nine healthy men (33 ± 9 yr). Cardiac output, heart rate, stroke volume, mean arterial pressure, and femoral blood flow of the passively moved leg and stationary (control) leg were evaluated second by second during 3 min of passive knee extension with and without a thigh cuff that occluded leg blood flow. Without the thigh cuff, significant transient increases in cardiac output (1.0 ± 0.6 l/min, Δ15%), heart rate (7 ± 4 beats/min, Δ12%), stroke volume (7 ± 5 ml, Δ7%), passive leg blood flow (411 ± 146 ml/min, Δ151%), and control leg blood flow (125 ± 68 ml/min, Δ43%) and a transient decrease in mean arterial pressure (3 ± 3 mmHg, 4%) occurred shortly after the onset of limb movement. Although the rise and fall rates of these variables differed, they all returned to baseline values within 45 s; therefore, continued limb movement beyond 45 s does not maintain an increase in cardiac output or net blood flow. Similar changes in the central variables occurred when blood flow to the passively moving leg was occluded. These data confirm the role of peripheral factors and reveal an essential supportive role of cardiac output in the hyperemia at the onset of passive limb movement. This cardiac output response provides an important potential link between the physiology of active and passive exercise.

Oxygen transport during steady-state submaximal exercise in chronic hypoxia

1991 ◽  
Vol 70 (3) ◽  
pp. 1129-1136 ◽  
Author(s):  
E. E. Wolfel ◽  
B. M. Groves ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
R. S. Mazzeo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Steady State ◽  
Sea Level ◽  
Vascular Resistance ◽  
Barometric Pressure ◽  
Submaximal Exercise ◽  
Leg Blood Flow ◽  
Total Body ◽  
O2 Delivery

Arterial O2 delivery during short-term submaximal exercise falls on arrival at high altitude but thereafter remains constant. As arterial O2 content increases with acclimatization, blood flow falls. We evaluated several factors that could influence O2 delivery during more prolonged submaximal exercise after acclimatization at 4,300 m. Seven men (23 +/- 2 yr) performed 45 min of steady-state submaximal exercise at sea level (barometric pressure 751 Torr), on acute ascent to 4,300 m (barometric pressure 463 Torr), and after 21 days of residence at altitude. The O2 uptake (VO2) was constant during exercise, 51 +/- 1% of maximal VO2 at sea level, and 65 +/- 2% VO2 at 4,300 m. After acclimatization, exercise cardiac output decreased 25 +/- 3% compared with arrival and leg blood flow decreased 18 +/- 3% (P less than 0.05), with no change in the percentage of cardiac output to the leg. Hemoglobin concentration and arterial O2 saturation increased, but total body and leg O2 delivery remained unchanged. After acclimatization, a reduction in plasma volume was offset by an increase in erythrocyte volume, and total blood volume did not change. Mean systemic arterial pressure, systemic vascular resistance, and leg vascular resistance were all greater after acclimatization (P less than 0.05). Mean plasma norepinephrine levels also increased during exercise in a parallel fashion with increased vascular resistance. Thus we conclude that both total body and leg O2 delivery decrease after arrival at 4,300 m and remain unchanged with acclimatization as a result of a parallel fall in both cardiac output and leg blood flow and an increase in arterial O2 content.(ABSTRACT TRUNCATED AT 250 WORDS)

Leg vasoconstriction during dynamic exercise with reduced cardiac output

1992 ◽  
Vol 73 (5) ◽  
pp. 1838-1846 ◽  
Author(s):  
J. A. Pawelczyk ◽  
B. Hanel ◽  
R. A. Pawelczyk ◽  
J. Warberg ◽  
N. H. Secher
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Dynamic Exercise ◽  
Adrenergic Blockade ◽  
Vascular Conductance ◽  
Leg Blood Flow ◽  
Norepinephrine Spillover

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Determinants of maximal oxygen uptake in severe acute hypoxia

2003 ◽  
Vol 284 (2) ◽  
pp. R291-R303 ◽  
Author(s):  
J. A. L. Calbet ◽  
R. Boushel ◽  
G. Rådegran ◽  
H. Søndergaard ◽  
P. D. Wagner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Acute Hypoxia ◽  
Cycle Ergometer ◽  
Pulmonary Gas Exchange ◽  
Leg Blood Flow ◽  
Ergometer Exercise

To unravel the mechanisms by which maximal oxygen uptake (V˙o 2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2(hypoxia, ∼5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31–34 mmHg and arterial O2 content (CaO2 ) was reduced by 35% ( P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (Pi O2 ) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia ( P < 0.05). Hypoxia caused a 47% decrease inV˙o 2 max (a greater fall than accountable by reduced CaO2 ). Peak cardiac output decreased by 17% ( P < 0.01), due to equal reductions in both peak heart rate and stroke volume ( P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia ( P < 0.001) correlating closely with V˙o 2 max( r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction ofV˙o 2 max in severe acute hypoxia: 1) reduction of Pi O2 , 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss inV˙o 2 max.

