Severity of Barotrauma Influences the Physiological Status,
Postrelease Behavior, and Fate of
Tournament-Caught Smallmouth Bass
MARIE-ANGE GRAVEL AND STEVEN J. COOKE*
Fish Ecology and Conservation Physiology Laboratory, Department of Biology, Carleton University,
1125 Colonel By Drive, Ottawa, Ontario K1S 5B6, Canada
Abstract.—Much research on the fish physiological consequences of tournaments has been conducted to
date and has provided anglers and tournament organizers with strategies for reducing stress and mortality.
However, one aspect of tournaments that has received little attention is barotrauma. At a fall competitive
angling event on Rainy Lake in northwestern Ontario, we evaluated the incidence of barotrauma among
tournament-caught smallmouth bass Micropterus dolomieu; we then tagged and released a subset of fish that
had severe barotrauma indicators and compared physiology, postrelease behavior, and fate between these fish
and those with negligible signs of barotrauma. Overall, 76% of fish had at least one sign of barotrauma (either
hemorrhaging or swim bladder distention), but only 32% of fish had two or more indicators and were thus
deemed to have severe barotrauma. When telemetered fish were released at a common site, we determined
that fish with negligible signs of barotrauma evacuated the release site more rapidly than fish with severe
barotrauma did. Some fish with barotrauma floundered at the surface when released, and one of these fish was
subsequently hit and killed by a boat. At the end of the monitoring period, 20% of fish with severe barotrauma
had died; two additional individuals (20%) that were still at the release site were moribund (failed to respond
to diver stimuli). Conversely, we failed to observe any mortality in fish with negligible signs of barotrauma.
All tournament fish had elevated levels of blood glucose and lactate. However, stress indices were higher in
fish with barotrauma and tended to be highest among fish with barotrauma that died after release. This study
revealed that the incidence of barotrauma in tournaments can be high; moreover, outside of a laboratory
environment, a significant proportion of fish with severe barotrauma may die after release. Additional research
is needed to determine the seasonal variation in incidence and consequences of barotrauma as well as the
effectiveness of different depressurization techniques in the field that could be used during fishing
In North America, live-release tournaments involv-
ing black basses Micropterus spp. are becoming
increasingly popular with recreational anglers
(Schramm et al. 1991; Kerr and Kamke 2003). Not
surprisingly, many researchers have examined the
biological effects of tournaments on black basses
(reviewed in Cooke et al. 2002; Siepker et al. 2007)
and have found that several factors, including water
temperature (Wilde 1998), live-well conditions (i.e.,
where the fish are held at ambient atmospheric pressure
for extended periods; Cooke et al. 2002; Suski et al.
2004, 2005, 2006), and weigh-in procedures (Suski et
al. 2003, 2004), can influence stress and mortality. By
adopting simple strategies such as refraining from
holding tournaments during the warmest times of the
year, providing fish with adequate live-well water
quality, and improving weigh-in procedures, anglers
and tournament organizers have the potential to reduce
stress and mortality. Other factors that can influence
stress and mortality are depth of capture and associated
barotrauma. Unfortunately, the incidence and conse-
quences of barotrauma are poorly understood in
relation to bass tournaments, especially those in which
live wells are used.
Barotrauma has been documented in many freshwa-
ter and marine game fish and is increasingly being
recognized as a serious conservation and management
issue in catch-and-release fisheries (Bartholomew and
Bohnsack 2005; Arlinghaus et al. 2007). Barotrauma
results from a process called decompression, where fish
are brought from depth to the surface quickly, leading
to rapid changes in ambient pressure. The decline in
ambient pressure can have profound physiological
(Morrissey et al. 2005) and physical (Feathers and
Knable 1983) consequences, especially in physoclis-
tous fishes (including black basses), in which the swim
bladder does not directly connect to the digestive tract
(Fa¨nge 1966). Beyond problems with swim bladder
distention (which, in some species, includes stomach or
anal eversion or swim bladder bursting; Feathers and
Knable 1983), fish that are exposed to decompression
can experience internal (peritoneum, kidneys, dorsal
* Corresponding author: email@example.com
Received January 22, 2007; accepted July 24, 2007
Published online March 24, 2008
North American Journal of Fisheries Management 28:607–617, 2008
Ó Copyright by the American Fisheries Society 2008
aorta; Feathers and Knable 1983) and external (fins,
gums, body surface; Feathers and Knable 1983;
Morrissey et al. 2005) hemorrhaging; ocular pressure;
formation of gas bubbles within the circulatory system,
gills, heart, and brain (Philp 1974; Casillas et al. 1975);
and general tissue damage (Morrissey et al. 2005;
Rummer and Bennett 2005). In fact, one study
documented over 70 injuries that could arise from
severe decompression (Rummer and Bennett 2005).
