The physiological responses of the rainbow trout to strenuous exercise: interactions of water hardness and environmental acidity

1982 ◽  
Vol 60 (12) ◽  
pp. 3153-3164 ◽  
Author(s):  
Mark S. Graham ◽  
Chris M. Wood ◽  
Jeffrey D. Turner

Cannulated adult rainbow trout were subjected to 6 min of exercise stress in four different water conditions: hard water ([Formula: see text] as CaCO3), control pH ([Formula: see text]); artificial soft water [Formula: see text], control pH; hard water, acid pH [Formula: see text]; and artificial soft water, acid pH. Physiological changes and postexercise mortalities were monitored over a 12-h recovery period. The physiological responses to exercise stress were qualitatively similar in all treatments and are discussed in detail. At control pH, water hardness had minimal influence on the magnitude of physiological response and postexercise mortality. When fish were exercised in hard water at acid pH, the symptoms of postexercise acidosis were actually ameliorated slightly and there was no increase in mortality. However, acid exposure in soft water greatly exacerbated most of the postexercise disturbances and caused a doubling of mortality.

1980 ◽  
Vol 88 (1) ◽  
pp. 109-132
Author(s):  
D. G. McDONALD ◽  
H. HŌBE ◽  
C. M. WOOD

The physiological responses of 1- to 2-year-old rainbow trout to low pH are dependent on the environmental calcium concentration. Trout, maintained for 5 days in moderately hard water ([Ca2+] = 1·6–2·7 m-equiv/1) at a mean pH of 4·3, developed a major blood acidosis but exhibited only a minor depression in plasma ion levels. In acidified soft water ([Ca2+] = 0·3 m-equiv/1), only a minor acidosis occurred, but plasma ion levels fell and there were substantially greater mortalities. Lethal bioassays performed on fingerling trout over a range of pH levels (3·0–4·8) revealed an important influence of external [Ca2+] on resistance to acid exposure. Terminal physiological measurements on adult fish succumbing to low pH in soft water indicate the singular importance of iono-regulatory failure as the toxic mechanism of action under these circumstances.


1963 ◽  
Vol 41 (5) ◽  
pp. 825-830 ◽  
Author(s):  
David E. Craigie

Two groups of Salmo gairdnerii were reared from fertilization in hard and soft waters, and the thermal resistance of the yearling trout was measured for both groups in soft and saline waters at 27, 28, and 29 °C. In all cases a history of rearing in soft water resulted in a greater resistance to thermal stress than did a history of rearing in hard water. Increased salinity of the testing medium resulted in an increase in thermal resistance.


1996 ◽  
Vol 69 (6) ◽  
pp. 1419-1441 ◽  
Author(s):  
S. F. Perry ◽  
S. G. Reid ◽  
E. Wankiewicz ◽  
V. Iyer ◽  
K. M. Gilmour

1988 ◽  
Vol 45 (12) ◽  
pp. 2206-2215 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood

At a waterborne [Zn] of 1.9 mg∙L−1 in hard water (~1 mmol Ca∙L−1), Zn influx across an isolated, saline-perfused head preparation of rainbow trout (Salmo gairdneri) was about 1.5 nmol∙kg−1∙h−1 through the lamellar pathway and about 1 nmol∙kg−1∙h−1 through the filamental route. Flux rates came rapidly to steady state in both pathways. Trout preexposed to artificial soft water (~0.05 mmol Ca∙L−1) for 5 d showed differential stimulation of flux rates to about 42 and 5 nmol Zn∙kg−1∙h−1 through the lamellar and filamental pathways, respectively. Under these conditions, steady-state fluxes across the lamellae did not occur until 15–20 min after the start of perfusion. Preparations from hardwater-acclimated trout tested in soft water gave typical hardwater fluxes showing that these changes in influx were not simply due to acute exposure of the gill surface to low waterborne [Ca]. Influxes in softwater trout, studied over [Zn] from 0.4 to 7.5 mg Zn∙L−1, revealed a saturable, first-order uptake with apparent Jmax and Km of 150 nequiv∙kg−1∙h−1 and 1.5 mg Zn∙L−1 (23 μmol∙L−1), respectively. Because the apparent Km is in the toxic range, Zn is clearly not the primary substrate. Scanning electron micrography revealed hypertrophy and increased apical exposure of chloride cells; this stimulation, coupled with the increase in Zn influx, suggests that chloride cells may be the site of entry of Zn across the gill.


1976 ◽  
Vol 33 (1) ◽  
pp. 173-176 ◽  
Author(s):  
William R. Driedzic ◽  
Joe W. Kiceniuk

Rainbow trout (Salmo gairdneri) were exercised to fatigue in a series of 60-min stepwise increasing velocity increments. There was no increase in blood lactate concentration, serially sampled during swimming by means of indwelling dorsal and ventral aortic catheters, at velocities as high as 93% of critical velocity of individuals. The data show that under these conditions the rate of production of lactate by white muscle, at less than critical velocities, is minimal or that the rate of elimination of lactate from white muscle is equal to its rate of utilization elsewhere. Immediately following fatigue blood lactate level increases rapidly. During the recovery period there appears to be a net uptake of lactate by the gills.