Leg blood flow during submaximal cycle ergometry is not reduced in healthy older normally active men

2003 ◽  
Vol 94 (5) ◽  
pp. 1859-1869 ◽  
Author(s):  
David N. Proctor ◽  
Sean C. Newcomer ◽  
Dennis W. Koch ◽  
Khoi U. Le ◽  
David A. MacLean ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Femoral Vein ◽  
Plasma Catecholamines ◽  
Older Men ◽  
Constant Load ◽  
Cycle Ergometry ◽  
Leg Blood Flow ◽  
Younger Men ◽  
Power Outputs

The purpose of the present study was to test the hypothesis that leg blood flow responses during submaximal cycle ergometry are reduced with age in healthy normally active men. Eleven younger (20–25 yr) and eight older (62–73 yr) normotensive, nonendurance-trained men performed both graded and constant-load bouts of leg cycling at the same absolute and relative [% of peak O2 consumption (V˙o 2 peak)] exercise intensities while leg blood flow (femoral vein thermodilution), mean arterial pressure (MAP; radial artery), cardiac output (acetylene rebreathing), blood O2 content, and plasma catecholamines were measured. Leg blood flow responses at the same absolute submaximal power outputs (20–100 W) and at a fixed systemic O2 demand (1.1 l/min) did not differ between groups ( P = 0.14–0.19), despite lower absolute levels of cardiac output in the older men ( P < 0.05). MAP at the same absolute power outputs was 8–12 mmHg higher ( P < 0.05) in the older men, but calculated leg vascular conductance responses (leg blood flow/MAP) were identical in the two groups ( P > 0.9). At the same relative intensity (60% V˙o 2 peak), leg norepinephrine spillover rates were approximately twofold higher in the older men ( P = 0.38). Exercise-induced increases in leg arterial-venous O2difference were identical between groups ( P > 0.9) because both arterial and venous O2 contents were lower in the older vs. younger men. These results suggest that the ability to augment active limb blood flow and O2 extraction during submaximal large muscle mass exercise is not impaired but is well preserved with age in healthy men who are normally active.

Influence of respiratory muscle work onV˙o 2 and leg blood flow during submaximal exercise

1999 ◽  
Vol 87 (2) ◽  
pp. 643-651 ◽  
Author(s):  
Thomas J. Wetter ◽  
Craig A. Harms ◽  
William B. Nelson ◽  
David F. Pegelow ◽  
Jerome A. Dempsey
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Work Of Breathing ◽  
Submaximal Exercise ◽  
Leg Blood Flow ◽  
Muscle Work ◽  
Resistive Loads ◽  
Resistive Forces ◽  
Norepinephrine Spillover ◽  
Ventilation Rates

The work of breathing (Wb) normally incurred during maximal exercise not only requires substantial cardiac output and O2 consumption (V˙o 2) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q˙leg). We wondered whether the Wbnormally incurred during submaximal exercise would also reduceQ˙leg. Therefore, we investigated the effects of changing the Wb onQ˙leg via thermodilution in 10 healthy trained male cyclists [maximalV˙o 2(V˙o 2 max) = 59 ± 9 ml ⋅ kg−1 ⋅ min−1] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% ofV˙o 2 max. Inspiratory muscle work was 1) reduced 40 ± 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 ± 8% by addition of inspiratory resistive loads. Increasing the Wb during submaximal exercise caused V˙o 2 to increase; decreasing the Wb was associated with lowerV˙o 2(ΔV˙o 2 = 0.12 and 0.21 l/min at 50 and 75% ofV˙o 2 max, respectively, for ∼100% change in Wb). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, orQ˙leg when Wb was reduced or increased. Why are LVR, norepinephrine spillover, andQ˙leg influenced by the Wb at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal Wbrequired makes insufficient demands forV˙o 2 and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50–70% increase in Wb during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR orQ˙leg.

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