Linking swimming performance, cardiac pumping ability and cardiac anatomy in rainbow trout
1 Centre de Recherche sur les Écosystèmes Marins et Aquacoles,
Place du Séminaire, BP 5, 17137 L'Houmeau, France
2 Ocean Sciences Centre, Memorial University of Newfoundland, Logy Bay, NL,
A1C 5S7 Canada
3 Station Expérimentale Mixte IFREMER-INRA, Barrage du Drennec, 29450
Sizun, France
4 UBC Centre for Aquaculture and the Environment, Faculty of Agricultural
Sciences and Department of Zoology, 2357 Main Mall, University of British
Columbia, Vancouver, BC, V6T 1Z4, Canada
* Author for correspondence (e-mail: farrellt{at}interchange.ubc.ca)
Accepted 10 March 2005
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Summary |
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Key words: swimming, metabolism, cardiovascular performance, heart morphology, domestication, rainbow trout, Oncorhynchus mykiss
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Introduction |
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While these data are compelling, they are not conclusive evidence and may
not even be applicable to other fish species. Indeed, Soofiani and Priede
(1985) and later Reidy et al.
(1995
) both showed that
O2 in Atlantic
cod Gadus morhua was greater post-exercise rather than during
exercise. In fact, the suggestion was made that metabolic scope for Atlantic
cod evolved to accommodate post-prandial and post-exercise peaks in oxygen
demand rather than those during locomotor activity
(Soofiani and Priede, 1985
).
However, while feeding greatly increases
O2 in all fish
including salmonids (Jobling,
1981
; Brett, 1983
;
Legrow and Beamish, 1986
),
active metabolic rate (AMR) in salmonids is typically 2-3 times higher than
the post-exercise
O2 measured in
Atlantic cod (Nelson et al.,
1996
). Furthermore, while feeding increases
O2 by 50-100% in
salmonids, AMR during post-prandial swimming is no higher than in unfed fish
(Thorarensen, 1994
;
Alsop and Wood, 1997
). In fact,
because Ucrit is compromised post-prandially, it seems
likely that there is no excess capacity for salmonids to pump blood to the
intestine and liver to maximise digestion, as well as to skeletal muscles to
maximise locomotion (Farrell et al.,
2001
). Indeed, gut blood flow decreases dramatically during
exercise (Thorarensen et al.,
1993
). Thus, while the weight of evidence supports the idea that
cardiac pumping is maximal during swimming at Ucrit, some
room for doubt still remains, especially given the recent finding that
exercising monitor lizards have a higher AMR post-prandially compared with in
the unfed state (Bennett and Hicks,
2001
) and that in Atlantic cod the post-prandial increase in
O2 for a fixed
meal size increased with swimming activity
(Blaikie and Kerr, 1996
).
A difficulty with interventional experiments is the degree of inherent
individual diversity that exists in physiological performance traits, which
can often be greater than the change elicited by the experimental
intervention. In the present study we exploited inherent individual diversity
and reasoned that if cardiac performance is indeed closely linked with
swimming performance, then poor swimmers should have poorer cardiac
performance than good swimmers. Therefore, we screened a large group of
hatchery-raised rainbow trout to identify good and poor swimmers within the
population. These fish were then individually tagged and allowed to grow
together for a further 9 months, at which point their cardiac performance was
measured both in vivo and in vitro to compare good and poor
swimmers. In addition, and because cardiac abnormalities are frequently
reported for cultured fish (Poppe and
Taksdal, 2000; Brocklebank and
Raverty, 2002
; Poppe et al.,
2002
,
2003
;
Gamperl and Farrell, 2004
), we
compared simple cardiac meristics to determine if differences in cardiac
morphology were associated with poor cardiac performance and swimming.
