Renal function in the freshwater rainbow trout after dietary cadmium acclimation and waterborne cadmium challenge

Renal function was examined in adult rainbow trout (Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 52 d and during a subsequent challenge to waterborne Cd (10 microg/L) for 72 h. Dietary Cd had no major effects on UFR (urine flow rate) and GFR (glomerular filtration rate) but caused increased renal excretion of glucose, protein, and major ions (Mg(2+), Zn(2+), K(+), Na(+), Cl(-) but Ca(2+)). However, dietary Cd did not affect any plasma ions except Na(+) which was significantly elevated in the Cd-acclimated trout. Plasma glucose and ammonia levels fell by 25% and 36% respectively, but neither plasma nor urine urea was affected in Cd-acclimated fish. Dietary Cd exposure resulted in a remarkable increase of Cd load in the plasma (48-fold, approximately 22 ng/mL) and urine (60-fold, 8.9 ng/mL), but Cd excretion via the kidney was negligible on a mass-balance basis. Clearance ratio analysis indicates that all ions, Cd, and metabolites were reabsorbed strongly (58-100%) in both na?ve and dietary Cd exposed fish, except ammonia which was secreted in both groups. Mg(2+), Na(+), Cl(-) and K(+) reabsorption decreased significantly (3-15%) in the Cd-exposed fish relative to the control. Following waterborne Cd challenge, GFR and UFR were affected transiently, and only Mg(2+) and protein excretion remained elevated with no recovery with time in Cd-acclimated trout. Urinary Ca(2+) and Zn(2+) excretion rates dropped with an indication of renal compensation towards plasma declines of both ions. Cadmium challenge did not cause any notable effects on urinary excretion rates of metabolites. However, a significant decrease in Mg(2+) reabsorption but an increase in total ammonia secretion was observed in the Cd-acclimated fish. The study suggests that dietary Cd acclimation involves physiological costs in terms of renal dysfunction and elevated urinary losses.     

Dietary Ca inhibits waterborne Cd uptake in Cd-exposed rainbow trout, Oncorhynchusmykiss

The effects of chronic exposure to waterborne Cd and elevated dietary Ca, alone and in combination, were examined in juvenile rainbow trout, Oncorhynchusmykiss. Fish were chronically exposed to 0.05 (control) or 2.56 μg/l Cd [as Cd(NO₃)₂·4H₂O] and were fed 2% body mass/day of control (29.6 mg Ca/g) or Ca-supplemented trout food (52.8 mg Ca/g as CaCl₂·2H₂O). Cd accumulated mainly in gill, liver, and kidney. Waterborne Cd inhibited unidirectional Ca uptake from water into the gill and induced hypocalcemia in the plasma on day 40. Waterborne Cd also induced an elevated Ca concentration on day 20 in the gill tissue of trout fed the Ca-supplemented diet and a decreased Ca concentration on day 35 in the gills of trout fed the control diet. Dietary Ca protected against Cd accumulation in gill, liver, and kidney, but did not protect against the inhibition of Ca uptake into the gill or plasma hypocalcemia. When fed Ca-supplemented diet and exposed to waterborne Cd, fish showed 35% mortality, compared to 0–2% in control fish and in the Cd-exposed fish with normal Ca in the diet. Growth, on the other hand, was not affected by any treatment.     

Influence of dissolved organic matter on copper binding, and calcium on cadmium binding, by gills of rainbow trout

