O2 extraction maintains O2 uptake during submaximal exercise with β-adrenergic blockade at 4,300 m

1998 ◽  
Vol 85 (3) ◽  
pp. 1092-1102 ◽  
Author(s):  
Eugene E. Wolfel ◽  
Mark A. Selland ◽  
A. Cymerman ◽  
George A. Brooks ◽  
Gail E. Butterfield ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
High Altitude ◽  
Sea Level ◽  
Submaximal Exercise ◽  
Whole Body ◽  
Exercise Heart Rate ◽  
Adrenergic Blockade ◽  
Mixed Venous

Whole body O2 uptake (V˙o 2) during maximal and submaximal exercise has been shown to be preserved in the setting of β-adrenergic blockade at high altitude, despite marked reductions in heart rate during exercise. An increase in stroke volume at high altitude has been suggested as the mechanism that preserves systemic O2 delivery (blood flow × arterial O2 content) and thereby maintainsV˙o 2 at sea-level values. To test this hypothesis, we studied the effects of nonselective β-adrenergic blockade on submaximal exercise performance in 11 normal men (26 ± 1 yr) at sea level and on arrival and after 21 days at 4,300 m. Six subjects received propranolol (240 mg/day), and five subjects received placebo. At sea level, during submaximal exercise, cardiac output and O2 delivery were significantly lower in propranolol- than in placebo-treated subjects. Increases in stroke volume and O2 extraction were responsible for the maintenance of V˙o 2. At 4,300 m, β-adrenergic blockade had no significant effect onV˙o 2, ventilation, alveolar Po 2, and arterial blood gases during submaximal exercise. Despite increases in stroke volume, cardiac output and thereby O2 delivery were still reduced in propranolol-treated subjects compared with subjects treated with placebo. Further reductions in already low levels of mixed venous O2 saturation were responsible for the maintenance ofV˙o 2 on arrival and after 21 days at 4,300 m in propranolol-treated subjects. Despite similar workloads and V˙o 2, propranolol-treated subjects exercised at greater perceived intensity than subjects given placebo at 4,300 m. The values for mixed venous O2 saturation during submaximal exercise in propranolol-treated subjects at 4,300 m approached those reported at simulated altitudes >8,000 m. Thus β-adrenergic blockade at 4,300 m results in significant reduction in O2delivery during submaximal exercise due to incomplete compensation by stroke volume for the reduction in exercise heart rate. Total bodyV˙o 2 is maintained at a constant level by an interaction between mixed venous O2 saturation, the arterial O2-carrying capacity, and hemodynamics during exercise with acute and chronic hypoxia.

Cardiovascular changes in the exercising emu

1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Oxygen Content ◽  
Body Mass ◽  
Fold Increase ◽  
Exercise Heart Rate ◽  
Rate Of Oxygen Consumption ◽  
Cardiovascular Variables

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.

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.

Cardio-respiratory and metabolic responses to different levels of compression during submaximal exercise

2011 ◽  
Vol 26 (3) ◽  
pp. 102-106 ◽  
Author(s):  
B Sperlich ◽  
M Haegele ◽  
M Krüger ◽  
T Schiffer ◽  
H-C Holmberg ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Stroke Volume ◽  
Oxygen Saturation ◽  
Arterial Oxygen Saturation ◽  
Peak Oxygen Uptake ◽  
Submaximal Exercise ◽  
Arterial Oxygen ◽  
Different Levels

Objective The effects of knee-high socks that applied different levels of compression (0, 10, 20, 30 and 40 mmHg) on various cardio-respiratory and metabolic parameters during submaximal running were analysed. Methods Fifteen well-trained, male endurance athletes (age: 22.2 ± 1.3 years; peak oxygen uptake: 57.2 ± 4.0 mL/minute/kg) performed a ramp test to determine peak oxygen uptake. Thereafter, all athletes carried out five periods of submaximal running (at approximately 70% of peak oxygen uptake) with and without compression socks that applied the different levels of pressure. Cardiac output and index, stroke volume, arterio-venous difference in oxygen saturation, oxygen uptake, arterial oxygen saturation, heart rate and blood lactate were monitored before and during all of these tests. Results Cardiac output ( P = 0.29) and index ( P = 0.27), stroke volume ( P = 0.50), arterio-venous difference in oxygen saturation ( P = 0.11), oxygen uptake ( P = 1.00), arterial oxygen saturation ( P = 1.00), heart rate ( P = 1.00) and arterial lactate concentration ( P = 1.00) were unaffected by compression (effect sizes = 0.00–0.65). Conclusion This first evaluation of the potential effects of increasing levels of compression on cardio-respiratory and metabolic parameters during submaximal exercise revealed no effects whatsoever.

