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Serotonergic modulation of swimming speed in the pteropod mollusc Clione limacina. III. Cerebral neurons.

Swim acceleration in Clione limacina can occur via central inputs to pattern generator interneurons and motor neurons and through peripheral inputs to the swim musculature. In the previous paper, peripheral modulation of the swim muscles was shown to increase wing contractility. In the present paper, central inputs are described that trigger an increase in swim frequency and an increase in motor neuron activity. In dissected preparations, spontaneous acceleration from slow to fast swimming included an increase in the cycle frequency, a baseline depolarization in the swim interneurons and an increase in the intensity of motoneuron firing. Similar effects could be elicited by bath application of 10(-5) mol l-1 serotonin. Two clusters of cerebral serotonin-immunoreactive interneurons were found to produce acceleration of swimming accompanied by changes in neuronal activity. Posterior cluster neurons triggered an increase in swim frequency, depolarization of the swim interneurons, an increase in general excitor motoneuron activity and activation of type 12 interneurons and pedal peripheral modulatory neurons. Cells from the anterior cerebral cluster also increased swim frequency, increased activity in the swim motoneurons and activated type 12 interneurons, pedal peripheral modulatory neurons and the heart excitor neuron. The time course of action of the anterior cluster neurons did not greatly outlast the duration of spike activity, while that of the posterior cluster neurons typically outlasted burst duration. It appears that the two discrete clusters of serotonin-immunoreactive neurons have similar, but not identical, effects on swim neurons, raising the possibility that the two serotonergic cell groups modulate the same target cells through different cellular mechanisms.

Animals↗

Swimming and the risk of cutaneous melanoma.

Recreational exposure to the sun may not explain fully current trends in melanoma incidence. The hypothesis was examined whether carcinogens in water play a role in the development of cutaneous melanoma. In a case-control study, 128 melanoma patients and 168 patients with other types of malignancy completed a detailed questionnaire on aquatic leisure time activities. All relative risk estimates were adjusted for age, gender, educational level, pigmentation characteristics, and exposure to sun habits. Regular swimming during the summer months in swimming pools and in open waters such as rivers and seas before the age of 15 years, was associated with odds ratios of 2.20 (95% confidence interval (CI), 1.05-4.62) and 2.41 (95% CI, 1.04-5.58), respectively, compared with no swimming at all or swimming in relatively unpolluted waters, such as lakes and fens. Melanoma patients learned to swim at a younger age; compared with those who never learned to swim or who learned to swim after the age of 12 years, the odds ratio was 1.87 (95% CI, 0.91-3.78) for those who learned to swim at ages 9-12 years, and 2.22 (95% CI, 1.16-4.26) for those who learned to swim before 9 years of age. Compared with persons who had no swimming certificates, an odds ratio of 1.25 (95% CI, 0.71-2.23) was found for persons with one or two certificates, and an odds ratio of 2.96 (95% CI, 1.25-6.96) for persons with three or more certificates. The positive association between a history of swimming and melanoma risk suggests that carcinogenic agents in water, possibly chlorination by products, play a role in melanoma aetiology.

Adolescent↗

The VO2 slow component in swimming.

All studies on the oxygen uptake (VO2) slow component have been carried out for the sporting disciplines of cycling or running, but never for swimming. Considering that front crawl swimming is a sport discipline that is fundamentally different from both running and cycling, the aim of this study was to verify whether this slow component also appears in swimming. Six elite pentathletes were tested in a swimming flume while front crawl swimming to exhaustion. Swimming velocity for the slow component test was determined as v50% delta = CV + [vVO2peak - CV)/2], where CV is the critical velocity and vVO2peak the lowest velocity at which peak VO2 occurred. To set the subject's CV, expressed as the slope of a straight line that describes the correlation between swimming distance and time, the record times over three swimming distances were recorded in a 50 m swimming pool. The vVO2peak was measured by means of an incremental test in the swimming flume. Gas exchange was measured by means of a telemetric metabolimeter (K4 RQ, Cosmed, Italy) that was connected to a snorkel. The slow component was found in all subjects, with a mean (SD) value of 239 (194) mlO2.min-1. Therefore, although front crawl swimming is fundamentally different from both running and cycling, it appears that it also incurs a VO2 slow component. The origin of this phenomenon, however, is even more uncertain than for the other sport disciplines.

Adolescent↗

Insulin and glucagon secretion in swimming mice: effects of autonomic receptor antagonism.

