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PubMed1987

Neural mechanisms generating the leech swimming rhythm: swim-initiator neurons excite the network of swim oscillator neurons.

This paper describes newly identified excitatory connections linking the segmentally iterated swim-initiator interneurons with the network of oscillator neurons that generates the leech swimming rhythm. Apparently monosynaptic excitatory chemical connections are made from one class of swim-initiator neurons (cells 204/205) to several members of the swim oscillator network, including cells 28, 115 and, as described by Weeks (1982c), cell 208. A second class of swim-initiator neurons, cells 21 and 61, also excites this subset of the oscillator neurons. The unpaired swim oscillator neuron, cell 208, also chemically excites cells 28 and 115, apparently directly. Thus, in addition to its role as a member of the swim oscillator, the excitatory output from cell 208 to the swim oscillator adds to that provided by the swim-initiator neurons. The results of this paper enlarge the subset of identified swim oscillator neurons synaptically excited by the swim-initiator neurons. These newly described targets of the swim-initiators strengthen the hypotheses that: 1) the swim-initiator neurons supply much of the tonic excitatory drive responsible for activation and maintenance of the swim central motor program, and 2) the two classes of swim-initiators, cells 204/205 and cells 21/61, act synergistically to initiate and maintain swimming.

Animals↗

PubMed2002

Swimming and ammonia toxicity in salmonids: the effect of sub lethal ammonia exposure on the swimming performance of coho salmon and the acute toxicity of ammonia in swimming and resting rainbow trout.

This study tested the hypothesis that swimming exacerbates ammonia toxicity in fish. Both sub-lethal and acute toxicity testing was conducted in a swim tunnel on swimming and resting coho salmon and rainbow trout, respectively. The sub lethal tests on coho salmon also considered the compartmentalization of ammonia within the fish. Coho salmon showed a significant linear decrease in U(crit) both with increasing water ammonia (0, 0.02, 0.04 and 0.08 mg per l NH3) and increasing plasma ammonia. Data collected included plasma pH and ammonia, muscle pH and ammonia and muscle membrane potential. Based on results found in these experiments it was concluded that the reduction in swimming performance was due to both metabolic challenges as well as depolarization of white muscle. Acute toxicity testing on swimming and resting rainbow trout revealed that swimming at (60% U(crit) or approximately 2.2 body lengths/s) decreased the LC50 level from 207+/-21.99 mg N per l in resting fish to 32.38+/-10.81. The LC50 for resting fish was significantly higher than that for swimming fish. The acute value set forth by the US EPA at the same pH is 36.1 mg N per l and may not protect swimming fish. In addition the effect of water hardness on ammonia toxicity was considered. It was found that increased water calcium ameliorates ammonia toxicity in fish living in high pH water.

Ammonia↗

PubMed1983

The freely-chosen swimming stroke rate in a maximal swim and on a biokinetic swim bench.

The purpose of this study was to investigate the significance of the freely-chosen stroke rate (S) in swimming to attain maximum velocity. Seven club swimmers swam five 366-m freestyle trials, the first three at low to maximum velocities and the next two at higher stroke rates in an attempt to increase velocity further. A clear "inverted U" pattern was observed, the optimal stroke rate (Sopt) being the median rate of 45.8 (range 42-49) S X min-1. Each subject then performed a maximal experimental test on five separate occasions, simulating the freestyle arm action on a biokinetic swim bench. Stroke rate was manipulated according to the five rates used by each subject in the swim trials. The mean VO2peak on the biokinetic bench also varied as an "inverted U" curvilinear function of S, with the correlation between Sopt and the S at the highest VO2peak being 0.98 (P less than 0.001). Peak values for VO2, VE, and heart rate in simulated swimming were, respectively, 73%, 52%, and 85% of the maximal rates determined on a cycle ergometer. Maximum swimming velocity was not significantly correlated with VO2max or with VO2peak on the swim bench (P greater than 0.05). Results confirm that freely-chosen S produces the top performance in swimming to attain maximum velocity and the highest peak VO2 values in simulated swimming on a biokinetic bench.

Adolescent↗

PubMed1990

Costs of swimming measured at optimum speed: scale effects, differences between swimming styles, taxonomic groups and submerged and surface swimming.