Complexation of Cu by 5 mg Cl⁻¹ dissolved organic matter (DOM) from a marsh kept Cu from binding to gills of small rainbow trout Oncorhynchus mykiss in 9-day exposures to 0.5 μM Cu in soft water. The protective effect of DOM occurs because the formation of Cu-DOM complexes reduces the amount of free Cu in the water, so the disruptive effects of Cu on ionoregulation, such as inhibited Na uptake, cannot develop. The Cu-DOM complexes themselves do not bind to the gills. Calcium (1100 μm) reduced the accumulation of Cd by trout gills in short, 2-h exposures through competition for gill binding sites but not over longer, 7-day exposures to 0–14 μM Cd. However, the protective effect of Ca against Cd toxicity persisted throughout the longer experiment, likely due to the decrease in the electrochemical gradient for diffusive loss of Ca from the fish to the water. Rainbow trout and fathead minnows Pimephales promelas accumulated Cu and Cd on their gills in a similar manner; thus, binding constants for metal-gill interactions determined for one species of fish can be generalized to other fish species. When literature binding constants determined for fathead minnows were applied to our studies with rainbow trout, computer modelling of Cu-gill and Cu-DOM interactions simulated our results well. In contrast Cd-gill and Ca-gill modelling predicted the initial competitive effect of Ca against Cd accumulation by trout gills, but did not predict the longer-term accumulation of Cd by trout gills.     

The effect of sub-lethal ammonia exposure on fed and unfed rainbow trout: the role of glutamine in regulation of ammonia

Many species of fishes have evolved mechanisms for coping with ammonia caused by either high ammonia environments or an inability to excrete nitrogenous wastes. Rainbow trout (Oncorhynchus mykiss), have not been known to have such a mechanism. The present study investigated whether rainbow trout can use amino acid synthesis and storage to cope with ammonia. Experiments were performed on fed and unfed rainbow trout under both control and elevated ammonia conditions (0 and 10 mgN/l (total ammonia nitrogen), pH 7.2). The results indicate that both feeding and ammonia exposure increased plasma ammonia significantly 6 h postprandial and post ammonia exposure. After 48 h the fed/ammonia exposed fish had plasma ammonia levels that were not significantly different than the fed/control fish. Plasma ammonia was reduced by more than 50%, attributable to ammonia being converted to glutamine in brain, liver and muscle tissue. Feeding alone also increased glutamine levels in brain tissue. Activity of glutamine synthetase in brain and liver was increased corresponding to an increase in glutamine concentrations when fish were exposed to ammonia. This is the first report showing that rainbow trout can detoxify endogenous and exogenous ammonia.     

Effects of copper on the acute cortisol response and associated physiology in rainbow trout

The aim of this study was to determine the effects of chronic waterborne copper (Cu) exposure on the acute stress-induced cortisol response and associated physiological consequences in rainbow trout (Oncorhynchus mykiss). Trout were exposed to 30 μg Cu/L in moderately hard water (120 mg/L as CaCO(3)) for 40 days, following which time the acute cortisol response was examined with a series of stressors. At 40 days, a 65% increase in Cu was observed in the gill, but no accumulation was observed in the liver, brain or head kidney. Stressors such as air exposure or confinement did not elicit an increase in circulating cortisol levels for Cu-exposed fish, in contrast to controls. However, this inhibitory effect on the acute cortisol response appeared to have few implications on the ability of Cu-exposed fish to maintain ion and carbohydrate homeostasis. For example, plasma Na(+), Ca(2+) and glucose levels as well as hepatic glycogen levels were the same post-stress in control and Cu-exposed fish. Trout were also challenged with exposure to 50% seawater for 48 h, where Cu-exposed trout maintained plasma Na(+), glucose and hepatic glycogen levels. However, Cu-exposed fish experienced decreased plasma K(+) levels throughout the Cu exposure and stress tests. In conclusion, chronic Cu exposure resulted in the abolition of an acute cortisol response post-stress. There was no Cu accumulation in the hypothalamus-pituitary-interrenal axis (HPI axis) suggesting this was not a direct toxic effect of Cu on the cortisol regulatory pathway. However, the lack of an acute cortisol response in Cu-exposed fish did not impair the ability of the fish to maintain ion and carbohydrate homeostasis. This effect on cortisol may be a strategy to reduce costs during the chronic stress of Cu exposure, and not endocrine disruption as a result of toxic injury.     

