It’s a good thing that severely hypoxic salmon (Salmo salar) havea limited capacity to increase heart rate when warmed

With climate change, fish are facing rising temperatures, an increase
in the frequency and severity of heat waves and hypoxia, sometimes
concurrently. However, only limited studies have examined the
combined effects of increases in temperature and hypoxia on
fish physiology and survival. We measured the cardiorespiratory
physiology of 12°C-acclimated Atlantic salmon when exposed
acutely to normoxia [100% air saturation (sat.)] versus 75 and 50%
air sat., and then warmed to their critical thermal maximum (CT max ) at
2°C h−1 . Fish exposed to 50% air sat. became bradycardic, were
unable to increase heart rate ( fH ) when warmed, and had lower
values for metabolic scope and CTmax (21.3 vs 26.1°C in normoxic
fish). The effects of 75% air sat. on cardiorespiratory parameters and
CTmax were intermediate. We then used atropine (1.2 mg kg−1
) and 8-
cyclopentyltheophylline (CPT; 50 nmol kg−1
) to investigate what
role(s) cholinergic tone on the heart and cardiac adenosinergic
effects, respectively, play in preventing severely hypoxic salmon
(40% air sat.) from increasing fH when warmed. CPT had no/limited
effects on salmon cardiorespiratory parameters and thermal
tolerance. However, atropine increased fH in hypoxic fish and
allowed it to rise with temperature, and this resulted in salmon
that were much less tolerant to warming. Collectively, these results:
(1) show that fish in severely hypoxic environments will be
very susceptible to climate change-associated heat waves; and
(2) suggest that cholinergic tone on the heart is not removed when
severely hypoxic fish are exposed to rising temperatures to protect
the heart’s pumping capacity.