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Materials and methods |
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In vivo swimming studies
In vivo studies were performed on six poor swimmers of mean
(± S.E.M.) mass 1204±105 g and
fork length 419±11 mm, and six good swimmers with a mean mass
1030±62 g and forklength 419±10 mm. The water temperature was
16±0.4°C during these experiments. Fish were anaesthetised in 0.1
mg l-1 MS-222 buffered with 0.1 mg l-1 NaHCO3
before being transferred to an operating table, where their gills were
irrigated with aerated water containing diluted anaesthetic (0.05 mg
l-1 MS-222 and NaHCO3). The ventral aorta was exposed
via an incision in the cleithrum, a Transonic flow probe (Transonic
Systems, Ithaca, NY, USA) placed around it and the incision closed with silk
sutures. The dorsal aorta (DA) was then cannulated using the technique
described by Soivio et al.
(1975). Following surgery,
fish were transferred to individual opaque PVC chambers, where they recovered
for 48 h in a continuous flow of normoxic water. The DA cannula was flushed
daily with heparinised (10 IU l-1) Cortland's saline
(Wolf, 1963
). Following this
recovery period, trout were carefully transferred, without air-exposure, into
a water-filled plastic bag and then into a swimming respirometer, where they
recovered for at least 4 h while swimming gently against a water velocity of
30 cm s-1.
The Ucrit swimming tests were performed using two
Brett-type swim-tunnel respirometers, designed to exercise individual fish in
a non-turbulent water flow with a uniform velocity profile
(Steffensen et al., 1984). One
respirometer constructed of PVC has been described in detail previously
(McKenzie et al., 2001
). The
second was of a similar design and size, but constructed in stainless steel,
with a total water volume of 48 l and a swim chamber with a square
cross-sectional area of 290 cm2. Water flow was generated by a
thermo plastic composite propeller downstream of the swim chamber, attached to
a variable speed, low inertia, brushless servo-motor (Ultact II, Phase Motion
Control S.R.L., Milan, Italy), calibrated to deliver water velocities in cm
s-1 and swimming speeds in body lengths s-1 (BL
s-1). The respirometer was thermostatted by immersion in a large
outer stainless steel tank that received a flow of aerated water. In both
respirometers, swimming speeds were corrected for the solid blocking effect of
the fish, as described by Bell and Terhune
(1970
).
Each trout was exposed to progressive water velocity increments of 10 cm
s-1 every 30 min, until fatigue. Fish were considered to be
fatigued when they were unable to remove themselves from the posterior screen
of the swimming chamber despite gentle encouragement with a sudden increase in
water velocity. Measurements of oxygen uptake
(O2) were
collected at each swimming speed, as described in McKenzie et al.
(2001
). These measurements
were used to derive: (i) the notional metabolic rate of the immobile fish
(IMR); (ii) the maximum metabolic rate of activity (AMR) during swimming (this
occurred at speeds approaching Ucrit); and (iii) net
aerobic scope relative to IMR (McKenzie et
al., 2003a
). Critical swimming speed was calculated in both
absolute (cm s-1) and relative (BL s-1) terms,
as described by Brett (1964
).
Three fish from each experimental group swam in each of the two respirometers.
Prior to actual experiments, preliminary Ucrit tests were
run on four, non-instrumented trout (two good swimmers, two poor swimmers) in
both the PVC and steel respirometers. There were no systematic differences in
either
O2 or
swimming performance linked to a particular respirometer (mean ±
S.E.M.): AMR was 181±39 µmol
kg-1 min-1 in the PVC tunnel and 195±37 µmol
kg-1 min-1 in the steel tunnel, while
Ucrit was 2.45±0.28 BL s-1 in
the PVC tunnel and 2.40±0.21 BL s-1 in the steel
tunnel.
Measurements of cardiac output ()
were made at each swimming speed. Data from the flow probe were acquired and
displayed real-time on a PC with LabVIEW software
(Axelsson et al., 2002
).