To study the regulation of islet hormone secretion in exercise-stress, we developed a swimming mouse model. Mice swam for 2, 6, or 10 minutes whereafter blood was sampled for analysis of plasma levels of insulin, glucagon, and glucose. Plasma insulin levels, which were not different from resting controls after 2 or 6 minutes of swimming, were slightly lower after 10 minutes of swimming (P less than .05). Plasma glucagon levels were increased after 2, 6, and 10 minutes of swimming (P less than .001), and plasma glucose levels were lower after 6 and 10 minutes of swimming (P less than .05). Glucose (5.6 mmol/kg)-stimulated insulin secretion was inhibited by 52% +/- 9% by the swimming (P less than .001). The mechanisms behind this inhibition of glucose-stimulated insulin secretion and the increase in basal plasma glucagon levels induced during 2 minutes of swimming were investigated by the use of autonomic receptor antagonists, administered intraperitoneally 20 minutes before the swimming period. The ganglionic antagonist hexamethonium (56 mumols/kg) prevented the swimming-induced inhibition of glucose-stimulated insulin secretion, indicating involvement of nerves in the inhibition. Also the nonselective alpha-adrenoceptor antagonist phentolamine (6.0 mumols/kg) and the alpha 2-adrenoceptor antagonist yohimbine (3.6 mumols/kg) prevented the inhibition of glucose-stimulated insulin secretion induced by swimming, whereas the beta-adrenoceptor antagonist L-propranolol (9.6 mumols/kg) had no effect. The swimming-induced increase in plasma glucagon levels was partially inhibited by hexamethonium by (58% +/- 24%, P less than .05). Phentolamine and yohimbine totally prevented the increase in plasma glucagon levels, whereas L-propranolol had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Role of mu-opioid and NMDA receptors in the development and maintenance of repeated swim stress-induced thermal hyperalgesia.

Repeated exposure to swimming stress induces a long-lasting hyperalgesia in the rat by mechanisms to be elucidated. Since opioid and glutamate neurotransmitter systems modulate pain, we now evaluated the effect of pharmacological blockade of opioid and glutamate receptors subtypes on forced swimming stress-induced hyperalgesia. Male rats were daily subjected to 10-20 min of forced or sham swimming for 3 days and thermal nociception was estimated twice, before each behavioral conditioning and 24 h after the last, using hot plate test. Selective opioid and NMDA receptor antagonists were administered i.p. either before each conditioning session or before the second nociception assessment. Unlike sham swimming rats, forced swimming rats showed significant reductions in hot plate response latencies (hyperalgesia) after the last swimming session, as compared to pre-stress values. Rats treated with the opioid receptor antagonists naloxone (0.1 mg/kg, non-subtype-selective) and naloxonazine (5 mg/kg, mu(1)-subtype-selective), before each forced swimming, did not become hyperalgesic, whereas those treated before the second post-stress assessment of nociception developed hyperalgesia. Naltrindole (0.5 mg/kg, delta-subtype-selective) and nor-binaltorphimine (0.5mg/kg, kappa-subtype-selective) were inactive in both administration schedules. The efficacy of morphine (3-7.5 mg/kg) to produce analgesia in forced swimming rats was lower than in sham swimming rats. Rats treated with the NMDA antagonist ketamine (5 mg/kg) before the forced swimming or the second post-stress assessment of nociception did not have hyperalgesia. Thus, swim stress-induced hyperalgesia might be initiated by the repeated stimulation of mu-opioid and NMDA receptors but maintained only by the activity of NMDA receptors.

Analysis of Variance↗

Ventilation tubes after surgery for otitis media with effusion or acute otitis media and swimming. Systematic review and meta-analysis.

OBJECTIVE: To determine if the use of ear protection when swimming of children with ventilation tubes modifies the risk of acute otitis media (AOM) compared to not swimming. METHODS: Systematic review. DATA SOURCES: Search conducted in MEDLINE, EMBASE and The Cochrane Library databases. STUDY SELECTION: Prospective cohort studies and controlled clinical trials of children with ventilation tubes, with a minimum follow-up of 2 months. DATA EXTRACTION: Two reviewers independently assessed trial quality and extracted data. RESULTS: 11 studies were selected. No difference was found in risk of AOM in children who swim without ear protection compared with those who do not swim: Odds ratio=0.78, 95% confidence interval 0.42-1.44; nor compared with those who use earplugs and swimming caps, odds ratio=0.75, 95% confidence interval 0.38-1.48; nor in those who use ear drops after swimming compared with those who used earplugs or swimming caps, odds ratio=0.76, 95% confidence interval 0.56 to 1.02. The use of ear drops after swimming increases the risk of AOM in children with ventilation tubes as compared with those who do not swim, odds ratio=3.14, 95% confidence interval 1.40 to 7.05. CONCLUSIONS: There is no evidence to suggest that protection when swimming with earplugs, swimming caps or ear drops in children with ventilation tubes reduces the risk of AOM. Ear drops may even increase this risk.