1. Data on swimming energy expenditure of 30 submerged and nine surface swimmers, covering different swimming styles and taxonomic groups, are selected from the literature. 2. The costs of transport at the optimum speed are compared and related to body mass and Re numbers. 3. Fish and turtles use relatively less and most surface swimmers slightly more energy than the other submerged swimmers; man and mink are poorly adapted to swimming. 4. The metabolic rate in W at optimum speed is approximately equal to the body mass in kg for fish and turtles and three times the mass figure for the other submerged swimmers.

Animals↗

PubMed1995

Termination of leech swimming activity by a previously identified swim trigger neuron.

Cell Tr2 is a neuron in the subesophageal ganglion of the leech that can trigger swim episodes. In this report, we describe the ability of Tr2 to terminate ongoing swim episodes as well as to trigger swimming. Stimulation of Tr2 terminated ongoing swim episodes in nearly every preparation tested, while Tr2 stimulation triggered swim episodes in only a minority of the preparations. We suggest that the primary role of Tr2 is in the termination rather than the initiation of swimming activity. The swim trigger neuron Tr3 and a swim-gating neuron, cell 21, hyperpolarized during Tr2-induced swim termination. Another swim-gating neuron, cell 204 was sometimes slightly excited, but more often, hyperpolarized during Tr2-induced swim termination. In contrast to these cells, Tr2 stimulation excited another swim-gating neuron, cell 61. The responses of the swim-gating cells were variable in amplitude and sometimes not evident during Tr2-induced swim termination. Hence, the effects of Tr2 stimulation on swim-gating neurons seem unlikely to be the direct cause of swim termination. Oscillator cells examined during Tr2-induced swim termination include: 27, 28, 33, 60, 115, and 208. The largest effect seen in an oscillator neuron was in cell 208, which was repolarized by up to 10 mV during Tr2 stimulation. Tr2 stimulation did not produce any obvious synaptic effects in motor neurons DI-1, VI-1, and DE-3. Our findings indicate that other, yet undiscovered, connections are likely to be important in Tr2-induced swim termination. Therefore, we propose that cell Tr2 is probably a member of a distributed neural network involved in swim termination.

Animals↗

PubMed2002

Energetics of median and paired fin swimming, body and caudal fin swimming, and gait transition in parrotfish (Scarus schlegeli) and triggerfish (Rhinecanthus aculeatus).

To determine the energetic costs of rigid-body, median or paired-fin (MPF) swimming versus undulatory, body-caudal fin (BCF) swimming, we measured oxygen consumption as a function of swimming speed in two MPF swimming specialists, Schlegel's parrotfish and Picasso triggerfish. The parrotfish swam exclusively with the pectoral fins at prolonged swimming speeds up to 3.2 total lengths per second (L s(-1); 30 min critical swimming speed, U(crit)). At higher speeds, gait transferred to a burst-and-coast BCF swimming mode that resulted in rapid fatigue. The triggerfish swam using undulations of the soft dorsal and anal fins up to 1.5 L s(-1), beyond which BCF undulations were recruited intermittently. BCF swimming was used continuously above 3.5 L s(-1), and was accompanied by synchronous undulations of the dorsal and anal fins. The triggerfish were capable of high, prolonged swimming speeds of up to 4.1 L s(-1) (30 min U(crit)). In both species, the rates of increase in oxygen consumption with swimming speed were higher during BCF swimming than during rigid-body MPF swimming. Our results indicate that, for these species, undulatory swimming is energetically more costly than rigid-body swimming, and therefore support the hypothesis that MPF swimming is more efficient. In addition, use of the BCF gait at higher swimming speed increased the cost of transport in both species beyond that predicted for MPF swimming at the same speeds. This suggests that, unlike for terrestrial locomotion, gait transition in fishes does not occur to reduce energetic costs, but to increase recruitable muscle mass and propulsive surfaces. The appropriate use of the power and exponential functions to model swimming energetics is also discussed.

Animals↗

PubMed1995

Relationship between oxygen uptake, stroke rate and swimming velocity in competitive swimming.