It is believed that some decompressed fish, if
released quickly, will be able to descend enough to
recompress the gases and minimize the negative
consequences of barotrauma. However, in bass tour-
naments, fish are retained in live wells at atmospheric
pressure, which allows gases to expand; when bloating
is severe, fish are unable to equilibrate. When released,
fish that are unable to return to depth immediately
because of the added buoyancy could face predation
(e.g., Keniry et al. 1996; St. John 2003); solar radiation
or thermal stress; involuntary transport to shore or
undesirable habitats via waves, currents, tides, or wind;
injury from impact with boats; or additional physio-
logical disturbances as they struggle to return to depth
(Morrissey et al. 2005). The magnitude of the
decompression and the potential for mortality appear
to increase with depth of capture (Feathers and Knable
1983; Gitschlag and Renaud 1994; St. John and Syers
2005) beyond a minimum of 3.5 m (Shasteen and
Sheehan 1997). Previous research has occurred pri-
marily in the laboratory environment (Shasteen and
Sheehan 1997) or in field cages (Gitschlag and Renaud
1994; St. John and Syers 2005) and thus has not
approximated the actual condi tions of live-release
tournaments. Only Morrissey et al. (2005) quantita-
tively assessed incidence and physiological conse-
quences of barotrauma in smallmouth bass Micropterus
dolomieu at a tournament; however, they did not assess
survival of the fish.
The purpose of this study was to evaluate the
incidence of barotrauma at a live-release smallmouth
bass tournament and the consequences of barotrauma
for physiology, pos trelease behavior, and fate of
affected individuals. Because the focus was on
barotrauma rather than other variables, we selected a
tournament conducted in the fall, when water (;148C)
and air (;108C) temperatures were low and thus when
environmental conditions during live-well retention
and weigh-in were expected to be reasonably benign
(Wilde 1998; Schreer et al. 2001). In addition, unlike
previous studies, we used biotelemetry to monitor the
behavior and fate of released fish. By taking nonlethal
biopsies before the fish were released (Cooke et al.
2005), we were able to conduct the first examination of
the relationship between individual physiological status
and fate in a recreational fishery.
Study site and tournament.—This study was con-
ducted at a live-release angling tournament (September
30 and October 1, 2006) in northwestern Ontario on
Rainy Lake at LaBelle’s Camp (48850
W; mean depth ¼ 9.8 m; maximum depth ¼
49.1 m). This annual tournament involves 75 boats and
150 tournament anglers. Each team may retain and
weigh in five smallmouth bass per competition day
(minimum tournament size ¼ 30 cm), competing for the
greatest combined weight over a 2-d period. Surface
water temperatures in the nearshore areas were between
13.68C and 14.7 8C during the tournament. Fish
captured during the event were kept in circulating live
wells of various sizes for up to 9 h. For the weigh-in,
fish were brought to shore in plastic bags filled with
water, transferred to water basins, and transported to
the weigh-in site in all-terrain vehicles (ATVs; trip
lasted ;1 min). At the weigh-in site, fish were held in
static-water-filled basins, dry weighed in air, and then
ATV-transported in water basins back to the dock
region. For our experiments, we intercepted fish as they
were delivered to the dock but before they were placed
in a pontoon boat, where they were held for up to 3 h
until release. During the 2-d period, tournament anglers
weighed in 592 smallmouth bass.
Assessment of barotrauma.—To assess incidence of
barotrauma at the tournament, we randomly intercepted
fish (N ¼ 64) after weigh-in over the 2-d period. Fish
were processed one at a time and were placed in a 30-L
container for an observation period of about 1 min.
Because barotrauma causes pressure changes that can
be visualized by expanded swim bladders (bloating)
and broken blood vessels (hemorrhaging; Feathers and
Knable 1983), we evaluated these indicators during the
observation period. We emulated the techniques of
Morrissey et al. (2005) to enable direct comparison of
barotrauma incidence and severity. A fish was
categorized as moderately bloated if the body was
slightly distended or severely bloated if the body was
greatly deformed (Morrissey et al. 2005). Fish of the
latter group were unable to maintain equilibrium and
some also showed signs of eye bulging. Fish were then
placed in a water trough, where gills were submerged
in fresh lake water. We then looked for signs of
hemorrhaging on the fins, gums, and body surface,
where broken blood vessels would be visible as
described by Morrissey et al. (2005). Hemorrhaging
was categorized as severe if it occurred in two or more
areas or moderate if it occurred in only one area.
