Development of adrenergic and cholinergic cardiac control in larvae of the African clawed frog Xenopus laevis

Cardiac responses (heart rate, stroke volume, and cardiac output) to cholinergic and adrenergic receptor stimulation were investigated in developing larvae of Xenopus laevis from Nieuwkoop and Faber (NF) stage 33/34 (newly hatched) to NF stage 53 (22 d after hatching). Effects on heart rate (fH), stroke volume (SV), and cardiac output (CO) were analyzed using in situ preparations and video-microscopic techniques to record the continually beating heart. The results show that administration of acetylcholine to the heart decreases heart rate as early as NF stage 40. A significant reduction in SV and CO following acetylcholine administration to the heart was found at NF stages 45-53. Epinephrine had no significant effect on fH, SV, or CO at any of the stages investigated. However, an adrenergic tonus on the heart is present already at NF stage 40 (11%). This tonus increases up to a maximum (44%) at NF stages 45-47, when the maximal heart rate is found during development of X. laevis. We conclude that acetylcholine has a negative chronotropic and possibly also inotropic effect on the heart very early in development of X. laevis. We also hypothesize that the high adrenergic tonus found at NF stages 45-47 is responsible, at least in part, for the peak in heart rate seen at these stages.     

Cardiovascular hemodynamics with increasing exercise intensities in postmenopausal women.

We sought to determine the cardiovascular responses to increasing exercise intensities in postmenopausal women with different physical activity levels and hormone replacement therapy (HRT) status. Forty-four women (11 sedentary, 19 physically active, 14 master athletes; 24 not on HRT, 20 on HRT) completed treadmill exercise at 40, 60, 80, and 100% of maximal oxygen consumption. Oxygen consumption, heart rate, blood pressure, and cardiac output, determined via acetylene rebreathing, were measured at each exercise intensity. HRT did not affect cardiovascular hemodynamics. Stroke volume (SV) decreased significantly between 40 and 100% of maximal oxygen consumption in all groups, and the decrease did not differ among groups. The greater oxygen consumption of the athletes at each intensity was due to their significantly greater cardiac output, which was the result of a significantly greater SV, compared with both of the less active groups. The athletes had significantly lower total peripheral resistance at each exercise intensity than did the two less active groups. There were no consistent significant hemodynamic differences between the physically active and sedentary women. These results indicate that SV decreases in postmenopausal women as exercise intensity increases to maximum, regardless of their habitual physical activity levels or HRT status.     

Fifteen-day cessation of training on selected physiological and performance variables in women runners

This study examined the effects of a 15-day cessation of training on maximal oxygen consumption and selected physiological variables (maximal heart rate, cardiac output [Q], stroke volume [SV], arteriovenous oxygen difference [(a-v)O2 diff], blood plasma concentration) in 15 women middle-distance competitive runners (.VO2max: 49.8 +/- 1.1 ml.kg(-1).min(-1)). Subjects were randomly assigned to a cessation training (CT, n = 7) or maintenance training (MT, n = 8) group and tested every 5 days. Q was measured by CO2 rebreathing from which SV and (a-v)O2 diff were calculated. No significant changes were found at day 5. After 10 days there was a significant decrement in .VO2max (3.8 ml.kg(-1).min(-1)) in the CT group, being significantly lower than MT but no changes thereafter in any physiological variables. Performance (2,400 m) times did not change for MT but was significantly slower (21.5 +/- 7.1 seconds) for the CT group after 15 days, corresponding to the 7.8% decrease in .VO2max. These findings suggest that in competitive women middle-distance runners, actual performance decrements found after 15 days of CT most likely are due to declines in .VO2max.     

Cardiovascular response to acute hypoxemia induced by prolonged breath holding in air

