Résumé: Most teleost fish reduce heart rate when exposed to acute hypoxia. This hypoxic bradycardia has been characterised for many fish species, but it remains uncertain whether this reflex contributes to the maintenance of oxygen uptake in hypoxia. Here we describe the effects of inhibiting the bradycardia on oxygen consumption (MO(2)), standard metabolic rate (SMR) and the critical oxygen partial pressure for regulation of SMR in hypoxia (Pcrit) in European eels Anguilla anguilla (mean +/- A SEM mass 528 +/- A 36 g; n = 14). Eels were instrumented with a Transonic flow probe around the ventral aorta to measure cardiac output (Q) and heart rate (f (H)). MO(2) was then measured by intermittent closed respirometry during sequential exposure to various levels of increasing hypoxia, to determine Pcrit. Each fish was studied before and after abolition of reflex bradycardia by intraperitoneal injection of the muscarinic antagonist atropine (5 mg kg(-1)). In the untreated eels, f (H) fell from 39.0 +/- A 4.3 min(-1) in normoxia to 14.8 +/- A 5.2 min(-1) at the deepest level of hypoxia (2 kPa), and this was associated with a decline in Q, from 7.5 +/- A 0.8 mL min(-1) kg(-1) to 3.3 +/- A 0.7 mL min(-1) kg(-1) in normoxia versus deepest hypoxia, respectively. Atropine had no effect on SMR, which was 16.0 +/- A 1.8 mu mol O(2) kg(-1) min(-1) in control versus 16.8 +/- A 0.8 mu mol O(2) kg(-1) min(-1) following treatment with atropine. Atropine also had no significant effect on normoxic f (H) or Q in the eel, but completely abolished the bradycardia and associated decline in Q during progressive hypoxia. This pharmacological inhibition of the cardiac responses to hypoxia was, however, without affect on Pcrit, which was 11.7 +/- A 1.3 versus 12.5 +/- A 1.5 kPa in control versus atropinised eels, respectively. These results indicate, therefore, that reflex bradycardia does not contribute to maintenance of MO(2) and regulation of SMR by the European eel in hypoxia.

Résumé: While many ectothermic species can withstand prolonged fasting without mortality, food deprivation may have sublethal effects of ecological importance, including reductions in locomotor ability. Little is known about how such changes in performance in individual animals are related to either mass loss during food deprivation or growth rate during re-feeding. This study followed changes in the maximum sprint swimming performance of individual European sea bass, Dicentrarchus labrax, throughout 45 days of food deprivation and 30 days of re-feeding. Maximum sprint speed did not show a significant decline until 45 days of food deprivation. Among individuals, the reduction in sprinting speed at this time was not related to mass loss. After 30 days of re-feeding, mean sprinting speed had recovered to match that of control fish. Among individuals, however, maximum sprinting speed was negatively correlated with growth rate after the resumption of feeding. This suggests that the rapid compensatory growth that occurs during re-feeding after a prolonged fast carries a physiological cost in terms of reduced sprinting capacity, the extent of which shows continuous variation among individuals in relation to growth rate. The long-term repeatability of maximum sprint speed was low when fish were fasted or fed a maintenance ration, but was high among control fish fed to satiation. Fish that had been previously food deprived continued to show low repeatability in sprinting ability even after the initiation of ad libitum feeding, probably stemming from variation in compensatory growth among individuals and its associated negative effects on sprinting ability. Together, these results suggest that food limitation can disrupt hierarchies of maximum sprint performance within populations. In the wild, the cumulative effects on locomotor capacity of fasting and re-feeding could lead to variable survival among individuals with different growth trajectories following a period of food deprivation.

Résumé: In teleosts, the regulation of hydromineral balance has a direct impact on several physiological functions, biochemical processes, and can influence behaviour, distribution and survival. As European sea bass Dicentrarchus labrax undertake seasonal migrations from seawater (SW) to brackish, estuarine and fresh water (FW) in their habitat, this study investigates their capacity to tolerate fresh water and explores intraspecific variations in physiological responses. Juvenile D. labrax were transferred from SW to FW at various ages. Freshwater-tolerant and non-tolerant phenotypes were discriminated according to behavioural and morphological characteristics. About 30% of the fish exposed to FW were identified as freshwater intolerant following FW challenges performed at different ages. Interestingly, intolerant fish exhibited the same phenotypic traits: erratic swimming, lower speed, isolation from the shoal and darker colour. Freshwater-intolerant fish were also characterised by a significant lower blood osmolality compared to tolerant fish, and significantly lower Na+/K+-ATPase alpha 1a expression in the posterior kidney. An imbalance in ion regulatory mechanisms was further confirmed by a blood Na+/Cl- ratio imbalance observed in some freshwater-intolerant fish. The analysis of glucocorticoid and mineralocorticoid receptor expression levels in gills and kidney revealed significant differences between freshwater-intolerant and -tolerant fish in both organs, suggesting differential stress-related responses. This study clearly shows an intraspecific difference in the responses following FW transfer with a decreased renal ion uptake capacity as a major cause for freshwater intolerance.