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The objective of this study was to determine whether individual variation in the swimming performance of northern squawfish was correlated with variation in cardiac performance. Critical velocity tests were conducted on fish either during the summer at 16°C or during the winter at 5°C. Fish were individually marked and, within 2 wk after the first swimming challenge, underwent surgery in which an ultrasonic flow probe was fitted around the ventral aorta. The day after surgery a second critical velocity test was conducted, during which heart rate, stroke volume (SV), and cardiac output (Q̇) were measured. The mean maximum prolonged swimming speed (Ucrit) of the fish following surgery dropped significantly relative to that of the intact fish; however, the rank orderperformance of the fish was maintained in both seasons (winter, P = 0.019; summer, P = 0 029). Exercise increased Q̇by a statistically significant 2 7 times at 16°C and 2.5 times at 5°C. When fish at either temperature were swimming near their Ucrit, Q̇and SV were strongly correlated with body mass, with heart mass, and with each other (r> 0.75, P< 0.01 for all pairs of variables). Maximum Q̇of northern squawfish appeared to depend upon maximum SV, which in turn appeared to depend upon heart mass; however, none of the cardiovascular traits measured in this study were significantly correlated with individual variation in swimming performance.

This is the first study to report absolute measurements of cardiac output (Q̇) with Transonic flow probes during prolonged swimming in a salmonid. Simultaneous measurements of hematocrit and arterial blood O₂ content in seawater-acclimated rainbow trout (Oncorhynchus mykiss) (body mass 401-1,025 g) at 10° ± 1° C indicated that the fish were in good physiological condition, while measurements of resting heart rate, arterial blood pressure, and systemic resistance suggested relatively low levels of stress. Maximum Q̇Q̇max(48. 7 mL · min⁻¹ · kg⁻¹) was reached at 97.3% of the maximum prolonged swimming speed and is similar to the Q̇maxestimated by the Fick principle during swimming in freshwater rainbow trout. Maximum Q̇was 84% greater than the resting Q̇(Q̇rest) (26.6 mL · min⁻¹ · kg⁻¹) and was brought about by a 38% increase in heart rate (fH) and a 25% increase in stroke volume (SVH). Correlation analysis showed that individual variability in Q̇maxwas mainly due to variability in maximum SVH; maximum fHwas relatively invariant among individuals. At rest, SVHand fH, were negatively correlated. Individual fish with a high Q̇maxwere characterized by a low resting fHand a high resting SVH.

Lactate utilization was studied in an in situ perfused trout heart preparation that was capable of performing at levels similar to in vivo maximum cardiac performance. Hearts were perfused with modified Cortland saline containing 0.5 mmol l-1 iodoacetic acid (to block endogenous glycolysis) and varying amounts of lactate (1 or 10 mmol l-1). We confirmed previous observations that lactate utilization is limited by substrate availability. However, contrary to previous observations, exogenous fuel availability did not limit cardiac performance, even at the high workload. Furthermore, when plentiful (i.e. 10mmoll-1), exogenous lactate was preferred over endogenous fuel and was able to supply the heart’s energy requirements at both the low and high workloads. Pyruvate at 10fold greater concentration, had no apparent effect on lactate utilization at the high workload. α-Cyano-4-hydroxycinnamate (α-CIN) (2.5 mmol l-1) proved to be an unsuitable probe of lactate transport in the trout heart as it caused a reduction in both lactate utilization and cardiac performance. However, addition of 20 μmol l-1 isobutyl carbonyl lactyl anhydride or 100μmoll-1 4-acetamido-4 ′-isothiocyano-stilbene-2,2 ′-disulphonic acid (putative lactate transport blockers) to the perfusate virtually abolished lactate oxidation at the high workload without affecting cardiac performance. These observations suggest that lactate uptake by the in situ perfused trout heart is carrier-mediated.

Cardiac output, ventral and dorsal aortic blood pressure and heart rate were recorded simultaneously in unanaesthetized hagfish, Myxine glutinosa L. Mean cardiac output was 8.7 ml min−1 kg−1 and mean heart rate 22.3 beats min−1. The absence of beat-to-beat oscillations in heart rate was consistent with the lack of an extrinsic cardiac innervation in hagfish. Mean blood pressures were 1.04 kPa (ventral aorta) and 0.77kPa (dorsal aorta). Injection of adrenaline into the caudal vein significantly increased cardiac output, stroke volume, heart rate and blood pressures of both aortas. Peak cardiac output was close to 25 ml min−1 kg−1. Injection of the β-adrenoreceptor antagonist sotalol decreased resting heart rate significantly. We conclude that endogenous catecholamines from chromaffin cells of the heart are instrumental in the regulation of cardiac function in Myxine. Injection of acetylcholine had little direct effect on the recorded cardiac variables, but caused marked branchial vasoconstriction. Heart rate increased as the pressor response subsided. The cholinergic antagonist atropine had no effect on any of the resting parameters. Injection of adenosine had no direct cardiac effects but reduced the systemic vascular resistance. Severe hypoxia (kPa for 15–35 min) had very little effect on the cardiovascular variables recorded. The remarkable ability of the hagfish heart to maintain normal cardiac output during severe hypoxia is discussed with respect to the anaerobic pumping capacity of the heart. Pump-perfused, in situ gill preparations were used to examine branchial vasoactivity. Acetylcholine and adrenaline produced dose-dependent vasoconstriction, whereas isoprenaline, noradrenaline and adenosine dilated the branchial vasculature.

