Status of alpha 1-adrenergic regulation of stroke volume during hypokinesia in the rat

The positive effect of phenylephrine (PE) on stroke volume (SV) was 3 to 5 times weaker in the rats exposed to hypokinesia for 30 days as compared to the controls. After obsidan blockade of beta-adrenoreceptors SV increased in both groups and the intergroup differences in the PE effect remained significant but less pronounced. This can be attributed to a greater effectiveness of PE after obsidan administration during hypokinesia. Correlation analysis showed that the weak effects of PE on SV were potentiated by obsidan (potentiation was the stronger the weaker the effects) while the distinct effects were on the contrary inhibited. This demonstrates the synergy--antagonism relationships in the PE and obsidan interaction and seems to indicate that the common site of their action is alpha 1-adrenoreceptors. After phentolamine injections the PE effect on SV was not found. In this situation SV decreased; the SV decrease as well as its increase under the action of obsidan was less significant in the hypokinetic than in the control rats. The above investigation suggests that the activity of alpha 1-adrenoreceptors involved in the actualization of positive effects of agonists on SV is considerably lower during hypokinesia.     

Cardiorespiratory responses to orthostasis and the effects of propranolol.

Cardiac output and gas exchange were determined serially using the single-breath method of Kim et al. before, during, and after orthostasis on six subjects after beta-adrenergic blockade and in duplicate controls. In the latter, heart rate increased and pulse pressure dropped immediately on tilting to 60 degrees and remained stable while cardiac output and stroke volume declined gradually over 21 min upright. On propranolol, heart rate was 10 bpm lower supine and 20 bpm less at 60 degrees but cardiac output was only slightly lower before and following tilt-up. However, after 15 min upright, stroke volume and cardiac output recovered on propranolol exceeding the controls after 21 min without change in heart rate. Returning to supine, heart rate dropped in all tests with a transitory increase in stroke volume, cardiac output and arterio-venous O2 difference. At the same time, apparent O2 uptake increased temporarily, reflecting the return of pooled venous blood to the lungs. Orthostatic tolerance did not appear to be affected by beta-adrenergic blockade.     

Central and regional hemodynamics in long space flights

This paper presents the results of studying central and regional hemodynamics in short-term (7 days) and long-term (65-237 days) space mission onboard Salyut-6--Soyuz and Salyut-7--Soyuz using the method of tetrapolar rheography. During space flights circulation changes were observed: variations in pulse blood filling and tone of regional vessels (head, forearm, leg) and insignificant changes of stroke volume and cardiac output. In response to exercise tests the contribution of stroke volume to cardiac output decreased and that of the chronotropic function of the heart increased. These changes were induced by variations in the hemodynamic status of the human body and were, to a certain extent, dependent on flight duration and position of the vascular area relative to the heart. The changes suggested that the circulation system retained its adaptive capabilities in flights of 237 days in duration.     

Left ventricular performance of the athletic heart during upright exercise: a heart rate-controlled study

This study compares the left ventricular performance of chronically conditioned pentathletes (N = 10) with less-conditioned subjects (N = 10) during dynamic upright exercise. The pentathletes were found to have a superior treadmill performance [24 +/- 4 vs 17 +/- 2 min (SD), P less than 0.01], reduced resting heart rate (41 +/- 13 vs 62 +/- 6 bpm, P less than 0.01), and increased left ventricular mass (254 +/- 85 vs 179 +/- 35 g, P less than 0.05) compared to the control group. Radionuclide ventriculography and heart rate controlled-bicycle ergometry were employed to examine changes in left ventricular ejection fraction, end-diastolic volume, end-systolic volume, and stroke volume. Heart rate was controlled by adjusting the resistance of the ergometer until stable heart rates of 90, 110, 130, and 150 bpm were achieved. Following heart rate stabilization, 99mTc images were acquired during 3-min stages at each target heart rate level. In the pentathletes, left ventricular ejection fraction, end-diastolic volume, and stroke volume increased (P less than 0.01) during exercise, and end-systolic volume tended to decrease. No difference was noted in left ventricular ejection fraction between groups when heart rates were matched. However, the exercise-induced changes in end-diastolic volume and stroke volume were greater (P less than 0.01) in the pentathletes. In conclusion, the athletes studied relied on the same mechanism as the less-conditioned subjects for improving pump performance during exercise stress, but the athletes' ability to mobilize a greater end-diastolic volume accounts for their larger stroke output during each stage of heart rate-matched exercise.     

