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The aims of this study were to assess whether thermal tolerance of brook trout (Salvelinus fontinalis) is affected during seawater (SW) acclimation and to investigate the role of cortisol in osmoregulation and thermal tolerance duringSWacclimation. Freshwater (FW)-acclimated brook trout at 18°C (Tacc) were exposed to SW for 16 days, whilst maintaining a FW control. Fish were examined for critical thermal maximum (CTmax) 0 (before), 2, 5 and 16 days afterSWexposure, and sampled at Tacc and CTmax for analysis of plasmacortisol, glucose and Cl-, gill Na+/K+-ATPase (NKA) activity and heat shock protein 70 (HSP70) abundance, and whitemusclewater content. At 2 days inSW, CTmax was significantly reduced (from 31 to 26°C), and then recovered by 16 days. This transient decrease in thermal tolerance coincided with a transient increase in plasma Cl- and decrease in muscle moisture content. Salinity itself had no effect on gill HSP70 abundance compared with the large and immediate effects of high temperature exposure during CTmax testing. To examine the role of cortisol in osmoregulation, brook troutwere administered a cortisol implant (5 and 25 μgg-1CORT) prior toSWexposure. Both CORT doses significantly increased their capacity tomaintain plasma Cl- during SW acclimation. Treatment with the 25 μg g-1 CORT dose was shown to significantly improve CTmax after 2 days in SW, and CTmax was associated with plasma Cl- and muscle moisture content. These findings indicate that brook trout are sensitive to temperature during SW acclimation and that thermal tolerance is associated with ion and water balance during SW acclimation. [ABSTRACT FROM AUTHOR]

The aims of this study were to assess whether thermal tolerance of brook trout (Salvelinus fontinalis) is affected during seawater (SW) acclimation and to investigate the role of cortisol in osmoregulation and thermal tolerance during SW acclimation. Freshwater (FW)-acclimated brook trout at 18 °C (Tacc) were exposed to SW for 16 d, whilst maintaining a FW control. Fish were examined for critical thermal maximum (CTmax) 0 (before), 2, 5, and 16 d after SW exposure, and sampled at Tacc and CTmax for analysis of plasma cortisol, glucose, and Cl-, gill Na+/K+-ATPase (NKA) activity and heat shock protein 70 (HSP70) abundance, and white muscle water content. At 2 d in SW, CTmax was significantly reduced (from 31 to 26 °C), then recovered by 16 d. This transient decrease in thermal tolerance coincided with a transient increase in plasma Cl- and decrease in muscle moisture content. Salinity itself had no effect on gill HSP70 abundance compared to the large and immediate effects of high temperature exposure during CTmax testing. To examine the role of cortisol in osmoregulation, brook trout were administered a cortisol implant (5 and 25 µg/g CORT) prior to SW exposure. Both CORT doses significantly increased their capacity to maintain plasma Cl- during SW acclimation. Treatment with the 25 µg/g CORT dose was shown to significantly improve CTmax after 2 d in SW, and CTmax was associated with plasma Cl-. These findings indicate that brook trout are sensitive to temperature during SW acclimation and that thermal tolerance is associated with ion and water balance during SW acclimation. [ABSTRACT FROM AUTHOR]