The purpose of this study was to determine the relationship between oxygen demand, stroke rate and swimming velocity in competitive swimmers. The subjects who volunteered for this study were ten trained male swimmers (age, 16.7 +/- 0.4 yrs). VO2peak, swimming velocities at 80% (V80% VO2peak) and 100% (V100% VO2peak) of VO2peak and swimming velocity at the onset of blood lactate accumulation (VOBLA) were determined during a swimming economy profile test in a swimming flume. In the swimming economy test, determined by studying the relationship between oxygen uptake and swimming velocity cubed, the subjects were instructed to swim for six minutes at five or six submaximal swimming velocities. Steady-state oxygen uptake and stroke rate were calculated during the final two minutes of swimming. Results indicated that there were significant correlations between oxygen uptake and swimming velocity cubed (r = 0.963 to 0.998, p < 0.01), between oxygen uptake and stroke rate (r = 0.925 to 0.998, p < 0.01) and between stroke rate and swimming velocity cubed (r = 0.897, p < 0.05; to 0.994, p < 0.01) for all subjects. Furthermore, it was found that the slopes of the regression lines between oxygen uptake and swimming velocity cubed and between oxygen demand and stroke rate were significantly correlated to swimming performance indices (V80% VO2peak, V100% VO2peak and VOBLA). The results of this study suggest that the slope of the regression line between oxygen uptake and stroke rate can be utilized as an effective index of evaluating swimming performance.

Adolescent↗

PubMed2000

Scratch-swim hybrids in the spinal turtle: blending of rostral scratch and forward swim.

Turtles with a complete transection of the spinal cord just posterior to the forelimb enlargement at the D2-D3 segmental border produced coordinated rhythmic hindlimb movements. Ipsilateral stimulation of cutaneous afferents in the midbody shell bridge evoked a rostral scratch. Electrical stimulation of the contralateral dorsolateral funiculus (DLF) at the anterior cut face of the D3 segment activated a forward swim. Simultaneous stimulation of the ipsilateral shell bridge and the contralateral DLF elicited a scratch-swim hybrid: a behavior that blended features of both rostral scratch and forward swim into each cycle of rhythmic movement. This is the first demonstration of a scratch-locomotion hybrid in a spinal vertebrate. The rostral scratch and the forward swim shared some characteristics: alternating hip flexion and extension, similar timing of knee extensor activity within the hip cycle, and a behavioral event during which force was exerted against a substrate. During each cycle, each behavior exhibited three sequential stages, preevent, event, and postevent. The rostral scratch event was a rub of the foot against the stimulated shell site. The forward swim event was a powerstroke, a hip extension movement with the foot held in a vertical position with toes and webbing spread. The two behaviors differed with respect to several features: amount of hip flexion and extension, electromyogram (EMG) amplitudes, and EMG duty cycles. Scratch-swim hybrids displayed two events, the scratch rub and the swim powerstroke, within each cycle. Hybrid hip flexion excursion, knee extensor EMGs, and hip flexor EMGs were similar to those of the scratch; hybrid hip extension excursion and hip extensor EMGs were similar to those of the swim. The hybrid also had three sequential stages during each cycle: 1) a combined scratch prerub and swim postpowerstroke, 2) a scratch rub that also served as a swim prepowerstroke, and 3) a swim powerstroke that also served as a scratch postrub. Merging of the rostral scratch with the forward swim was possible because of similarities between the sequential stages of the two forms, making them biomechanically compatible for hybrid formation. Kinematic and myographic similarities between the rostral scratch and the forward swim support the hypothesis that the two behaviors share common neural circuitry. The common features of the sequential stages of each behavior and the production of scratch-swim hybrids provide additional support for the hypothesis of a shared core of spinal cord neurons common to both rostral scratch and forward swim.

Afferent Pathways↗

PubMed2003

To swim or not to swim: regional effects of serotonin, octopamine and amine mixtures in the medicinal leech.