608 GRAVEL AND CO OKE
To assess physiological condition, we placed the fish
in supine position in the trough and obtained a 1.5-mL
nonlethal blood sample (Cooke et al. 2005) by caudal
venipuncture with a Vacutainer (3-mL tube containing
lithium heparin anticoagulant; Becton Dickinson, Inc.,
Franklin Lakes, New Jersey); samples were immedi-
ately placed in a water–ice slurry. The fish were then
transferred to the live-release pontoon boat. Within 2
min of blood sample collection, we measured lactate
and glucose levels in whole blood by adding 10 lLof
blood to a handheld glucose meter (Roche Diagnostics
Corp., Indianapolis, Indiana; Accu-Chek) and lactate
meter (Arkray, Inc., Kyoto, Japan; Lactate Pro LT-
1710 Analyzer). Appropriate standards and calibrations
were used with the meters before analysis according to
the manufacturers’ guidelines. These field meters have
been shown to produce results c omparable with
laboratory values for fish and other animals (e.g.,
Morgan and Iwama 1997; Wells and Pankhurst 1999;
Pyne et al. 2000; Venn Beecham et al. 2006); even if
the values show minor deviations from results of
laboratory assays, the relative differences among
treatments are useful (Morgan and Iwama 1997;
Mizock 2002; Venn Beecham et al. 2006). Within 2
h, the Vacutainers were gently inverted several times
and some of the remaining blood was placed in
microhematocrit tubes for 6 min of centrifugation at
10,000 revolutions/min to assess packed cell volume
(i.e., hematocrit). The above procedures were per-
formed again during two posttournament dates (Octo-
ber 4and 5, 2006) on a pseudo-control group (N ¼ 11)
containing fish that were angled from Rainy Lake
(maximum capture depth ¼ 8 m), landed within 30 s,
and immediately sampled for blood while being held in
a water-filled trough to provide context for other
physiological values. The pseudo-control fish were
Assessing posttournament behavior and survival.—
In addition to the randomly chosen fish described
above, we also nonrandomly selected tournament-
caught fish that had either negligible (one or no signs
of) barotrauma (N ¼ 12 fish) or severe (two or more
signs of) barotrauma (N ¼ 10; Morrissey et al. 2005)
toward the end of each sampling period on each day.
All of the fish with severe barotrauma exhibited loss of
equilibrium in addition to bloating and hemorrhaging.
The nonrandomly selected additional fish were used to
assess posttournament behavior and survival in relation
to barotrauma severity. The blood collection protocol
was identical to that described above, but fish were also
equipped with small, flattened, external radio transmit-
ters (2.4 g in air; ,1 g in water; ;4 3 15 3 18 mm;
20-cm trailing antennas; frequency ¼ 148–151 MHz)
according to the techniques described by Cooke
(2003). Stainless steel wires were passed through the
fish by using paired hypodermic needles. The wires
were connected to the transmitters and formed a
harness when the wires were twisted and flattened
against a backing plate. The transmitters were placed
near the dorsal surface (;5 mm ventral to the dorsal
midline), at the interface of the soft and spiny dorsal
fins. Transmitters had a life expectancy of 10 d. Fish
were also affixed with anchor tags (Floy Manufactur-
ing, Inc.) to identify individual fish externally.
Telemetered fish were transported to a common
release site in a 200-L transport tank to simulate normal
tournament release procedures. The release site was a
rocky point (depth ;4 m) in a distinct bay that was off-
limits to anglers participating in the tournament. After
release on day 1, fish had to swim roughly 1 km before
moving into a region where they could be targeted by
anglers on day 2. Using three-element Yagi antennas
and several radiotelemetry receivers, we tracked the
fish by radiotelemetry for 5–6 d or until they left the
study site (.2 km). To track fish from shore and by
boat (with a trolling motor), we used a combination of
triangulation and successive gain reductions (i.e., zero-
point tracking). At night, fish were tracked from shore
from several high vantage points, enabling general
assessment of the presence or absence of fish within
different spatial scales from the release point. This was
particularly necessary during the day of release so that
we could assess immediate postrelease beha vior.
Tracking calibrations were conducted to assess the
reception range of the receiver with different gain
settings from the release point. During the day, when
the boat could be used, fish positions were marked on
scale maps and the positions were noted by using a
handheld Global Positioning System unit. At night,
observations focused on using maps to determine fish
position relative to the release site. When a transmitter
had not moved (,5 m), possibly indicating mortality, a
snorkeler was deployed to look for the fish or its
Statistical analysis.—The mean concentrations of
metabolites (i.e., blood lactate and glucose) and
hematocrit were compared using one-way analysis of
variance (ANOVA) and Tukey–Kramer post hoc tests.