Measurements of dorsal aortic blood pressure (PDA) were
also made at each speed by connecting the saline-filled DA cannula to a
physiological pressure transducer (Statham P23XL, Statham Instruments, Oxnard,
CA, USA), with the amplified (Gould Universal amplifier, Gould Instruments,
Valley View, OH, USA) signal then acquired and displayed on the PC with
LabVIEW software (Axelsson et al.,
2002
). Heart rate (fH) was calculated
automatically from the flow probe signal, and used to derive cardiac stroke
volume (VS)
(Gallaugher et al., 2001
).
Total systemic vascular resistance (Rsys) during swimming
was calculated from the measurements of
and PDA
(Gallaugher et al., 2001
).
Maximum values for
,
fH and VS were identified from the
cardiovascular measurements made at each swimming speed, as was the minimum
value for Rsys. These extreme values always occurred at
speeds near Ucrit.
Arterial blood samples (100 µl) were collected from the DA cannula (and
replaced with an equal volume of saline) at swimming speeds of 40 cm
s-1 and 80 cm s-1, as well as just prior to fatigue
(i.e. at Ucrit). Arterial blood total O2
content (CaO2) was measured using the method of
Tucker (1967), as described in
McKenzie et al. (2003b
). The
measurements of CaO2 and maximum
(see above) were then used to
calculate maximum rates of arterial blood O2 transport
(
O2), as
described by Gallaugher et al.
(2001
).
In vitro perfused heart studies
The in vitro studies were performed on 15 fish (good swimmers:
body mass=1148±63 g, ventricular mass=0.87±0.07 g; poor
swimmers: body mass=1106±59 g, ventricular mass=0.92±0.08 g).
The in situ heart preparation used to assess maximum cardiac
performance has been described in detail by Farrell et al.
(1986) and included the
modifications outlined by Farrell et al.
(1988
). Briefly, fish were
anaesthetised, transferred to an operating sling where their gills were
irrigated with aerated buffered anaesthetic at 4°C, and injected with 0.6
ml of heparinised (100 IU ml-1) saline via the caudal
vessels. A stainless steel input cannula was secured into the sinus venosus
through a hepatic vein and perfusion begun immediately with oxygenated saline
containing a tonic level of adrenaline (5 nmol l-1 adrenaline).
Silk threads were used to occlude any remaining hepatic veins and the ducti
Cuvier. A stainless steel output cannula was advanced into the ventral aorta
until the tip was in the bulbus arteriosus and tied firmly in place. These
procedures, which were completed in 15-20 min, isolated the heart in terms of
saline input and output, while leaving the pericardium intact. The preparation
was then immersed in a saline-filled, temperature-controlled organ bath at
16°C, where the input and output cannulae were attached to constant
pressure heads. The heart was perfused with an oxygenated physiological saline
(Farrell et al., 1988
) and
filling (input) pressure of the heart was adjusted to give a routine
of 25 ml min-1
kg-1 body mass. Mean output pressure was set at
5 kPa to
simulate routine in vivo mean ventral aortic blood pressures
(Stevens and Randall, 1967
).
The heart maintained this control level of performance for a period of 15-20
min before the assessment protocol began.