Adolescent↗

Neither forced running nor forced swimming affect acute pyridostigmine toxicity or brain-regional cholinesterase inhibition in rats.

Stress-induced change in the distribution of the drug pyridostigmine (PYR) has been proposed as a contributing factor to unexplained illnesses in Persian Gulf War veterans. We evaluated the effects of two stress models, forced running and forced swimming, on acute PYR (30 mg/kg, p.o.) toxicity and cholinesterase (ChE) inhibition in the blood and selected brain regions of young adult male Sprague-Dawley rats (6 weeks of age). Plasma corticosterone levels were measured at 0, 1 and 3 h after termination of forced swimming or forced running to confirm the induction of stress. PYR was given either immediately before stress (15 min swimming; 20 min running) or immediately after stress (15 min swimming; 90 min running) and cholinergic toxicity and ChE inhibition were evaluated at 1, 2 or 4 h after PYR exposure. Additionally, rats were subjected to either swimming (15 min) or running (90 min) stress, anesthetized, injected with horseradish peroxidase (HRP, 100 mg/kg, transcardial) and brain-regional HRP activity measured as an indicator of altered blood-brain barrier integrity. Both forced swimming and forced running resulted in significant elevations of plasma corticosterone levels. PYR caused cholinergic toxicity at all time-points evaluated. Swimming and running stress had little influence on expression of PYR-induced toxicity, however. Blood ChE activity was generally inhibited 77-91% at 1-4 h after PYR, but rats pretreated with PYR prior to forced swimming showed lesser inhibition (64%) 1 h after dosing, possibly because of swimming-induced hypothermia and delayed absorption of the drug. Minimal changes in ChE activity were noted in frontal cortex, cerebellum and hippocampus following PYR exposure (maximal inhibition 28%), and neither swimming nor running stress affected the degree of inhibition. Neither stress model increased HRP accumulation in any brain region. The results suggest that stress associated with forced running or forced swimming has little effect on acute PYR toxicity, entry of PYR into the brain or PYR-induced brain-regional ChE inhibition.

Administration, Oral↗

Validation of the 12-minute swim as a field test of peak aerobic power in young women.

The purposes of this study were to validate the 12-min swim as a field test of VO2 peak in female recreational swimmers and to compare its validity with that of the 12-min run. The results are contrasted with those previously reported on a comparable group of male recreational swimmers. Thirty-four young women completed 12-min swim, 12-min run, tethered swimming VO2 peak, and treadmill running VO2 peak tests within 3 weeks. Mean (+/- SD) 12-min swim and run distances were 597 +/- 82 and 2,313 +/- 317 m, and mean tethered swim and treadmill run VO2 peak values were 39.2 +/- 4.9 and 45.4 +/- 6.3 ml.kg BW-1.min-1, respectively. Correlation coefficients and standard errors of estimate for predictions of swimming VO2 peak from the 12-min swim (.42 and 4.5 ml.kg BW-1.min-1) and run (.58 and 4.1 ml.kg BW-1.min-1) and for predictions of treadmill run VO2 peak from the 12-min swim (.34 and 6.0 ml.kg BW-1.min-1) and run (.87 and 3.2 ml.kg BW-1.min-1) indicated that the 12-min run was a more accurate predictor of tethered swim or treadmill run VO2 peak than the 12-min swim. These data are in close agreement with our previous study on young male recreational swimmers. We conclude that the 12-min swim has relatively low validity as a field test of peak aerobic power and that it is not an equally valid alternative to the 12-min run in young adult female recreational swimmers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Effects of swimming on functional recovery after incomplete spinal cord injury in rats.