For telemetered fish, differences in the probability of
survival between fish with negligible barotrauma and
those with severe barotrauma were assessed by using a
univariate survival analysis with censoring. The same
analysis method was used to compare the probability
that fish of each group were within a specified distance
(25 and 250 m) of the release site at the termination of
the monitoring period. Only fish that survived during
the entire study period were included in the distance
BAROTRAUMA EFFECTS ON SMALLMOU TH BASS 609
analysis. All statistical tests were performed in JMPIN
version 5.1 (SAS Institute), and a for all tests was 0.05.
Of the 64 randomly selected tournament fish (mean
total length 6 SE ¼ 435 6 5.7 mm), 64% showed
signs of hemorrhaging (gums, body, or fins) and 42%
showed signs of bloating (Figure 1). All fish that
showed signs of bloating also had problems with
equilibrium. We conservatively defined fish as expe-
riencing barotrauma if they showed signs of bloating
and one or more signs of hemorrhaging (Morrissey et
al. 2005) or if they showed signs of severe bloating
(hereafter, severe barotrauma group). This represented
31% of the randomly selected fish. Fish of the severe
barotrauma group were also significantly larger than
the other groups (ANOVA: P ¼ 0.01; Figure 2). The
severe and negligible barotrauma groups had elevated
blood lactate and glucose levels relative to those of
angled controls (ANOVA: P , 0.001; Figure 3A).
Hematocrit also varied across treatments, and there was
evidence of hemoconcentration in the tournament fish
(severe and negligible barotrauma groups) relative to
controls (ANOVA: P , 0.0001; Figure 4A). Despite
clear physiological disturbance and signs of barotrau-
ma, all handled fish were alive when placed into the
live-release pontoon boat.
The mean length of radio-tagged fish with negligible
barotrauma (N ¼ 12; 463 6 7 mm) did not differ
significantly from that of radio-tagged fish with severe
barotrauma (N ¼ 10; 447 6 11 mm; t-test: P ¼ 0.25).
The survival probability for radio-tagged fish with
severe barotrauma was significantly lower than that for
fish with negligible barotrauma (v
¼ 5.66, df ¼ 1, P ¼
0.017). Specifically, we observed no mortality in fish
with negligible barotrauma and 40% mortality in fish
with severe barotrauma. In calculating mortality, we
included two moribund fish that were still within 25 m
of the release site at the end of monitoring (i.e., after 5
or 6 d) and that did not respond to diver stimulation.
One of the dead fish was found floating on the surface
14 h after release; impact with a boat had severed the
pelvic fins, scarred the body externally, and ruptured
the stomach and liver internally. The other fish was
found dead on the bottom of the lake after 24 h. All
mortalities were located in close proximity (25 m) to
the release site.
By 16 h postrelease, no floating fish were observed,
although most of the severely barotraumatized fish
were indeed floundering at the surface until low light
levels prevented further observation (;3 h postre-
lease). Telemetered fish with severe barotrauma and
those with negligible barotrauma differed in the time
required to disperse 25 m from the common release site
¼ 4.78, df ¼ 1, P ¼ 0.029). After 15 h, all fish with
negligible barotrauma had left the release site, whereas
live fish with severe barotrauma took as much as 70 h
to leave the site (Figure 5A). We observed the same
trend in the time taken by fish to travel more than 250
m from the release site (v
¼ 4.62, df ¼ 1, P ¼ 0.032;
Figure 5B). The probability of a fish being within 250
m of the release site at 115 h postrelease was 8% for
fish with negligible barotrauma but 57% for fish with
severe barotrauma. At the end of the study period, 70%
of fish with negligible barotrauma were able to exit the
bay of release (.2 km), but only 30% of fish with
severe barotrauma were able to do so. Furthermore, the
FIGURE 1.—Percent of smallmouth bass (N ¼ 64 fish)
showing signs of hemorrhaging (none ¼ no visible broken
blood vessels; moderate ¼ broken blood vessels visible in only
one area of the body; severe ¼ broken blood vessels in more
than one area) or bloating (none ¼ no distension of the body;
moderate ¼ slight distention; severe ¼ great distention) after a
fall tournament on Rainy Lake, Ontario, in 2006.
FIGURE 2.—Size-specific patterns (mean total length 6 SE)
in number of barotrauma signs observed in smallmouth bass
caught during a fall tournament on Rainy Lake, Ontario, 2006.