Prolonged breath hold (BH) represents a valid model for studying the cardiac adaptation to acute hypoxemia in humans. Cardiac magnetic resonance (CMR) allows a three-dimensional, high-resolution, noninvasive, and nonionizing anatomical and functional evaluation of the heart. The aim of the study was to assess the adaptation of the cardiovascular system to prolonged BH in air. Ten male volunteer diving athletes (age 30 +/- 6 yr) were studied during maximal BH duration with CMR. Four epochs were studied: I, rest; II and III, intermediate BH; and IV, peak BH. Oxygen saturation (So(2)), heart rate (HR), blood pressure (BP), systemic vascular resistance (VR), end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), ejection fraction (EF), maximal elastance index (EL), systolic wall thickening (SWT), and end-systolic wall stress (ESWS) of the left ventricle (LV) were measured in all four BH epochs. Average BH duration was 3.7 +/- 0.3 min. So(2) was reduced (I: 97 +/- 0.2%, range 96-98%, vs. IV: 84 +/- 2.0%, range 76-92%; P < 0.00001). BP, EDV, ESV, SV, CO, and ESWS linearly increased from epochs I to IV, whereas EF, EL, and SWT showed an opposite behavior, decreasing from resting to epoch IV (all trends are P < 0.01). During prolonged BH in air, a marked enlargement of the LV chamber occurs in healthy diving athletes. This response to acute hypoxemia allows SV,CO, and arterial pressure to be maintained despite the severe reduction in LV contractile function.     

Cardiovascular responses in paraplegic subjects during arm exercise

The purpose of this study was to examine cardiovascular responses during arm exercise in paraplegics compared to a well-matched control group. A group of 11 male paraplegics (P) with complete spinal cord-lesions between T6 and T12 and 11 male control subjects (C), matched for physical activity, sport participation and age performed maximal arm-cranking exercise and submaximal exercise at 20%, 40% and 60% of the maximal load for each individual. Cardiac output (Qc) was determined by the CO2 rebreathing method. Maximal oxygen uptake was significantly lower and maximal heart rate (fc) was significantly higher in P compared to C. At the same oxygen uptakes no significant differences were observed in Qc between P and C; however, stroke volume (SV) was significantly lower and fc significantly higher in P than in C. The lower SV in P could be explained by an impaired redistribution of blood and, therefore, a reduced ventricular filling pressure, due to pooling of venous blood caused by inactivity of the skeletal muscle pump in the legs and lack of sympathetic vasoconstriction below the lesion. In conclusion, in P maximal performance appears to have been limited by a smaller active muscle mass and a lower SV despite the higher fc,max. During submaximal exercise, however, this lower SV was compensated for by a higher fc and, thus at the same submaximal oxygen uptake, Qc was similar to that in the control group.     

Acidaemia reduces cardiac output and left ventricular contractility in conscious lambs

We studied the effects of HCI-induced metabolic acidaemia on cardiac output, contractile function, myocardial blood flow, and myocardial oxygen consumption in nine unanaesthetized newborn lambs. Through a left thoracotomy, catheters were placed in the aorta, left atrium and coronary sinus. A pressure transducer was placed in the left ventricle. Three to four days after surgery, we measured cardiac output, dP/dt, left ventricular end diastolic and aortic mean blood pressures, heart rate, aortic and coronary sinus blood oxygen contents, and left ventricular myocardial blood flow during a control period, during metabolic acidaemia, and after the aortic pH was restored to normal. We calculated systemic vascular resistance, myocardial oxygen consumption and left ventricular work. Acidaemia was associated with reduction in cardiac output, maximal dP/dt, and aortic mean blood pressure. Left ventricular end diastolic pressure and systemic vascular resistance increased, and heart rate did not change significantly. The reduction in myocardial blood flow and oxygen consumption was accompanied by fall in cardiac work. Cardiac output returned to control levels after the pH had been normalized but maximal dP/dt was incompletely restored. Myocardial blood flow and oxygen consumption increased beyond control levels. This study demonstrates that HCI-induced metabolic acidaemia in conscious newborn lambs is associated with a reduction in cardiac output which could have been mediated by the reduction in contractile function and/or the increase in systemic vascular resistance. The decreases in myocardial blood flow and oxygen consumption appear to reflect diminished cardiac work. The restoration of a normal cardiac output after normalization of the pH appears to have resulted from the increases in heart rate and left ventricular filling pressures in conjunction with an incomplete restoration of contractile function.     

