| Summary: | Thesis (Ph.D.)--Memorial University of Newfoundland, 2010. Biology Includes bibliographical references Currently, little information exists on how chronic hypoxia influences fish physiology. Thus, a comprehensive examination of how this ecologically-relevant environmental challenge affects the cardiorespiratory physiology, exercise performance and hypoxia tolerance of Atlantic cod ( Gadus morhua ) was performed. -- Exposure to acute hypoxia (Pw O2 8-9 kPa) lowered the Ucrit of normoxic-acclimated cod by approx. 30%, and this was associated with large decreases in max. oxygen consumption (MO2 ), metabolic scope (≥ 50%), and maximum heart rate (f H) and cardiac output (Q) (by 16 and 22%). Hypoxic acclimation (6-12 weeks at 10°C; Pw O2 8-9 kPa) elevated normoxic MO2 (standard by 27 %; routine by 44%) compared with normoxic controls, but did not influence Ucrit , max. MO2 or metabolic scope under either normoxia or hypoxia. Further, although, resting and maximum values for Q were significantly diminished in hypoxic-acclimated cod due to lower values for stroke volume (Sv ), increased fH partially compensated for the latter, and hypoxic-acclimated cod were able to consume more oxygen for a given cardiac output. -- This lower in vivo cardiac pumping capacity proved not to be a regulated decrease as hypoxic acclimation reduced in situ values for maximum Sv , the scope for Sv , and consequently maximum cardiac output (Qmax ) (by 19%). However, hypoxic-acclimated fish were able to sustain Q better under hypoxia, and the recovery of Q max (compared to initial Qmax ) was significantly improved (94 vs. 83%) as compared with normoxic controls. -- Although several physiological adjustments had taken place during the 6-12 weeks of hypoxic acclimation [increased fH elevated hematocrit (Hct) by 11 % and [Hb] by 14 %; enhanced tissue oxygen extraction efficiency by ∼ 15%; and a more robust stress response (2-8 fold higher levels of plasma catecholamines at Pw O2 's of 5.3 and 2.7 kPa)], these adjustments were only successful in improving the cod's critical oxygen tension (Pcrit of normoxic and hypoxic-acclimated cod 8.1 ± 0.5 vs. 6.6 ± 0.6 kPa, respectively), not the cod's hypoxia tolerance (Hcrit = 4.3 ± 0.2 vs. 4.8 ± 0.3 kPa). Finally, the significance of the enhanced stress response in hypoxic-acclimated cod for cardiac function is uncertain as this species' heart is minimally responsive to adrenergic stimulation, and hypoxic-acclimation reduced the heart's adrenergic responsiveness further.
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