Sample sizes are given inside bars. Letter assignments denote
significant differences in means between categories (Tukey–
Kramer post hoc test: P , 0.05).
GRAVEL AND CO OKE
remaining fish with severe barotrauma (70%) had not
traveled further than 1 km from the release site.
Stress indicators varied according to barotrauma
severity and fate. Similar to the broader tournament
assessment (above), blood glucose and lactate values
varied significantly (P , 0.0001 for both; Figure 3B);
the tournament fish had significantly higher values than
the angled controls. Fish with negligible barotrauma
had blood glucose levels that were significantly lower
than those of severely barotraumatized fish that died
during the study period (P , 0.05); fish with severe
barotrauma that survived had intermediate levels. Fish
with negligible barotrauma had blood lactate levels that
were significantly lower (P , 0.05) than those of fish
with severe barotrauma irrespective of fate. Similarly,
hematocrit levels also varied by treatment (P ¼ 0.0002;
FIGURE 3.—Blood lactate and glucose levels (mean 6 SE) in smallmouth bass of varying fates and varying barotrauma
severity caught during a fall tournament on Rainy Lake, Ontario, in 2006: (A) fish with unknown fates from three severity groups
(control; NB ¼ negligible barotrauma; B ¼ severe barotrauma); and (B) radio-tagged fish with known fates (control; NB; B ¼
severely barotraumatized fish that lived; BD ¼ severely barotraumatized fish that died. Letter assignments (a and b for lactate; x–
z for glucose) denote significant differences in means between groups (Tukey–Kramer post hoc test: P , 0.05). Sample size is
indicated within each bar.
BAROTRAUMA EFFECTS ON SMALLMOU TH BASS 611
Figure 4B); the lowest levels were observed in angled
controls, and consistently higher values were recorded
in all tournament fish irrespective of barotrauma status
Barotrauma is increasingly being recognized as a
factor that can affect the condition and survival of fish
captured from depth and released (reviewed by
Arlinghaus et al. 2007). In a recent meta-analysis,
Bartholomew and Bohnsack (2005) reported that
capture depth was a highly significant factor in
mortality of angled fish, such that mortality was higher
in deepwater captures than in shallow-water captures.
To our knowledge, however, all of the studies they
analyzed were based on experiments conducted in the
laboratory, where fish are artificially decompressed in
barochambers (e.g., Shasteen and Sheehan 1997),
captured in the field and then monitored for survival
in tanks or pens (e.g., Keniry et al. 1996), or held in
cages at various depths (e.g., St. John and Syers 2005).
Several mark–recapture tagging studies have been
conducted that evaluate barotrauma issues (e.g., Lee
1992; Burns and Restrepo 2002), but these studies
provide little information on fish behavior and are
subject to several limitations. In addition, only a
limited amount of work has assessed barotrauma at
fishing tournaments (see Morrissey et al. 2005), where
fish are subjected to multiple stressors (see Cooke et al.
2002; Suski et al. 2004). Our study revealed that at a
smallmouth bass tournament in northwestern Ontario,
32% of fish had clear indications of severe barotrauma
after weigh-in. In addition, using telemetry coupled
with nonlethal physiological sampling, we found that
fish with severe barotrauma were slower to disperse
from the release site than those with negligible
barotrauma. Mortality rates were significant (40%)in
fish with severe barotrauma, and those that died were
FIGURE 4.—Hematocrit levels (mean 6 SE) in smallmouth
bass of varying fates and varying barotrauma severity caught
during a fall tournament on Rainy Lake, Ontario, in 2006: (A)
fish with unknown fates from three severity groups (control;
NB ¼ negligible barotrauma; B ¼ severe barotrauma); and (B)
radio-tagged fish with known fates (control; NB; B ¼ severely
barotraumatized fish that lived; BD ¼ severely barotrauma-
tized fish that died). Letter assignments denote significant
differences in means between groups (Tukey–Kramer post hoc
test: P , 0.05). Sample size is indicated within each bar.
FIGURE 5.—Probability of being located (A) within 25 m or
(B) within 250 m of the release site for radio-tagged
smallmouth bass that exhibited severe or negligible barotrau-
ma after capture during a fall tournament on Rainy Lake,
Ontario, in 2006.
GRAVEL AND CO OKE
clearly stressed, as indicated by blood chemistry (i.e.,
extremely elevated blood glucose). The concept of
linking behavior, physiology, and fate with nonlethal
physiol ogical s ampling and biotelemetry is novel
among catch-and-release assessments but has been
done previously to assess migration failure in salmo-
nids (Cooke et al. 2006; Young et al. 2006) and
bycatch fate in marine pelagic species (Moyes et al.
