Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SWIMMING”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1987

Intracellular stimulation of sensory cells elicits swimming activity in the medicinal leech.

Intracellular stimulation of each of three different types of mechanoreceptors, the T, P and N cells, evokes swimming behavior in leech preparations. Stimulation of an individual N cell or P cell evoked swimming in 75% and 53% respectively, of the preparations tested. Stimulation of an individual T cell was ineffective in eliciting swimming; however, simultaneous stimulation of two T cells evoked swimming in 59% of our preparations. Stimulation of mechanosensory neurons elicited swimming activity for a limited number of trials; i.e. the response habituated. The number of swim episodes evoked before habituation to criterion did not differ significantly for the different types of mechanoreceptors. The duration of swim episodes declined significantly over the course of N cell stimulation. The tendency for swim length to decline with repeated stimulation was present as well for swim episodes elicited by P or T cell stimulation. Swim initiation recovered spontaneously following habituation resulting from T cell stimulation. Spontaneous recovery following N cell stimulation was not demonstrated. However, N cell stimulation evoked swimming again after DP nerve shock or to a limited extent, after cell 204 stimulation. Spontaneous recovery of swim initiation to P cell stimulation was not investigated. A previous study detailed habituation of swimming activity to mechanical stimulation of the body wall (Debski and Friesen 1985). Only the T cells are activated significantly by this stimulus. Stimulation of sensory receptors other than mechanoreceptors was not effective in eliciting swimming in our preparation. We conclude that T cells mediate swim initiation elicited by stroking of the body wall and that the cessation of swimming to this stimulus is not due to sensory adaptation.

Action Potentials↗
PubMed2006

Simulations of optimized anguilliform swimming.

The hydrodynamics of anguilliform swimming motions was investigated using three-dimensional simulations of the fluid flow past a self-propelled body. The motion of the body is not specified a priori, but is instead obtained through an evolutionary algorithm used to optimize the swimming efficiency and the burst swimming speed. The results of the present simulations support the hypothesis that anguilliform swimmers modify their kinematics according to different objectives and provide a quantitative analysis of the swimming motion and the forces experienced by the body. The kinematics of burst swimming is characterized by the large amplitude of the tail undulations while the anterior part of the body remains straight. In contrast, during efficient swimming behavior significant lateral undulation occurs along the entire length of the body. In turn, during burst swimming, the majority of the thrust is generated at the tail, whereas in the efficient swimming mode, in addition to the tail, the middle of the body contributes significantly to the thrust. The burst swimming velocity is 42% higher and the propulsive efficiency is 15% lower than the respective values during efficient swimming. The wake, for both swimming modes, consists largely of a double row of vortex rings with an axis aligned with the swimming direction. The vortex rings are responsible for producing lateral jets of fluid, which has been documented in prior experimental studies. We note that the primary wake vortices are qualitatively similar in both swimming modes except that the wake vortex rings are stronger and relatively more elongated in the fast swimming mode. The present results provide quantitative information of three-dimensional fluid-body interactions that may complement related experimental studies. In addition they enable a detailed quantitative analysis, which may be difficult to obtain experimentally, of the different swimming modes linking the kinematics of the motion with the forces acting on the self-propelled body. Finally, the optimization procedure helps to identify, in a systematic fashion, links between swimming motion and biological function.

Animals↗
PubMed2001

Thermoregulatory responses to low-intensity prolonged swimming in water at various temperatures and treadmill walking on land.