Interaction between dietary calcium supplementation and chronic waterborne zinc exposure in juvenile rainbow trout, Oncorhynchus mykiss

This study investigated the effects of dietary Ca2+ on branchial Ca2+ and Zn2+ uptake, new and total zinc accumulation in target tissues (gill, liver and kidney), calcium and zinc homeostasis, and acute tolerance to waterborne zinc in fish chronically exposed to waterborne zinc. Juvenile rainbow trout (Oncorhynchus mykiss) were maintained on a calcium-enriched diet [41.2 mg vs. 21.2 mg (control) calcium/g dry wt. of food] and chronic waterborne zinc exposure (2.3 micromol/L), both separately and in combination, for 28 days. Calcium-supplemented diet in the absence of waterborne zinc significantly reduced branchial Ca2+ and Zn2+ influx rates, and new and total zinc accumulations in target tissues relative to control. However it did not protect against the acute zinc challenge. In contrast, waterborne zinc exposure significantly increased branchial Ca2+ and Zn2+ influx rates, new and total zinc concentrations in target tissues, and acute zinc tolerance relative to control. Interestingly, no such changes in any of these parameters were recorded in fish treated simultaneously with elevated dietary Ca2+ and waterborne zinc, except acute zinc tolerance which was highest among all the treatments. Thus, we conclude that the interactions between elevated dietary Ca2+ and waterborne zinc can protect freshwater fish against waterborne zinc toxicity.     

Reevaluation of dietary methionine requirement by plasma methionine and ammonia concentrations in surgically modified rainbow trout,Oncorhynchus mykiss

This study aimed to reevaluate the dietary methionine requirement by means of the plasma methionine and ammonia concentrations in surgically modified rainbow trout, Oncorhynchus mykiss. A total of 35 rainbow trout averaging 505 ± 6.5 g (initial body weight, mean ± SD) were randomly distributed into seven groups with five fish in each group. After 48 h of food deprivation, each group was fed one of seven L‐amino acid‐based diets containing graded levels of methionine (0.25, 0.40, 0.50, 0.60, 0.70, 0.80 or 0.95% of diet, dry matter bases) by intubation at 1% bodyweight. Blood samples were taken at 0, 5 and 24 h after intubation. Post‐prandial plasma free methionine concentrations (PPmet, 5 h after intubation) and post‐absorptive plasma free methionine concentrations (PAmet, 24 h after intubation) of fish fed diets containing 0.60% or more methionine were significantly (P < 0.05) higher than those of fish fed diets containing 0.50% or less methionine. PPmet and PAmet in fish fed diets containing 0.60% or higher methionine were not significantly different except the PPmet of fish fed a diet containing 0.95% methionine. Post‐prandial plasma ammonia concentrations (PPA, 5 h after intubation) of fish fed diets containing 0.70% or more methionine were significantly higher than those of fish fed diets containing 0.60% or less methionine, and PPA of fish fed diets containing 0.25% and up to 0.60% methionine were not significantly different from each other. Broken‐line model analyses on PPmet, PAmet, and PPA indicated that the dietary methionine requirement of rainbow trout was between 0.59% (1.69) and 0.67% (1.91) of diets (% dietary protein bases) when the diets contained 0.5% cystine.     

Acute waterborne cadmium uptake in rainbow trout is reduced by dietary calcium carbonate

The effects of elevated dietary calcium (as CaCO3) and acute waterborne Cd exposure (50 microg/l) on whole body uptake, tissue uptake, and internal distribution of newly accumulated Cd, Ca2+, and Na+ in juvenile rainbow trout were examined. Fish were fed with three diets (mg Ca2+/g food): 20 (control), 30 and 60 for 7 days before fluxes were measured with radiotracers. The highest dietary Ca2+ elevation reduced waterborne whole body Ca2+ uptake, but did not protect against inhibition of waterborne Ca2+ uptake by waterborne Cd. Both Ca2+-supplemented diets reduced newly accumulated Ca2+ in the gills in relation to the control treatment, but did not prevent the Cd-inhibiting effect against accumulation of new Ca2+ in most compartments. Fish fed with Ca2+-supplemented diets showed markedly lower rates of whole body uptake and internalization (in some tissues) of waterborne Cd, illustrating that, while dietary Ca2+ supplementation did not protect against the impact of waterborne Cd on waterborne Ca2+ uptake, it did protect against the uptake of Cd. Waterborne Cd had no effect on Na+ fluxes, total Cl-, and in most body compartments, newly accumulated Na+ and total Na+ were also not affected. Dietary supplementation with CaCO3 had the same protective effect as demonstrated by dietary supplementation with CaCl2 in an earlier study. Thus, the reduction of waterborne Cd uptake and internalization by dietary Ca2+ was specifically due to Ca2+ and not to the anion.     