Despite the threat of climate change, the physiological mechanisms responsible for reduced performance at high temperatures remain unclear for most species. Elevated but sublethal temperatures may act via endocrine and cellular stress responses to limit performance in important life-history traits such as growth. Here, brook trout (Salvelinus fontinalis) subjected to chronically elevated or daily oscillating temperatures were monitored for growth and physiological stress responses. Growth rate decreased at temperatures above 16°C and was negative at 24°C, with an estimated upper limit for positive growth of 23.4°C. Plasma cortisol increased with temperature and was 12- and 18-fold higher at 22 and 24°C, respectively, than at 16°C, whereas plasma glucose was unaffected by temperature. Abundance of heat shock protein 70 (HSP70) in the gill increased with temperature and was 11- and 56-fold higher at 22°C and 24°C, respectively, than at 16°C. Therewas no relationship between temperature and plasma Cl-, but there was a 53% and 80% decrease in gill Na+/K+-ATPase activity and abundance at 24°C in comparison with 16°C. Daily temperature oscillations of 4°C or 8°C (19-23°C or 17-25°C) were compared with 21°C controls. Growth rate decreased with temperature and was 43% and 35% lower by length and mass, respectively, in the 8°C daily oscillation treatment than in the controls. There was no effect of temperature oscillation on plasma cortisol or glucose levels. In contrast, gill HSP70 abundance increased with increasing daily oscillation and was 40- and 700-fold greater at 4°C and 8°C daily oscillation, respectively, than in the constant temperature controls. In individuals exposed to 17-25°C diel oscillations for 4 days and then allowed to recover at 21°C, gill HSP70 abundance was still elevated after 4 days recovery, but not after 10 days. Our results demonstrate that elevated temperatures induce cellular and endocrine stress responses and provide a possible mechanism by which growth is limited at elevated temperatures. Temperature limitations on growth may play a role in driving brook trout distributions in the wild. [ABSTRACT FROM AUTHOR]

Organisms experience a wide range of environmental factors such as temperature, salinity and hydrostatic pressure, which pose challenges to biochemical processes. Studies on adaptations to such factors have largely focused on macromolecules, especially intrinsic adaptations in protein structure and function. However, micromolecular cosolutes can act as cytoprotectants in the cellular milieu to affect biochemical function and they are now recognized as important extrinsic adaptations. These solutes, both inorganic and organic, have been best characterized as osmolytes, which accumulate to reduce osmotic water loss. Singly, and in combination, many cosolutes have properties beyond simple osmotic effects, e.g. altering the stability and function of proteins in the face of numerous stressors. A key example is the marine osmolyte trimethylamine oxide (TMAO), which appears to enhance water structure and is excluded from peptide backbones, favoring protein folding and stability and counteracting destabilizers like urea and temperature. Co-evolution of intrinsic and extrinsic adaptations is illustrated with high hydrostatic pressure in deep-living organisms. Cytosolic and membrane proteins and G-protein-coupled signal transduction in fishes under pressure show inhibited function and stability, while revealing a number of intrinsic adaptations in deep species. Yet, intrinsic adaptations are often incomplete, and those fishes accumulate TMAO linearly with depth, suggesting a role for TMAO as an extrinsic 'piezolyte' or pressure cosolute. Indeed, TMAO is able to counteract the inhibitory effects of pressure on the stability and function of many proteins. Other cosolutes are cytoprotective in other ways, such as via antioxidation. Such observations highlight the importance of considering the cellular milieu in biochemical and cellular adaptation. [ABSTRACT FROM AUTHOR]

Growth hormone (GH)-transgenic Atlantic salmon display accelerated growth rates compared with non-transgenics. GH-transgenic fish also display cardiorespiratory and metabolic modifications that accompany the increased growth rate. An elevated routine metabolic rate has been described for pre- and post-smolt GH-transgenic salmon that also display improvements in oxygen delivery to support the increased aerobic demand. The early ontogenic effects of GH transgenesis on the respiratory and cellular physiology of fish, especially during adverse environmental conditions, and the effect of polyploidy are unclear. Here, we investigated the effects of GH transgenesis and polyploidy on metabolic, heart and ventilation rates and heat shock protein (HSP) levels after exposure to acute hypoxia in post-hatch Atlantic salmon yolk-sac alevins. Metabolic rate decreased with decreasing partial pressures of oxygen in all genotypes. In normoxia, triploid transgenics displayed the highest mass-specific metabolic rates in comparison to diploid transgenics and non-transgenic triploids, which, in contrast, had higher rates than diploid non-transgenics. In hypoxia, we observed a lower massspecific metabolic rate in diploid non-transgenics compared with all other genotypes. However, no evidence for improved O2 uptake through heart or ventilation rate was found. Heart rate decreased in diploid non-transgenics while ventilation rate decreased in both diploid non-transgenics and triploid transgenics in severe hypoxia. Regardless of genotype or treatment, inducible HSP70 was not expressed in alevins. Following hypoxia, the constitutive isoform of HSP70, HSC70, decreased in transgenics and HSP90 expression decreased in all genotypes. These data suggest that physiological changes through GH transgenesis and polyploidy are manifested during early ontogeny in Atlantic salmon. [ABSTRACT FROM AUTHOR]

