Effects of chronic hypoxia on the cardiorespiratory physiology of Atlantic cod (Gadus morhua)

Petersen, Lene Hebsgaard (2010) Effects of chronic hypoxia on the cardiorespiratory physiology of Atlantic cod (Gadus morhua). Doctoral (PhD) thesis, Memorial University of Newfoundland.

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Abstract

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 morhud) was performed. -- Exposure to acute hypoxia (PwO₂ 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 (ƒH) and cardiac output (Q) (by 16 and 22%). Hypoxic acclimation (6-12 weeks at 10 °C; PwO₂ 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 ƒH 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 Qmax (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 ƒH; 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 PwO₂'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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