Respiratory plasticity is insufficient to alleviate blood acid-base disturbances after acclimation to ocean acidification in the estuarine red drum, Sciaenops ocellatus.
The changes in ocean chemistry stemming from anthropogenic CO2 release--termed ocean acidification (OA)--are predicted to have wide-ranging effects on fish and ultimately threaten global populations. The ability of fish to adapt to environmental change is currently unknown, but phenotypic plasticity has been highlighted as a crucial factor in determining species resilience. Here we show that red drum, a long-lived estuarine-dependent fish species native to the Gulf of Mexico, exhibit respiratory plasticity that increases CO2 excretion capacity when acclimated to OA conditions. Specifically, fish exposed to 14 days of 1000 µatm CO2 had a 32% reduction in branchial diffusion distance and increased expression of two putative CO2 channel proteins--rhag and rhcg1. No changes were observed in the erythrocyte CO2 transport pathways. Surprisingly, no significant changes in blood chemistry were observed between acclimated and acutely challenged animals; however, a non-significant 30 % drop in the magnitude of plasma C(CO2) elevation was observed. Reduced diffusion distance also comes with the cost of increased diffusive water loss, which would require greater osmoregulatory investment by the animal. OA exposure induced increased gill Na(+), K(+) ATPase activity and intestinal nkcc2 expression, supporting both the presumed osmotic stress and increased osmoregulatory investment. However, no differences in standard metabolic rate, maximum metabolic rate or aerobic scope were detected between control and OA acclimated individuals. Similarly, no differences in critical swim speed were detected between groups, suggesting the energetic cost related to respiratory plasticity is negligible against background metabolism. The current study demonstrated that red drum exhibit respiratory plasticity with only mild physiological trade-offs; however, this plasticity is insufficient to fully offset the OA-induced acid-base disturbance and as such is unlikely to impact species resilience.
Andrew J
AJ
Esbaugh
Rasmus
R
Ern
Wiolene M
WM
Nordi
Abbey S
AS
Johnson
D000064:Acclimatization / Q000502:physiology*; D000137:Acid-Base Imbalance / Q000097:blood / Q000662:veterinary*; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D017753:Ecosystem; D063366:Estuaries; D005393:Fish Diseases / Q000097:blood* / Q000378:metabolism; D005399:Fishes / Q000097:blood / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D009792:Oceans and Seas; D010101:Oxygen Consumption / Q000502:physiology*
D002245:Carbon Dioxide