The activin type IIB receptor (Acvr2b) is the cell surface receptor for multiple transforming growth factor ß (TGF-ß) superfamily ligands, several of which regulate muscle growth in mammals. To investigate the role of the Acvr2b signaling pathway in the growth and development of skeletal muscle in teleost fish, transgenic rainbow trout (RBT; Oncorhynchus mykiss) expressing a truncated form of the acvr2b-2a (acvr2bᅀ) in muscle tissue were produced. High levels of acvr2bᅀ expression were detected in the majority of P1 transgenic fish. Transgenic P1 trout developed enhanced, localized musculature in both the epaxial and hypaxial regions (dubbed 'six pack'). The F1 transgenic offspring did not exhibit localized muscle growth, but rather developed a uniform body morphology with greater girth, condition factor and increased muscle fiber hypertrophy. There was a high degree of variation in the mass of both P1 and F1 transgenic fish, with several fish of each generation exhibiting enhanced growth compared with other transgenic and control siblings. The 'six pack' phenotype observed in P1 transgenic RBT overexpressing acvr2bᅀ and the presence of F1 individuals with altered muscle morphology provides compelling evidence for the importance of TGF-ß signaling molecules in regulating muscle growth in teleost fish. [ABSTRACT FROM AUTHOR]

Teleost muscle first arises in early embryonic life and its development is driven by molecules present in the egg yolk and modulated by environmental stimuli including temperature and oxygen. Several populations of myogenic precursor cells reside in the embryonic somite and external cell layer and contribute to muscle fibres in embryo, larval, juvenile and adult stages. Many signalling proteins and transcription factors essential for these events are known. In all cases, myogenesis involves myoblast proliferation, migration, fusion and terminal differentiation. Maturation of the embryonic muscle is associated with motor innervation and the development of a scaffold of connective tissue and complex myotomal architecture needed to generate swimming behaviour. Adult muscle is a heterogeneous tissue composed of several cell types that interact to affect growth patterns. The development of capillary and lymphatic circulations and extramuscular organs - notably the gastrointestinal, endocrine, neuroendocrine and immune systems - serves to increase information exchange between tissues and with the external environment, adding to the complexity of growth regulation. Teleosts often exhibit an indeterminate growth pattern, with body size and muscle mass increasing until mortality or senescence occurs. The dramatic increase in myotomal muscle mass between embryo and adult requires the continuous production of muscle fibres until 40-50% of the maximum body length is reached. Sarcomeric proteins can be mobilised as a source of amino acids for energy metabolism by other tissues and for gonad generation, requiring the dynamic regulation of muscle mass throughout the life cycle. The metabolic and contractile phenotypes of muscle fibres also show significant plasticity with respect to environmental conditions, migration and spawning. Many genes regulating muscle growth are found as multiple copies as a result of paralogue retention following whole-genome duplication events in teleost lineages. The extent to which indeterminate growth, ectothermy and paralogue preservation have resulted in modifications of the genetic pathways regulating muscle growth in teleosts compared to mammals largely remains unknown. This review describes the use of compensatory growth models, transgenesis and tissue culture to explore the mechanisms of muscle growth in teleosts and provides some perspectives on future research directions. [ABSTRACT FROM AUTHOR]