Lurman, G.J.;Petersen, L.H.; Gamperl, A.K. (2012). In situ cardiac performance of Atlantic cod (Gadus morhua) at cold temperatures: long-term acclimation, acute thermal challenge and the role of adrenaline. Journal of Experimental Biology. 215 (22) 4006-4014.
The resting and maximum in situ cardiac performance of Newfoundland Atlantic cod (Gadus morhua) acclimated to 10, 4 and 0 degrees C were measured at their respective acclimation temperatures, and when acutely exposed to temperature changes: i.e. hearts from 10 degrees C fish cooled to 4 degrees C, and hearts from 4 degrees C fish measured at 10 and 0 degrees C. Intrinsic heart rate (f(H)) decreased from 41 beats min(-1) at 10 degrees C to 33 beats min(-1) at 4 degrees C and 25 beats min(-1) at 0 degrees C. However, this degree of thermal dependency was not reflected in maximal cardiac output (Q(max) values were similar to 44, similar to 37 and similar to 34 ml min(-1) kg(-1) at 10, 4 and 0 degrees C, respectively). Further, cardiac scope showed a slight positive compensation between 4 and 0 degrees C (Q(10)=1.7), and full, if not a slight over compensation between 10 and 4 degrees C (Q(10)=0.9). The maximal performance of hearts exposed to an acute decrease in temperature (i.e. from 10 to 4 degrees C and 4 to 0 degrees C) was comparable to that measured for hearts from 4 degrees C- and 0 degrees C-acclimated fish, respectively. In contrast, 4 degrees C-acclimated hearts significantly out-performed 10 degrees C-acclimated hearts when tested at a common temperature of 10 degrees C (in terms of both Q(max) and power output). Only minimal differences in cardiac function were seen between hearts stimulated with basal (5 nmol l(-1)) versus maximal (200 nmol l(-1)) levels of adrenaline, the effects of which were not temperature dependent. 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.