Plasma ghrelin levels in rainbow trout in response to fasting, feeding and food composition, and effects of ghrelin on voluntary food intake

Ghrelin, a peptide hormone which stimulates growth hormone (GH) release, appetite and adiposity in mammals, was recently identified in fish. In this study, the roles of ghrelin in regulating food intake and the growth hormone (GH)-insulin-like growth factor I (IGF-I) system of rainbow trout (Oncorhynchus mykiss) were investigated in three experiments: 1) Pre- and postprandial plasma levels of ghrelin were measured in relation to dietary composition and food intake through dietary inclusion of radio-dense lead-glass beads, 2) the effect of a single intraperitoneal (i.p.) injection with rainbow trout ghrelin on short-term voluntary food intake was examined and 3) the effect of one to three weeks fasting on circulating ghrelin levels and the correlation with plasma GH and IGF-I levels, growth and lipid content in the liver and muscle was studied. There was no postprandial change in plasma ghrelin levels. Fish fed a normal-protein/high-lipid (31.4%) diet tended to have higher plasma ghrelin levels than those fed a high-protein/low-lipid (14.1%) diet. Plasma ghrelin levels decreased during fasting and correlated positively with specific growth rates, condition factor, liver and muscle lipid content, and negatively with plasma GH and IGF-I levels. An i.p. ghrelin injection did not affect food intake during 12-hours post-injection. It is concluded that ghrelin release in rainbow trout may be influenced by long-term energy status, and possibly by diet composition. Further, in rainbow trout, ghrelin seems to be linked to growth and metabolism, but does not seem to stimulate short-term appetite through a peripheral action.     

Serotonin, but not melatonin, plays a role in shaping dominant-subordinate relationships and aggression in rainbow trout

The aim of this study was to clarify to what extent the effects of elevated dietary L-tryptophan (Trp) on aggressive behavior and stress responsiveness in rainbow trout are mediated by circulating melatonin and central serotonin (5-HT), respectively. Isolated rainbow trout were paired for 1h a day for 7 days in order to create fish with experience of being dominant and subordinate. Following this week, the fish were tested for aggressive behavior using a resident-intruder test after which they were subjected to one of four treatments: (1) tryptophan, (2) the selective serotonin reuptake inhibitor (SSRI) citalopram, (3) melatonin, and (4) no treatment (controls). After 7 days of treatment, the fish were subjected to a second resident-intruder test. Trp-supplemented feed resulted in a suppression of aggressive behavior in fish with experience of being dominant. Moreover, fish fed Trp-supplemented feed, regardless of social experience, also displayed lower plasma cortisol levels than controls. These effects of elevated dietary Trp were closely mimicked by citalopram treatment, whereas exogenous melatonin had no effect on either aggressive behavior or plasma cortisol. Thus, the effect of elevated dietary Trp on aggressive behavior and stress responses does not appear to be mediated by melatonin even though elevated dietary intake of Trp resulted in an increase in plasma melatonin concentrations.     

Effect of dietary tryptophan on plasma and brain tryptophan, brain serotonin, and brain 5-hydroxyindoleacetic acid in rainbow trout

In order to determine the effect of dietary tryptophan level on plasma and brain tryptophan, brain serotonin, and brain 5-hydroxyindoleacetic acid levels, juvenile rainbow trout (Salmo gairdneri) were raised for 16 weeks on semipurified diets containing 0.06%, 0.16%, 0.21%, 0.26%, 0.39%, or 0.59% tryptophan. After 14 weeks, feed intake was depressed in fish fed the diets containing 0.06% or 0.16% tryptophan. No further differences in feed intake were noted between the remaining treatments. In addition, body weight was lower in fish fed diets containing 0.06%, 0.16%, or 0.21% tryptophan compared with fish fed higher levels. After 16 weeks of feeding the test diets, plasma tryptophan levels were found to be directly related to dietary tryptophan levels. Similarly, increased dietary levels of tryptophan resulted in increased brain levels of tryptophan, serotonin, and 5-hydroxyindoleacetic acid. These results demonstrate that in rainbow trout, as in mammals, altered dietary levels of tryptophan result in alterations in plasma and brain tryptophan, brain serotonin, and brain 5-hydroxyindoleacetic acid.     

