Increase In Maximal Cardiac Output Research Articles

Effect of E-OJ-01 on Cardiac Conditioning in Young Exercising Adults: A Randomized Controlled Trial.

Cardiac health is a determinant of athletic performance. A body of data suggests that in healthy young adults, an increase in maximal cardiac output leads to an increase in endurance. Terminalia arjuna (TA) has been studied for multiple benefits in cardiovascular health although its effects as a cardioprotective ergogenic aid require further exploration. The current trial was planned to study the effect of the proprietary TA extract (E-OJ-01) on the markers of cardiac conditioning in healthy young adults. No study has assessed the effect of TA extract on cardiac conditioning by improvement of left ventricular ejection fraction (LVEF) in young exercising individuals. A randomized, double-blind, placebo-controlled, parallel group study was conducted to determine the efficacy and safety of E-OJ-01 for use as an ergogenic supplements in young exercising adults. This trial was registered at ClinicalTrials.gov (NCT02207101) and reported according to Consolidated Standards of Reporting Trials (CONSORT) requirements. Thirty-two healthy males, aged 18-40 years performing regular endurance exercise, were randomly assigned to 400 mg of E-OJ-01 or placebo for 56 days. LVEF, right and left ventricular Myocardial Performance Index, and Borg Rated Perceived Exertion (RPE) were assessed at baseline, day 28, and day 56; creatine kinase-MB and troponin-T were assessed at baseline and at day 56. As compared with placebo, 56 days of E-OJ-01 supplementation significantly improved the LVEF (P = 0.0001) and decreased the right ventricular Myocardial Performance Index (P = 0.001). The fatigue level captured by Borg Scale after completion of exercise showed a greater decrease in the E-OJ-01 group as compared with placebo. Creatine kinase-MB and troponin-T did not change significantly. TA (E-OJ-01) significantly increased cardiovascular efficiency and improved the cardiac conditioning in young healthy adults.

Limiting factors for maximum oxygen uptake and determinants of endurance performance.

In the exercising human, maximal oxygen uptake (VO2max) is limited by the ability of the cardiorespiratory system to deliver oxygen to the exercising muscles. This is shown by three major lines of evidence: 1) when oxygen delivery is altered (by blood doping, hypoxia, or beta-blockade), VO2max changes accordingly; 2) the increase in VO2max with training results primarily from an increase in maximal cardiac output (not an increase in the a-v O2 difference); and 3) when a small muscle mass is overperfused during exercise, it has an extremely high capacity for consuming oxygen. Thus, O2 delivery, not skeletal muscle O2 extraction, is viewed as the primary limiting factor for VO2max in exercising humans. Metabolic adaptations in skeletal muscle are, however, critical for improving submaximal endurance performance. Endurance training causes an increase in mitochondrial enzyme activities, which improves performance by enhancing fat oxidation and decreasing lactic acid accumulation at a given VO2. VO2max is an important variable that sets the upper limit for endurance performance (an athlete cannot operate above 100% VO2max, for extended periods). Running economy and fractional utilization of VO2max also affect endurance performance. The speed at lactate threshold (LT) integrates all three of these variables and is the best physiological predictor of distance running performance.

Effects of exercise training on limb blood flow in patients with reduced ventricular function