Effects of Imposed Acid–Base Derangement on the Cardiovascular Effects and Pharmacokinetics of Bupivacaine and Thiopental

2004 ◽  
Vol 100 (6) ◽  
pp. 1457-1468 ◽  
Author(s):  
Laurence E. Mather ◽  
Leigh A. Ladd ◽  
Susan E. Copeland ◽  
Dennis H.-T. Chang
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Myocardial Contractility ◽  
Cardiovascular Effects ◽  
Whole Body ◽  
Coronary Perfusion ◽  
Acid Base ◽  
Blood Concentrations ◽  
Blood Ph

Background By changing physicochemical properties such as effective lipophilicity, changes in blood pH could alter the distribution, elimination, and effects of weakly ionizing drugs. The authors examined the outcome of imposed acid-base derangement on cardiovascular effects and myocardial and whole body pharmacokinetics of bupivacaine, a weak base, and thiopental, a weak acid. Methods Intravenous infusions of rac-bupivacaine HCl (37.5 mg) or rac-thiopental sodium (250 mg, subanesthetic dose) were administered over 3 min to previously instrumented conscious ewes with normal blood pH, acidemia imposed by lactic acid infusion, or alkalemia imposed by bicarbonate infusion. Hemodynamic and electrocardiographic effects were recorded; arterial and coronary sinus drug blood concentrations were analyzed by chiral high-performance liquid chromatography. Results Bupivacaine decreased myocardial contractility, coronary perfusion, heart rate, and cardiac output; however, cardiac output and stroke volume were not as affected by bupivacaine with acidemia. Thiopental decreased myocardial contractility and stroke volume and increased heart rate; acidemia enhanced the tachycardia and produced a greater decrease in stroke volume than with alkalemia. Taken as a whole, the cardiovascular changes were not systematically modified by acid-base derangement. Overall, the tissue distribution of bupivacaine was favored by alkalemia, but thiopental pharmacokinetics were essentially unaffected by acid-base derangement. Acid-base derangement did not influence the kinetics of either drug enantioselectively. Conclusions At the doses used, the hemodynamic and electrocardiographic effects of bupivacaine and thiopental were not systematically modified by acid-base derangement, nor were there changes in regional or whole body pharmacokinetics of either drug that were clearly related to acid-base status.

Effects of chronic beta-adrenergic blockade on exercise training in dogs

1988 ◽  
Vol 64 (5) ◽  
pp. 1960-1967 ◽  
Author(s):  
E. E. Wolfel ◽  
J. Lindenfeld ◽  
J. Smoak ◽  
L. D. Horwitz
Keyword(s):  
Heart Rate ◽  
Submaximal Exercise ◽  
Peak Exercise ◽  
Exercise Heart Rate ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Exercise Time ◽  
Adrenergic Blocker

To assess the role of beta-adrenergic stimulation in cardiovascular conditioning we examined the effects of a beta-adrenergic blocker, propranolol, in mongrel dogs during an 8-wk treadmill-training program. Seven dogs were trained without a drug (NP), six were trained on propranolol 10 mg.kg-1.day-1 (P), and five served as caged controls (C). Effective beta-adrenergic blockade was documented by a decrease in peak exercise heart rate of 54 +/- 11 (SE) beats/min (P less than 0.05) and a one-log magnitude of increase in the isoproterenol-heart rate dose-response curve. Testing was performed before drug treatment or training and again after training without the drug for 5 days. Submaximal exercise heart rate decreased similarly in both NP and P (-26 +/- 4 NP vs. -25 +/- 9 beats/min P, P less than 0.05 for both) but peak heart rate decreased only with NP (-33 +/- 9 beats/min, P less than 0.05). Treadmill exercise time increased similarly in both groups: 3.4 +/- 0.6 min in NP and 3.0 +/- 0.2 min in P (both P less than 0.05). Blood volume also increased after training in both groups: 605 +/- 250 ml (26%) in NP and 377 +/- 140 ml (17%) in P (both P less than 0.05). Submaximal exercise arterial lactates were reduced similarly in both groups but peak exercise lactate was reduced more in NP (-1.4 +/- 0.3 NP vs -0.3 +/- 0.12 mmol/l P, P less than 0.05). Lactate threshold increased in both groups but the increase was greater in NP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of high-altitude exposure for 10 days on stroke volume and cardiac output

1977 ◽  
Vol 42 (5) ◽  
pp. 722-727 ◽  
Author(s):  
R. S. Hoon ◽  
V. Balasubramanian ◽  
O. P. Mathew ◽  
S. C. Tiwari ◽  
S. C. Sharma ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
High Altitude ◽  
Sea Level ◽  
Impedance Plethysmography ◽  
Noninvasive Technique ◽  
Electrical Impedance Plethysmography ◽  
Group A ◽  
Group B ◽  
Permanent Residents

Resting stroke volume and cardiac output of 50 normal healthy sea-level residents (group A) were estimated by the noninvasive technique of electrical impedance plethysmography. They were then airlifted to an altitude of 3,658 m and serial estimations carried out at 0–4 h and 5–8 h and on the 2nd, 3rd, 4th, 5th, and 10th days. The subjects were brought back to sea level and studied for up to 5 days. Thirty permanent residents of high altitude (group B) and sixteen lowlanders temporarily resident at high altitude (group C) were also subjected to similar studies. It was found that resting stroke volume and cardiac output of group A started falling immediately on arrival at high altitude, reached the minimum on the 3rd day and tended to improved on the 4th and 5th day, but showed a secondary fall on the 10th day. The reduction in stroke volume in this group was not fully compensated by tachycardia. On return to sea level the cardiac output normalized immediately, the stroke volume on the 2nd day. At sea level goup A had values similar to group B and at high altitude to group C.