Ischemic preconditioning of the muscle improves maximal exercise performance but not maximal oxygen uptake in humans

Brief episodes of nonlethal ischemia, commonly known as "ischemic preconditioning" (IP), are protective against cell injury induced by infarction. Moreover, muscle IP has been found capable of improving exercise performance. The aim of the study was the comparison of standard exercise performances carried out in normal conditions with those carried out following IP, achieved by brief muscle ischemia at rest (RIP) and after exercise (EIP). Seventeen physically active, healthy male subjects performed three incremental, randomly assigned maximal exercise tests on a cycle ergometer up to exhaustion. One was the reference (REF) test, whereas the others were performed after the RIP and EIP sessions. Total exercise time (TET), total work (TW), and maximal power output (W(max)), oxygen uptake (VO(2max)), and pulmonary ventilation (VE(max)) were assessed. Furthermore, impedance cardiography was used to measure maximal heart rate (HR(max)), stroke volume (SV(max)), and cardiac output (CO(max)). A subgroup of volunteers (n = 10) performed all-out tests to assess their anaerobic capacity. We found that both RIP and EIP protocols increased in a similar fashion TET, TW, W(max), VE(max), and HR(max) with respect to the REF test. In particular, W(max) increased by ～ 4% in both preconditioning procedures. However, preconditioning sessions failed to increase traditionally measured variables such as VO(2max), SV(max,) CO(max), and anaerobic capacity(.) It was concluded that muscle IP improves performance without any difference between RIP and EIP procedures. The mechanism of this effect could be related to changes in fatigue perception.     

Myocardial oxygen consumption and mechanical efficiency of a perfused dogfish heart preparation

Summary Oxygen consumption of an in-pericardium heart preparation from the spiny dogfish (Squalus acanthias) was linearly related to cardiac power output. Basal oxygen consumption, predicted from the regression, was 0.127 l · s^-1 · g ventricle mass^-1 and increased by 0.189 l · s^-1 · g ventricle mass^-1 per milliwatt of power generated. From the relationship between cardiac power output and mechanical efficiency, mechanical efficiency was predicted to increase with cardiac power output to a maximum of 21 %. Mechanical efficiency was measured during volume loading and pressure loading at two power outputs (50% and 72% of maximum power output). At 50% of maximum power output, mechanical efficiency increased significantly by 2.87%, from 11.9±0.3% to 14.8±0.5% (n=7), when flow was halved and output pressure doubled to achieve the same power output. Similarly, at 72% of maximum power output, mechanical efficiency increased from 14.74±0.92% to 17.61±0.84% (n=6) when flow was halved and output pressure doubled to generate the same higher level of power output. The increased mechanical efficiency at higher output pressures is believed to result from cardiac myocytes working within a length range where they are able to generate the most tension during contraction and are most efficient. We speculate that the loss of mechanical efficiency associated with large changes in sarcomere length, when stroke volume is large, is a driving force behind the use of frequency as the principal means of increasing cardiac output as observed in more active fishes, birds and mammals.Abbreviations BM body mass - CO cardiac output - HR heart rate - P _i mean cardiac input pressure - P _o mean cardiac output pressure - PO partial pressure of oxygen - SV stroke volume of heart - VM ventricle mass     

Fluid replacement and glucose infusion during exercise prevent cardiovascular drift.

This study examined the influence of both hydration and blood glucose concentration on cardiovascular drift during exercise. We first determined if the prevention of dehydration during exercise by full fluid replacement prevents the decline in stroke volume (SV) and cardiac output (CO) during prolonged exercise. On two occasions, 10 endurance-trained subjects cycled an ergometer in a 22 degrees C room for 2 h, beginning at 70 +/- 1% maximal O2 uptake (VO2max) and in a euhydrated state. During one trial, no fluid (NF) replacement was provided and the subject's body weight declined 2.09 +/- 0.19 kg or 2.9%. During the fluid replacement trial (FR), water was ingested at a rate that prevented body weight from declining after 2 h of exercise (i.e., 2.34 +/- 0.17 1/2 h). SV declined 15% and CO declined 7% during the 20- to 120-min period of the NF trial while heart rate (HR) increased 10% and O2 uptake (VO2) increased 6% (all P less than 0.05). In contrast, SV was maintained during the 20- to 120-min period of FR while HR increased 5% and thus CO actually increased 7% (all P less than 0.05). Rectal temperature, SV, and HR were similar during the 1st h of exercise during NF and FR. However, after 2 h of exercise, rectal temperature was 0.6 degree C higher (P less than 0.05) and SV and CO were 11-16% lower (P less than 0.05) during NF compared with FR.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular characteristics of two resting marsupials: An insight into the cardio-respiratory allometry of marsupials