One of the most promising rehabilitation strategies for spinal cord injury is weight-supported treadmill training. This strategy seeks to re-train the spinal cord below the level of injury to generate a meaningful pattern of movement. However, the number of step cycles that can be accomplished is limited by the poor weight-bearing capability of the neuromuscular system after injury. We have begun to study swimming as a rehabilitation strategy that allows for high numbers of steps and a high step-cycle frequency in a standard rat model of contusive spinal cord injury. The purpose of the present study was to evaluate the effect of swimming as a rehabilitation strategy in rats with contusion injuries at T9. We used a swimming strategy with or without cutaneous feedback based on original work in the chick by Muir and colleagues. Adult female rats (n=27) received moderately-severe contusion injuries at T9. Walking and swimming performance were evaluated using the Open-Field Locomotor Scale (BBB; Basso et al., 1995) and a novel swimming assessment, the Louisville Swimming Scale (LSS). Rats that underwent swim-training with or without cutaneous feedback showed a significant improvement in hindlimb function during swimming compared to untrained animals. Rats that underwent swim-training without cutaneous feedback showed less improvement than those trained with cutaneous feedback. Rats in the non-swimming group demonstrated little improvement over the course of the study. All three groups showed the expected improvement in over-ground walking and had similar terminal BBB scores. These findings suggest that animals re-acquire the ability to swim only if trained and that cutaneous feedback improves the re-training process. Further, these data suggest that the normal course of recovery of over-ground walking following moderately-severe contusion injuries at T9 is the result of a re-training process.

Animals↗

Differential metabolic capacity of mice selected for magnitude of swim stress-induced analgesia.

Maximum oxygen consumption (Vo(2)) elicited by swimming in 20 degrees C water or by exposure to -2.5 degrees C in helium-oxygen (Helox) atmosphere is higher in mice selected for low (LA) than for high (HA) stress-induced analgesia (SIA) produced by swimming. However, this line difference is greater with respect to swim- than to cold-elicited Vo(2). To study the relationship between the analgesic and thermogenic mechanisms, we acclimated HA and LA mice to 5 degrees C or to daily swimming at 20 or 32 degrees C. Next, the acclimated mice were exposed to a Helox test at -2.5 degrees C and to a swim test at 20 degrees C to compare Vo(2) and hypothermia (DeltaT). Cold acclimation raised Vo(2) and decreased DeltaT. These effects were similar in both lines in the Helox test but were smaller in the HA than in the LA line in the swim test. HA and LA mice acclimated to 20 or 32 degrees C swims increased Vo(2) and decreased DeltaT elicited by swimming, but only HA mice acclimated to 20 degrees C swims increased Vo(2) and decreased DeltaT in the Helox test. We conclude that the between-line difference in swim Vo(2) results from a stronger modulation of thermogenic capacities of HA mice by a swim stress-related mechanism, resulting in SIA. We suggest that the predisposition to SIA observed in laboratory as well as wild animals may significantly affect both the results of laboratory measurements of Vo(2) and the interpretation of its intra- and interspecific variation.

Acclimatization↗

Changes in electrophysiological properties of lamprey spinal motoneurons during fictive swimming.

Electrophysiological properties of lamprey spinal motoneurons were measured to determine whether their cellular properties change as the spinal cord goes from a quiescent state to the active state of fictive swimming. Intracellular microelectrode recordings of membrane potential were made from motoneurons in the isolated spinal cord preparation. Electrophysiological properties were first characterized in the quiescent spinal cord, and then fictive swimming was induced by perfusion with D-glutamate and the measurements were repeated. During the depolarizing excitatory phase of fictive swimming, the motoneurons had significantly reduced rheobase and significantly increased input resistance compared with the quiescent state, with no significant changes in these parameters during the repolarizing inhibitory phase of swimming. Spike threshold did not change significantly during fictive swimming compared with the quiescent state. During fictive swimming, the slope of the spike frequency versus injected current (F-I) relationship decreased significantly as did spike-frequency adaptation and the amplitude of the slow after-spike hyperpolarization (sAHP). Serotonin is known to be released endogenously from the spinal cord during fictive swimming and is known to reduce the amplitude of the sAHP. Therefore the effects of serotonin on cellular properties were tested in the quiescent spinal cord. It was found that, in addition to reducing the sAHP amplitude, serotonin also reduced the slope of the F-I relationship and reduced spike-frequency adaptation, reproducing the changes observed in these parameters during fictive swimming. Application of spiperone, a serotonin antagonist, significantly increased the sAHP amplitude during fictive swimming but had no significant effect on F-I slope or adaptation. Because serotonin may act in part through reduction of calcium currents, the effect of calcium-free solution (cobalt substituted for calcium) was tested in the quiescent spinal cord. Similar to fictive swimming and serotonin application, the calcium-free solution significantly reduced the sAHP amplitude, the slope of the F-I relationship, and spike-frequency adaptation. These results suggest that there are significant changes in the firing properties of motoneurons during fictive swimming compared with the quiescent state, and it is possible that these changes may be attributed in part to the endogenous release of serotonin acting via reduction of calcium currents.