2006). We believe that this approach has much value
for catch-and-release studies, particularly those con-
cerning barotrauma; cage and laboratory experiments
fail to expose fish to the suite of predators, environ-
mental conditions, boating traffic, and other variables
that exist in actual live-release angling scenarios.
Of our examined fish, 64% showed signs of
hemorrhaging and 42% showed signs of extreme
bloating. Our analyses also showed that fish with
severe barotrauma tended to be larger than other fish.
However, the effect of fish size on barotrauma was not
the focus of this study because tournament anglers tend
to target the largest individuals. All fish with extreme
bloating also had problems maintaining equilibrium
and were floating on the water surface during
observations. In addition, when placed in the live-
release boats, many of these same fish floated upside
down but continued to ventilate their gills, similar to
the tournament-caught largemouth bass M. salmoides
observed by Lee (1992). A previous study (Morrissey
et al. 2005) investigated posttournament barotrauma in
smallmouth bass in several lakes in southern Ontario
and used the same criteria used here to classify fish
with severe barotrauma (i.e., two or more signs). In
shallow Rice Lake (mean depth ¼ 3 m; maximum depth
¼ 7.9 m), they observed a low incidence of severe
barotrauma (1.9%); however, they found a much higher
incidence (56.5%) in a deeper lake (i.e., western basin
of Lake Erie; mean depth ¼ 7.4 m; maximum depth ¼
18.9 m). In contrast, Rainy Lake has a mean depth of
9.8 m and a maximum depth of 49.1 m, and 32% of
observed fish had severe barotrauma. Because Rainy
Lake is deeper than Rice Lake or Lake Erie, we would
expect barotrauma to be more prevalent in Rainy Lake.
The fact that it was not suggests that mean or
maximum depth of a water body cannot alone explain
the extent of barotrauma observed in tournament-
caught fish; other factors, such as fishing techniques,
tournament protocol, available habitat, depth of fish,
water temperature, and season, probably also play a
role. Anecdotal discussions with anglers at the
tournament on Rainy Lake revealed that a substantial
range of depths was targeted (1–10 m) by anglers. In
some cases, anglers reported fishing shallowly (;3m)
in deep water (;7 m) and having fish come from depth
to strike the lure. Future work is needed to elucidate the
various factors that influence variation in barotrauma
incidence at tournaments.
Unlike previous assessments of postrelease mortality
of fish with barotrauma, we used telemetry to study
fish fate in the wild. This also enabled us to assess the
sublethal behavioral consequences of barotrauma for
the first time. For this aspect of the study, we exploited
previous knowledge that smallmouth bass disperse
from a release site after being displaced from the site of
capture (information obtained either from experiments
or after tournaments; e.g., Stang et al. 1996; Bunt et al.
2002; Wilde 2003). Given that no angling was
permitted within 1 km of the release site, we expected
that all fish would evacuate the release site. Indeed, all
fish with negligible barotrauma evacuated the imme-
diate release site (i.e., 25 m) within 15 h and most
(92%) evacuated the 250-m zone within 27 h. Fish with
severe barotrauma took substantially longer to leave
the release site; at the end of the monitoring period (5–
6 d), two moribund individuals were still within 25 m
of the site. Although no other studies provide data
appropriate for comparison, fish with severe barotrau-
ma were clearly impaired in some way that delayed
their departure, perhaps reflecting energetic exhaustion
or physiological disturbance. In fact, most fish with
severe barotrauma were floating on the surface at the
time of release. In general, behaviors (including loss of
equilibrium and slow dispersal) tend to be sensitive
indicators of animal condition and stress (Schreck et al.
1997). Although potential effects of transmitters or
attachment procedures on fish behavior cannot be
excluded, the small size of the transmitters and the
recapture of one tagged fish by angling within several
days indicate that any effects were probably minimal.
At the tournament, all 592 fish that were weighed in
were deemed to be alive; based on clinical indicators,
such as gill ventilation, this assessment is correct.
Given that most tournaments monitor only initial
mortality (e.g., Wilde et al. 2002), the presumption is
that tournament mortality rates are low. In our study, it
was apparent that groups of the live-released fish did
die within hours to days of release. No evidence of
mortality was seen in fish with negligible barotrauma,
and one of these fish was actually recaptured by an
angler several days after release. Conversely, 40% of
smallmouth bass with severe barotrauma died after
release. Two fish died within the first 48 h postrelease.
Although we did not observe any predation, in some
systems or in certain species, fish with signs of
barotrauma would be extremely susceptible to preda-
tors (e.g., Keniry et al. 1996).