1983 ◽  
Vol 40 (6) ◽  
pp. 824-828 ◽  
Author(s):  
D. W. Rodgers ◽  
F. W. H. Beamish

We measured the efficiency of uptake of waterborne methylmercury relative to oxygen consumption for rainbow trout, Salmo gairdneri, in hard or soft water and during exposure to sublethal concentrations of mercuric chloride or zinc sulphate. The relative efficiency of methylmercury uptake in soft water was more than double that measured in hard water. When mercuric chloride was added with waterborne methylmercury, uptake efficiency was further increased, with similar values obtained in hard and soft water. In contrast, addition of zinc sulphate decreased the relative efficiency of methylmercury uptake. Water quality thus significantly affects the accumulation of waterborne methylmercury by fish. In particular, calcium-dependent changes in gill permeability may explain elevated methylmercury residues observed in fish from lakes of low alkalinity and pH.


1983 ◽  
Vol 105 (1) ◽  
pp. 1-14
Author(s):  
PETER NEUMANN ◽  
GEORGE F. HOLETON ◽  
NORBERT HEISLER

Rainbow trout (Salmo gairdneri) were electrically stimulated to exhausting activity and the changes in cardiac output and blood flow distribution to gills and systemic tissues resulting from the developing severe lactacidosis were repeatedly measured by the microsphere method (15 μm). Determination of cardiac output by application of the Fick principle resulted in values not significantly different from cardiac output measured by the indicator dilution technique, suggesting that cutaneous respiration, oxygen consumption, and arterio-venous shunting were insignificant under these conditions. Following muscular activity, cardiac output was elevated by up to 60%. In the gills, the blood flow distribution in the gill arches showed a consistent pattern, even during lactacidosis, with a higher perfusion in gill arches II and III, and in the middle sections of individual gills. Blood flow to white and red muscle was increased much more than cardiac output (+230 and +490%, respectively) such that blood flow to other tissues was actually reduced. We conclude that the elimination of lactate from muscle cells during the recovery period from strenuous exercise is delayed, not as a result of an impaired post-exercise muscle blood flow, but probably as a result of a high diffusion resistance in the cell membrane. Note: Deceased.


1981 ◽  
Vol 59 (8) ◽  
pp. 1518-1526 ◽  
Author(s):  
Mark S. Graham ◽  
Chris M. Wood

Classical 7-day lethality tests were used to establish the influence of water hardness [Formula: see text], acid type (HCl versus H2SO4) and activity level (rest versus exhaustive exercise) on acid toxicity to fingerling rainbow trout (Salmo gairdneri) at 15 °C. Seven-day mean lethal concentration (LC50) pH's ranged from 4.1 to 4.5. Hardness reduced H2SO4 toxicity at all pH levels during both rest and exericise, but reduced HCl toxicity only at very low pH levels. Hardness increased HCl toxicity at pH's > 3.8. H2SO4 was generally less toxic than HCl, except at pH's > 3.8 in soft water. Exchaustive exercise markedly potentiated H2SO4 toxicity in both hard and soft water except at very low pH levels. Below pH = 4.4–4.6, critical swimming speed declined linearly by about 4% per 0.1 pH unit. Possible physiological mechanisms responsible for these modifying influences and their ecological significance are discussed.


2014 ◽  
Vol 12 (4) ◽  
pp. 817-823 ◽  
Author(s):  
Nevenka J. Knezović ◽  
Mustafa Memić ◽  
Mirela Mabić ◽  
Jasna Huremović ◽  
Ivanka Mikulić

The aim of this study was to determine the association of cardiovascular disease (CVD) of selected human subjects with the hardness of water they consume. Laboratory testing of physical and chemical parameters of water were made using standardized methods: Standard Methods 19th edn, 1995 (APHA, AWWA & WEF, Washington, DC), and ISO 7888:1985, ISO 10523:1998. Pearson's chi-squared test was used for the statistical analysis of data, with the significance level of 0.05. The obtained data were analysed using the statistical program SPSS 16.0. The study sample consisted of 1,021 individuals divided into two groups: soft water consumers, 603 individuals, and, hard water consumers, 618 individuals. Results indicate that a statistically significant (χ2 = 5.315; df = 1; p = 0.021) number of individuals with CVD drink soft water. The prevalence of CVD in the age group 45–60 years in the study area where soft water is consumed was 21.3% and in the study area where hard water is consumed the prevalence of CVD was 13.7%. The summary results indicate significant correlation between the prevalence of CVD in the population group who drink soft water. The value of the relative risk is 1.127.


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