Action Potentials↗

Neuronal elements that mediate escape swimming and suppress feeding behavior in the predatory sea slug Pleurobranchaea.

1. The white, bilaterally paired A1 interneurons of the cerebropleural ganglion of Pleurobranchaea californica fire rhythmic bursts of action potentials during escape swimming behavior. We studied the role of the A1s in swimming behavior and pattern generation in whole animal and isolated CNS preparations. 2. The escape swim is a cyclic sequence of dorsal and ventral flexions of the body. During the swim, A1 bursts precede and accompany the dorsal flexion phase of the cycle. Hyperpolarization of A1 to prevent spike activity interrupts swimming behavior in the whole animal and fictive swimming in the isolated CNS. Stimulated A1 activity was not observed to cause swimming in whole animals, and was only occasionally sufficient to trigger fictive swimming activity in the isolated CNS. 3. In quiescent whole animal preparations, stimulation of a single A1 normally causes a single dorsal flexion followed by body flexion to the side contralateral to the stimulated cell; characteristically, A1 spike activity stimulates feedback inhibition coinciding with the end of dorsal flexion and the onset of contralateral flexion. 4. A1 spike activity suppresses feeding behavior and causes proboscis retraction in whole animal preparations induced to feed. A1 activity also suppresses fictive feeding driven by stimulation of the critical phasic paracerebral neurons (PCps) of the motor network of feeding in the isolated CNS. Concomitantly, A1 spikes cause potent inhibition of the PCp interneurons. 5. The A1s are specifically excited by noxious mechanical and chemical stimuli, but are not affected by feeding stimuli or the occurrence of feeding behavior. 6. We conclude that the A1 neurons are elements of an escape swimming pattern generator, and that they are probably homologous to the similar C2 neurons of the nudibranch Tritonia diomedea. One of their functions outside of generating the swim pattern may be the suppression of feeding behavior in response to noxious stimulation. These observations provide a neural mechanism for the original observations of the dominance of escape swimming behavior over feeding.

Action Potentials↗

Coordination of startle and swimming neural systems in the pteropod mollusk Clione limacina: role of the cerebral cholinergic interneuron.

The holoplanktonic pteropod mollusk Clione limacina has a unique startle system that provides a very fast, ballistic movement of the animal during escape or prey capture behaviors. The startle system consists of two groups of large pedal motoneurons that control ventral or dorsal flexions of the wings. Although startle motoneurons innervate the same musculature used during normal swimming, they are independent of the swim central pattern generator and swim motoneurons. This study demonstrates that a cerebral startle (Cr-St) interneuron, which provides prominent excitatory inputs to startle motoneurons, plays a very important role in coordination of the startle and swimming neural systems. The Cr-St interneuron produces, simultaneously with monosynaptic excitatory inputs to dorsal startle motoneurons, monosynaptic inhibitory inputs to all types of swim neurons, including interneurons of the central pattern generator, general excitor motoneurons, small motoneurons, and modulatory pedal serotonergic wing neurons. The inhibitory synaptic transmission between the Cr-St interneuron and swim interneurons and motoneurons, as well as excitatory transmission between the Cr-St interneuron and startle motoneurons, appears to be cholinergic because it is blocked by the cholinergic antagonists atropine and d-tubocurarine, mimicked by exogenous acetylcholine in very low concentrations, and enhanced by the cholinesterase inhibitor eserine (physostigmine). The Cr-St-neuron-mediated inhibitory inputs to the swimming system are strong enough to completely terminate swimming activity while the Cr-St interneuron is active. Mechanosensory inputs are capable of triggering Cr-St neuron firing at rates sufficient to suppress fictive swimming in reduced preparations. Thus the Cr-St interneuron can temporally remove the swimming system from the control over the swim musculature while simultaneously activating the startle system to produce a powerful, short-latency response.