The maximum pumping ability of the heart was assessed first by measuring
maximum when filling pressure was
increased (i.e. a Starling response) and then by increasing output pressure to
8 and 9 kPa to elicit an increase in cardiac power output while the heart
continued to pump maximally. When rainbow trout swim, or when they are given
an intra-arterial adrenaline injection, both
and diastolic ventral aortic pressure
increase, but mean pressure rarely exceeds 8
kPa(Kiceniuk and Jones, 1977
;
Gamperl et al., 1994
). The
heart was then returned to the control perfusion conditions for a 15 min
recovery and equilibration with a new adrenaline concentration (1 µmol
l-1) in the perfusate, which was then used to assess the effect of
maximum adrenergic stimulation of the heart (see
Mercier et al., 2000
). The two
adrenaline concentrations used (5 nmol l-1 and 1 µmol
l-1) span the range for circulating catecholamine levels observed
in resting and stressed trout, respectively
(Milligan et al.,
1989
; Randall and Perry,
1992
; Gamperl et al.,
1994
). An in-line Transonic flow probe (Transonic Systems, Ithaca,
NY, USA) was used to record
(=
ventral aortic flow in the output cannula). Pressures in the sinus venosus
(input) and ventral aorta (output) were measured using DP6100 pressure
transducers (Medizintechnik, Dusslingen, Germany), through saline-filled tubes
placed at the tip of the cannulae. The pressure transducers were calibrated
against a static water column for each preparation. Pressure and flow signals
were amplified and filtered using a Model MP100A-CE data acquisition system
(BIOPAC Systems Inc., Santa Barbara, CA, USA). The acquired signals were then
analysed and stored using Acknowledge Software (BIOPAC Systems Inc., Santa
Barbara, CA, USA) installed on a Dell laptop computer.
Myocardial power output (mW g-1 ventricle mass) was calculated
from the product of [ (ml
min-1)x(output-input pressure) (kPa)x(0.0167 min
s-1)]/ventricular mass (g)]. Ventricular mass was determined at the
conclusion of the experiment when the cannulae were checked for correct
positioning.
Physiological saline and chemicals
The physiological saline used for the perfused heart preparations (pH 7.8
at 15°C) contained (in mmol l-1): NaCl 124, KCl 3.1,
MSO4.7H2O 0.93, CaCl2.2H2O 2.52,
glucose, 5.6 Tes salt 6.4 and Tes acid 3.6
(Keen and Farrell, 1994). The
saline was equilibrated with 100% oxygen for at least 30 min prior to
experimentation. The coronary artery, which supplies the outer compact
myocardium of the ventricle, was not perfused and so oxygenated saline was
used to ensure that a sufficient amount of oxygen diffused from the
ventricular lumen to the compact myocardium. The oxygen gradient from the
lumen to the myocardium of the perfused heart was at least 20-times greater
than that in vivo. Preliminary experiments have shown that this
rainbow trout heart preparation can perform maximally even when the oxygen
tension is reduced to
8 kPa. Adrenaline bitartrate was purchased from
Sigma-Aldrich (St Quentin-Fallavier, France).
Cardiac anatomy
In vivo cardiac morphology were assessed for an additional 9 fish
per group (good swimmers: mass=1104±47 g, length=425±7 mm; poor
swimmers: mass=1167±33 g, length=423±4 mm) using echo-Doppler
imaging (Esaote-Pie Medical FalcoVet 100 scanner and 7.5 MHz probe,
Fontenaysous-Bois, France; accuracy ±0.3 mm). Fish were lightly
anaesthetised and placed in an operating sling where a hand-held probe
provided a lateral image of the ventricle, bulbus arteriosus and ventral
aorta. The image was stored and subsequently analysed. After calibration, the
machine software allowed the measurement of ventricular height (H)
and length (L), as well as the angle () subtended between the
ventral aorta and the ventral surface of the ventricular wall
(Fig. 1).
|
Data analysis and statistics
Comparisons between good and bad swimmers for single variables were
performed using a Student t-test. The effect of swimming speed on
in vivo variables was assessed and compared between the two groups
using a two-way ANOVA with repeated measures. A probability less than 5%
(P<0.05) was taken as the limit for statistical significance.
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Results |
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In vivo performance
Fish that swam poorly in the screening test had a significantly (27%) lower
Ucrit (both in absolute and relative terms) 9 months later
(Table 2).
Fig. 2 compares
O2 and
cardiovascular variables during the Ucrit protocol for
good and poor swimmers. There was no difference in derived IMR
(Table 2). Oxygen uptake
increased significantly with each increase in swimming speed in both groups,
and at common speeds there were no significant differences between the good
and poor swimmers (Fig. 2).