Given that mortality was 40% for telemetered fish
with severe barotrauma and that 32% of all tourna-
ment-sampled fish exhibited severe barotrauma, we
BAROTRAUMA EFFECTS ON SMALLMOU TH BASS 613
calculate an overall tournament mortality rate of 12.8%
(i.e., 76 of the 592 smallmouth bass that were weighed
in). Relative to contemporary studies of catch-and-
release mortality at tournaments (summarized by
Cooke et al. 2002), this value is not remarkable.
However, relatively few studies have used telemetry to
assess delayed postrelease survival in black bass
tournaments. Usually, studies quantify initial mortality
(e.g., Wilde et al. 2002) or hold fish in pens or cages to
assess delayed mortality (see Wilde 1998); such
procedures may not be representative of conditions in
the wild (see Cooke and Schramm 2007). Considering
that water temperatures during the study period were
moderate for smallmouth bass (i.e., 148C; Schreer et al.
2001) and given the strong relationship between water
temperature and tournament mortality (Wilde 1998),
the level of mortality we documented would probably
have been higher at a summer tournament. However,
whether the incidence and consequences of barotrauma
vary seasonally is currently unclear. Interestingl y,
evidence to date suggests that tournament-related
mortality in black bass fisheries has negligible effects
at the population level (Hayes et al. 1995; Kwak and
Henry 1995; Edwards et al. 2004).
Blood samples obtained from smallmouth bass at the
tournament were used to characterize the physiological
condition of fish with negligible or severe barotrauma
and that of angled controls. The angled controls were
not subjected to tournament conditions, but some were
captured from depth. However, control fish, sampled
within seconds of capture, were intended to provide a
benchmark for background physiological condition.
Even tournament-caught fish with negligible barotrau-
ma had blood lactate and glucose levels that were
greater than those of controls. This is not surprising
given the immediate sampling of fish after a dry weigh-
in procedure that included exposure to air. Dry weigh-
in procedures have been shown to mobilize glucose,
deplete tissue energy stores (e.g., glycogen, ATP,
phosphocreatine), and lead to accumulation of muscle
and blood lactate in largemouth bass (Suski et al.
2004). In the analysis focused on telemetered fish with
known fates, severely barotraumatized fish that died
clearly had the highest blood glucose concentrations.
The fish that died also tended to have the highest levels
of blood lactate and the most elevated hematocrit;
however, these results were not significant. We suggest
that continued efforts by fish with severe barotrauma to
right themselves and maintain equilibrium and their
continued upside-down swimming led to mobilization
of glucose (hyperglycemia) and accumulation of the
anaerobic metabolite, lactate. Elevated blood lactate
could also be a result of hypoxia, which is produced by
gas bubbles that impair circulation (Beyer et al. 1976;
Morrissey et al. 2005). Cooke et al. (2004) noted
similar problems in largemouth bass exposed to low
levels of clove oil for transportation: fish that lost
equilibrium had greater cardiac disturbance as they
worked continually in an attempt to regain equilibrium.
The actual levels of glucose and lactate in the blood of
smallmouth bass at this tournament were often twice
those values recorded for smallmouth and largemouth
bass after exposure to a range of thermal, exercise, and
hypoxic stressors (e.g., Furimsky et al. 2003; Suski et
al. 2003, 2004, 2006) suggesting that the relative or
combined effects of tournament practices and baro-
trauma are significant.
Our study appears to be the first documentation of
elevated hematocrit associated with tournaments and
barotrauma. Although Morrissey et al. (2005) did not
measure hematocrit, they did measure plasma hemo-
globin and found evidence (i.e., elevated hemoglobin)
that red blood cells (RBCs) may be damaged by
decompression, potentially compromising their ability
to transport respiratory gases. The elevated hematocrit
may also reflect the fact that teleost fish regulate RBC
pH in the presence of a stress-induced acidosis (e.g.,
tournament- and barotrauma-induced lactate levels) by
activating RBC Na
exchange to minimize impair-
ment to oxygen transport (Nikinmaa et al. 1984; Perry
and Kinkead 1989). Given the concentrations of lactate
observed in this study, release of RBCs may also be a
compensatory mechanism to provide more capacity for
oxygen transport in the face of acidotic conditions. Our
work tends to support these conclusions, in that
elevated hematocrit could arise from the secretion of
splenic red blood cells in an effort to compensate for
damaged RBCs (which themselves can swell and
increase hematocrit) or the acidotic state of RBCs.
