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Journal of Experimental Biology, Vol 201, Issue 21 2961-2970, Copyright © 1998 by Company of Biologists


JOURNAL ARTICLES

Relative contribution of quantitative and qualitative changes in mitochondria to metabolic compensation during seasonal acclimatisation of rainbow trout Oncorhynchus mykiss

J. St-Pierre, P. M. Charest and H. Guderley

This study examined whether changes in the properties of mitochondria from red muscle of rainbow trout Oncorhynchus mykiss are accompanied by ultrastructural changes during cold acclimatisation. We compared measurements at five levels of organisation in red muscle of winter- (1 °C) and summer- (16 °C) acclimatised trout. We examined (1) maximal rates of pyruvate and palmitoyl carnitine oxidation by isolated mitochondria, (2) enzymatic activities [cytochrome c oxidase (CCO), citrate synthase (CS), carnitine palmitoyl transferase (CPT) and phosphofructokinase (PFK)] of the muscle and isolated mitochondria, (3) mitochondrial protein content in the muscle, (4) the ultrastructure of muscle fibres, and (5) the cristae surface density of the mitochondria. All variables were measured on each trout sampled. The mitochondria from winter-acclimatised trout possessed higher maximal capacities for the oxidation of pyruvate and palmitoyl carnitine than those from summer-acclimatised trout. Muscle activities of CCO, CS and CPT were greater in winter than in summer trout, whereas the levels of PFK did not differ seasonally. Similarly, the mitochondria from winter trout had elevated levels of CCO, CS and CPT compared with those isolated from summer trout. The cristae surface density of the mitochondria from winter trout (40.2+/-0.6 micrometre2 micrometre-3; mean +/- s.e.m.) was significantly higher than that from summer trout (36.4+/-1.2 micrometre2 micrometre-3), whereas there was no difference in the mitochondrial volume densities of muscle fibres from winter and summer trout. Thus, the considerable compensation of muscle aerobic capacity at low temperatures in trout is not accompanied by changes in mitochondrial volume density, but rather by shifts in enzyme levels and cristae surface density.


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