Dynamic exercise training in foxhounds. I. Oxygen consumption and hemodynamic responses

1985 ◽  
Vol 59 (1) ◽  
pp. 183-189 ◽  
Author(s):  
T. I. Musch ◽  
G. C. Haidet ◽  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Maximal Exercise ◽  
Submaximal Exercise ◽  
Maximal Heart Rate ◽  
O2 Consumption

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8–12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.

scholarly journals Hemodynamic Changes Associated with Spinal Anesthesia for Cesarean Delivery in Severe Preeclampsia

2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Spinal Anesthesia ◽  
Cesarean Delivery ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Severe Preeclampsia

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Cardiovascular Effects of Moxibustion at Jen Chung (Go-26) during Halothane Anesthesia in Dogs

1975 ◽  
Vol 03 (03) ◽  
pp. 245-261 ◽  
Author(s):  
Do Chil Lee ◽  
Myung O. Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Halothane Anesthesia

The cardiovascular effects of moxibustion at Jen Chung (Go-26) in 10 dogs under halothane anesthesia were compared to 5 dogs under halothane anesthesia without moxibustion and 5 dogs under halothane anesthesia in which moxibustion was effected at a neutral or non-acupuncture site. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two-hour period. A significant increase in cardiac output and stroke volume and a significant decrease in the total peripheral resistance were observed in the group which was stimulated by moxibustion at Jen Chun (Go-26). Heart rate, mean arterial pressure and pulse pressure were significantly increase during the early part of the two-hour period in the same group. The cardiovascular effects of moxibustion at Jen Chung (Go-26) which were observed at the end of the two hours were also present in two dogs in which measurements were continued for two additional hours.

Effects of beta-adrenergic blockade on O2 uptake during submaximal and maximal exercise

1983 ◽  
Vol 54 (4) ◽  
pp. 901-905 ◽  
Author(s):  
P. A. Tesch ◽  
P. Kaiser
Keyword(s):  
Heart Rate ◽  
Maximal Exercise ◽  
Pulmonary Ventilation ◽  
Submaximal Exercise ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
O2 Consumption ◽  
O2 Uptake ◽  
Beta Adrenergic

Changes in cardiorespiratory variables and perceived rate of exertion (RPE) were studied in 13 trained men performing cycling exercise before and after beta-adrenergic blockade. Propranolol (Inderal, 80 mg) was administered orally 2 h prior to standardized maximal and submaximal exercises. Muscle biopsies were obtained from vastus lateralis at rest for subsequent histochemical analyses of muscle fiber type distribution and capillary supply. During submaximal exercise O2 consumption decreased from 2.76 to 2.59 l . min-1 following blockade (P less than 0.01), whereas heart rate decreased from 157 to 113 beats . min-1 (P less than 0.001). Maximal O2 uptake was lowered from 3.79 to 3.26 l . min-1 (P less than 0.001) and maximal heart rate was reduced from 192 to 142 beats . min-1 (P less than 0.001) as a result of the blockade. Pulmonary ventilation was unaltered in both exercise conditions. “Local” RPE was higher (P less than 0.001) than “central” RPE after beta-blockade in both submaximal and maximal exercise. During normal condition this difference did not appear. Changes in both local and central RPE during submaximal exercise were positively correlated to changes in O2 uptake. Individual variations in the metabolic profile of the exercising muscle had no influence on beta-blockade-induced changes in O2 uptake. It is concluded that blockade of beta-adrenergic receptors reduces O2 consumption during submaximal (approximately 73% maximal O2 uptake) and maximal exercise in habitually trained men.

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.

scholarly journals Central and peripheral hemodynamic responses to passive limb movement: the role of arousal

2012 ◽  
Vol 302 (1) ◽  
pp. H333-H339 ◽  
Author(s):  
Massimo Venturelli ◽  
M. Amann ◽  
J. McDaniel ◽  
J. D. Trinity ◽  
A. S. Fjeldstad ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Visual Feedback ◽  
Passive Movement ◽  
Afferent Feedback ◽  
Hemodynamic Responses

The exact role of arousal in central and peripheral hemodynamic responses to passive limb movement in humans is unclear but has been proposed as a potential contributor. Thus, we used a human model with no lower limb afferent feedback to determine the role of arousal on the hemodynamic response to passive leg movement. In nine people with a spinal cord injury, we compared central and peripheral hemodynamic and ventilatory responses to one-leg passive knee extension with and without visual feedback (M+VF and M-VF, respectively) as well as in a third trial with no movement or visual feedback but the perception of movement (F). Ventilation (V̇e), heart rate, stroke volume, cardiac output, mean arterial pressure, and leg blood flow (LBF) were evaluated during the three protocols. V̇e increased rapidly from baseline in M+VF (55 ± 11%), M-VF (63 ± 13%), and F (48 ± 12%) trials. Central hemodynamics (heart rate, stroke volume, cardiac output, and mean arterial pressure) were unchanged in all trials. LBF increased from baseline by 126 ± 18 ml/min in the M+VF protocol and 109 ± 23 ml/min in the M-VF protocol but was unchanged in the F protocol. Therefore, with the use of model that is devoid of afferent feedback from the legs, the results of this study reveal that, although arousal is invoked by passive movement or the thought of passive movement, as evidenced by the increase in V̇e, there is no central or peripheral hemodynamic impact of this increased neural activity. Additionally, this study revealed that a central hemodynamic response is not an obligatory component of movement-induced LBF.

