Abstract
Variations in respiratory and acid-base status were studied in turbot (Scophthalmus maximus) during progressive severe hypoxia followed by recovery under normoxic conditions. The first behavioural strategy of turbot under hypoxia was an increase in amplitude and frequency of ventilation. Consequently, standard O2 consumption remained unchanged over a broad range of O2 tensions, until a low critical level of 30 mmHg. The hyperventilation induced a moderate blood alkalosis, compensated by a lactic acidosis. The fact that blood pH did not decrease below control values could be explained by the retention in white muscle of most of the lactate produced and by a high capacity for H+ excretion. During the recovery period, the marked increase in O2 uptake corresponding to an oxygen debt repayment, was partly related to the lactate elimination. When total energy contributions of aerobic and anaerobic processes were assessed in terms of ATP, the anaerobic contribution, estimated at the deepest hypoxia level, was higher than 20% of the total energy budget and appeared to totally compensate for the decline in aerobic metabolism. Moreover, the high value of O2 tension in arterial blood in normoxia and during recovery from hypoxia showed high diffusing capacity of gills in turbot. Our results explain the high tolerance of turbot for O2 deficient waters.
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Maxime, V., Pichavant, K., Boeuf, G. et al. Effects of hypoxia on respiratory physiology of turbot, Scophthalmus maximus. Fish Physiology and Biochemistry 22, 51–59 (2000). https://doi.org/10.1023/A:1007829214826
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DOI: https://doi.org/10.1023/A:1007829214826
- acid-base status
- ATP
- hypoxia
- lactate production
- respiratory homeostasis
- Scophthalmus maximus
- turbot
- ventilation