Atlantic cod (Gadus morhua L.) in situ cardiac performance at cold temperatures: long-term acclimation, acute thermal challenge and the role of adrenaline

• Published in: Journal of Experimental Biology
• Main Authors: Lurman, Glenn J., Petersen, Lene H., Gamperl, A. Kurt
• Format: Text
• Language: English
• Published: Company of Biologists 2012
• Subjects: Research Article; atlantic cod; Gadus morhua; Newfoundland
• Online Access: http://jeb.biologists.org/cgi/content/short/jeb.069849v1; https://doi.org/10.1242/jeb.069849

The resting and maximum in situ cardiac performance of Newfoundland Atlantic cod ( Gadus morhua L.) acclimated to 10, 4 and 0°C were measured at their respective acclimation temperatures, and when acutely exposed to temperature changes: i.e. hearts from 10°C fish cooled to 4°C, and hearts from 4°C fish measured at 10°C and 0°C. Intrinsic heart rate ( f H ) decreased from 41 beats min-1 (bpm) at 10°C to 33 bpm at 4°C and to 25 bpm at 0°C. However, this degree of thermal dependency was not reflected in maximal cardiac output. Q max values were ~44, ~37 and ~34 ml min-1 kg-1 at 10, 4 and 0°C, respectively. Further, cardiac scope showed a slight positive compensation between 4 and 0°C (Q 10 = 1.7), and full, if not a slight over compensation between 10 and 4°C (Q 10 = 0.9). The maximal performance of hearts exposed to an acute decrease in temperature (i.e. from 10°C to 4°C and 4°C to 0°C) was comparable to that measured for hearts from 4 and 0°C acclimated fish, respectively. In contrast, 4°C acclimated hearts significantly out-performed 10°C acclimated hearts when tested at a common temperature of 10°C (in terms of both Q max and power output). Only minimal differences in cardiac function were seen between hearts stimulated with basal (5 nM) vs. maximal (200 nM) levels of adrenaline, the effects of which were not temperature dependant. These results: 1) show that maximum performance of the isolated cod heart is not compromised by exposure to cold temperatures; and 2) support data from other studies which show that, in contrast to salmonids, cod cardiac performance/myocardial contractility is not dependent upon humoral adrenergic stimulation.