Relationship between stress, feeding and plasma ghrelin levels in rainbow trout, Oncorhynchus mykiss

Sexually immature rainbow trout were acclimated to small-volume (1 m³) holding tanks and then exposed to short-term stress to examine the relationship between feeding, stress, plasma ghrelin levels and other plasma stress parameters. Plasma ghrelin levels showed an increase 24 h after a single feed, plasma lactate and glucose levels decreased over the same period and plasma cortisol levels were low and constant. One hour of confinement stress resulted in elevations of plasma cortisol, glucose and lactate and depression of plasma ghrelin levels. In a separate experiment, 2 h of confinement stress also depressed feeding immediately after stress, concomitant with increases in plasma cortisol, lactate and glucose; however, in this case there was no change in plasma ghrelin concentrations. A repeat of the 2-h confinement experiment using fish that had not been acclimated to small-volume holding tanks produced a more marked elevation in plasma cortisol and a stronger suppression of feeding post-stress but in this case also, there was no change in plasma ghrelin levels. The results of this study confirm that feeding in rainbow trout is suppressed by confinement stress although the effect is transitory in this domesticated stock. Similar to that in other fishes, plasma ghrelin levels appear to be modulated by feeding status and may be influenced by stress, suggesting an orexigenic role for ghrelin in rainbow trout.     

Acid-base balance during social interactions in rainbow trout (Oncorhynchus mykiss)

Socially subordinate rainbow trout (Oncorhynchus mykiss) experience chronic stress that impacts upon a variety of physiological functions, including Na(+) regulation. Owing to the tight coupling between Na(+) and Cl(-) uptake and, respectively, H(+) and HCO(3)(-) loss at the gill, ionoregulatory changes associated with social status may affect acid-base regulation. The present study assessed the responses of dominant, subordinate and control trout to hypercapnia (1% CO(2)) to test this hypothesis. Social status appeared to impact net acid excretion (J(net)H(+)) as subordinate individuals failed to increase net acid flux in response to hypercapnia. However, blood acid-base status was found to be unaffected by social status before or during hypercapnic exposure, indicating that subordinate fish were as effective as dominant or control trout in achieving compensation for the acid-base disturbance induced by hypercapnic exposure. Compensation in all groups involved decreasing Cl(-) uptake in response to hypercapnia. The branchial activities of both Na(+),K(+)-ATPase (NKA) and V-type H(+)-ATPase were affected by social interactions and/or exposure to hypercapnia. Branchial NKA activity was higher but V-ATPase activity was lower in control fish than in dominant or subordinate trout. In addition, control and subordinate but not dominant trout exposed to 24h of hypercapnia exhibited significantly higher branchial V-ATPase activity than fish maintained in normocapnia. Collectively, the data suggest that subordinate trout are able to regulate blood pH during a respiratory acidosis.     

Dietary tissue cadmium accumulation in an amazonian teleost (Tambaqui, Colossoma macropomum Cuvier, 1818).

Understanding the effects of metal contamination in the Amazon basin is important because of the potential impact on this region of high biodiversity. In addition, the significance of fish as the primary source of protein for the local human population (living either alongside the Amazon River or in the city of Manaus) highlights the need for information on the metal transfer through the food chain. Bioaccumulation of metals in fish can occur at significant rates through the dietary route, without necessarily resulting in death of the organism. The goal of this work was to expose an economic relevant species from the Amazon basin (tambaqui, Colossoma macropomum) to dietary cadmium (Cd) at concentrations of 0, 50, 100, 200, and 400 microg.g-1 dry food. Fish were sampled on days 15, 30, and 45 of the feeding trials. Tissues were collected for analysis of Cd concentration using graphite furnace atomic absorption spectrophotometry. Cd accumulation in the tissues occurred in the following order: kidney > liver > gills > muscle. Relative to other freshwater fish (e.g., rainbow trout, tilapia), tambaqui accumulated remarkably high levels of Cd in their tissues. Although Cd is known to affect Ca2+ homeostasis, no mortality or growth impairment occurred during feeding trials.     