Cycling exercise with functional electrical stimulation improves postural control in stroke patients

The aim of this study is to determine whether short term functional electrical stimulation (FES)-assisted cycling training can affect the postural control of stroke patients, and whether the application of FES can enhance the effect of cycling training. 20 stroke patients were randomly assigned to the FES-cycling group (FES-CG) or the cycling group (CG). Measurements were completed before and immediately after each 20 min training sessions. The measurements included a balance test (to quantify the postural control ability), a Hoffmann's reflex/motor response ratio (H/M ratio) test and a pendulum test (to quantify the muscle tone). In the balance test, some parameters in all directions exhibited significant intervention effects between the FES-CG group and the CG group. The H/M ratios (p=.014; .005, FES-CG and CG respectively) and relaxation index (p=.005; .047, FES-CG and CG respectively) revealed significant difference between FES-CG and CG group. The change ratios of directional control in the forward direction and H/M ratio revealed significant difference (p=.022; .015) between FES-CG and CG among subjects with higher muscle tone. The stroke subjects' postural control was improved while their muscle tone was reduced after the 20 min cycling training program both with and without FES. We conclude that cycling training, with or without FES may reduce spasticity in stroke patients. The application of FES in cycling exercise was shown to be more effective in stroke patients with higher muscle tone.     

Plasma norepinephrine, blood pressure and heart rate response to graded change in body position

In this study, 44 human subjects underwent either an orthostatic postural change (supine to stand, n = 17) or a graded change in body position (head-up) on a tilt-table (n = 27). No significant changes in systolic blood pressure or mean blood pressure were observed during either maneuver; significant increases, under both conditions, were observed in diastolic blood pressure and heart rate. Plasma norepinephrine concentrations after orthostatic position change increased significantly (supine 181 +/- 14 (S.E.M.) pg X ml-1; stand, 472 +/- 35 pg X ml-1, p less than 0.01). Plasma norepinephrine concentrations during graded postural change increased proportionately with increasing degrees of tilt (r = 0.76, p less than 0.01). A significant correlation between plasma norepinephrine and heart rate was observed during both positional change maneuvers (graded tilt-table, r = 0.80, p less than 0.01; orthostatic, r = 0.50, p less than 0.01). These results suggest that the degree of sympathetic nervous system activity for blood pressure regulation during graded postural change is appropriately reflected by plasma norepinephrine concentrations.     

Does exercise alter anaerobic threshold in coronary artery disease during beta blockade?