However, the good swimmers achieved a significantly 19% higher AMR by
achieving a higher Ucrit and, consequently, had a
significantly 24% higher aerobic scope
(Table 2).
|
|
Swimming significantly increased
and, at any common speed,
was similar
in both good and poor swimmers (Fig.
2). However, maximum
was
significantly (30%) higher for the good swimmers
(Table 2). fH and VS increased significantly in
both groups during swimming and in both groups the increase in
during swimming was predominantly a
result of increased VS rather than fH
(Fig. 2). Nevertheless, the
maximum values of fH and VS were not
significantly different between the good and poor swimmers
(Table 2). Both groups of fish
maintained PDA during exercise
(Fig. 2), but the decrease in
Rsys induced by exercise
(Fig. 2) was significantly
(35%) greater in good vs poor swimmers
(Table 2).
The oxygen content of arterial blood did not differ significantly between
good and poor swimmers and was unchanged during the exercise protocol when
measured at 40 cm s-1 and 80 cm s-1, which was just
prior to fatigue for the poor swimmers. The resting and two exercise values
for CaO2 were averaged for each fish prior to
calculating the group mean for CaO2
(Table 2). Maximum
O2 was
significantly (39%) higher in good swimmers compared with poor swimmers, as a
direct result of the former group's higher maximum
(Table 2).
In vitro performance
Under tonic adrenergic stimulation, maximum
was not statistically different
between the good and poor swimmers (48.0±2.7 ml min-1
kg-1 and 42.2±2.3 ml min-1 kg-1,
respectively; Fig. 3). Maximum
stimulation with adrenaline (1 µmol l-1) significantly increased
maximum
in both good and poor
swimmers, but that increase was significantly greater in good swimmers than in
poor swimmers (maximum
increased to
56.4±2.3 ml min-1 kg-1 and 45.9±1.9 ml
min-1 kg-1, respectively). Under control (tonic
adrenergic stimulation) conditions, fH was similar for
good and poor swimmers, as was the modest elevation in fH
produced by maximum adrenergic stimulation (an increase from 87.1±5.4
beats min-1 to 100.9±3.9 beats min-1 in poor
swimmers and from 89.1±4.4 beats min-1 to 97.5±2.8
beats min-1 in good swimmers). Similarly, VS
was not statistically different between the two swim groups under tonic
adrenergic stimulation (0.54±0.03 ml in good swimmers vs
0.49±0.03 ml in poor swimmers). However, under maximum adrenergic
stimulation, VS increased significantly in good swimmers
(0.58±0.02 ml), whereas it decreased significantly in poor swimmers
(0.46±0.03 ml). Thus, the maximum cardiac pumping ability of poor
swimmers was significantly (26%) lower than that of good swimmers.
|
Cardiac power output was calculated from the product of
and output pressure. The effect of
increasing output pressure while the heart was pumping maximally is shown in
Fig. 4. Overall, cardiac power
output in good swimmers was significantly higher than in poor swimmers. When
output pressure was progressively raised from 8 kPa to 9 kPa, power output was
unchanged in good swimmers. In contrast, the same increase in output pressure
from 8 kPa to 9 kPa in poor swimmers resulted in a significant decrease in
power output from 4.77±0.97 mW g-1 to 3.96±0.58 mW
g-1, which was 32% lower than the 5.97 mW g-1 for good
swimmers. Thus, the hearts from poor swimmers were less able to tolerate a
high cardiac afterload compared with good swimmers, as well as having a lower
maximum
.
|
Cardiac anatomy
The ventricle was significantly longer in good swimmers compared with poor
swimmers, although there were no differences in ventricular width or the
subtended angle (Table 3). As a
result, the ventricular length to width ratio was smaller in the poor swimmers
(Table 3).