Alterations of tissue glutathione levels and metallothionein mRNA in rainbow trout during single and combined exposure to cadmium and zinc

The objective of this study was to assess the effects of Cd and Zn exposure of rainbow trout (Oncorhynchus mykiss) on (a) hepatic glutathione (GSH) levels; and (b) hepatic and branchial metallothionein (MT) mRNA expression. Juvenile rainbow trout were exposed to waterborne Cd (nominal concentrations: 1.5 or 10 microg Cd l(-1)), Zn (150 or 1000 microg Zn l(-1)) or Cd/Zn mixtures (1.5 microg Cd l(-1) with 200 microg Zn l(-1) or 10 microg Cd l(-1) with 1000 microg Zn l(-1)). After 14 and 28 days of treatment, hepatic concentrations of total glutathione, oxidized glutathione (GSSG) and cysteine were determined by means of fluorometric high performance liquid chromatography (HPLC). Branchial and hepatic expression of MT mRNA was measured by means of semi-quantitative RT-PCR. Exposure of trout to Zn did not result in significantly elevated tissue levels of Zn, whereas Cd accumulation factors changed significantly with time and concentration. Despite of the absence of Zn accumulation, hepatic GSH but not MT mRNA levels were significantly altered in Zn-exposed fish. Cd, on the contrary, affected mainly the MT response but not GSH. Also tissue specific differences in the regulation of the two thiol pools were expressed. The thiol response after exposure to metal mixtures could not be explained by simple addition of the effects of the individual metals. The results indicate that cellular thiol pools show different reaction patterns with respect to specific metals and metal mixtures. Under conditions of long-term, low dose metal exposure, the function of GSH appears to go beyond that of a transitory, first line defense.     

Evidence of complement-mediated killing of Discocotyle sagittata (Platyhelminthes, Monogenea) oncomiracidia

Discocotyle sagittata oncomiracidia were rapidly killed when incubated in na?ve plasma and immune sera from both rainbow trout (Oncorhynchus mykiss) and brown trout (Salmo trutta), the killing proceeding at a faster rate with blood material from the latter fish species. The lethal activity of na?ve plasma and immune sera was comparable. This was abolished after incubation at 45 degrees C for 30 min and by the addition of EDTA but not EGTA supplemented with Mg(2+), indicating that complement acting via the alternative pathway is responsible for the parasiticidal effect observed. Scanning electron micrographs showed varying degrees of surface disruption in larvae exposed to fish plasma, suggesting that complement acts by breaching the oncomiracidial tegument. Control (untreated) oncomiracidia showed no damage. Ultrastructural damage was more extensive in oncomiracidia exposed to brown trout plasma than to rainbow trout plasma for equal periods, suggesting that the complement cascade may be involved in mediating host susceptibility.     

Hepatic glucokinase is induced by dietary carbohydrates in rainbow trout, gilthead seabream, and common carp

Glucokinase (GK) plays a central role in glucose homeostasis in mammals. The absence of an inducible GK has been suggested to explain the poor utilization of dietary carbohydrates in rainbow trout. In this context, we analyzed GK expression in three fish species (rainbow trout, gilthead seabream, and common carp) known to differ in regard to their dietary carbohydrate tolerance. Fish were fed for 10 wk with either a diet containing a high level of digestible starch (>20%) or a diet totally deprived of starch. Our data demonstrate an induction of GK gene expression and GK activity by dietary carbohydrates in all three species. These studies strongly suggest that low dietary carbohydrate utilization in rainbow trout is not due to the absence of inducible hepatic GK as previously suggested. Interestingly, we also observed a significantly lower GK expression in common carp (a glucose-tolerant fish) than in rainbow trout and gilthead seabream, which are generally considered as glucose intolerant. These data suggest that other biochemical mechanisms are implicated in the inability of rainbow trout and gilthead seabream to control blood glucose closely.     