The purpose of the present study was to examine the effect of water temperature on the human body during low-intensity prolonged swimming. Six male college swimmers participated in this study. The experiments consisted of breast stroke swimming for 120 minutes in 23 degrees C, 28 degrees C and 33 degrees C water at a constant speed of 0.4 m.sec-1 in a swimming flume. The same subjects walked on a treadmill at a rate of approximately 50% of maximal oxygen uptake (VO2max) at the same relative intensity as the three swimming trials. Rectal temperature (Tre) in 33 degrees C water was unchanged during swimming for 120 minutes. Tre during treadmill walking increased significantly compared to the three different swimming trials. Tre, mean skin temperature (Tsk) and mean body temperature (Tb) in 23 degrees C and 28 degrees C water decreased significantly more than in both the 33 degrees C water and walking on land. VO2 during swimming in 23 degrees C water increased more than during swimming in the 28 degrees C and 33 degrees C trials; however, there were no significant differences in VO2 between the 23 degrees C swimming trial and treadmill walking. Heart rate (HR) during treadmill walking on land increased significantly compared with HR during the three swimming trials. Plasma adrenaline concentration at the end of the treadmill walking was higher than that at the end of each of the three swimming trials. Noradrenaline concentrations at the end of swimming in the 23 degrees C water and treadmill walking were higher than those during the other two swimming trials. Blood lactate concentration during swimming in 23 degrees C water was higher than that during the other two swimming trials and walking on land. These results suggest that the balance of heat loss and heat production is maintained in the warm water temperature. Therefore, a relatively warm water temperature may be desirable when prolonged swimming or other water exercise is performed at low intensity.

Adolescent↗
PubMedDate not supplied

Applied physiology of swimming.

Scientific research in swimming over the past 10 to 15 years has been oriented toward multiple aspects that relate to applied and basic physiology, metabolism, biochemistry, and endocrinology. This review considers recent findings on: 1) specific physical characteristics of swimmers; 2) the energetics of swimming; 3) the evaluation of aerobic fitness in swimming; and 4) some metabolic and hormonal aspects related to swimmers. Firstly, the age of finalists in Olympic swimming is not much different from that of the participants from other sports. They are taller and heavier than a reference population of the same age. The height bias in swimming may be the reason for lack of success from some Asian and African countries. Experimental data point toward greater leanness, particularly in female swimmers, than was seen 10 years ago. Overall, female swimmers present a range of 14 to 19% body fat whereas males are much lower (5 to 10%). Secondly, the relationship between O2 uptake and crawl swimming velocity (at training and competitive speeds) is thought to be linear. The energy cost varies between strokes with a dichotomy between the 2 symmetrical and the 2 asymmetrical strokes. Energy expenditure in swimming is represented by the sum of the cost of translational motion (drag) and maintenance of horizontal motion (gravity). The cost of the latter decreases as speed increases. Examination of the question of size-associated effects on the cost of swimming using Huxley's allometric equation (Y = axb) shows an almost direct relationship with passive drag. Expressing energy cost in litres of O2/m/kg is proposed as a better index of technical swimming ability than the traditional expression of VO2/distance in L/km. Thirdly, maximal direct conventional techniques used to evaluate maximal oxygen consumption (VO2 max) in swimming include free swimming, tethered swimming, and flume swimming. Despite the individual peculiarities of each method, with similar experimental conditions similar results for VO2 max will be found. Free swimming (unimpeded) using the backward extrapolation method will, however, lead to reliable and valid results obtained in a condition that is closer to the competitive situation than with a direct test. A maximal indirect field-test has been recently made available. This test can predict VO2 max with an acceptable accuracy (r = 0.877), and provides a mean to evaluate the functional maximal aerobic power in swimming which corresponds to the maximal aerobic swimming velocity.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed2003

Analgesia induced by swim stress: interaction between analgesic and thermoregulatory mechanisms.