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Discussion |
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The in vivo values for maximum
in the current study are consistent
with other reports for rainbow trout exercising to Ucrit
(Kiceniuk and Jones, 1977
;
Taylor et al., 1996
). Kiceniuk
and Jones (1977
) measured
indirectly by the Fick equation and
found a maximum
value of 51 ml
min-1 kg-1 at 11°C. Similarly, Thorarensen et al.
(1996a
) and Brodeur et al.
(2001
) report maximum
values for rainbow trout of 49 ml
min-1 kg-1 at 10°C and 65 ml min-1
kg-1 at 12°C, respectively. Taylor et al.
(1996
) also measured blood
flow indirectly, with microspheres, and found that maximum
was very sensitive to temperature,
being 20 ml min-1 kg-1 at 4°C, 69 ml
min-1 kg-1 at 11°C and decreasing to 42 ml
min-1 kg-1 at 18°C. Thus, both the good and the poor
swimmers in the current study had maximum
values at 16°C that were
intermediate between those for 11°C and 18°C reported by Taylor et al.
(1996
).
The present study, which used individual diversity in swimming performance
as a means of segregating two groups of fish, shows similarities with earlier
studies in which fish were exercise-trained in an attempt to improve their
aerobic capacity. For example, training of rainbow trout at 50% of
Ucrit for 1 month increased maximum
and power output by 17% and 26%,
respectively, as measured in perfused hearts
(Farrell et al., 1991
). In
chinook salmon Oncorhynchus tshawytscha, training at 1.5 BL
s-1 did not improve either Ucrit or AMR
(Thorarensen et al., 1993
),
but a more vigorous training protocol that involved them swimming to
Ucrit on alternate days for 4 months did elicit a
significant 50% increase in AMR
(Gallaugher et al., 2001
). In
the present study, similar differences in maximum
between good and poor swimmers (26%
in vitro and 30% in vivo) were associated with a 19% higher
AMR and a 27% higher Ucrit. Given this quantitative
agreement, it appears that the extremes of inherent individual diversity in
maximum
and associated swimming
ability, within a large group of hatchery-raised rainbow trout, are
approximately equivalent to the effects of intensive and prolonged training
protocols aimed at remodelling salmonid cardiac and aerobic performance.
The finding that rainbow trout retained a swimming performance trait over a
9 month period was not surprising. Numerous studies have demonstrated that
swimming performance is a repeatable trait in salmonid and non-salmonid
fishes, both in the short term (Randall et
al., 1987; Brauner et al.,
1994
; Kolok and Farrell,
1994
; Jain et al.,
1998
; Farrell et al.,
2003
) and the long term
(Kolok, 1992
;
Martinez et al., 2002
).
Although individual diversity in swimming performance has been related to
muscle biochemistry (Kolok,
1992
; Martinez et al.,
2002
), we are unaware of any previous linkages of individual
diversity in maximum
, AMR, aerobic
scope and Ucrit, as revealed in the present study. While
the basis for this diversity awaits further study of potential genetic,
environmental or even social influences, we believe that the in vitro
work, by providing definitive information about maximum cardiac pumping
capacity, lends direct support for the contention that rainbow trout utilise
their maximum cardiac pumping ability at or near
Ucrit.
One concern encountered in the present study was that the fish grew faster
than anticipated, which resulted in experimental fish that were larger than
the preferred optimal for perfused heart work. Because approximately 30% of
the outer ventricular wall receives oxygen from a coronary circulation and
this was not perfused in the heart preparation, the expectation was that the
oxygenated perfusate, which has an oxygen tension nearly 50-times higher than
that measured in venous blood passing through the heart at
Ucrit (1.6 kPa;
Farrell and Clutterham, 2003
),
would provide sufficient oxygen delivery to the compact myocardium. This was
certainly the case for the poor swimmers because there was an excellent
agreement between the maximum
measured in vivo (47.3 ml min-1 kg-1) and that
measured in vitro (45.9 ml min-1 kg-1).
