Effect of acute and chronic hypoxia on the swimming performance, metabolic capacity and cardiac function of Atlantic cod (Gadus morhua)

Abstract

Low water oxygen content (hypoxia) is a common feature of many freshwater and marine environments. However, we have a poor understanding of the degree to which diminished cardiac function contributes to the reduction in fish swimming performance concomitant with acute exposure to hypoxia, or how fish cardiorespiratory physiology is altered by, or adapts to, chronic hypoxia. Thus, we acclimated adult Atlantic cod (Gadus morhua) to either approximately 8-9 kPa O(2) (40-45% air saturation) or approximately 21 kPa O(2) (100% air saturation; normoxia) for 6-12 weeks at 10 degrees C, and subsequently measured metabolic variables [routine oxygen consumption (M(O(2)), maximum (M(O(2)), metabolic scope] and cardiac function (cardiac output, Q; heart rate, f(H); and stroke volume, V(S)) in these fish during critical swimming speed (U(crit)) tests performed at both levels of water oxygenation. Although surgery (flow probe implantation) reduced the U(crit) of normoxia-acclimated cod by 14% (from 1.74 to 1.50 BL s(-1)) under normoxic conditions, exposure to acute hypoxia lowered the U(crit) of both groups (surgery and non-surgery) by approximately 30% (to 1.23 and 1.02 BL s(-1), respectively). This reduction in swimming performance was associated with large decreases in maximum M(O(2)) and metabolic scope (> or = 50%), and maximum f(H) and Q (by 16 and 22%), but not V(S). Long-term acclimation to hypoxia resulted in a significant elevation in normoxic metabolic rate as compared with normoxia-acclimated fish (by 27%), but did not influence normoxic or hypoxic values for U(crit), maximum M(O(2)) or metabolic scope. This was surprising given that resting and maximum values for Q were significantly lower in hypoxia-acclimated cod at both levels of oxygenation, because of lower values for V(S). However, hypoxia-acclimated cod were able to consume more oxygen for a given cardiac output. These results provide important insights into how fish cardiorespiratory physiology is impacted by short-term and prolonged exposure to hypoxia, and further highlight the tremendous capacity of the fish cardiorespiratory system to deal with environmental challenges.