Summary Minimum resting values for several cardiovascular and respiratory characteristics were established for two marsupial species,Trichosurus vulpecula andMacropus eugenii. Certain characteristics including heart rate, stroke volume and cardiac output varied significantly with body mass and allometric equations of the formy=aM ^b were derived to describe the relationships. The exponents of body mass,b, were generally similar to those for eutherian mammals, but in the marsupials they intercept,a, differed significantly from reported eutherian values.Although resting cardiac output in the marsupials appeared reduced in proportion to their lower resting oxygen consumption this pattern was not repeated for other variables. The stroke volume of the marsupials was 156% of eutherian levels while heart rate was less than 50% of the eutherian values.Initial data for respiratory variables also indicated comparable differences in this aspect of oxygen transport between marsupials and eutherians. Minimum respiratory rates of the marsupials were much lower than those of eutherians and tidal volumes appear larger in marsupials. The results are interpreted as suggesting that marsupials may have a large aerobic capacity.     

Does fitness level modulate the cardiovascular hemodynamic response to exercise?

Subjects with greater aerobic fitness demonstrate better diastolic compliance at rest, but whether fitness modulates exercise cardiac compliance and cardiac filling pressures remains to be determined. On the basis of maximal oxygen consumption (VO2max), healthy male subjects were categorized into either low (LO: VO2max=43+/-6 ml.kg-1.min-1; n=3) or high (HI: VO2max=60+/-3 ml.kg-1.min-1; n=5) aerobic power. Subjects performed incremental cycle exercise to 90% Vo(2max). Right atrial (RAP) and pulmonary artery wedge (PAWP) pressures were measured, and left ventricular (LV) transmural filling pressure (TMFP=PAWP-RAP) was calculated. Cardiac output (CO) and stroke volume (SV) were determined by direct Fick, and LV end-diastolic volume (EDV) was estimated from echocardiographic fractional area change and Fick SV. There were no between-group differences for any measure at rest. At a submaximal workload of 150 W, PAWP and TMFP were higher (P<0.05) in LO compared with HI (12 vs. 8 mmHg, and 9 vs. 4 mmHg, respectively). At peak exercise, CO, SV, and EDV were lower in LO (P<0.05). RAP was not different at peak exercise, but PAWP (23 vs. 15 mmHg) and TMFP (12 vs. 6 mmHg) were higher in LO (P<0.05). Compared with less fit subjects, subjects with greater aerobic fitness demonstrated lower LV filling pressures during exercise, whereas SV and EDV were either similar (submaximal exercise) or higher (peak exercise), suggesting superior diastolic function and compliance.     

Non-invasive assessment of cardiac output and stroke volume in patients during exercise. Evaluation of a CO2-rebreathing method

A one-step CO2 rebreathing method for the determination of cardiac output and stroke volume (SV) has been evaluated by comparison with the direct Fick technique during recumbent exercise (10-90 W) in 13 patients. In an initial analysis, the influence of different rebreathing times and of correction for haemoglobin concentration was studied. The best correlation with the direct Fick technique was obtained with the longest analysis time, i.e. 21 s, and correction for variations in haemoglobin concentration further improved the correlation. Consequently, an analysis time of 21 s and correction for haemoglobin have been used. At low cardiac outputs, the CO2-rebreathing method overestimated the flow compared to the Fick technique. The correlation between the methods, however, was so good that a valid estimate of cardiac output could be obtained from the CO2 rebreathing method with appropriate corrections (Cardiac output, CO2 method = 2.7 + 0.77. Cardiac output, Fick; r = 0.91; Residual Standard deviation (SD res) = 0.77 l X min-1). Stroke volumes measured with the CO2 rebreathing method did not differ significantly from those obtained with the direct Fick technique, although there was a tendency to overestimate stroke volume with the CO2 rebreathing method (SV, CO2 method = 12 + 0.89 X SV, Fick; r = 0.82; SD res = 11 ml).     