The effect of propranolol on cardiac patients undergoing exercise training is reported to increase exercise tolerance and maximum oxygen uptake (VO2 max) but its effect on anaerobic threshold (AT) is unknown. It was the purpose of this study to determine the role of exercise training with propranolol on AT in patients with coronary artery disease (CAD). Eight men and one woman with significant (CAD) were selected for this study. Each patient completed a maximum treadmill stress test (MTST) following the Bruce protocol on propranolol 40-160 mg/day as a control study. Cardiorespiratory variables were measured at rest and at each stage of the treadmill test. These patients underwent an exercise training programme for 12-16 weeks on the same dose of propranolol. Training sessions were for a minimum of 30-40 minutes, 3 times a week, with training heart rate of 75%-85% of the pretraining peak heart rate. Training heart rate ranged from 98 to 128 beats/min. They were retested with a MTST after the training programme, on the same dose of propranolol. AT was calculated noninvasively by measuring respiratory variables every 30 seconds in relation to work increment. AT was identified by measuring the time course of VE, VCO2, VE/VO2, etc. in relation to incremental work. The mean values of VO2, O2P and % VO2 max at AT before and after training on propanolol were as follows: VO2 = 1.43 L/min +/- .25 and 1.86 L/min +/- .44, O2P = 14.35 +/- 2.40 and 18.73 +/- 4.00 ml/beat, % of VO2 max = 68.20 +/- 6.31 and 73.59 +/- 5.84. The mean changes of VO2 O2P, and % of VO2 max were + 0.43 L/min +/- 0.20 (P < .003), + 4.38 +/- 2.55 (P < .003) and +/- 5.07% +/- 4.84 (P < .001). After exercise training on propanolol, the mean peak exercise tolerance time and absolute VO2 max increased by 2.8 min (from 9.0 to 11.8 min) (P < .001) and 22.7% (P < .007), respectively. We conclude that the increase in anaerobic threshold in patients with coronary artery disease may be due to improvement in VO2 max, increased stroke volume, and peripheral O2 extraction.     

Interval and strength training in CAD patients

This study sought to study the effect of high intensity aerobic interval endurance training on peak stroke volume and maximal strength training on mechanical efficiency in coronary artery disease (CAD) patients. 8 CAD patients (age 61.4 ± 3.7 years) trained 30 interval training sessions with 4 × 4 min intervals at 85-95% of peak heart rate while 10 CAD patients (age 66.5 ± 5.5 years) trained 24 sessions of maximal horizontal leg press. In the interval training group peak stroke volume increased significantly by 23% from 94.1 ± 23.0 mL · beat (-1) to 115.8 ± 22.4 mL · beat (-1) (p<0.05). Peak oxygen uptake increased significantly by 17% from 27.2 ± 4.5 mL · kg (-1) · min (-1) to 31.8 ± 5.0 mL · kg (-1) min (-1) (p<0.05) in the same group. In contrast, there was no such exercise training-induced change in peak stroke volume or peak oxygen uptake in the maximal strength training group, despite a 35% improvement in sub maximal walking performance.     

Dynamics of changes in the fluids of the extremities in man in different body positions

Anthropometric measurements and occlusion venous plethysmography were used to investigate fluid inflow and outflow in the limbs of human subjects who kept normal motor activity for 4 hrs, remained in recumbency or were in the head-down position at an angle of -12 degrees and -22 degrees (to simulate effects of zero G). During these exposures diuresis, heart rate and blood pressure according to Korotkoff were also measured. In the horizontal and, to a greater extent, head-down position, when motor activity was diminished, volume blood flow velocity in the limbs decreased, i. e. blood inflow to them became smaller. Arm volume varied insignificantly since inflow and outflow were in balance whereas leg volume decreased because fluid outflow was larger than inflow. In the head-down position the tone of leg veins also declined. Thus the peripheral vascular bed developed a complex of mechanisms that were to prevent volume overload of the central bed. Fluid shifts from the legs to the central bed were made up for by the renal excretion of water in the horizontal and head-down (-12 degrees C) (-22 degrees) produced a stressful effect on compensatory mechanisms which manifested as a greater rise of diastolic pressure and bradycardia. The data obtained indicate an active involvement of the peripheral vascular bed in the adaptation to diminished motor activity in the horizontal and head-down position of human subjects.     

Athletic Performance in Children With Cardiovascular Problems

The effects of physical training include cardiovascular and specific muscle adaptation, decreased resting heart rate, and increased cardiac size, stroke volume, maximum cardiac output, blood volume, vagal tone, and maximum breathing capacity. Young athletes with heart disease can generally participate in sports, but there is a wide spectrum of ability among them. The treadmill exercise test should be used to establish exercise norms. Children with severe mitral stenosis, aortic stenosis, idiopathic hypertrophic subaortic stenosis, active myocarditis, pulmonary hypertension, and significant arrhythmias should not participate in strenuous sports. Others with cardiac problems should be encouraged to participate for enjoyment rather than winning.     