Background Among the factors that contribute to limiting exercise tolerance in chronic heart failure are reduced peripheral blood flow and impaired vasodilatory capacity. Exercise training improves vasodilatory capacity in normal subjects, but controlled studies of exercise training evaluating upper and lower limb blood flow rates have not been performed in patients with reduced ventricular function. Improved vasodilatory capacity could help explain how training increases exercise capacity in these patients. Methods Twenty patients (mean age 55 ± 6 years) with reduced left ventricular function (mean ejection fraction 32% ± 6%) after a myocardial infarction were randomized to a 2-month high-intensity residential rehabilitation program or to a control group and were monitored over the subsequent year. Both groups were treated according to current practice with angiotensin-converting enzyme inhibition therapy. Training began 1 month after myocardial infarction. Baseline and postischemic flow rates were measured by plethysmography in both the upper and lower limbs 1 month, 3 months, and 1 year after the infarction. Peak oxygen uptake (V o 2) and cardiac output were measured before and after training, and peak V o 2 was determined again after 1 year. Results After 2 months of training peak V o 2 increased 25%, V o 2 at the lactate threshold increased 40%, and maximal cardiac output increased from 12.1 ± 1.6 L/min to 13.9 ± 2.4 L/min in the exercise group (all p < 0.05), whereas no differences were observed in the control group. At the 1-year follow-up no further increases in peak V o 2 were noted in either group, but the higher value persisted in the trained group. However, changes in limb flow rates were poorly related to changes in both peak V o 2 and maximal cardiac output. Improvements in baseline and postischemic flow rates occurred mainly in the lower limbs and were observed in the two groups to a similar degree. Conclusion Exercise training is highly effective in improving exercise capacity in patients with reduced ventricular function after myocardial infarction. These improvements parallel an increase in maximal cardiac output, but they are unrelated to vasodilatory capacity. In patients with reduced ventricular function after myocardial infarction, lower limb vasodilatory capacity improves gradually over the subsequent year, and these improvements occur irrespective of exercise training. (Am Heart J 1998;136:22-30.)

901-70 Central Hemodynamic and Gas Exchange Adaptions to Training in Chronic Heart Failure

Exercise Training has just recently been recognized as an important therapeutic modality in patients with chronic heart failure (CHF). However, central hemodynamic adaptations to exercise training in patients with CHF remain unclear. Seventeen patients with first diagnosis of CHF (56 ± 5 years, mean EF = 32 ± 6%) were randomized to an exercise raining group (N = 8), or a control group (N = 9). Patients in the exercise group performed two hours of daily walking along with five sessions per week of high intensity monitored stationary cycling (40 minutes at 70 to 80% peak capacity) at a residential rehabilitation center for a period of two months. Control patients received usual community care. Ventilatory gas exchange and upright hemodynamic measurements (rest and peak exercise cardiac output, pulmonary artery, wedge, and mean arterial pressures, and systemic vascular resistance) were performed before and after the study period. Changes in oxygen uptake at maximal exercise and the lactate threshold (LT) were as follows: Exercise group Control group PRE POST PRE POST VO 2 max (ml/kg/min) 19.6 ± 3 24.9 ± 3 * 19.6 ± 4 19.3 ± 5 VO 2 LT (ml/kg/min) 13.0 ± 3 17.8 ± 2 * 12.3 ± 2 12.0 ± 2 * p &lt; 0.5 within and between groups The increase in VO 2 max in the trained group paralleled an increase in maximal cardiac output (11.8 pre vs. 12.8 l/min post p &lt; 0.05), but maximal cardiac output did not change in controls. None of the hemodynamic pressures at rest or during exercise differed within or between groups. All of the increase in VO 2 max occurred during the first month of training, whereas significant increases in VO 2 LT were observed after both months. Both blood lactate and perceived exertion levels were significantly lower at matched ramp work rates after raining. Training benefits occur early in the course of rehabilitation in CHF and are mediated through increases in maximal cardiac output, but not central hemodynamic status. Training longer than one month after the onset of CHF does not increase VO 2 max further, but may provide further increases in VO 2 LT.

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.