However, the agreement was not quite as good for the good swimmers, where
maximum
in vivo was 68.0 ml
min-1 kg-1 vs 56.4 ml min-1
kg-1 in vitro. This concern is unlikely to invalidate our
main finding that maximum cardiac pumping ability was significantly lower in
poor compared with good swimmers, since if anything we underestimated maximum
in vitro.
The difference observed in cardiac anatomy between good and poor swimmers
did not translate into a significantly larger VS for good
swimmers under a condition of tonic adrenergic stimulation. However, hearts
from poor swimmers were less sensitive to adrenergic stimulation, which did
not increase maximum in vitro, a fact
that may underlie the lower in vivo maximum
. Mechanistically, it seems that while
a modest positive chronotropic response to adrenergic stimulation was common
to good and poor swimmers, the consequence of this elevated
fH was to modestly decrease maximum VS
in the poor swimmers. This indicates a limited inotropic action of adrenaline
in the poor swimmers, a response that was not observed in the good swimmers.
An inotropic deficiency in poor swimmers was further manifested as a lower
maximum power output (i.e. maximum VS was not maintained
when either output pressure or fH was increased). Given
this shortcoming, the inability of poor swimmers to decrease
Rsys (which sets cardiac afterload) during swimming may
have contributed to their lower maximum
in
vivo. A limited cardiac response to adrenergic stimulation was expected
at 16°C because earlier work has shown that adrenergic sensitivity of
rainbow trout hearts falls off at temperatures approaching 18°C (Farrell
et al., 1986
,
1996
), unlike at colder
temperatures when adrenergic stimulation may be critical for basic cardiac
rhythmicity (Graham and Farrell,
1989
) and calcium channel function
(Shiels et al., 2003
).
Between 20 and 60% of farmed triploid brown trout Salmo trutta
have been observed with a bent aorta, depending on the origin of the fish (G.
Claireaux and J. Aubin, personal observations;
Poppe et al., 2003), with an
value of >100° in the worst cases. In the present work with
rainbow trout, aortic deformities were not observed. Hatchery-raised salmonids
are also characterised by having a more rounded ventricle than those captured
from the wild (Poppe et al.,
2003
; Gamperl and Farrell,
2004
) and this would mean that the L/H ratio for
the ventricle would tend towards unity. The present finding of a reduced
ventricular L/H ratio for poor swimmers is consistent with a
more rounded ventricular shape. Furthermore, amongst the individual fish used
in the present study, this ventricular ratio was negatively correlated with
fish condition factor, i.e. the higher the condition factor, the more rounded
the ventricle (Fig. 5).
Moreover, when data for wild anadromous rainbow trout (steelhead) from the
Clearwater River, Idaho, USA (Poppe et
al., 2003
) are included on this graph, it becomes clear that
condition factor and ventricular shape may be more generally related. There
are a variety of potential reasons why these correlations might exist and
further work is needed to tease them apart. For example, there is likely an
optimum condition factor for swimming performance that would lie somewhere
between the states of starvation and obesity. The fish in the present study
were very well fed and their condition factors indicated that they were near
or above this optimum. Until the relationships between cardiac shape, swimming
performance, condition factor, reduced maximum cardiac pumping ability and
reduced cardiac sensitivity to adrenaline among cultured rainbow trout are
resolved, it remains probable that specific culture conditions and practices
(e.g. fast growth, lack of physical exercise, nutrition, phenotype and
genotype selection, etc.) play a role in the more rounded ventricle of farmed
salmonids, and within this aquaculture context, knowledge of ventricular shape
in relation to condition factor may have potential to be a predictor of
swimming ability. Nevertheless, future studies would do well to consider how a
change in relative ventricular mass might affect ventricular shape, given that
cold temperature acclimation and sexual maturation (in males) are both known
to increase relative ventricular mass in rainbow trout.
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List of symbols and abbreviations |
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Acknowledgments |
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References |
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