Exposure of an animal to stressful stimuli, perceived by the animal as a threatening, emergency condition, elicits a transient decrease of pain sensitivity, which often affects thermoregulatory mechanisms in the threatened organism. We studied the interaction between emergency and thermoregulatory components of swim stress in developing swim stress-induced analgesia (SSIA). The subjects were mice selectively bred for high analgesia (HA) induced by swimming in 20 degrees C water, and displaying profound swim hypothermia. The mice were acclimated to one of the following conditions: (1) ambient cold (5 degrees C, mimicking the thermal component of swim stress); (2) daily 3-min swimming at 32 degrees C (mimicking the emergency, emotional in nature, component of swim stress), or (3) daily swimming at 20 degrees C (a combination of both emergency and thermal component of swim stress). Following each of the procedures the analgesia induced by swimming in 20 degrees C water and by acute exposure to -2.5 degrees C in helium/oxygen (Helox) atmosphere was measured. Analgesia was also assessed in a group of naive mice immersed in 20 degrees C shallow water with the purpose of eliminating the emergency condition, but assuring the animal's contact with the cold water environment. Cold acclimation markedly attenuated Helox-induced analgesia (HIA) without affecting SSIA, whereas repeated swims attenuated SSIA without affecting HIA. The results suggest that hypothermia is the only stimulus eliciting HIA, while the emergency condition of swimming is essential for inducing SSIA. The significantly lower magnitude of SSIA in mice acclimated to repeated swims in 20 degrees C than in 32 degrees C water suggests that SSIA develops due to an interaction between the emergency and hypothermic components of swim stress. This is further supported by a greater hypothermia and greater analgesia in freely swimming than in immersed naive mice.

Acclimatization↗
PubMed2006

Dopamine receptor mechanism(s) and antinociception and tolerance induced by swim stress in formalin test.

In the present study, involvement of D1 and D2 dopamine receptors in the antinociception and tolerance induced by water swim stress in the formalin test has been investigated. Water swim stress at 20 degrees C temperature induced antinociception in both phases of the formalin test. Intraperitoneal administration of the D2 dopamine receptor antagonist, sulpiride (25 and 50 mg/kg) reduced swim stress-induced antinociception in the second phase of the formalin test. A higher dose of the D1 dopamine receptor antagonist, SCH23390 (0.1 mg/kg, intraperitoneal) also reduced swim stress-induced antinociception in both phases of the test. Exposure to 3 min water swimming stress, once daily for 3 days, induced tolerance to swim stress-induced antinociception in the second phase of the formalin test. Administration of sulpiride (12.5, 25 and 50 mg/kg), during exposure to water swimming stress (once daily for 3 days), decreased tolerance in the second phase, whereas the antagonist (12.5 and 50 mg/kg) increased pain scores in the first phase of the formalin test. Sulpiride (25 mg/kg) treatment however, once daily for 3 days with no water swimming stress, did not alter swim stress-induced antinociception (0.5, 1 and 3 min tests). Similarly, repeated treatment with SCH23390 (0.05 mg/kg) and water swimming stress did not alter tolerance induced by water swimming stress. Repeated administration of the antagonist in the absence of water swimming stress also did not change swim stress-induced antinociception. The results may indicate a possible involvement of both dopamine D1 and D2 receptors in the antinociception induced by swim stress and D2 receptor mechanism in the tolerance induced by repeated swim stress.

Analgesia↗
PubMed1980

Maximal oxygen uptake during free, tethered, and flume swimming.

The purpose of this study was 1) to compare the maximal oxygen uptake (VO2max) obtained in swimmers during tethered swimming, free swimming, and flume swimming, and 2) to determine whether an arm-ergometer test would provide comparable results. In the first experiments the VO2max for tethered swimming (2.67 +/- 0.26 l/min) and flume swimming (2.62 +/- 0.26 l/min) were not different (P greater than 0.05) and were highly correlated (r = 0.99). However, with arm ergometry a significantly lower VO2max (2.36 +/- 0.24 l/min) occurred from those found in the two swimming tests (P less than 0.05). Other experiments demonstrated that the tethered swimming VO2max (3.53 +/- 0.27 l/min) and the free swimming VO2max (3.55 +/- 0.28 l/min) also provide results that were similar (P greater than 0.05) and highly correlated with each other (r = 0.99). Differences between tethered and flume swimming, and tethered and free swimming were small, being 1.2 +/- 1.6% and 0.6 +/- 0.9%, respectively. Differences between tethered swimming and arm ergometry VO2max were large, 14.7 +/- 2.4%, despite the high correlation (r = 0.97) between these measurements. Predictions of a swimming VO2max from the arm-ergometer data yielded a considerable error (+/-7.1% and +/-7.4%). The present results indicate that flume swimming, free swimming, and tethered swimming yield essentially identical VO2max results.