Unfortunately, we did not measure ions or osmolality,
so we cannot explore alternative explanations associ-
ated with hydromineral balance. Notably, however,
Morrissey et al. (2005) did not find plasma Cl
osmola lity differenc es between decompressed and
nondecompressed fish, which suggests that the most
parsimonious explanation for the elevated hematocrit
was release of additional RBCs. This indication of
tissue damage builds on the ideas presented by
Morrissey et al. (2005) and Rummer and Bennett
(2005) that decompression c an have catastrophic
physiological and anatomical consequences. Our study,
however, is the first to provide evidence that the
physiological disturbances in severely barotraumatized
fish that die are greater than those in barotraumatized
fish that survive.
Barotrauma has been identified as an important issue
in catch-and-release fisheries, including live-release
tournaments. We provide the first documentation of
614 GRAVEL AND CO OKE
behavioral impairments associated with barotrauma;
specifically, we demonstrated that not all fish with
barotrauma will survive when released in the wild. The
observation that one fish with severe barotrauma was
hit and killed by a boat has implications for live-release
tournament organizers. There is a need to consider the
release location and ensure that the site is proximal to
deep water and appropriate habitat and that it contains
minimal boat traffic. Tournament organizers should be
able to rapidly assess the magnitude of the barotrauma
issues by (1) examining the incidence of severe
bloating and loss of equilibrium during fish holding
in the live-release boat and (2) making decisions about
where to release the fish. Not all competitive angling
events for black basses result in barotrauma, and
although our focus is on a specific fishery, the findings
and research approach may have relevance to other
fisheries (e.g., for reef fishes).
This work also points to the need to develop
strategies for recompressing fish. Despite several
assessments of fizzing (i.e., use of hypodermic needles
to deflate distended swim bladders; reviewed in Kerr
2001), including several focused on black basses
(Shasteen and Sheehan 1997), few field assessments
of the long-term survival effects of fizzing have been
conducted aside from some mark–recapture studies
(e.g., Lee 1992). Telemetry studies are required to
compare the behavior and fate of fizzed fish with those
of nonfizzed individuals, including appropriate controls
and shams. In addition, other techniques that do not
require use of needles are needed, because needles can
puncture vital organs (Kerr 2001). Despite the fact that
other options exist (e.g., using milk crates or cages to
lower fish to depth or attaching weighted clips to fish;
see Kerr 2001; Theberge and Parker 2005), few
rigorous comparative assessments of these different
decompression techniques have been made (but see
study of rockfishes Sebastes spp. by Hannah and
Matteson 2007). In terms of live-release tournaments,
any solution must consider the realities of tournaments.
For example, as noted here and by Morrissey et al.
(2005), a substantial number of fish at tournaments can
suffer from barotrauma. Is it realistic to try to
individually recompress up to several hundred fish?
Some tournaments targeting walleyes Sander vitreus
penalize or prohibit fish with distended swim bladders
at weigh-in (Kerr 2001). This means that anglers must
either fish in shallow waters or must fizz their fish
before weigh-in. Again, without knowing the conse-
quences of fizzing on long-term survival, this regula-
tory approach contains inherent risk. In tournaments,
culling is a common practice; if fizzing is to be
encouraged, it should probably be done for culled fish
prior to release. In instances when tournament anglers
recognize that they are consistently landing barotrau-
matized fish, they should consider focusing their
angling efforts on shallower waters to maintain fish
welfare. Although placing the burden on the angler,
this approach is the most prudent given the lack of
current options. In addition, efforts to reduce all
stressors associated with competitive angling events
should continue (see Suski et al. 2004); such efforts
should focus on minimizing mortality, reducing
sublethal disturbances, and maintaining fish welfare
during the capture event, retention, weigh-in, and
release. Because stress is additive in fish, stress
preventative efforts are particularly important in
systems where barotrauma is common. Although the
focus of the paper was on a black bass competitive
angling event, the techniques used in this study (i.e.,
using telemetry and nonlethal physiological biopsy to
assess fate of angled fish) are relevant to other fisheries
and environments (e.g., coastal marine fisheries).
Primary support for this research activity was
provided by the Rainy Lake Fisheries Charity Trust.
Additional support was provided by the Canadian
Foundation for Innovation, the Ontario Research Fund,
and Carleton University. All research was conducted in
accordance with the Canadian Council for Animal Care
administered through Carleton University. The Ontario
Ministry of Natural Resources kindly supplied neces-
sary permits and logistic support. In particular, we
thank Linda Wall, Darryl McLeod, D. J. Mackintosh,
and Eric Fontaine. Dale LaBelle and Jody Shypit from
LaBelle’s Birch Point Camp kindly provided accom-
modations and a boat for tracking. Cory Suski provided
valuable comments on an earlier version of this
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