Focally treating the head brain of the medicinal leech Hirudo medicinalis with various biogenic amines affected the initiation, termination and maintenance of fictive swimming (i.e., the neural correlate of swimming). Application of serotonin to saline surrounding only the head brain inhibited fictive swimming, whereas removing serotonin induced swimming. This contrasts sharply with previous observations that serotonin applied to the nerve cord induces swimming. Although application of octopamine to the brain activated swimming, a mixture of octopamine and serotonin inhibited swimming. Subsequent removal of this mixture from the brain activated robust swimming and was more potent for activating swimming than either the removal of serotonin or the application of octopamine. Swim episodes induced by brain-specific manipulations of octopamine had more swim bursts per episode than those induced by serotonin. These brain-specific effects of the amines on fictive swimming are probably due to the modulation of higher-order circuits that control locomotion in the leech. We observed that serotonin or a mixture of serotonin and octopamine hyperpolarized an identified descending brain interneuron known as Tr2. Removal of the mixture caused Tr2 to exhibit membrane potential depolarizations that correlated in time with the expression of swim episodes.

Amines↗

PubMed1992

A simple method for determining critical speed as swimming fatigue threshold in competitive swimming.

The purpose of this investigation was to determine whether the concept of the critical power could be applied to competitive swimming by using critical swimming speed (CS) as determined both in the swimming flume (CS-flume) and in the normal swimming pool (CS-pool) and whether CS could be utilized as a practical index for assessing a swimmer's endurance performance. CS defined as the swimming speed which could be theoretically maintained continuously without exhaustion was expressed as the slope of a regression line between swimming distance (D) and its duration (T) obtained at various swimming speeds. Eight highly trained swimmers were instructed to swim until onset of fatigue at four predetermined swimming speed levels in the swimming flume and at maximal effort over four different swimming distances in the swimming pool. In the results of CS-flume and CS-pool, the regression relations between D and T were expressed in the general form, D = a+b x T, with r2 being higher than 0.998 (p less than 0.01), respectively. These results both from the flume and the pool indicated extremely good linearity. Furthermore, maximal oxygen uptake (VO2max) during the incremental exercise test, swimming speed corresponding 4 mM of blood lactate concentration (V-OBLA) and mean velocity in the 400 m freestyle (V-400) were measured on each subject.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1998

Swimming performance of delta smelt: maximum performance, and behavioral and kinematic limitations on swimming at submaximal velocities.

Swimming performance, measured as critical swimming velocity (Ucrit) and endurance, and swimming behavior and kinematics were measured in delta smelt Hypomesus transpacificus, a threatened estuarine planktivore. Most fish (58 % of the Ucrit test group) were capable of achieving and sustaining moderately high velocities: mean Ucrit was 27.6±5.1 cm s-1 (s.d.). Ucrit was not affected by either acclimation temperature (1221 °C) or fish size (3.26.8 cm standard length) and was generally comparable with values measured for other similarly sized fishes. The remaining 42 % of the fish failed to swim at velocities above 1015 cm s-1. Interestingly, of the fish that provided a Ucrit measurement, 62 % experienced at least one temporary swimming failure between 10 and 20 cm s-1. Endurance was highly variable and, for all velocities, not normally distributed; the only significant decrease, from 6 h to 64 min, occurred between 10 and 15 cm s-1. Kinematic analyses of stroke frequency, stroke amplitude, stride length, glide frequency, glide duration, proportion of time spent stroking and the number of strokes between successive glides showed that delta smelt employed three velocity-dependent swimming gaits: a discontinuous 'stroke-and-glide' swimming behavior below 10 cm s-1; a continuous swimming behavior above 15 cm s-1 and up to Ucrit; and a discontinuous 'burst-and-glide' swimming behavior at velocities above Ucrit. Swimming failure at velocities between 10 and 20 cm s-1 coincided with the transition from 'stroke-and-glide' swimming to continuous swimming; delta smelt were unable or unwilling to swim steadily in the flume within this transition velocity range. These results underscore the importance of monitoring and quantifying behavior in experiments intended as physiological performance tests of whole animals.

Journal Article↗

PubMed1986

Initiation of swimming activity by trigger neurons in the leech subesophageal ganglion. II. Role of segmental swim-initiating interneurons.