Adolescent↗
PubMed2001

Synaptic drive to motoneurons during fictive swimming in the developing zebrafish.

The development of swimming behavior and the correlated activity patterns recorded in motoneurons during fictive swimming in paralyzed zebrafish larvae were examined and compared. Larvae were studied from when they hatch (after 2 days) and are first capable of locomotion to when they are active swimmers capable of capturing prey (after 4 days). High-speed (500 Hz) video imaging was used to make a basic behavioral characterization of swimming. At hatching and up to day 3, the larvae swam infrequently and in an undirected fashion. They displayed sustained bursts of contractions ('burst swimming') at an average frequency of 60-70 Hz that lasted from several seconds to a minute in duration. By day 4 the swimming had matured to a more frequent and less erratic "beat-and-glide" mode, with slower (approximately 35 Hz) beats of contractions for approximately 200 ms alternating with glides that were twice as long, lasting from just a few cycles to several minutes overall. In whole cell current-clamp recordings, motoneurons displayed similar excitatory synaptic activity and firing patterns, corresponding to either fictive burst swimming (day 2-3) or beat-and-glide swimming (day 4). The resting potentials were similar at all stages (about -70 mV) and the motoneurons were depolarized (to about -40 mV) with generally non-overshooting action potentials during fictive swimming. The frequency of sustained inputs during fictive burst swimming and of repetitive inputs during fictive beat-and glide swimming corresponded to the behavioral contraction patterns. Fictive swimming activity patterns were eliminated by application of glutamate antagonists (kynurenic acid or 6-cyano-7-nitroquinoxalene-2,3-dione and DL-2-amino-5-phosphonovaleric acid) and were modified but maintained in the presence of the glycinergic antagonist strychnine. The corresponding synaptic currents underlying the synaptic drive to motoneurons during fictive swimming could be isolated under voltage clamp and consisted of cationic [glutamatergic postsynaptic currents (PSCs)] and anionic inputs (glycinergic PSCs). Either sustained or interrupted patterns of PSCs were observed during fictive burst or beat-and-glide swimming, respectively. During beat-and-glide swimming, a tonic inward current and rhythmic glutamatergic PSCs (approximately 35 Hz) were observed. In contrast, bursts of glycinergic PSCs occurred at a higher frequency, resulting in a more tonic pattern with little evidence for synchronized activity. We conclude that a rhythmic glutamatergic synaptic drive underlies swimming and that a tonic, shunting glycinergic input acts to more closely match the membrane time constant to the fast synaptic drive.

Animals↗
PubMed2005

Submerged swimming of the great cormorant Phalacrocorax carbo sinensis is a variant of the burst-and-glide gait.

Cormorants are water birds that forage by submerged swimming in search and pursuit of fish. Underwater they swim by paddling with both feet simultaneously in a gait that includes long glides between consecutive strokes. At shallow swimming depths the birds are highly buoyant as a consequence of their aerial lifestyle. To counter this buoyancy cormorants swim underwater with their body at an angle to the swimming direction. This mechanical solution for foraging at shallow depth is expected to increase the cost of swimming by increasing the drag of the birds. We used kinematic analysis of video sequences of cormorants swimming underwater at shallow depth in a controlled research setup to analyze the swimming gait and estimate the resultant drag of the birds during the entire paddling cycle. The gliding drag of the birds was estimated from swimming speed deceleration during the glide stage while the drag during active paddling was estimated using a mathematical ;burst-and-glide' model. The model was originally developed to estimate the energetic saving from combining glides with burst swimming and we used this fact to test whether the paddling gait of cormorants has similar advantages. We found that swimming speed was correlated with paddling frequency (r=0.56, P<0.001, N=95) where the increase in paddling frequency was achieved mainly by shortening the glide stage (r=-0.86, P<0.001, N=95). The drag coefficient of the birds during paddling was higher on average by two- to threefold than during gliding. However, the magnitude of the drag coefficient during the glide was positively correlated with the tilt of the body (r=0.5, P<0.003, N=35) and negatively correlated with swimming speed (r=-0.65, P<0.001, N=35), while the drag coefficient during the stroke was not correlated with tilt of the body (r=-0.11, P>0.5, N=35) and was positively correlated with swimming speed (r=0.41, P<0.015, N=35). Therefore, the difference between the drag coefficient during the glide and during propulsion diminished at lower speeds and larger tilt. The mean drag of the birds for a single paddling cycle at an average swimming speed of 1.5 m s(-1) was 5.5+/-0.68 N. The burst-and-glide model predicts that energy saving from using burst-and-glide in the paddling cycle is limited to relatively fast swimming speeds (>1.5 m s(-1)), but that as the birds dive deeper (>1 m where buoyancy is reduced), the burst-and-glide gait may become beneficial even at lower speeds.

