Fish larvae are the world's smallest vertebrates, and their high rates of mortality may be partially owing to a very limited aerobic scope. Unfortunately, however, no complete empirical dataset exists on the relationship between minimal and maximal metabolism (and thus aerobic scope) for any fish species throughout ontogeny, and thus such an association is hard to delineate. We measured standard and maximal metabolism in three marine fish species over their entire life history, and show that while aerobic scope depends greatly on body size and developmental trajectory, it is extremely small during the early life stages (factorial aerobic scope%1.5). Our findings strongly suggest that limited scope for aerobic activity early in life is likely to constrain physiological function and ultimately impact behaviour and possibly survival. Furthermore, our results have important implications for ecological models that incorporate metabolic scaling, and provide additional evidence against the existence of 'universal' scaling exponents.

With over 20·000 species of teleost fish, considerable interspecific diversity in cardiac anatomy and physiology is expected. This is the outcome of evolutionary adaptation to different habits, modes of life and activity levels. For example, athletic species have a more powerful heart than sedentary species, and fish such as hagfish, carp and eel normally show a much higher degree of myocardial hypoxia tolerance than species such as salmonids (Farrell, 1991;Farrell and Jones, 1992). Plasticity in cardiac form and function has also been demonstrated during ontogeny, and the cardiovascular flexibility exhibited during embryonic and larval development, is nicely reviewed by Pelster (2003). What is less well appreciated, however, is the high degree of intraspecific cardiac plasticity displayed by post-larval fishes. Accordingly, this review explores what is known about intraspecific cardiac plasticity among juvenile and adult fishes. This intraspecific plasticity, like that exhibited during development, may well reflect individual variability on which natural selection could act.In this review, we focus primarily on temperature effects, which are relatively well studied, and on the effects of other environmental and biological factors that modify cardiac anatomy and physiology, including food deprivation, sexual maturation, exercise training and rearing under aquaculture conditions. Further, we summarize recent work on cardiac preconditioning and myocardial hypoxia tolerance in fishes, and discuss the potential implications of this work.Preconditioning is a short-term form of cardiac plasticity that has the potential to protect the heart from insults that might normally lead to cardiac damage, dysfunction or death. Preconditioning has been the focus of several thousand mammalian studies (e.g. see review by Yellon and Downey, 2003), and so the handful of recent studies in fish, which already point to important intraspecific differences, may find application outside the piscine world. Similarly, researchers who wish to stimulate cardiac growth to replace damaged myocardial tissue in mammals, may be heartened to discover that fish cardiac tissue, unlike the mammalian heart, does not lose its ability for hyperplastic growth with age. In fact, we suspect that the high degree of intraspecific plasticity that we Fish cardiac physiology and anatomy show a multiplicity of intraspecific modifications when exposed to prolonged changes in environmentally relevant parameters such as temperature, hypoxia and food availability, and when meeting the increased demands associated with training/increased activity and sexual maturation. Further, there is evidence that rearing fish under intensive aquaculture conditions significantly alters some, but not all, aspects of cardiac anatomy and physiology. This review focuses on the responses of cardiac physiology and anatomy to these challenges, highlighting where applicable, the importance of hyperplastic (i.e. the production of new cells) vs hypertrophic (the enlargement of existing cells...

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 (fH) increased until near the fish's CTM (22.2±0.2°C), and then declined rapidly. Q 10 values for Q and fH were 2.48 and 2.12, respectively, and increases in both parameters were tightly correlated with O 2 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.

Temperature-induced limitations on the capacity of the cardiorespiratory system to transport oxygen from the environment to the tissues, manifested as a reduced aerobic scope (maximum minus standard metabolic rate), have been proposed as the principal determinant of the upper thermal limits of fishes and other waterbreathing ectotherms. Consequently, the upper thermal niche boundaries of these animals are expected to be highly sensitive to aquatic hypoxia and other environmental stressors that constrain their cardiorespiratory performance. However, the generality of this dogma has recently been questioned, as some species have been shown to maintain aerobic scope at thermal extremes. Here, we experimentally tested whether reduced oxygen availability due to aquatic hypoxia would decrease the upper thermal limits (i.e. the critical thermal maximum, CT max ) of the estuarine red drum (Sciaenops ocellatus) and the marine lumpfish (Cyclopterus lumpus). In both species, CT max was independent of oxygen availability over a wide range of oxygen levels despite substantial (>72%) reductions in aerobic scope. These data show that the upper thermal limits of waterbreathing ectotherms are not always linked to the capacity for oxygen transport. Consequently, we propose a novel metric for classifying the oxygen dependence of thermal tolerance; the oxygen limit for thermal tolerance (P CTmax ), which is the water oxygen tension (Pw O2 ) where an organism's CT max starts to decline. We suggest that this metric can be used for assessing the oxygen sensitivity of upper thermal limits in water-breathing ectotherms, and the susceptibility of their upper thermal niche boundaries to environmental hypoxia.

No abstract