Acetylcholine↗

Development and role of GABA(A) receptor-mediated synaptic potentials during swimming in postembryonic Xenopus laevis tadpoles.

We have investigated the contribution of GABA(A) receptor activation to swimming in Xenopus tadpoles during the first day of postembryonic development. Around the time of hatching stage (37/8), bicuculline (10-50 microM) causes a decrease in swim episode duration and cycle period, suggesting that GABA(A) receptor activation influences embryonic swimming. Twenty-four hours later, at stage 42, GABA(A) receptor activation plays a more pronounced role in modulating larval swimming activity. Bicuculline causes short, intense swim episodes with increased burst durations and decreased cycle periods and rostrocaudal delays. Conversely, the allosteric agonist, 5beta-pregnan-3alpha-ol-20-one (1-10 microM) or the uptake inhibitor, nipecotic acid (200 microM) cause slow swimming with reduced burst durations and increased cycle periods. These effects appear to be mainly the result of GABA release from the spinal terminals of midhindbrain reticulospinal neurons but may also involve spinal GABAergic neurons. Intracellular recordings were made using KCl electrodes to reverse the sign and enhance the amplitude of chloride-dependent inhibitory postsynaptic potentials (IPSPs). Recordings from larval motoneurons in the presence of strychnine (1-5 microM), to block glycinergic IPSPs, provided no evidence for any GABAergic component to midcycle inhibition. GABA potentials were observed during episodes, but they were not phase-locked to the swimming rhythm. Bicuculline (10-50 microM) abolished these sporadic potentials and caused an apparent decrease in the level of tonic depolarization during swimming activity and an increase in spike height. Finally, in most larval preparations, GABA potentials were observed at the termination of swimming. In combination with the other evidence, our data suggest that midhindbrain reticulospinal neurons become involved in an intrinsic pathway that can prematurely terminate swim episodes. Thus during the first day of larval development, endogenous activation of GABA(A) receptors plays an increasingly important role in modulating locomotion, and GABAergic neurons become involved in an intrinsic descending pathway for terminating swim episodes.

Animals↗

Childhood drowning: barriers surrounding private swimming pools.

OBJECTIVE: To investigate the causes of child drowning and determine the need for changes in the legislation as well as improvements to the inspection and enforcement of current legislation related to barriers surrounding private swimming pools. METHODS: There were 3 stages to the study: a retrospective review of coroner's data, an audit of swimming pool inspections, and in-depth interviews with swimming pool inspectors in Western Australia. The incidence of childhood drowning (per population) and compliance rates of swimming pools (per 1000 swimming pools) to the legislation were measured. RESULTS: During the 12-year observational period (1988-2000) 50 children younger than 5 years drowned in private swimming pools in Western Australia with an overall incidence of drowning of 4.4 per 100 000 children per year. Sixty-eight percent of drownings occurred in pools that did not have 4-sided fencing with an almost 2-fold increased risk (incidence rate ratio: 1.78; 95% confidence interval: 1.40-1.79) of a child's drowning in a swimming pool with 3-sided versus 4-sided fencing. The compliance rate of swimming pools (compliance to the current legislation) at first inspection was approximately 400 per 1000 swimming pools. CONCLUSIONS: Almost two thirds of the swimming pools in which children drowned had only 3-sided fencing. With a combination of a change in legislation, enhanced inspection processes, and public education, the incidence of drowning in private swimming pools in Western Australia could be reduced in the coming years.

Architectural Accessibility↗

Validity of ratings of perceived exertion as an index of exercise intensity in swimming training.