Animals↗
PubMed2000

Simple mechanisms organise orientation of escape swimming in embryos and hatchling tadpoles of Xenopus laevis.

Many amphibian tadpoles hatch and swim before their inner ears and sense of spatial orientation differentiate. We describe upward and downward swimming responses in hatchling Xenopus laevis tadpoles from stages 32 to 37/38 in which the body rotates about its longitudinal axis. Tadpoles are heavier than water and, if touched while lying on the substratum, they reliably swim upwards, often in a tight spiral. This response has been observed using stroboscopic photography and high-speed video recordings. The sense of the spiral is not fixed for individual tadpoles. In 'more horizontal swimming' (i.e. in directions within +/-30 degrees of the horizontal), the tadpoles usually swim belly-down, but this position is not a prerequisite for subsequent upward spiral swimming. Newly hatched tadpoles spend 99 % of their time hanging tail-down from mucus secreted by a cement gland on the head. When suspended in mid-water by a mucus strand, tadpoles from stage 31 to 37/38 tend to swim spirally down when touched on the head and up when touched on the tail. The three-dimensional swimming paths of stage 33/34 tadpoles were plotted using simultaneous video images recorded from the side and from above. Tadpoles spiralled for 70 % of the swimming time, and the probability of spiralling increased to 1 as swim path angles became more vertical. Tadpoles were neutrally buoyant in Percoll/water mixtures at 1.05 g cm(-)(3), in which anaesthetised tadpoles floated belly-down and head-up at 30 degrees. In water, their centre of mass was ventral to the muscles in the yolk mass. A simple mathematical model suggests that the orientation of tadpoles during swimming is governed by the action of two torques, one of which raises the head (i.e. increases the pitch) and the other rotates (rolls) the body. Consequently, tadpoles (i) swim belly-down when the body is approximately horizontal because the body is ballasted by dense yolk, and (ii) swim spirally at more vertical orientations when the ballasting no longer stabilises orientation. Measurements in tethered tadpoles show that dorsal body flexion, which could produce a dorsal pitch torque, is present during swimming and increases with tailbeat frequency. We discuss how much of the tadpole's behaviour can be explained by our mathematical model and suggest that, at this stage of development, oriented swimming responses may depend on simple touch reflexes, the organisation of the muscles and physical features of the body, rather than on vestibular reflexes.

Animals↗
PubMed1993

Dry-land resistance training for competitive swimming.

To determine the value of dry-land resistance training on front crawl swimming performance, two groups of 12 intercollegiate male swimmers were equated based upon preswimming performance, swim power values, and stroke specialties. Throughout the 14 wk of their competitive swimming season, both swim training group (SWIM, N = 12) and combined swim and resistance training group (COMBO, N = 12) swam together 6 d a week. In addition, the COMBO engaged in a 8-wk resistance training program 3 d a week. The resistance training was intended to simulate the muscle and swimming actions employed during front crawl swimming. Both COMBO and SWIM had significant (P < 0.05) but similar power gains as measured on the biokinetic swim bench and during a tethered swim over the 14-wk period. No change in distance per stroke was observed throughout the course of this investigation. No significant differences were found between the groups in any of the swim power and swimming performance tests. In this investigation, dry-land resistance training did not improve swimming performance despite the fact that the COMBO was able to increase the resistance used during strength training by 25-35%. The lack of a positive transfer between dry-land strength gains and swimming propulsive force may be due to the specificity of training.