Inhibition of the Cardiovascular Effects of Acupuncture (Moxibustion) by Phenotolamine in Dogs During Halothane Anesthesia

1976 ◽  
Vol 04 (02) ◽  
pp. 153-161 ◽  
Author(s):  
Myung O. Lee ◽  
Do Chil Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Blocking Agent ◽  
Halothane Anesthesia

The cardiovascular effects of acupuncture, moxibustion by electrocautery, at Jen Chung (Go-26) and phentolamine (0.1 mg/kg-i.v.) alone were compared to phentolamine (0.1 mg/kg-i.v.) prior to moxibustion at Go-26 in groups of ten dogs under 0.75 percent halothane anesthesia. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressue, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two hour period. A significant increase (5% level) in cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure and significant decrease in total peripheral resistance were observed following acupuncture, moxibustion with electrocautery, at Jen Chung (Go-26) in dogs under halothane anesthesia. These effects were inhibited by pretreatment with the alpha blocking agent, phentolamine (0.1mg/kg-i.v.). The cardiovascular effects of phentolamine (0.1mg/kg-i.v.) alone were similar to those of dogs in which phenotolamine was administered prior to moxibustion.

scholarly journals Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

1999 ◽  
Vol 86 (6) ◽  
pp. 1890-1896 ◽  
Author(s):  
D. Slamowitz ◽  
L. Chen ◽  
S. M. Scharf
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Mechanical Effects

There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 ± 25%, P < 0.05), systemic vascular resistance (SVR; +33 ± 16%, P < 0.0005), and heart rate (HR; +5 ± 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; −16 ± 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater (∼14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes.

Long-term bed rest-induced reductions in stroke volume during rest and exercise: cardiac dysfunction vs. volume depletion

2005 ◽  
Vol 98 (2) ◽  
pp. 648-654 ◽  
Author(s):  
Jonas Spaak ◽  
Stéphanie Montmerle ◽  
Patrik Sundblad ◽  
Dag Linnarsson
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Cardiac Dysfunction ◽  
Bed Rest ◽  
Volume Depletion ◽  
Rest And Exercise

Long-term head-down-tilt bed rest (HDT) causes cardiovascular deconditioning, attributed to reflex dysfunctions, plasma volume reduction, or cardiac impairments. Our objective with the present study was to evaluate the functional importance and relative contribution of these during rest and exercise in supine and upright postures. We studied six subjects before (baseline), during [ days 60 (D60) and 113 (D113)], and after [recovery days 0 (R0), 3 (R3), and 15 (R15)] 120 days of −6° HDT. We determined cardiac output, stroke volume (SV), mean arterial pressure, and heart rate during rest and exercise in supine and upright postures. Cardiac output and SV decreased significantly in all four conditions, but the time courses differed for rest and exercise. Upright resting SV was decreased by 24 ± 9% at D60 compared with baseline but had recovered already at R3. Supine exercise SV decreased more slowly (by 5 ± 8% at D60 and by 18 ± 4% at D113) and recovered more slowly after HDT termination. Steady-state mean arterial pressure showed no changes. Heart rate had increased by 18 ± 4% at D60 and had recovered partially at R3. Our data indicate that long-term HDT causes both a rapid, preload-dependent reduction in SV, most evident during rest in the upright position, and a more slowly developing cardiac dysfunction, most evident during supine exercise. However, the ability to maintain blood pressure and to perform sustained low levels of dynamic exercise is not influenced by HDT.

Hemodynamic responses to acute carboxyhemoglobinemia in the rat

1983 ◽  
Vol 244 (3) ◽  
pp. H320-H327 ◽  
Author(s):  
W. E. Kanten ◽  
D. G. Penney ◽  
K. Francisco ◽  
J. E. Thill
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Cardiac Index ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work

The effects of carbon monoxide on the hemodynamics of the adult rat were investigated. A number of parameters were measured using an open-chest, chloralose-urethan anesthetized preparation. Our experiments showed this anesthetic agent to have several advantages over pentobarbital sodium. One group inhaled 150 ppm CO for 0.5-2 h, carboxyhemoglobin (HbCO) reaching 16%. Heart rate, cardiac output, cardiac index, dF/dtmax (aortic), and stroke volume rose significantly; mean arterial pressure, total peripheral resistance, and left ventricular systolic pressure fell, whereas stroke work, left ventricular dP/dtmax, and stroke power changed little. These effects were evident at a HbCO saturation as low as 7.5% (0.5 h). A second group inhaled 500 ppm CO for 5-48 h, HbCO reaching 35-38%. The same parameters changed in the same direction as in the first group, with mean arterial pressure and peripheral resistance remaining depressed, while heart rate, cardiac output, cardiac index, and stroke volume remained elevated. Heart rate and arterial systolic pressure were also monitored in conscious rats; rats in one group inhaled 500 ppm CO for 24 h, and rats in a second group were injected with a bubble of pure CO ip. In both cases heart rate was sharply elevated and blood pressure depressed as HbCO saturation increased. Both parameters recovered on CO washout. There was no significant difference between the response to inhaled vs. injected CO.

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