Body, eye, and chorioallantoic vessel growth are not dependent on cardiac output level in day 3-4 chicken embryos

Normal aerobic metabolic rates persist in the early chicken embryo after elimination of cardiac output, but the dependence of tissue growth and differentiation on blood flow is unknown in these early stages. We partially ligated (25-50% occlusion) the ventricular outflow tract of Hamburger-Hamilton stage (HH) 16-18 embryos, producing a wide range of cardiac output. For the next approximately 48 h (to HH 24), we measured heart rate (HR), stroke volume (SV), and cardiac output (CO), as well as these growth indicators: eye diameter, chorioallantoic vessel density, and body mass. Acutely, HR declined with partial ligation (from 108 to 98 beats/min). Paradoxically, SV and CO decreased sharply in most embryos but increased in others, collectively producing the desired large variation (up to 25-fold) in CO and permitting assessment of tissue growth over a very large range of blood perfusion. Eye diameter doubled (from 0.6 to 1.2 mm) with development from HH 16 to HH 24, but within a developmental cohort there was no significant correlation between eye diameter and CO over a 25-fold range of CO. Similarly, chorioallantoic membrane vessel index was independent of CO over the CO range at all stages. Finally, body mass increase during development was not significantly affected by partial conal truncal ligation. Collectively, these data suggest that normal eye and vessel growth and body mass accumulation occur independent of their rate of blood perfusion, supporting the hypothesis of prosynchronotropy-that the heart begins to beat and generate blood flow in advance of the actual need for convective blood flow to tissues.     

正常人左心室功能指标的参考值及其预计公式的初步研究报告*

目的: 当前评估左心室容量和功能仍常用正常值范围,个体化分析也仅使用体表面积进行校正。尚缺少个体化因素相关的大样本参考值和预计公式。方法: 本研究纳入美国加州洛杉矶县南湾地区1200名健康志愿者,其中男807女393,年龄20岁-94岁,心脏CT造影（CTA）,经过高精度三维成像技术处理,计算左心室容积在收缩和舒张过程中的连续动态变化,测定左心室（LV）容量和功能指标：舒张末期容积（EDV)、收缩末期容积(ESV)、每搏输出量(SV)、射血分数(EF)和心输出量(CO)。将以上指标与一般特征指标进行多因素相关分析,以探索正常人预计值计算公式。结果: 男性除LVEF小于女性外（P<0.001）,其余各指标均大于女性（P<0.001）。多元线性回归分析提示, 性别、年龄、身高和体质量均为EDV、ESV、SV的独立影响因子(P<0.001); 而CO仅受年龄、性别、体质量显著影响(P<0.001),但与身高无关(P>0.05)。CO的预测公式CO (L·min^-1)= 6.963+0.446(Male) -0.037×年龄(yr)+0.013×体质量(kg)。结论: 性别、年龄、身高、体质量均影响左心室容量和功能,建立预测值计算公式,对心血管疾病的无创评估和个体化精准医疗具有重要参考价值。     

Left ventricular mechanical limitations to stroke volume in healthy humans during incremental exercise

During incremental exercise, stroke volume (SV) plateaus at 40-50% of maximal exercise capacity. In healthy individuals, left ventricular (LV) twist and untwisting ("LV twist mechanics") contribute to the generation of SV at rest, but whether the plateau in SV during incremental exercise is related to a blunting in LV twist mechanics remains unknown. To test this hypothesis, nine healthy young males performed continuous and discontinuous incremental supine cycling exercise up to 90% peak power in a randomized order. During both exercise protocols, end-diastolic volume (EDV), end-systolic volume (ESV), and SV reached a plateau at submaximal exercise intensities while heart rate increased continuously. Similar to LV volumes, two-dimensional speckle tracking-derived LV twist and untwisting velocity increased gradually from rest (all P < 0.001) and then leveled off at submaximal intensities. During continuous exercise, LV twist mechanics were linearly related to ESV, SV, heart rate, and cardiac output (all P < 0.01) while the relationship with EDV was exponential. In diastole, the increase in apical untwisting was significantly larger than that of basal untwisting (P < 0.01), emphasizing the importance of dynamic apical function. In conclusion, during incremental exercise, the plateau in LV twist mechanics and their close relationship with SV and cardiac output indicate a mechanical limitation in maximizing LV output during high exercise intensities. However, LV twist mechanics do not appear to be the sole factor limiting LV output, since EDV reaches its maximum before the plateau in LV twist mechanics, suggesting additional limitations in diastolic filling to the heart.     