Adult↗
PubMed1995

Neuronal control of leech swimming.

Leech swimming is produced by the antiphasic contractions of dorsal and ventral longitudinal muscles that travel rearward along the animal and propel it forward. Research over the past three decades has focused on identifying the underlying neuronal circuit and mechanisms that produce and control this coordinated movement pattern. Investigations have also tested whether leech swimming is modifiable, both by experience and by neuromodulators. One outcome has been the identification of several functional classes of neurons associated with swimming. Systematic analysis of the interactions between these neurons had led to the elucidation of a neuronal circuit that adequately accounts for the generation of the swim motor program cord. The swim motor program appears to be produced by a chain of coupled segmental oscillators whose intrinsic properties and intersegmental connections ensure the coordinated expression of swimming along the nerve cord. In addition, neurons identified in the head ganglion comprise two parallel, but opposite-acting, systems that control the initiation of swimming in response to sensory input. Also, the pathway by which body wall stimulation initiates swimming shows a simple form of learning, that is habituation. Repeatedly stroking the leech body wall decreases both the probability of initiating swimming and the length of elicited swim episodes. Finally, the biogenic amine serotonin, which is found in the nerve cord, affects leech swimming in a number of ways. Serotonin's modulation of swimming is due, in part, to its effect of the membrane properties of swim-initiating interneurons and several swim motor neurons.

Animals↗
PubMed1994

Modulation of swimming in Tritonia: excitatory and inhibitory effects of serotonin.

1. In the mollusc Tritonia escape swimming is produced by a network of central pattern generator (CPG) neurons. The purpose of this study was to determine which neurotransmitters might be involved in the swim system. 2. Injection of serotonin (5HT) into whole animals elicited swimming followed by a long-lasting inhibition of swimming. In isolated brain preparations, bath-applied 5HT elicited a swim pattern at short latency and also caused a long-lasting inhibition of the swim pattern. The activation of swimming by 5HT was associated with a tonic depolarization of cerebral cell 2 (C2) and the dorsal swim interneurons (DSI) which form part of the swim CPG network. 3. In isolated brain preparations, bath applied glycine, histamine, proctolin, and FMFRamide had no effect on the swim motor pattern elicited by electrical stimulation of a peripheral nerve. Aspartate, carbacol, dopamine, glutamate, octopamine, pilocarpine, and small cardioactive peptide-B (SCPB) inhibited the activation of swimming by nerve stimulation. 4. The 5HT antagonists cyproheptidine, tryptamine, and 7-methyltryptamine had no effect on swimming, but methysergide and fenfluramine inhibited swimming to both normal sensory stimuli and exogenously applied 5HT. 5. Staining with a polyclonal antibody indicated that one class of CPG neurons, the dorsal swim interneurons (DSI), was immunoreactive for 5HT.

Animals↗
PubMed2006

The contribution of the pleural type 12 interneuron to swim acceleration in Clione limacina.

The pteropod mollusc, Clione limacina, swims by alternate dorsal-ventral flapping movements of its wing-like parapodia. The basic swim rhythm is produced by a network of pedal swim interneurons that comprise a swim central pattern generator (CPG). Serotonergic modulation of both intrinsic cellular properties of the swim interneurons and network properties contribute to swim acceleration, the latter including recruitment of type 12 interneurons into the CPG. Here we address the role of the type 12 interneurons in swim acceleration. A single type 12 interneuron is found in each of the pleural ganglia, which contributes to fast swimming by exciting the dorsal swim interneurons while simultaneously inhibiting the ventral swim interneurons. Each type 12 interneuron sends a single process through the pleural-pedal connective that branches in both ipsilateral and contralateral pedal ganglia. This anatomical arrangement allowed us to manipulate the influence of the type 12 interneurons on the swim circuitry by cutting the pleural-pedal connective followed by a "culture" period of 48 h. The mean swim frequency of cut preparations was reduced by 19% when compared to the swim frequency of uncut preparations when stimulated with 10(-6) M serotonin; however, this decrease was not statistically significant. Additional evidence suggests that the type 12 interneurons may produce a short-term, immediate effect on swim acceleration while slower, modulatory inputs are taking shape.