Effects of high-intensity sprint training on skeletal muscle blood flow in rats

The regional blood flow response (via radioactive microspheres) was determined for female rats after 6 wk of high-intensity sprint training (HIST) or limited cage activity as the animals exercised at work loads that would elicit maximal O2 uptake. Blood flow to the different organs of the abdominal region was greatly reduced during maximal exercise conditions, and the magnitude of the reduction appeared to be similar for both the HIST group of rats and their sedentary (SED) control counterparts. Of the 20 different hindlimb muscles examined in the present study, blood flow to the soleus, plantaris, gastrocnemius, flexor hallicus longus, vastus lateralis, rectus femoris, biceps femoris, and adductor magnus and brevis muscles was significantly greater (P less than 0.05) in the HIST rats during maximal exercise conditions than in the SED control rats. Correspondingly, blood flow to the total hindlimb during maximal exercise was also significantly greater in the HIST rats than in the SED control rats [240 +/- 18 vs. 192 +/- 15 (SE) ml.min-1.100 g-1]. These results support the contention that the increase in maximal cardiac output that is produced by HIST in the rat is primarily directed toward the working skeletal muscle and not toward the organs found in the abdominal region. We conclude from these experiments that HIST will produce significant adaptations in central cardiac function and skeletal muscle blood flow in the rat.

Exercise Physiology and Cardiovascular Fitness

Endurance exercise training produces numerous metabolic and cardiovascular effects. Metabolic adaptations include an increase in oxidative capacity of skeletal muscle (greater number and size of mitochondria); an increase in skeletal muscle myoglobin concentration; a greater ability to oxidize fatty acids for energy; and an increase in stored glycogen. Cardiovascular effects of training include a decrease in resting heart rate and heart rate response to submaximal exercise; an increase in resting and exercise stroke volume; an increase in maximal cardiac output; an increase in VO2max; and an increase in arteriovenous oxygen difference. Aerobic exercise training contributes to cardiovascular fitness, because it beneficially alters the coronary artery disease risk profile. An inverse relationship exists between physical fitness and resting heart rate, body weight, percent body fat, serum cholesterol, triglycerides, glucose, and systolic blood pressure. In addition, exercise training increases the high-density lipoprotein fraction of total cholesterol. Endurance exercise is any activity that uses large muscle groups, can be performed continuously, and is rhythmic and aerobic in nature. To develop and maintain cardiovascular fitness, this exercise should be performed at a frequency of 3 to 5 days per week, an intensity of 60% to 90% HRmax or 50% to 85% HRmax reserve, and a duration of 20 to 60 minutes.

Cardiac adaptations to endurance training in rats with a chronic myocardial infarction

The hemodynamic response to maximal exercise was determined in sedentary and trained rats with a chronic myocardial infarction (MI) produced by coronary artery ligation and in rats that underwent sham operations (SHAM). Infarct size in the MI groups of rats comprised 28-29% of the total left ventricle and resulted in both metabolic and hemodynamic changes that suggested that these animals had moderate compensated heart failure. The training regimen used in the present study produced significant increases in maximal O2 uptake (VO2max) when expressed in absolute terms (ml/min) or when normalized for body weight (ml.min-1.kg-1) and consisted of treadmill running at work loads that were equivalent to 70-80% of the animal's VO2max for a period of 60 min/day, 5 days/wk over an 8- to 10-wk interval. This training paradigm produced two major cardiocirculatory adaptations in the MI rat that had not been elicited previously when using a training paradigm of a lower intensity. First, the decrement in the maximal heart rate response to exercise (known as "chronotropic incompetence") found in the sedentary MI rat was completely reversed by endurance training. Second, the downregulation of cardiac myosin isozyme composition from the fast ATPase V1 isoform toward the slower ATPase (V2 and V3) isoforms in the MI rat was partially reversed by endurance training. These cardiac adaptations occurred without a significant increase in left ventricular pump function as an increase in maximal cardiac output (Qmax) and maximal stroke volume (SVmax) did not occur in the trained MI rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Determinants of VO2max in rats after high-intensity sprint training.

