Sundin, J., Amcoff, M.,
Mateos-González, F.,
Raby, G.D. and Clark, T.D.
2019
Long-term acclimation
to near-future
ocean acidification
has negligible effects
on energetic attributes
in a juvenile coral reef fish.
Oecologia 190: 689-702.
NOTE:
Sundin et al. (2019) note that
so-called ocean acidification
is projected to increase
the energy use of
marine fish by means of
various physiological
and behavioral mechanisms.
This hypothesis, they say, is
"based on a theoretical framework
suggesting that detrimental effects
on energy use are caused by
plasma acid-base disruption
in response to hypercapnic acidosis,
potentially in combination
with a malfunction of the
gamma aminobutyric
acid type A (GABAA)
receptors in the brain."
But they note that
"the existing
empirical evidence
testing these effects
primarily stems
from studies
that exposed fish
to elevated CO2
for a few days and
measured [only] a
small number of traits."
SUMMARY:
Sundin et al. say
that their findings
"demonstrate that
end-of-century levels
of CO2 may have
negligible effects
on a variety of
energetic traits
in at least some fishes,
and they add to a
growing dichotomy
across studies
in this field
of research."
DETAILS:
The work focused on
juvenile spiny
chromis damselfish
(Acanthochromis poluacanthus).
Following three months
of acclimation to projected
CO2 levels at the end of
this century (i.e., 1000 µatm)
they examined a range
of energetic traits,
comparing responses
to juveniles reared u
nder ambient seawater pH.
The authors report that:
(1)
"somatic growth and otolith size
and shape were unaffected
by the CO2 treatment
across 3 months
of development
in comparison with
control fish (~420 µatm),"
(2)
"swimming activity
during behavioral assays
was initially higher
in the elevated CO2 group,
but this effect dissipated
within ~25 minutes
following handling,"
and
(3)
"the transient higher activity
of fish under elevated CO2
was not associated with
a detectable difference
in the rate of oxygen uptake
nor was it mediated by GABAA
neurotransmitter interference
because treatment with
a GABAA antagonist (gabazine)
did not abolish the CO2
treatment effect."