Animals↗
PubMed1999

Immersion deaths and deterioration in swimming performance in cold water.

BACKGROUND: General hypothermia (deep body temperature <35 degrees C) has been implicated in immersion-related deaths, but many deaths occur too quickly for it to be involved. We investigated changes in swimming capability in cold water to find out whether such changes could lead to swim failure and drowning. METHODS: Ten volunteers undertook three self-paced breaststroke swims in a variable-speed swimming flume, in water at 25 degrees C, 18 degrees C, and 10 degrees C, for a maximum of 90 min. During each swim, we measured oxygen consumption, rectal temperature, swim speed and angle, and stroke rate and length. Swim failure was defined as being unable to keep feet off the bottom of the flume. FINDINGS: All ten swimmers completed 90 min swims at 25 degrees C, eight completed swims at 18 degrees C, and five at 10 degrees C. In 10 degrees C water, one swimmer reached swim failure after 61 min and four were withdrawn before 90 min with rectal temperatures of 35 degrees C when they were close to swim failure. Swimming efficiency and length of stroke decreased more and rate of stroke and swim angle increased more in 10 degrees C water than in warmer water. These variables seemed to characterise impending swim failure. INTERPRETATION: Impaired performance and initial cardiorespiratory responses to immersion probably represent the major dangers to immersion victims. Consequently, treatment should be aimed at symptoms resulting from near-drowning rather than severe hypothermia.

Adult↗
PubMed2006

Effect of pool length on blood lactate, heart rate, and velocity in swimming.

Exercise testing in water has been used to follow the progression of conditioning during regular training in swimmers. The present study examined the effects of pool length in eleven male swimmers on a set of 5 x 200-m freestyle swims with increasing speed from submaximal to maximal. Mean velocity of swimming, blood lactate and heart rate were examined in both 25-m and 50-m pools. Turning benefit as a marker for turning skill was measured separately by a underwater video system (speed difference between pre- and post-turning) during short all-out swims. Maximum force during swimming was measured in tethered swimming and explosive strength of leg extensor muscles was evaluated by a counter movement jump. The significantly higher (p=0.033 - 0.000) blood lactate values for the 50-m pool as compared to the 25-m pool were found at each point of swimming velocity versus blood lactate curve. The highest post-test lactate level was 7.36 +/- 1.47 mmol x l (-1) in the short course and 8.24 +/- 1.55 mmol x l (-1) (p=0.033) in the long course. The maximum swimming velocity was significantly greater (4.5 %) in the 25-m pool swimming (1.38 +/- 0.11 m x s (-1) vs. 1.32 +/- 0.12 m x s (-1); p=0.000). The heart rate values were significantly (p=0.020 - 0.000) lower in the short course than in the long course at all points of submaximal velocity with a mean difference of 7.3 +/- 0.7 bpm. Heart rate was equal (172 +/- 14 vs. 172 +/- 14 bpm) after the maximum swims in both short and long course. The turning benefit in the short maximum swim was 0.12 +/- 0.05 m x s (-1) (8.1 +/- 3.2 %), correlating positively with the difference in maximal swimming velocity between the short and long-pool swims (r = 0.59; p = 0.029), with the maximum force during tethered swimming (r=0.75; p=0.004) and with the vertical jumping height in the counter movement jump (r=0.55; p=0.039). We conclude that the pool length has a strong effect on blood lactate concentration and heart rate with greater swimming velocity in the short course pool.

Environment↗
PubMed1986

Role of central interneurons in habituation of swimming activity in the medicinal leech.