The hemodynamic response to maximal exercise was determined in rats that were subjected to high-intensity sprint training (HIST) and rats that served as sedentary controls. Training consisted of five 1-min bouts of treadmill running at work loads (15% grade, 97 m/min) in excess of the animals' maximal O2 uptake (VO2max) interspersed with 90 s of rest. Training was performed 6 days/wk for 6 wk. After the training regimen, all rats were acutely instrumented with catheters in the right carotid artery and right ventricle. O2 uptakes, hemodynamic parameters, arterial and mixed venous O2 concentrations, blood gases, and acid-base status were determined at rest and during submaximal and maximal exercise. Results demonstrated that VO2max of HIST rats was significantly greater than that found for sedentary control rats. This increase in VO2max was due to an increase in maximal cardiac output (Qmax), since maximal arteriovenous O2 difference was similar between trained and sedentary rats. The increase in Qmax was due to an increase in maximal stroke volume (SVmax), because maximal heart rate in trained rats was similar to that in sedentary control rats. Citrate synthase and phosphofructokinase activities measured in the white gastrocnemius, plantaris, and soleus muscles of trained and sedentary rats were similar. These results suggest that the increase in VO2max produced with HIST in rats is strongly linked to an increase in central cardiac function as indicated by an increase in Qmax and SVmax.

Cardiovascular and respiratory responses to submaximal exercise training in the thoroughbred horse

Cardiovascular and respiratory responses to submaximal exercise training were investigated in 6 thoroughbred racehorses. Oxygen uptake, heart rate (HR) and arteriovenous oxygen content difference were measured during incremental treadmill exercise tests, before and after 7 weeks of treadmill training. Cardiac output during exercise was calculated by the direct Fick technique. Maximal oxygen uptake (VO2max) was increased by 23% after training, from 129.7 ml/kg/min to 160.0 ml/kg/min. The treadmill speed at which VO2max was attained increased by 19%. The increased aerobic power after training was associated with an increase in maximal cardiac output and stroke volume, a decrease in arteriovenous oxygen difference and no change in HR. There was no change in pulmonary ventilation during exercise at VO2max. Mean mixed venous oxygen content (CvO2) at VO2max before training was 2.8 +/- 1.0 ml/100 ml blood (mean +/- SE). After training the value was 8.6 +/- 1.4 ml/100 ml blood. It is concluded that the increase in VO2max after training in the horse is dependant on augmented blood flow, and is not dependant on either increased arterial oxygen content or arteriovenous oxygen content difference. Cardiac capacity to pump blood is therefore of primary importance as a determinant of increases in VO2max due to training in the horse.

Training effects on regional blood flow response to maximal exercise in foxhounds.

The effect of training on the regional blood flow response to maximal exercise was investigated in the foxhound. Training consisted of 8-12 wk of treadmill running at 80% of maximal heart rate 1 h/day for 5 days/wk and resulted in a 31% increase in maximal O2 consumption, a 28% increase in maximal cardiac output, and a 23% decrease in systemic vascular resistance during maximal exercise. Blood flow to the heart, diaphragm, brain, skin, and 9 of 10 muscles investigated was similar during maximal exercise pre- and posttraining; however, blood flow to the gastrocnemius muscle was greater posttraining than it was pretraining. Blood flow to the stomach, small intestine, and pancreas decreased during maximal exercise pre- and posttraining; however, blood flow to the large intestine, spleen, liver, adrenal glands, and kidneys decreased during maximal exercise only posttraining. In addition, a larger decrease in blood flow to the stomach during maximal exercise was found posttraining compared with pretraining. These results demonstrate that blood flow to skeletal muscle, the kidneys, and the splanchnic region of the foxhound during maximal exercise can be significantly altered by dynamic exercise training.

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

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.

Dynamic exercise training in foxhounds. II. Analysis of skeletal muscle.