The validity of ratings of perceived exertion (RPE), proposed by Borg (1962), as an index of exercise intensity in swimming training was discussed based on the following four experiments. Experiment I: VO2 and heart rate (HR) were measured and RPE was asked in ten female and seven male physical education students with different levels of swimming skill performing submaximal and maximal work in tethered swimming. The increases in HR and RPE with increase in %VO2max were fitted well by straight lines with high correlation coefficients of r = 0.957-0.999 and r = 0.893-0.988, respectively. RPE was increased in a linear fashion with increase in HR except for a few subjects. The correlation coefficients for linear regression for individuals were 0.862-0.987. Experiment II: Swimming velocity and HR were measured in four groups with different levels of swimming skill. The breast stroke in a 50-m pool for 5 min at three RPE ratings, i.e., very light (RPE 9), somewhat hard (RPE 13) and very hard (RPE 17) was requested of these groups. In good skilled well trained college swimmers, %HRmax was fairly higher than the RPE at the RPE 9 and RPE 13 levels but coincided with the RPE at the RPE 17 level. In skilled trained physical education students, the HR increased with a corresponding increase in RPE. But in the group with low or lower levels of swimming skill, the HR kept about the same values in spite of the increase in RPE. Experiment III: Two male and six female low skilled physical education students took the swimming training in the swimming pool for 2.0-2.5 hours a day, 6 days a week, for 2 weeks. The students also received the swimming training in the sea which lasted for 2 hours each in the morning and in the afternoon for 6 days. The same RPE test, as mentioned in Experiment II, was done before, during and after swimming training. Mean swimming velocity during and after training was slightly higher than that before training at the RPE 9 and RPE 13 levels, and was much higher at the RPE 17 level. Before training, the HR was fairly higher than the RPE at the RPE 9 and RPE 13 level. But during and after training, the HR was much closer to the RPE at the RPE 9 and RPE 13 levels. Experiment IV: Two male and three female lower skilled middle-aged swimmers performed the same RPE test as mentioned in Experiment II.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Neural adaptation in imipramine-treated rats processed in forced swim test: assessment of time course, handling, rat strain and amine uptake.

The intent of the present series of experiments was to better understand the events that produce a rapid adaptation of beta adrenergic and serotonin-2 (5-HT2) receptors when imipramine treatment and forced swim are combined in Sprague-Dawley rats. Beta adrenergic and 5-HT2 receptors were evaluated at specific stages of the forced swim test with and without imipramine treatment. Rapid changes in receptor binding were observed in saline-treated rats during specific stages of the test. The changes observed during forced swim could not be attributed to the transport-novelty that occurs during forced swim. Binding for both monoamine receptors was reduced in hippocampus and frontal cortex before the test swim in imipramine-treated rats as they were 10 min, 3 hr and 24 hr after the test swim. The increase in corticosterone induced by the second forced swim was not altered by imipramine, indicating that imipramine was not interfering with this measure of the stress response. In the Fisher-344 rat strain, imipramine did not produce a behavioral change during the test swim. In contrast to this lack of a behavioral change in the Fischer-344 rats, beta adrenergic and 5-HT2 receptor down-regulation was facilitated in this rat strain, similar to that found in imipramine-treated Sprague-Dawley rats subjected to swim. This latter finding suggests that beta adrenergic or 5-HT2 receptor adaptation alone is insufficient to cause an imipramine-induced behavioral change in the swim test. Studies with specific norepinephrine- and serotonin-uptake inhibitors, nisoxetine and fluoxetine, respectively, indicate that the behavioral effects of imipramine in the forced swim test are dependent upon norepinephrine uptake inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Rapid down regulation of beta adrenergic receptors by combining antidepressant drugs with forced swim: a model of antidepressant-induced neural adaptation.

The hypothesis that behavioral responses to antidepressant drugs in the forced swim test are related to a rapid neural adaptation produced by the combination of drug treatment and swim stress was explored. As a measure of adaptation, brain beta adrenergic receptors were assayed using [3H]dihydroalprenolol [( 3H]DHA) binding to brain membranes from rats that were processed in the forced swim test. The combination of swim stress and imipramine treatment antagonized immobility induced by forced swimming and resulted in a reduction in [3H] DHA binding to membranes from forebrain preparations which did not include the corpus striatum. Administration of antidepressant drugs from other chemical classes, including pargyline, iprindole and nomifensine, also reduced immobility induced by the forced swim and produced a reduction in [3H]DHA binding to forebrain membranes. In homogenates of the corpus striatum, [3H]DHA binding was not altered by swim stress combined with antidepressant drug treatment. Chlordiazepoxide was without an effect on immobility or beta receptor binding when combined with forced swim. Even though atropine and amphetamine exhibited a positive activity in the forced swim test, they did not reduce [3H]DHA binding. Therefore, by combining behavioral and neurochemical analysis of animals processed in the forced swim test, it may be possible to differentiate, with greater confidence, potential antidepressant drugs from "false positives." The present studies support the hypothesis that antidepressant drug action in the forced swim test involves a rapid neural adaptation as reflected by the down regulation of beta adrenergic receptors. Thus, this behavioral paradigm may serve as a model of adaptive mechanisms induced by antidepressant drugs.

Adaptation, Physiological↗