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Recent in vivo experiments on Atlantic cod (Gadus morhua) acclimated to chronic hypoxia (6-12weeks at 10°C; Pwo2 -8-9kPa) revealed a considerable decrease in the pumping capacity of the heart. To examine whether this diminished cardiac performance was due to the direct effects of chronic moderate hypoxia on the myocardium (as opposed to alterations in neural and/or hormonal control), we measured the resting and maximum in situ function of hearts from normoxiaand hypoxia-acclimated cod: (1) when initially perfused with oxygenated saline; (2) at the end of a 15min exposure to severe hypoxia (Po2 ∼0.6kPa); and (3) 30min after the hearts had been reperfused with oxygenated saline. Acclimation to hypoxia did not influence resting (basal) in situ cardiac performance during oxygenated or hypoxic conditions. However, it caused a decrease in maximum cardiac Output (Omax) under oxygenated conditions (from 49.5 to 40.3mlmin-1kg-1 by 19%), that was due to diminished values for maximum stroke volume (Vs) and scope for Vs. Severe hypoxia reduced in both groups to -20mlmin-1 kg-1, yet, the hearts of hypoxiaacclimated fish were better able to sustain this level of under hypoxia, and the recovery of Omax (as compared with initial values under oxygenated conditions) was significantly improved (94% vs 83%). These data show that acclimation to hypoxia has a direct effect on cod myocardial function and/or physiology, and suggest that the cod heart shows some adaptations to prolonged hypoxia. [ABSTRACT FROM AUTHOR]

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 ∼8-9kPa O2 (40-45% air saturation) or ∼21 kPaO2 (100% air saturation; normoxia) for 6-12 weeks at 10°C, and subsequently measured metabolic variables [routine oxygen consumption (Mo2), maximum Mo2, metabolic scope] and cardiac function (cardiac output, Q heart rate, fH; and stroke volume, Ucrit) in these fish during critical swimming speed (Ucrit) tests performed at both levels of water oxygenation. Although surgery (flow probe implantation) reduced the Ucrit of normoxia-acclimated cod by 14% (from 1.74 to 1.50 BLs-1) under normoxic conditions, exposure to acute hypoxia lowered the Ucrit of both groups (surgery and non-surgery) by ∼30% (to 1.23 and 1.02 BLs-1, respectively). This reduction in swimming performance was associated with large decreases in maximum Mo2 and metabolic scope (⩾50%), and maximum fH and O (by 16 and 22%), but not Ucrit. 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 Llcrit, maximum Mo2 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 Ucrit 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. [ABSTRACT FROM AUTHOR]

Oxygen consumption, as an indicator of routine metabolic rate (RoMR), and tissue-specific changes in protein synthesis, as measured by ³H-labelled phenylalanine incorporation rates, were determined in Astronotus ocellatus to investigate the cellular mechanisms behind hypoxia-induced metabolic depression and recovery. RoMR was significantly depressed, by approximately 50%, when dissolved oxygen levels reached 10% saturation (0.67±0.01 mg l-1 at 28±1°C). This depression in RoMR was accompanied by a 50-60% decrease in liver, heart and gill protein synthesis, but only a 30% decrease in brain protein synthesis. During recovery from hypoxia, an overshoot in RoMR to 270% of the normoxic rate was observed, indicating the accumulation of an oxygen debt during hypoxia. This conclusion was consistent with significant increase in plasma lactate levels during the hypoxic exposure, and the fact that lactate levels rapidly returned to pre-hypoxic levels. In contrast, a hyperactivation of protein synthesis did not occur, suggesting the overshoot in oxygen consumption during recovery is attributed to an increase in cellular processes other than protein synthesis. [ABSTRACT FROM AUTHOR]

For fish to survive large acute temperature increases (i.e. >10.0°C) that may bring them close to their critical thermal maximum (CTM), oxygen uptake at the gills and distribution by the cardiovascular system must increase to match tissue oxygen demand. To examine the effects of an acute temperature increase (∼1.7°C h-1 to CTM) on the cardiorespiratory physiology of Atlantic cod, we (1) carried out respirometry on 10.0°C acclimated fish, while simultaneously measuring in vivo cardiac parameters using Transonic® probes, and (2) constructed in vitro oxygen binding curves on whole blood from 7.0°C acclimated cod at a range of temperatures. Both cardiac output (Q) and heart rate (ƒʜ) increased until near the fish's CTM (22.2±0.2°C), and then declined rapidly. Q10 values for Q and ƒH were 2.48 and 2.12, respectively, and increases in both parameters were tightly correlated with O2 consumption. The haemoglobin (Hb)-oxygen binding curve at 24.0°C showed pronounced downward and rightward shifts compared to 20.0°C and 7.0°C, indicating that both binding capacity and affinity decreased. Further, Hb levels were lower at 24.0°C than at 20.0°C and 7.0°C. This was likely to be due to cell swelling, as electrophoresis of Hb samples did not suggest protein denaturation, and at 24.0°C Hb samples showed peak absorbance at the expected wavelength (540 nm). Our results show that cardiac function is unlikely to limit metabolic rate in Atlantic cod from Newfoundland until close to their CTM, and we suggest that decreased blood oxygen binding capacity may contribute to the plateau in oxygen consumption. [ABSTRACT FROM AUTHOR]

In recent years, there has been a great deal of interest in how growth hormone (GH) transgenesis affects fish physiology. However, the results of these studies are often difficult to interpret because the transgenic and non-transgenic fish had very different environmental/rearing histories. This study used a stable line of size-matched GH Atlantic salmon (Salmo salar) that were reared in a shared tank with controls (at 10°C, for -9 months) to perform a comprehensive examination of the cardiorespiratory physiology of GH transgenic salmon, and serves as a novel test of the theory of symmorphosis. The GH transgenic salmon had a 3.6× faster growth rate, and 21 and 25% higher values for mass-specific routine and standard oxygen consumption (ṀO2), respectively. However, there was no concurrent increase in their maximum ṀO2, which resulted in them having an 18% lower metabolic scope and a 9% reduction in critical swimming speed. This decreased metabolic capacity/performance was surprising given that the transgenics had a 29% larger heart with an 18% greater mass-specific maximum in situ cardiac output, a 14% greater post-stress blood haemoglobin concentration, 5–10% higher red muscle and heart aerobic enzyme (citrate synthase or cytochrome oxidase) activities, and twofold higher resting and 1.7× higher post-stress, catecholamine levels. However, gill surface area was the only cardiorespiratory parameter that was not enhanced, and our data suggest that gill oxygen transfer may have been limiting. Overall, this research: (1) shows that there are significant metabolic costs associated with GH transgenesis in this line of Atlantic salmon; (2) provides the first direct evidence that cardiac function is enhanced by GH transgenesis; (3) shows that a universal upregulation of post-smolt (adult) GH transgenic salmon cardiorespiratory physiology, as suggested by symmorphosis, does not occur; and (4) supports the idea that whereas differences in arterial oxygen transport (i.e. cardiac output and blood oxygen carrying capacity) are important determinants of inter-specific differences in aerobicity, diffusion-limited processes must be enhanced to achieve substantial intra-specific improvements in metabolic and swimming performance. [ABSTRACT FROM AUTHOR]