The purpose of this study was to determine whether 8-12 wk of endurance training produces biochemical and histochemical adaptations in skeletal muscle in foxhounds. Analyses were performed on samples removed from gastrocnemius, triceps, and semitendinosus muscles of foxhounds before and after a treadmill running program. Biochemical analysis showed that training did not alter the activities of phosphofructokinase, beta-hydroxyacyl-CoA dehydrogenase, succinate dehydrogenase, or total phosphorylase. Histochemical analysis of myofibrillar actomyosin ATPase demonstrated three distinct classes of type II fibers and one type I fiber in the semitendinosus and triceps muscles and two type II and two type I fibers in the gastrocnemius muscle. Fiber type distribution and oxidative and glycolytic potentials, as indicated by nicotinamide adenine dinucleotide tetrazolium reductase or alpha-glycerophosphate dehydrogenase staining intensity, were unaltered by training. Similarly, capillary density, capillary-to-fiber ratios, and capillary area-to-fiber area ratios did not change with training. Thus, unlike humans and other mammals (i.e., rat), these foxhounds did not manifest biochemical or histochemical adaptations in skeletal muscle as the result of endurance training. This is consistent with the results of the study in which endurance training produced a 27% increase in maximal cardiac output and a 4% increase in maximal arteriovenous O2 extraction in foxhounds.

Hemodynamic effects of felodipine at rest and during exercise in exertional angina pectoris

To examine the antianginal effects of felodipine, a new calcium antagonist, 8 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 30 minutes after oral administration of 0.1 mg/kg of felodipine. Angina pectoris was always prevented after the drug was given and the exercise intensity was increased until recurrence of angina (5 patients) or exhaustion (3 patients). Hemodynamic data were also recorded at this higher exercise capacity. At rest and during submaximal exercise, felodipine increased heart rate and decreased arterial blood pressure and systemic vascular resistance. The prevention of angina pectoris was accompanied by lower mean pulmonary capillary wedge pressure, systemic vascular resistance and ST-segment depression; the pressure-rate product was unchanged. The 20% greater exercise capacity after felodipine was attended by a 20% increase in maximal cardiac output, a 17% increase in maximal heart rate and a 13% increase in maximal pressure-rate product; the maximal arterial blood pressure and ST-segment abnormalities were unchanged and the systemic vascular resistance was lower. The relation between ST-segment depression and the pressure-rate product during exercise was favorably influenced by felodipine. Thus, felodipine is an active antianginal drug; its major mechanism of action is to lower the systemic vascular resistance. The data also suggest that it improves coronary blood flow during exercise.

Physiologic improvement following coronary artery bypass surgery.

In this study the effects of coronary artery bypass surgery on ventricular function were evaluated at rest by quantitative analysis of segmental wall motion on cineventriculography, and during maximal treadmill exercise by measurement of serial cardiac outputs (Fick method) with the use of indwelling pulmonary artery and radial artery catheters. The patient had single vessel coronary disease and exertional angina. Following placement of a bypass graft to the proximally occluded left anterior descenting coronary artery, and despite the presence of arterial hypoxemia secondary to interstitial pulmonary fibrosis, a striking increase in maximal cardiac output occurred, mediated by a rise in both maximal heart rate and stroke volume. In this patient, resting ventricular volumes and ejection fraction were normal both before and after surgery, but preoperative abnormalities in extent of segmental wall motion, identified quantitatively, were restored to normal after bypass grafting. These investigations indicate that bypass surgery can provide substantial physiologic benefits in addition to providing subjective relief of anginal symptoms.

Physical training in sedentary middle-aged and older men. 3. Cardiac output and gas exchange asubmaximal and maximal exercise.

Fifteen previously sedentary men (38–55 years old) participated in an endurance training program which consisted of running for 2–3 half-hours a week for 8–10 weeks. Maximal oxygen uptake increased in all subjects, mean increase from 2.68 to 3.06 l/min, i.e. 14 per cent. This increase was brought about by a 13 per cent increase in maximal cardiac output, from 18.7 to 21.1 l/min. Heart rate was 8–17 beats/min lower during submaximal exercise. The maximal heart rate decreased by 6 (from 182 to 176) beats/min. Thus stroke volume was increased 7–17 ml at submaximal and 17 ml (16 per cent) at maximal exercise. Heart volume determined from X-rays did not change. After the training, mean arterial blood pressure was on the average 5 mm Hg lower at a given submaximal oxygen uptake; no change was observed at maximal exercise.