scholarly journals ACE insertion/deletion polymorphism and submaximal exercise hemodynamics in postmenopausal women

2002 ◽  
Vol 92 (3) ◽  
pp. 1083-1088 ◽  
Author(s):  
James M. Hagberg ◽  
Steve D. McCole ◽  
Michael D. Brown ◽  
Robert E. Ferrell ◽  
Kenneth R. Wilund ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Women Athletes ◽  
Peripheral Resistance ◽  
Submaximal Exercise ◽  
Exercise Heart Rate ◽  
Physically Active ◽  
Cardiovascular Hemodynamics ◽  
Ace Genotype

We sought to determine whether the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism is associated with submaximal exercise cardiovascular hemodynamics. Postmenopausal healthy women (20 sedentary, 20 physically active, 22 endurance athletes) had cardiac output (acetylene rebreathing) measured during 40, 60, and 80%V˙o 2 max exercise. The interaction of ACE genotype and habitual physical activity (PA) level was significantly associated with submaximal exercise systolic blood pressure, with only sedentary women exhibiting differences among genotypes. No significant effects of ACE genotype or its interaction with PA levels was observed for submaximal exercise diastolic blood pressure. ACE genotype was significantly associated with submaximal exercise heart rate (HR) with ACE II having ∼10 beats/min higher HR than ACE ID/DD genotype women. ACE genotype did not interact significantly with habitual PA level to associate with submaximal exercise HR. ACE genotype was not independently, but was interactively with habitual PA levels, associated with differences in submaximal exercise cardiac output and stroke volume. For cardiac output, ACE II genotype women athletes had ∼25% greater cardiac output than ACE DD genotype women athletes, whereas for stroke volume genotype-dependent differences were observed in both the physically active and athletic women. ACE genotype was not significantly associated, either independently or interactively with habitual PA levels, with submaximal exercise total peripheral resistance or arteriovenous O2 difference. Thus the common ACE locus polymorphic variation is associated with many submaximal exercise cardiovascular hemodynamic responses.

Cardiac output in muscular exercise at 5,800 m (19,000 ft)

1964 ◽  
Vol 19 (3) ◽  
pp. 441-447 ◽  
Author(s):  
L. G. C. E. Pugh
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Sea Level ◽  
Indirect Evidence ◽  
Mean Value ◽  
Muscular Exercise ◽  
Maximum Output ◽  
Work Intensity ◽  
Maximum Heart Rate ◽  
Sea Level Pressure

Cardiac output during muscular exercise was estimated by the acetylene technique on four members of the Himalayan Scientific and Mountaineering expedition 1960–1961 at sea level and 5,800 m (19,000 ft). The output for a given work intensity at 5,800 m (19,000 ft) was comparable with the output at the same work intensity at sea level, but the maximum output was reduced, the mean value being 16 liters/min, compared with 23 liters/min at sea level. Heart rates during light and moderate exercise were higher than the rates observed at the same work intensity at sea level. The maximum heart rate during exercise was limited to 130–150 beats/min compared with 180–196 beats/min at sea level. The stroke volume at altitude was lower than at sea level at each work rate. On breathing oxygen at sea-level pressure, heart rate for a given work intensity was reduced; but the maximum heart rate increased. Indirect evidence suggested that maximum cardiac output increased but probably not to the sea-level values because of the increased hemoglobin and lower heart rate. altitude acclimatization; cardiac function, work and altitude; hypoxia and cardiac output Submitted on July 29, 1963

Physiological factors associated with the lower maximal oxygen consumption of master runners

1989 ◽  
Vol 66 (2) ◽  
pp. 949-954 ◽  
Author(s):  
A. M. Rivera ◽  
A. E. Pels ◽  
S. P. Sady ◽  
M. A. Sady ◽  
E. M. Cullinane ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Maximal Oxygen Consumption ◽  
Maximal Heart Rate ◽  
Distance Runners ◽  
Physiological Factors ◽  
Factors Associated ◽  
Older Athletes ◽  
Maximal Cardiac Output

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.

Cardiac Response During Trumpet Playing

2010 ◽  
Vol 25 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Donald U Robertson ◽  
Lynda Federoff ◽  
Keith E Eisensmith
Keyword(s):  
College Students ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Cardiac Response ◽  
Physiological Efficiency ◽  
Rest Periods ◽  
Upper Register

Heart rate, heart rate variability, stroke volume, and cardiac output were measured while six college students and six professionals played trumpet. One-minute rest periods were followed by 1 minute of playing exercises designed to assess the effects of pitch and articulation. Heart rate and heart rate variability increased during playing, but stroke volume decreased. Changes in heart rate between resting and playing were greater for students, although beat-to-beat variability was larger for professionals in the upper register. These results suggest that expertise is characterized by greater physiological efficiency.

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