Cardiac growth in rainbow trout, Salmo gairdneri

Reducing temperature below the optimum of most vertebrate hearts impairs contractility and reduces organ function. However, a number of fish species, including the rainbow trout, can seasonally acclimate to low temperature. Such ability requires modification of physiological systems to compensate for the thermodynamic effects of temperature on biological processes. The current study tested the hypothesis that rainbow trout compensate for the direct effect of cold temperature by increasing cardiac contractility during cold acclimation. We examined cardiac contractility, following thermal acclimation (4, 11 and 17°C), by measuring the Ca 2+ sensitivity of force generation by chemically skinned cardiac trabeculae as well as ventricular pressure generation using a modified Langendorff preparation. We demonstrate, for the first time, that the Ca 2+ sensitivity of force generation was significantly higher in cardiac trabeculae from 4°C-acclimated trout compared with those acclimated to 11 or 17°C, and that this functional change occurred in parallel with a decrease in the level of cardiac troponin T phosphorylation. In addition, we show that the magnitude and rate of ventricular pressure generation was greater in hearts from trout acclimated to 4°C compared with those from animals acclimated to 11 or 17°C. Taken together, these results suggest that enhanced myofilament function, caused by modification of existing contractile proteins, is at least partially responsible for the observed increase in pressure generation after acclimation to 4°C. In addition, by examining the phenotypic plasticity of a comparative model we have identified a strategy, used in vivo, by which the force-generating capacity of cardiac muscle can be increased.

Section: Variation In Morphological Remodellingsupporting

confidence: 80%

Cold acclimation increases cardiac myofilament function and ventricular pressure generation in trout

Klaiman

Pyle

Gillis

2014

“…Although many studies report that RVM increases in rainbow trout at cold temperatures (e.g. Farrell et al, 1988;Graham and Farrell, 1989), Sephton and Driedzic (Sephton and Driedzic, 1995) did not observe any increase in heart size when trout were acclimated to 5°C for 4weeks.…”

Section: Temperature Effects On Cardiac Functionmentioning

confidence: 83%

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

Lurman

Petersen

Gamperl

2012

SUMMARYThe resting and maximum in situ cardiac performance of Newfoundland Atlantic cod (Gadus morhua) 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 and 0°C. Intrinsic heart rate (f H ) decreased from 41beatsmin -1 at 10°C to 33beatsmin -1 at 4°C and 25beatsmin -1 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 to 4°C and 4 to 0°C) was comparable to that measured for hearts from 4°C-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nmoll ) 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.

“…Salmonids apparently have an upper limit to f H of approximately 2Hz, which is purported to be related to calcium handling by cardiomyocytes during excitation-contraction coupling (Farrell, 1991). Indeed, a limited involvement of the sarcoplasmic reticulum in delivering activator calcium is associated with fish cardiomyocytes retaining a large surface area to volume ratio by undergoing hyperplasia to a greater degree than hypertrophy during cardiac growth (Farrell et al, 1988;Sun et al, 2009). Consequently, salmon maintain a near-constant cardiomyocyte surface area to volume ratio despite isometric ventricular growth, a situation that contrasts diametrically with the situation in mammalian hearts, where postnatal growth of cardiomyocytes is largely through hypertrophy, resulting in a progressively smaller surface area to volume ratio with isometric cardiac growth.…”

Section: F H Scaling In Fishmentioning

confidence: 99%

Effects of body mass on physiological and anatomical parameters of mature salmon: evidence against a universal heart rate scaling exponent

Farrell

2011

Clark et al., 2010) and took advantage of the diverse life history of Chinook salmon (Oncorhynchus tshawytscha), the largest of the Pacific salmonids (Groot and Margolis, 1991). After emerging from the egg with a M b of <1g (Kinnison et al., 1998), juvenile Chinook salmon typically remain in freshwater for around 1year prior to commencing an ocean migration to grow and mature. Whereas the majority of individuals spend around 3years in the ocean and return to freshwater spawning grounds as 4year olds, some individuals leave the ocean as 2 or 3year olds (primarily males), or late as 5 or 6year olds. These different intra-specific life history strategies,