Impaired muscle metaboreflex-induced increases in ventricular function in heart failure

We investigated to what extent heart failure alters the ability of the muscle metaboreflex to improve ventricular function. Dogs were chronically instrumented to monitor mean arterial pressure (MAP), cardiac output (CO), heart rate (HR), stroke volume (SV), and central venous pressure (CVP) at rest and during mild treadmill exercise (3.2 km/h) before and during reductions in hindlimb blood flow imposed to activate the muscle metaboreflex. These control experiments were repeated at constant heart rate (ventricular pacing 225 beats/min) and at constant heart rate coupled with a beta-adrenergic blockade (atenolol, 2 mg/kg iv) in normal animals and in the same animals after the induction of heart failure (HF, induced via rapid ventricular pacing). In control experiments in normal animals, metaboreflex activation caused tachycardia with no change in SV, resulting in large increases in CO and MAP. At constant HR, large increases in CO still occurred via significant increases in SV. Inasmuch as CVP did not change in this setting and that beta-adrenergic blockade abolished the reflex increase in SV at constant HR, this increase in SV likely reflects increased ventricular contractility. In contrast, after the induction of HF, much smaller increases in CO occurred with metaboreflex activation because, although increases in HR still occurred, SV decreased thereby limiting any increase in CO. At constant HR, no increase in CO occurred with metaboreflex activation even though CVP increased significantly. After beta-adrenergic blockade, CO and SV decreased with metaboreflex activation. We conclude that in HF, the ability of the muscle metaboreflex to increase ventricular function via both increases in contractility as well as increases in filling pressure are markedly impaired.     

Determination of cardiac output by the CO2 - rebreathing method in fifteen-year-old boys subjected to graduated loading.

The dynamics of cardiac output changes were studied in 23 15-year-old boys subjected to graduated loading up to maximum on an bicycle ergometer and relationships between cardiac output and other indexes of cardiorespiratory functions were determined. The correlation between cardiac output (Q in 1/min) and oxygen consumption (VO2 in 1/min) was Q = 6.84 + 5.64. VO2. CO2-rebreathing was found to be a suitable non-invasive method for determining cardiac output in loading tests in adolescents. Maximum cardiac output correlated with maximum oxygen consumption, maximum pulmonary ventilation, body weight, lean body mass and physical working capacity W 170 and did not correlate with systolic volume, the arteriovenous oxygen difference, the pulse rate and ballistocardiographic force. The absence of any statistically significant differences between the various functional indexes of the physical fitness of trained and untrained boys indicates that training was not very effective.     

Increased pulmonary vascular resistance and reduced stroke volume in association with CO2 retention and inferior vena cava dilatation.

Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO(2) and O(2) were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO(2) increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (approximately 4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO(2) retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.     

An allometric analysis of oxygen consumption rate and cardiovascular function in the cockroach, Blaberus discoidalis.

The interrelationship of metabolic rate and cardiovascular function has been well documented in vertebrates through allometric analyses. However, similar studies are lacking in insects. Unlike vertebrates, the cardiovascular system of insects does not play a significant role in oxygen transport. A comparison of the interrelationship in insects and vertebrates might provide insight into the nature of the connection between metabolic rate and the cardiovascular system. Oxygen consumption, heart rate and heart dimensions were measured in the nymphs of the cockroach Blaberus discoidalis over a mass range of 0.03-5 g. Oxygen consumption rate scaled with an exponent of 0.83. The relationship between heart rate and body mass scaled negatively, however, it did not appear to be linear. Using measurements of heart widths, abdominal length and heart rate, stroke volume and cardiac output were estimated. Cardiac output appeared to scale linearly with an exponent of 0.85, which was not significantly different from the exponent observed for the rate of oxygen consumption. Thus, the observed similarity between the exponents for oxygen consumption rate and cardiac output in vertebrates also appears to be present in insects.     

Assessment of cardiac output as a predictor of metabolic rate in rainbow trout

When water temperature was increased from 12 to 27°C at a rate of 2°C h⁻¹, oxygen consumption of rainbow trout Oncorhynchus mykiss was correlated strongly with both heart rate and blood oxygen extraction but the relationship with cardiac output was variable and weak. On the other hand, when water temperature was decreased from 21 to 12°C at a rate of 0·5°C h⁻¹, oxygen consumption was correlated with both heart rate and cardiac output but not with blood oxygen extraction. When fish were forced to swim increasingly faster, heart rate, cardiac output and blood oxygen extraction all correlated positively with oxygen consumption. For both cardiac output and heart rate, the slope of the regression line with oxygen consumption was elevated significantly more when the fish were forced to swim at increasingly higher swimming speeds than when water temperature was increased or decreased. The variation of the regression lines between cardiac output and oxygen consumption indicated that cardiac output presents few advantages over heart rate as a predictor of metabolic rate.