用脉图方法观察2.5h头低位15°倾斜期间心血管系统的变化

为了解航天员航天初期心血管功能的动态变化，用脉图方法观察了１９名被试者在２．５ｈ头低位１５°倾斜期间的心血管功能。结果表明，ＨＤＴ期间心血管指标变化可分为现时期：急性反应期和反应期。     

Exercise cardiac function in young through elderly endurance trained women.

PURPOSE: To clarify the physiological reasons for the decline in aerobic power of endurance trained (ET) women with aging. METHODS: Blood volume, VO2max, and exercise cardiac function were examined in 23 ET women; six age 20-29 yr, six age 40-45 yr, six age 49-54 yr, and five age 58-63 yr. RESULTS: Blood volume was unchanged with aging. VO2max declined progressively at a rate of 0.51 mL x kg(-1) x min(-1) x yr(-1). During maximal exercise, there was an increase in total peripheral resistance (TPR) and a decrease in heart rate, stroke volume, and cardiac output with increasing age. At all ages, cardiac filling (diastole) was significantly faster than cardiac emptying (systole). Stroke volume did not plateau at a submaximal work rate but increased progressively to maximum. CONCLUSIONS: The decline in VO2max with age in ET women is due to decreases in maximal heart rate, stroke volume and cardiac output, and the primary advantage in the exercise cardiac performance of ET women of all ages is diastolic rather than systolic function.     

Noninvasive measurement of cardiovascular function in mice with high-temporal-resolution small-animal PET.

The aim of this study was to explore the feasibility of determining parameters of cardiovascular function in mice noninvasively by high-temporal-resolution imaging with a dedicated small-animal PET system. METHODS: Twenty-five anesthetized mice (28.8 +/- 4.6 g) were injected via an intravenous catheter with a 30-microL bolus of (18)F-FDG (8-44 MBq). The first 9 s of data were reconstructed into 30 frames of 0.3 s using filtered backprojection. The time-activity curve derived from a left ventricle volume of interest was corrected for tracer recirculation and partial volume. Cardiac output was calculated by the Stewart-Hamilton method, in which cardiac output is total injected activity divided by the area under the left ventricle time-activity curve. Cardiac output divided by body weight was defined as cardiac index; cardiac output divided by heart rate yielded the stroke volume. In 5 mice, measurements were repeated 2-4 times to assess reproducibility. In 4 mice, the hemodynamic response to dobutamine was examined by measuring heart rate, cardiac output, and stroke volume. RESULTS: The cardiac output averaged 20.4 +/- 3.4 mL/min; in the repeated measurements, the parameter displayed a mean percentage SD per mouse of 10% +/- 6%. The cardiac index averaged 0.73 +/- 0.19 mL/min/g and the stroke volume 45.0 +/- 6.9 microL, and both correlated with heart rate (r = 0.53, P = 0.007, and r = 0.49, P = 0.01, respectively). During dobutamine stress, heart rate increased from 423 +/- 50 to 603 +/- 30 beats/min (P = 0.002) and cardiac output increased from 18.5 +/- 1.9 to 32.0 +/- 4.2 mL/min (P = 0.008). CONCLUSION: Parameters of cardiovascular function can be measured in mice noninvasively by radionuclide angiography using high-temporal-resolution small-animal PET. Measured values of cardiac output and stroke volume are reproducible and comparable to those obtained with MRI. The approach permits the monitoring of changes in cardiovascular function in response to pharmacologic intervention.     

