How the efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle changes with cycle frequency

2002 ◽  
Vol 205 (5) ◽  
pp. 697-706 ◽  
Author(s):  
Claire L. Harwood ◽  
Iain S. Young ◽  
John D. Altringham

SUMMARYDifferent species of animals require different cardiac performance and, in turn, their cardiac muscle exhibits different properties. A comparative approach can reveal a great deal about the mechanisms underlying myocardial contraction. Differences in myocardial Ca2+ handling between fish and mammals suggest a greater energy cost of activation in fish. Further, while there is considerable evidence that heart rate (or cycle frequency) should have a profound effect on the efficiency of teleost cardiac muscle, this effect has been largely overlooked. We set out to determine how cycle frequency affects the power output and efficiency of rainbow trout (Oncorhynchus mykiss) ventricular muscle and to relate this to the heart’s function in life. We measured power output and the rate of oxygen consumption (V̇O2) and then calculated efficiency over a physiologically realistic range of cycle frequencies.In contrast to mammalian cardiac muscle, in which V̇O2 increases with increasing heart rate, we found no significant change in V̇O2 in the teleost. However, power output increased by 25 % as cycle frequency was increased from 0.6 to 1.0 Hz, so net and total efficiency increased. A maximum total efficiency of 20 % was achieved at 0.8 Hz, whereas maximum power output occurred at 1.0 Hz. We propose that, since the heart operates continuously, high mechanical efficiency is a major adaptive advantage, particularly at lower heart rates corresponding to the more commonly used slower, sustainable swimming speeds. Efficiency was lower at the higher heart rates required during very fast swimming, which are used during escape or prey capture.If a fixed amount of Ca2+ is released and then resequestered each time the muscle is activated, the activation cost should increase with frequency. We had anticipated that this would have a large effect on the total energy cost of contraction. However, since V̇O2 remains constant, less oxygen is consumed per cycle at high frequencies. We suggest that a constant V̇O2 would be observed if the amount of activator Ca2+ were to decrease with frequency. This decrease in activation energy is consistent with the decrease in the systolic intracellular Ca2+ ([Ca2+]i) transient with increasing stimulation frequency seen in earlier studies.

1998 ◽  
Vol 201 (19) ◽  
pp. 2723-2733 ◽  
Author(s):  
CL Harwood ◽  
IS Young ◽  
JD Altringham

This study investigates the effects of cycle frequency, strain and length on work and power output of isolated rainbow trout (Oncorhynchus mykiss) ventricular preparations using the work loop technique. These effects are discussed in the context of the whole heart using analogies with heart rate, stroke volume and end-diastolic volume. Power output was dependent on cycle frequency, increasing threefold beween 0.3 and 1.1 Hz. The frequency for maximum power output was approximately 1.1 Hz, corresponding to the frequency for maximum power in perfused heart experiments. The length for maximum work production (Lopt) was found to be the same as the length for maximum isometric force production (Lmax). The decline in net work at lengths greater than Lopt/Lmax was attributed to an increase in passive work (the work done on an unstimulated muscle) or to hysteresis and to a large increase in lengthening work. The strain yielding maximum work decreased with increasing frequency. This is discussed in the context of the decline in stroke volume observed at increased heart rates in vivo. Muscle strain in intact hearts paced at 0.3 Hz was +/-11.9 % (23.8 % peak to peak), a value similar to the optimum strain at 0.3 Hz in vitro (+/-12 %).


2020 ◽  
Vol 223 (12) ◽  
pp. jeb215210 ◽  
Author(s):  
Rachel L. Sutcliffe ◽  
Shaorong Li ◽  
Matthew J. H. Gilbert ◽  
Patricia M. Schulte ◽  
Kristi M. Miller ◽  
...  

Aquaculture ◽  
2019 ◽  
Vol 509 ◽  
pp. 188-197 ◽  
Author(s):  
J. Brijs ◽  
E. Sandblom ◽  
M. Rosengren ◽  
K. Sundell ◽  
C. Berg ◽  
...  

2006 ◽  
Vol 291 (3) ◽  
pp. R711-R718 ◽  
Author(s):  
Erik Sandblom ◽  
Michael Axelsson

Central venous blood pressure (Pven) increases in response to hypoxia in rainbow trout ( Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including Pven, dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (PWO2 = ∼9 kPa), where PWO2 is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80–100, 90–110, and 100–120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure Pven during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by α-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80–100% blood volume, whereas vascular capacitance decreased significantly at 90–110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, Pven always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an α-adrenergic mechanism with both humoral and neural components.


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