Contrasting seasonal modulation of the stress response in male and female rainbow trout

Between June and September the magnitude of the plasma cortisol response of maturing male and female rainbow trout to confinement was indistinguishable. A progressive increase in confinement-induced cortisol levels in both sexes occurred during May to September, associated with the seasonal rise in water temperature. Between September and January a reduction of >50% in the magnitude of the cortisol response to confinement in male fish (but no decline in females) coincided with declining water temperature and significant increases in plasma 11-ketotestosterone and elevated plasma testosterone levels. Plasma oestradiol-17β levels were significantly greater in females than males throughout the study period and this difference was maximal between September and January. However, plasma testosterone was also elevated in females during this period and levels overall were higher than those in male fish. Previous studies have shown oestradiol-17β and testosterone to have diametrically opposed effects on stress responsiveness in trout, with the former enhancing, and the latter suppressing, the cortisol response to a stressor. The relative roles of androgens, estrogen and water temperature in modulating the stress responsiveness of rainbow trout are discussed.     

Exercise training and the stress response in rainbow trout, Salmo gairdneri Richardson

Plasma levels of catecholamines, cortisol, and glucose were monitored in rainbow trout during a 6-week forced swimming exercise programme. Compared to resting non-exercised controls, resting trained fish had lower levels of epinephrine, norephinephrine, cortisol, and glucose during the last 3 weeks of training. Initially, trained fish that were swimming had higher levels of epinephrine than resting trained fish. After 2 weeks of exercise, swimming did not significantly elevate epinephrine levels in trained fish. Glucose levels were consistently greater in swimming fish than in resting fish. At the end of the training period, exercised trout had lower (15–20%) oxygen consumption rates while resting or swimming than unexercised fish.
After a 5-month forced swimming exercise programme plasma levels of catecholamines and glucose were monitored in trained and untrained cannulated rainbow trout after 2 min of mild agitation. Trained fish showed an immediate (within 1 min) increase in the levels of epinephrine, but not norepinephrine and a delayed (within 15 min) increase in the levels of plasma glucose. Epinephrine levels returned to pre-stress levels within 15 min. Untrained fish had no significant increase in the plasma levels of norepinephrine, epinephrine, or glucose.     

Sub-lethal plasma ammonia accumulation and the exercise performance of salmonids

The proposal that plasma ammonia accumulation might impair the swimming performance of fish was first made over a decade ago, and has now proven to be the case for a number of salmonid species. The first experimental evidence was indirect, when a negative linear relationship between plasma ammonia concentrations and maximum sustainable swimming speed (U(crit)) was found following the exposure of brown trout (Salmo trutta) to sub-lethal concentrations of copper in soft acidic water. Since then, negative linear relationships between plasma ammonia concentration and U(crit) have been demonstrated following exposure of brown trout, rainbow trout (Oncorhynchus mykiss) and coho salmon (Oncorhynchus kisutch) to elevated water ammonia. For brown trout, the relationships between plasma ammonia and U(crit) were remarkably similar following either exposure to elevated water ammonia or to sub-lethal copper. This indicates that the impairment of swimming performance resulting from exposure to sub-lethal concentrations of heavy metals may be attributable in large part to an accumulation of endogenous ammonia. The negative relationship between plasma ammonia concentration and U(crit) was similar in size-matched rainbow and brown trout but, under similar regimes of ammonia exposure, rainbow trout were able to maintain a significantly lower plasma ammonia concentration, revealing inter-specific differences in ammonia permeability and/or transport. One primary mechanism by which ammonia accumulation may impair exercise performance is a partial depolarisation of membrane potential in tissues such as the brain and white muscle. This may prejudice the co-ordination of swimming movements and reduce or abolish the development of muscle tension, thus, compromising swimming efficiency and performance at the top end of the range.