Swim training improves myocardial resistance to ischemia in rats

As the relationship between training and ischemic heart disease is not yet unraveled, we test the hypothesis that, in a model free from environmental, behavioural, and neuro-hormonal factors, endurance training improves myocardial resistance to ischemia. As carbohydrate metabolism is relevant for myocardial resistance to ischemia, we also test whether hyperglycemia blunts the protective effect of training. Eight-week old rats were randomly assigned to four groups (n = 6-8): sedentary or trained (3-week swim program, up to 2 h/day), and normal or high-carbohydrate diet (50 g/l sucrose in drinking water). Excised hearts were perfused isovolumically (flow = 15 ml/min) with Krebs-Henseleit (2 mM free Ca++, 11 mM glucose, pH 7.38 +/- 0.02, PO2 = 670 +/- 6 mmHg, PCO2 = 43 +/- 1 mmHg, mean +/- SE), exposed to 60 min low-flow (1.5 ml/min) ischemia, and then reperfused for 30 min (15 ml/min). In normally fed rats training increased the stroke volume index (97.5 +/- 13.0 vs. 72.6 +/- 6.2 microl, P = 0.05), depressed diastolic contracture (+2.3 +/- 2.0 vs. +24.2 +/- 6.7 mmHg, P = 0.02), improved the recovery of developed pressure x heart rate (33.8 +/- 2.3 vs. 24.1 +/- 3.3 mmHg/min/1000, P = 0.05), and decreased arrhythmias (P = 0.05). In high-carbohydrate-fed rats training induced myocardial hypertrophy (1.95 +/- 0.08 vs. 1.67 +/- 0.03 g, P = 0.02) and decreased arrhythmias but did not affect stroke volume, developed pressure x heart rate, and diastolic contracture. Thus endurance training improves myocardial resistance to ischemia but a high-carbohydrate diet partially blunts this protection. The occurrence of an inducible alteration able to modulate myocardial tolerance to ischemia may give clues to extend our knowledge of ischemic preconditioning.     

Comparison of ventricular volumes in normal and post-myocardial infarction subjects

In an effort to determine left ventricular volume changes between upright rest and exercise, 15 male late post-infarction patients (group A) and 13 normal matched volunteers (group B) were studied. Patients were at least 12 months post-cardiac event. Upright two-dimensional echocardiographic recordings were performed by the same cardiac sonographer using the apical four-chamber view at rest and immediately post-exercise after the subject reached 85% of measured maximal heart rate. Single-plane planimetry of the cross-sectional area was used for calculation of left ventricular volumes. Two subjects in each group failed to demonstrate adequate (i.e., measurable) echocardiograms and were excluded from the statistical analyses. Two-way analysis of variance for repeated measures was followed by the Newman-Kuels multiple comparison procedure to determine statistically significant differences between means (P less than 0.05). The results indicated no differences in any of the measured parameters at rest between the groups. Exercise values demonstrated a significant increase in end-diastolic volume, stroke volume, and ejection fraction with exercise only in group B. End-systolic volume did not change in either group. Cardiac output and heart rate increased in both groups. These data suggest that in the upright position, cardiac output increases in normal males due to an increase in heart rate and stroke volume (increases in end-diastolic volume) and by increases in heart rate alone in the post-infarction group.     

运动性窦性心动过缓和病态窦房结综合征——阿托品试验在鉴别诊断中的价值

<正> 运动员特别是从事耐力训练者常有窦性心动过缓,文献报告运动员安静时出现的心动极缓可达到29次/分、25次/分,睡眠中可达到21次/分。有少数出现窦房传导阻滞,与一般临床所见不典型的病态窦房结综合征相似,唯训练良好的运动员虽有心动过缓但多无     

Assessment of cardiovascular regulation during head-up tilt and suspension in swimmers