An in situ heart preparation was used to evaluate cardiac performance in the sea raven, Hemitripterus americanus, under physiological inflow and outflow pressure conditions. Winter and summer fish were subjected to an acute 10 °C temperature change from the seasonal ambient value. The maximum cardiac output under each temperature condition was determined by altering inflow pressure to the heart. Acute temperature increase produced positive chronotropic and inotropic effects in winter fish. Acute temperature decrease produced a negative chronotropic and inotropic effect in summer fish. The inotropic and chronotropic states of the heart were different in winter and summer fish. Intrinsic heart rate was higher in summer fish at all experimental temperatures. The sensitivity of the summer fish hearts to input pressure was also greater, especially during the warm experimen-tal temperatures. It was evident from heartbeat rate measurements and power output calculations that the advent of summer and winter seasons did not promote any compensatory ability in intrinsic heart function.

The effects of adrenaline, noradrenaline, substance P and vasoactive intestinal polypeptide (VIP) on dorsal aortic blood pressure, coeliac artery blood flow and heart rate were studied in unrestrained dogfish, Squalus acanthias. Changes in the coeliac vascular bed were calculated from these variables. Perfused tail preparations were used to study the effects of the various drugs on the somatic vascular bed. Corrosion casts were made to study the gross architecture of the coeliac vascular bed. Adrenaline and noradrenaline increased dorsal aortic pressure and reduced the coeliac artery blood flow. Adrenaline caused a small increase in heart rate while noradrenaline caused a small decrease. Both drugs increased the resistance in the coeliac vascular bed. VIP increased dorsal aortic pressure, heart rate and resistance in the coeliac vascular bed. Substance P caused an increase in heart rate, cardiac output and, in particular, in coeliac artery blood flow; dorsal aortic pressure was simultaneously reduced. Voluntary swimming or fright immediately caused a pronounced reduction in blood flow in the coeliac artery, even though cardiac output and dorsal aortic pressure increased. It is concluded that adrenergic mechanisms and possibly VIP are involved in reducing the blood flow to the gut, while substance P increases the flow to the gut.

We examined cardiac pacemaker rate resetting in rainbow trout following a reciprocal temperature transfer. In the original experiment, performed in winter, 4°C-acclimated fish transferred to 12°C reset intrinsic heart rate after just 1 h (from 56.8±1.2 to 50.8±1.5 beats min−1); 12°C-acclimated fish transferred to 4°C reset intrinsic heart rate after 8 h (from 33.4±0.7 to 37.7±1.2 beats min−1). However, in a replicate experiment, performed in the summer using a different brood year, intrinsic heart rate was not reset, even after 10 weeks at a new temperature. Using this serendipitous opportunity, we compared mRNA expression changes of a suite of proteins in sinoatrial node (SAN), atrial and ventricular tissues after both 1 h and longer than 3 weeks for both experimental acclimation groups to identify those changes only associated with pacemaker rate resetting. Of the changes in mRNA expression occurring after more than 3 weeks of warm acclimation and associated with pacemaker rate resetting, we observed downregulation of NKA α1cin the atrium and ventricle, and upregulation of HCN1in the ventricle. However, in the SAN there were no mRNA expression changes unique to the fish with pacemaker rate resetting after either 1 h or 3 weeks of warm acclimation. Thus, despite identifying changes in mRNA expression of contractile cardiac tissues, there was an absence of changes in mRNA expression directly involved with the initial, rapid pacemaker rate resetting with warm acclimation. Importantly, pacemaker rate resetting with thermal acclimation does not always occur in rainbow trout.

The cardiovascular system is critical for delivering O2to tissues. Here, we examined the cardiovascular responses to progressive hypoxia in four high-altitude Andean duck species compared with four related low-altitude populations in North America, tested at their native altitude. Ducks were exposed to stepwise decreases in inspired partial pressure of O2while we monitored heart rate, O2consumption rate, blood O2saturation, haematocrit (Hct) and blood haemoglobin (Hb) concentration. We calculated O2pulse (the product of stroke volume and the arterial–venous O2content difference), blood O2concentration and heart rate variability. Regardless of altitude, all eight populations maintained O2consumption rate with minimal change in heart rate or O2pulse, indicating that O2consumption was maintained by either a constant arterial–venous O2content difference (an increase in the relative O2extracted from arterial blood) or by a combination of changes in stroke volume and the arterial–venous O2content difference. Three high-altitude taxa (yellow-billed pintails, cinnamon teal and speckled teal) had higher Hct and Hb concentration, increasing the O2content of arterial blood, and potentially providing a greater reserve for enhancing O2delivery during hypoxia. Hct and Hb concentration between low- and high-altitude populations of ruddy duck were similar, representing a potential adaptation to diving life. Heart rate variability was generally lower in high-altitude ducks, concurrent with similar or lower heart rates than low-altitude ducks, suggesting a reduction in vagal and sympathetic tone. These unique features of the Andean ducks differ from previous observations in both Andean geese and bar-headed geese, neither of which exhibit significant elevations in Hct or Hb concentration compared with their low-altitude relatives, revealing yet another avian strategy for coping with high altitude.