Cell Tr1, a trigger neuron found in the subesophageal ganglion of the leech, Hirudo medicinalis, is part of a network of subesophageal ganglion neurons which control swimming activity, and makes apparently direct connections to swim-initiating interneurons (SIIs; cells 204 and 205). In this study, we investigated the role of SIIs in swim initiation by cell Tr1. We also examined how brief Tr1 activity controls swim initiation at the levels of the SIIs and of the oscillator neurons. We found: In shortened nerve cord preparations consisting of the head ganglion (supra- and subesophageal ganglia) through segmental ganglia 11 or 12, the effectiveness of swim initiation by Tr1 stimulation was highly correlated with the concurrent injection of depolarizing or hyperpolarizing current into a single cell 204. Tr1 stimulation causes sustained excitation in SIIs, serotonin-containing interneurons and Retzius cells, independent of whether or not swimming is initiated. A short, depolarizing current pulse injected simultaneously into as many as three 204 cells does not replicate the sustained excitation evoked in these cells by Tr1 stimulation. An oscillator neuron, cell 208, is inhibited when Tr1 stimulation fails to elicit swimming, but receives excitatory input from Tr1 otherwise. In another oscillator neuron, cell 115, stimulation of Tr1 suppressed an unidentified source of inhibitory synaptic potentials only on trials which resulted in swim initiation. We conclude that Tr1 stimulation triggers swimming by activating a long-lasting ramp depolarization in the SIIs which, in turn, provide excitatory drive to the swim oscillator. Moreover, Tr1 initiates swimming only when inhibitory inputs to the swim oscillator are suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2002

Evidence for corticotropin-releasing factor regulation of serotonin in the lateral septum during acute swim stress: adaptation produced by repeated swimming.

RATIONALE: Swim stress decreases extracellular serotonin (5-HT) levels in the rat lateral septum, and adaptation to this effect occurs with repeated swimming. Corticotropin-releasing factor (CRF) administered into the dorsal raphe nucleus (DRN) also decreases 5-HT release in the lateral septum, suggesting that CRF may mediate the effects of swim stress. OBJECTIVES: The hypothesis that endogenous CRF mediates the reduction of 5-HT levels in the lateral septum evoked by swim stress and is involved in the adaptation that occurs with repeated swim stress was tested. METHODS: Extracellular 5-HT levels in rat lateral septum were quantified by means of in vivo microdialysis. Extracellular single unit activity was recorded from the DRN. RESULTS: Intracerebroventricular (i.c.v.) administration of a CRF receptor antagonist prevented the ability of swim stress to decrease 5-HT release in the lateral septum. Prior exposure to swim stress reduced the ability of both CRF (i.c.v.) and a subsequent swim stress to decrease lateral septum 5-HT release (cross adaptation). Additionally, the effects of CRF, administered into the DRN, on DR neuronal discharge were attenuated in rats with a history of swim stress. Finally, administration of a CRF receptor antagonist (i.c.v.) between two swim stress sessions restored the neurochemical response to swim stress (i.e., 5-HT levels were reduced during the second exposure to swim). CONCLUSIONS: Endogenous CRF modulates 5-HT transmission during acute environmental stress and is also integral to adaptation of the 5-HT response produced by repeated stress. Modulation of the 5-HT system by CRF during acute stress may underlie certain coping behaviors, while stress-induced adaptation of this effect may be involved in psychiatric manifestations of repeated stress.

Analysis of Variance↗

PubMed2002

Effects of temperature on sustained swimming performance and swimming kinematics of the chub mackerel Scomber japonicus.

