Juvenile rainbow trout were chronically exposed to acidified softwater, alone and in combination with a slight temperature increase in order to understand the possible effects of global warming and environmental acidification in freshwater fish. The second goal was to determine the role of diet in the response to acid stress and elevated temperatures. In the first two exposures, a simulated global warming scenario (+2°C) was applied for 90 days in winter (8-12 °C), in the presence and absence of sublethal acidity (pH 5.2). In the first trial, fish were fed to satiation twice daily, while in the second trial, fish were fed only 1% of their wet body weight every four days (~0.25% daily). A slight increase in temperature caused a marked increase in oxygen consumption, nitrogenous waste excretion and growth, although there did not appear to be any specific pH effects. During the Satiation Exposure, fish exposed to low pH especially at slightly elevated temperatures had increased appetites compared to non-acid exposed fish. This increased appetite suggested that NaCl losses brought about by low pH exposure, stimulated appetite in some way, thereby alleviating any ionoregulatory disturbances. During the Limited Ration Exposure, ionoregulatory disturbances occurred during low pH exposure, with more dramatic effects in fish at slightly elevated temperatures. Trout maintained on a limited diet had a higher mortality rate, lower plasma and whole body Na⁺ and Cl⁻ concentrations, and elevated cortisol levels compared with fish fed to satiation. Thus, it became clear that fish could use food to compensate for the stresses of increased temperature and low pH. The third exposure was conducted to determine whether food simply provided the necessary fuel to meet the increased cost of living in a low pH environment, or whether food directly provided the dietary salts necessary to replace branchial ion loss. Diets were formulated at two levels of energy (regular: 16.31MJ/kg or low: 9.77MJ/kg) and two levels of NaCl (regular: 263 mmols/kg or low: 43 mmols/kg) using a factorial design (2x2=4 treatments). In addition, a fifth group of fish were not fed during the exposure. All five groups of fish were challenged with pH 4.0 to induce a rapid ionoregulatory disturbance and then held at pH 5.2 for the next 28 days. During this month, fish were fed 0.6% of their body weight of one of the four diets. Fish fed the low salt diets incurred typical long-term ionoregulatory disturbances with decreased whole body Na+, K+ and Cl concentrations. These effects were not seen in fish fed regular salt diets, regardless of energy content, showing that it is the salt content of the food rather than the energy content which is critical in protecting against the deleterious effects of low environmental pH. Interestingly, fish fed the regular energy/low salt diet had high cortisol levels and increased mortality while fish fed the regular salt diets, low energy/low salt diets and starved fish did not have a high rate of mortality. These results may have been due to differences in metabolic rate and therefore oxygen consumption (M₀₂). Starved fish had the lowest M₀₂. Fish fed the regular energy diet had increased post-prandial M₀₂ due to the specific dynamic action evoked in fish by ingestion of protein-rich food. An increase in oxygen consumption may have caused an increase in branchial ion loss, thereby exacerbating the ionoregulatory deficit associated with chronic acid exposure. This is detrimental when dietary salts are unavailable to replace branchial losses. Overall, the salt content of food may play an important role in ameliorating the deleterious effects of chronic low pH, while the energy content of food may complicate the response. / Thesis / Master of Science (MS)
| Identifer | oai:union.ndltd.org:mcmaster.ca/oai:macsphere.mcmaster.ca:11375/23063 |
| Date | 04 1900 |
| Creators | D'Cruz, Leela |
| Contributors | Wood, C. M., Biology |
| Source Sets | McMaster University |
| Language | English |
| Detected Language | English |
| Type | Thesis |
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