PURPOSE: The purpose of the present study was to compare cardiovascular responses in competitive swimmers with those in track and field (T and F) athletes during head-up tilt with engagement of the antigravity muscles in the lower extremities and during passive head-up suspension without the engagement of the antigravity muscles. METHODS: Blood pressure and heart rate during head-up tilt were compared among T and F athletes (N = 11), competitive swimmers (N = 15), and untrained subjects (N = 11). Moreover, stroke volume, cardiac output, and total peripheral resistance during head-up tilt and head-up suspension were also measured in T and F athletes and competitive swimmers. RESULTS: The heart rate increased significantly in all subject groups during head-up tilt; however, the MBP decreased in untrained subjects but did not change significantly in T and F athletes or competitive swimmers. Moreover, the DBP did not change significantly in untrained subjects or T and F athletes but increased significantly in swimmers. As with the head-up tilt, during the head-up suspension, the SBP decreased significantly and the heart rate increased significantly in both types of athletes, though the MBP decreased significantly. The ratios of decrease in stroke volume and cardiac output were significantly larger in swimmers than in T and F athletes during head-up tilt, but no significant difference was noted during head-up suspension. In T and F athletes, the ratios of decrease in stroke volume and cardiac output were significantly larger during head-up suspension than during head-up tilt, but no significant difference was noted in swimmers. CONCLUSION: The action of the antigravity muscles on cardiovascular regulation during upright standing is smaller in competitive swimmers than in T and F athletes.     

Time course of endotoxemia and cardiovascular changes in heat-stressed primates

Heat stress causes a marked reduction in splanchnic blood flow in order to compensate for the increased flow to the skin. Splanchnic ischemia causes a leakage of endotoxins from the gut lumen into the portal circulation and, especially in the presence of a compromised reticuloendothelial system, may cause severe systemic endotoxemia. Since many of the pathological features of heat stroke are similar to the shock state produced by LPS, we examined whether heat-stress causes endotoxemia. Five anesthetized monkeys were subjected to an environmental temperature of 41 degrees +/- 0.3 degrees C and relative humidity of 100%, until death. Rectal temperatures were recorded continuously, blood pressure and ECG were recorded at 5-min intervals, and arterial blood samples were taken at 15-30 min intervals. A decline in mean arterial pressure and rapid rise in heart rate occurred at about 42 degrees C. Plasma LPS remained at 0.071 +/- 0.006 ng.ml-1 until a rectal temperature of +/- 42 degrees C. Thereafter, it increased slowly until beyond 43 degrees C when it rose rapidly to 0.347 +/- 0.024 prior to death. Endotoxemia may have been a contributing factor in the pathogenesis of heat stroke. If so, then the use of anti-LPS antibodies may be expected to be beneficial.     

Ambulatory monitoring of left ventricular function in patients with Parkinson's disease and postural hypotension

Left ventricular (LV) function was continuously monitored using a radionuclide detector (VEST) after intravenous injection of 25 mCi technetium-99m labelled red blood cells in nine patients with Parkinson's disease and postural hypotension (group 1) and ten patients with Parkinson's disease but without postural hypotension (group 2). LV function and blood pressure were monitored in the supine position for 15 min (period A), upon changing posture from the supine to the upright position for 10 min (period B), and upon returning to the supine position for 10 min (period C). In group 1, the passage from period A to period B induced a significant decrease in end-diastolic volume, end-systolic volume and ejection fraction (allP<0.01). In group 2, ejection fraction increased (P<0.05) upon changing posture from the supine to the upright position. Ejection fraction (F=33,P<0.01), end-diastolic volume (F=9,P<0.05) and end-systolic volume (F=10,P<0.05) were significantly different between the two groups. In group 1, stroke volume, cardiac output and vascular peripheral resistance decreased from period A to period B (allP<0.001). In group 2, no changes in stroke volume, cardiac output and vascular peripheral resistance were observed from period A to period B. All parameters were similar in the two groups during the periods A and C. Upon changing posture from the supine to the upright position, patients with Parkinson's disease and postural hypotension showed marked changes in parameters of LV function induced by vascular abnormalities. The results of this study may help to clarify the potential risk of sudden postural changes in such patients, which may cause fainting, syncope and increased risk of ischaemic coronary and cerebrovascular attacks and of lower limb fractures.