The effects of a 6 degrees C difference in water temperature on maximum sustained swimming speed, swimming energetics and swimming kinematics were measured in the chub mackerel Scomber japonicus (Teleostei: Scombridae), a primarily coastal, pelagic predator that inhabits subtropical and temperate transition waters of the Atlantic, Pacific and Indian Oceans. New data for chub mackerel acclimated to 18 degrees C are compared with published data from our laboratory at 24 degrees C. Twelve individuals acclimated to each of two temperatures (15.6-26.3 cm fork length, FL, and 34-179 g at 18 degrees C; 14.0-24.7 cm FL and 26-156 g at 24 degrees C) swam at a range of speeds in a temperature-controlled Brett-type respirometer, at the respective acclimation temperature. At a given fish size, the maximum speed that S. japonicus was able to maintain for a 30-min period, while swimming steadily using slow, oxidative locomotor muscle (U(max,c)), was significantly greater at 24 than at 18 degrees C (52.5-97.5 cm s(-1) at 18 degrees C and 70-120 cm s(-1) at 24 degrees C). At a given speed and fish size, the rate of oxygen consumption (VO(2)) was significantly higher at 24 than at 18 degrees C because of a higher net cost of transport (1073-4617 J km(-1) kg(-1) at 18 degrees C and 2708-14895 J km(-1) kg(-1) at 24 degrees C). Standard metabolic rate, calculated by extrapolating the logO(2) versus swimming speed relationship to zero speed, did not vary significantly with temperature or fish mass (126.4+/-67.2 mg O(2) h(-1) kg(-1) at 18 degrees C and 143.2+/-80.3 mg O(2) h(-1) kg(-1) at 24 degrees C; means +/- S.D., N=12). Swimming kinematics was quantified from high-speed (120 Hz) video recordings analyzed with a computerized, two-dimensional motion-analysis system. At a given speed and fish size, there were no significant effects of temperature on tail-beat frequency, tail-beat amplitude or stride length, but propulsive wavelength increased significantly with temperature as a result of an increase in propulsive wave velocity. Thus, the main effects of temperature on chub mackerel swimming were increases in both U(max,c) and the net cost of swimming at 24 degrees C. Like other fishes, S. japonicus apparently must recruit more slow, oxidative muscle fibers to swim at a given sustainable speed at the lower temperature because of the reduced power output. Thus, the 24 degrees C mackerel reach a higher speed before they must recruit the fast, glycolytic fibers, thereby increasing U(max,c) at 24 degrees C. By quantifying in vivo the effects of temperature on the swimming performance of an ectothermic species that is closely related to the endothermic tunas, this study also provides evidence that maintaining the temperature of the slow, oxidative locomotor muscle at 6 degrees C or more above ambient water temperature in tunas should significantly increase sustainable swimming speeds, but also increase the energetic cost of swimming, unless cardiac output limits muscle performance.

Animals↗

PubMed1999

Effects of moderate dietary manipulations on swim performance and on blood lactate-swimming velocity curves.

Blood lactate responses are commonly employed for evaluation and prescription of training programmes. The purpose of the present studies was to examine the effects of dietary manipulations on both swim performance and on the relationship between blood lactate and swimming velocity. The first study engaged 8 subjects in a regimen to reduce muscle glycogen by a combination of diet and training. Subjects were monitored under a normal mixed diet comprising 53.6+/-7.8% carbohydrate (CHO) and under a decreased CHO condition (39.4+/-10.7% CHO) over 3 days. Mean swim performance decreased significantly (P<0.05) over 400 yards as a result of the carbohydrate reduction regimen. Mean blood lactates were reduced as a consequence of the glycogen depletion regimen following swims at 85% and 100% of maximum velocities. The swimming velocity corresponding to 4 mM blood lactate (V-4 mM) was altered from 0.67+/-0.04 m x s(-1) on a mixed diet to 0.70+/-0.05 m x s(-1) on a CHO-reduced diet. The second study employed 7 subjects in a regimen to enhance muscle glycogen stores. Subjects were monitored over 3 days under a normal diet (52.7+/-4.4% CHO) and on a separate occasion under an increased CHO intake (59.2+/-3.7% CHO). In contrast to the first study, mean swim performance improved over 100 yards and 400 yards (P<0.05). Mean blood lactates were evaluated after the carbohydrate-rich regimen at both 85% and 100% swim velocities (P<0.05). The mean swim velocity associated with V-4mM was paradoxically reduced from 0.69+/-0.05 to 0.67+/-0.04 m x s(-1) as a result of the increased CHO condition. The results indicate that a moderate reduction in CHO intake alters swimming performance adversely whereas a moderate elevation in CHO intake above the normal diet improves performance. The dietary manipulations affected the response of blood lactate to both submaximal and maximal swimming velocities. The observations highlight the limitations of applying lactate response curves to swim training.

Adolescent↗

PubMed1988

Forced swimming test in rats: effect of desipramine administration and the period of exposure to the test on struggling behavior, swimming, immobility and defecation rate.