Swimming activity evoked by light tactile stimulation of a body wall flap in dissected leech preparations undergoes habituation (5). In this study, we examine the activity of several interneurons (cell 204, cell 205, the S cell, and cell 208) during habituation trials to study further the neuronal mechanisms that mediate this decline in responsiveness. Light tactile stimulation of the leech body wall evoked initially a marked excitatory response in cell 204 homologs (segmental swim-initiating neurons) that preceded the initiation of swimming activity. This response decreased over the course of repeated stimulus trials; however, no marked decline in cell 204 activity accompanied the cessation of swim initiation. A similar activity pattern was observed in cell 205. Thus the habituation of swimming activity to stroking of the body wall is not due solely to reduced input to cell 204 and cell 205. The early activity of cell 204 was not correlated to the duration of subsequent swim episodes. However, the impulse frequency of cell 204 during swim episodes was negatively correlated to the period of swim cycles. This correlation between cell 204 activity and cycle period occurred both within individual episodes as well as between trials in a habituation series. Direct stimulation of cell 204 with current pulses evoked swimming activity reliably for an average of 72 trials. Therefore, habituation that results from stroking the body wall (which occurs after approximately 6 trials) is not mediated by plasticity in the connections between cell 204 and the swim oscillator. The S cell fired repeatedly in response to light tactile stimulation. This response declined with repeated trials. Intense intracellular stimulation of the S cell was sufficient to initiate swimming activity in some preparations. The magnitude and duration of the excitation required to initiate swimming by this means were far greater, however, than that which occurred during stroking the body wall. The response of cell 208 (a swim oscillator cell) to body wall stimulation during habituation trials was variable; usually an initial hyperpolarization was followed by some depolarization. No aspect of this response correlated with the onset of habituation. Our results are consistent with the idea that cell 204 and cell 205 are part of the pathway that mediates swimming activity in response to light tactile stimulation of the leech body wall, and that habituation occurs, in part, as the result of reduced sensory input to this cell.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1995

Regulation of the segmental swim-generating system by a pair of identified interneurons in the leech head ganglion.

1. The aim of this study was to identify neurons that modulate activity of segmental swim gating interneurons. We found a pair of bilaterally symmetrical interneurons, cells SE1, whose activity level directly influences three groups of segmental neurons associated with generating swimming in the medicinal leech. 2. The somata of cells SE1 are located on the dorsal surface of the subesophageal ganglion. Their axons extend most, if not the entire, length of the ventral nerve cord and appear to make identical connections with the same group of swim-generating neurons in all segmental ganglia. 3. Cells SE1 excite monosynaptically all segmental swim gating interneurons, cells 204, examined. The level of excitation in cell 204 is directly correlated with the firing frequency of cell SE1. In most quiescent preparations (when the preparation is not swimming) hyperpolarization of a single cell SE1 eliminates all excitatory synaptic input to cells 204. 4. Cells SE1 excite monosynaptically three swim oscillatory interneurons, cells 115, 28, and 208. The strength of the connection from cell SE1 to cell 115 is stronger than the connection from cell SE1 to either cells 28 or 208. The level of excitation in cell 115 is directly correlated with the firing frequency of cell SE1. In most quiescent preparations, hyperpolarization of a single cell SE1 eliminates all excitatory synaptic input to cell 115 but has only a minor effect on the level of activity in cells 208 and 28. 5. Due most likely to the strong and direct connections cells SE1 have with swim gating and oscillatory interneurons, brief stimulation of cell SE1 can elicit swimming. Swimming generally occurs within 1 s after stimulation of cell SE1. During swimming, the membrane potential of cell SE1 depolarizes by 2-5 mV, and its firing frequency increases. Brief depolarization of cell SE1 during swimming reliably shifts the phase of the swimming rhythm, whereas longer periods of depolarization increase both swim period and burst duration. 6. Excitatory motor neurons to the dorsal longitudinal muscles, cells 3, 5, and 7, are strongly excited by stimulation of cell SE1. The firing frequency of cell 3 is positively correlated with the firing frequency of cell SE1. 7. The results of this study indicate that cells SE1 can modulate the level of excitation in three groups of neurons associated with generating leech swimming.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