The effect of desipramine administration and the duration of the daily exposure to forced swimming on some variables has been studied in adult male rats. Desipramine administration (15 mg/kg) significantly increased struggling behavior in the first and second 5-min periods of a single exposure to forced swimming. Swimming was reduced in the first 5 min and remained unchanged thereafter. Immobility was decreased in the second and the third 5-min periods. After a pre-exposure to forced swimming for 15 min the day before, the drug was effective in increasing struggling behavior and reducing immobility during a subsequent 5-min test. Swimming was not modified. Daily exposure to forced swimming for 3 days caused a decline in struggling behavior and swimming, while increasing immobility and the defecation rate. The duration of daily exposure to forced swimming did not alter the changes in the variables measured. The present results indicate that a one-day test can be used to discriminate between saline- and desipramine-treated rats, and that struggling behavior could be a reliable measure of the positive action of antidepressants. The finding that behavioral changes over the 3 days were independent of the duration of exposure to swimming argues against the interpretation of the results which suggest that the responses are caused by the appearance of a behavioral despair state, and suggests that these behaviors might be trait-markers in the rat. In addition, the changes in struggling behavior and immobility over the 3 days cannot be attributed to a behavioral adaptation to the test because the defecation rate increased rather than decreased during successive forced swimming tests.

Animals↗

PubMed1998

Prolonged swimming, recovery and repeat swimming performance of mature sockeye salmon Oncorhynchus nerka exposed to moderate hypoxia and pentachlorophenol.

Mature, wild sockeye salmon (Oncorhynchus nerka) demonstrated their remarkable stamina and recovery abilities by performing three consecutive critical swimming speed tests with only a 45 min interval for recovery between subsequent tests. Although the repeated swimming challenges were performed without a full recovery, normoxic fish swam just as well on the second swim, and the majority of fish swam only marginally more poorly on the third swim. In addition, metabolic loading in these fish, as measured by the rate of oxygen consumption, ventilation rate and plasma lactate levels during recovery, did not appear to be cumulative with successive swims. Fish, however, did not recover as well after a similar level of initial swimming performance under moderately hypoxic conditions (water PO2>100 mmHg; 1 mmHg=0.1333 kPa). Four out of the five fish did not swim again and their high plasma lactate levels indicated a greater anaerobic effort. In another group of fish, metabolic loading (elevated control rates of oxygen consumption) was induced with an overnight sublethal exposure to pentachlorophenol, but these fish swam as well as normoxic fish on the first swim, and five of the six fish swam for a third time at a marginally lower critical swimming speed. In contrast to expectations, pentachlorophenol pretreatment and moderate hypoxia were not additive in their effects. Instead, the effects resembled those of pentachlorophenol pretreatment alone. The results are discussed in terms of what aspects of fatigue might impair the repeat swimming performance of sockeye salmon.

Animals↗

PubMed2003

Effect of cold acclimation and repeated swimming on opioid and nonopioid swim stress-induced analgesia in selectively bred mice.

Swiss-Webster mice selectively bred for high swim stress-induced analgesia (SSIA) were exposed to continuous ambient cold (5 degrees C) for 6 weeks or to daily 3-min swims for 14 consecutive days either in 20 or 32 degrees C water. Thereafter, mice subjected to the particular procedure were injected intraperitoneally with 10 mg/kg of naltrexone HCl and were tested for modification of the opioid and nonopioid component of SSIA. SSIA was reduced following swims at either water temperature and was antagonized by naltrexone to greater extent than in nonswimming mice. Thus, the nonopioid (i.e. naltrexone-resistant) portion of the overall SSIA was significantly reduced, whereas the opioid (naltrexone-sensitive) portion became relatively augmented. In contrast, SSIA differed neither in magnitude nor in sensitivity to naltrexone between cold-acclimated and unacclimated mice. Swim hypothermia as well as the nonopioid component of SSIA were decreased after repeated swimming at 32 and 20 degrees C, but remained unchanged after cold acclimation. This argues for the essential role of an extrathermal, probably emotional in nature, factor not only in the elicitation of nonopioid SSIA, but also in the modulation of thermoregulatory processes during swimming. We suggest that the emergency component of swim stress, together with initial moderate hypothermic challenge, first produces the opioid form of SSIA, and subsequently, as the swim continues, also affects the thermoregulatory processes maintaining thermal homeostasis. This causes further increase in swim hypothermia and raises its stressing property to induce the nonopioid form of SSIA.

Acclimatization↗