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PubMed1996

Functional classification of antidepressants based on antagonism of swim stress-induced fos-like immunoreactivity.

Autoradiographic analysis of 14C-2-deoxyglucose (2-DG) uptake and immunocytochemical assessment of Fos-like immunoreactivity (Fos-LI) were used to assess swim stress-induced changes in metabolic activity in brain and to define the effect of chronic treatment with antidepressants from different pharmacological classes. Saline-treated rats processed in the forced swim test exhibited marked increases in Fos-LI in limbic cortical regions, lateral septum, medial amygdala and paraventricular nucleus of the hypothalamus (PVN). Uptake of 2-DG was increased by swim stress in some of the same brain regions where Fos-LI was induced, with the notable exception of a lack of a change in the PVN. Rats received injections for 3 wk with imipramine, desipramine, fluoxetine, nisoxetine, tranylcypromine or mianserin before being processed in the forced swim test. Chronic treatment with imipramine and desipramine alone induced Fos-LI in the central nucleus of the amygdala and the dorsolateral bed nucleus of the stria terminalis. After tranylcypromine treatment, Fos-LI was induced in many brain regions including limbic cortex, amygdala and paraventricular nucleus of the hypothalamus. None of the other antidepressants induced Fos-LI in any brain region examined. Chronic administration of imipramine, desipramine and nisoxetine antagonized the swim induced expression of Fos-LI in the PVN and in limbic cortical regions, including the medial prefrontal ventrolateral orbital and cingulate cortices. Chronic treatment with fluoxetine, tranylcypromine and mianserin did not alter swim stress-induced Fos-LI in any brain region. Thus, only antidepressant drugs that affect norepinephrine uptake (i.e., imipramine, desipramine and nisoxetine) antagonized swim stress-induced Fos-LI. In contrast to the action of chronic imipramine on Fos-LI induced by swim, chronic administration of imipramine did not antagonize the stress-induced changes in 2-DG uptake in limbic cortical regions. Acute administration of propranolol, which blocks beta-adrenergic receptors, reduced the number of cells staining for Fos-LI in limbic cortical regions, resembling the effects produced by chronic imipramine, desipramine and nisoxetine. In the PVN, neither propranolol nor prazosin (an alpha 1 antagonist) blocked the swim-induced Fos-LI, suggesting that swim-induced Fos-LI in the PVN is not under control of beta- or alpha 1-adrenergic receptors. These latter results imply that adaptation of noradrenergic receptors by chronic imipramine may not be related to the antagonism of stress-induced Fos-LI. The clear functional differences of the various antidepressant agents on swim stress-induced Fos-LI after chronic administration provide a functional classification of antidepressant drug action not previously identified.

Animals↗
PubMed1997

Applying physiological principles and assessment techniques to swimming the English Channel. A case study.

BACKGROUND: This study presents the use of physiological principles and assessment techniques in addressing four objectives that can enhance a swimmer's likelihood of successfully swimming the English Channel. The four objective were: (1) to prescribe training intensities and determine ideal swimming pace; (2) to determine the amount of insulation needed, relative to heat produced, to diminish the likelihood of the swimmer suffering from hypothermia; (3) to calculate the caloric expenditure for the swim and the necessary glucose replacement required to prevent glycogen depletion; and (4) to determine the rate of acclimatization to cold water (15.56 C/60 F). METHODS: The subject participated in several pool swimming data collection sessions including a tethered swim incremental protocol to determine peak oxygen consumption and onset of lactate accumulation and several steady state swims to determine ideal swimming pace at 4.0 mM/L of lactate. Additionally, these swims provided information on oxygen consumption, which in combination with ultrasound assessment of subcutaneous fat was used to assess heat production and insulation capabilities. Finally, the subject participated in 18 cold water immersions to document acclimatization rate. RESULTS: The data demonstrated the high fitness level of this subject and indicated that at a stroke rate of 63 stokes/min, HR was 130 heats/min and lactate was 4 mM/L. At this swimming pace the swimmer would need to consume 470 kcal of glucose/hr. In addition, the energy produced at this swim pace was 13.25 kcal/min while the energy lost at the present subcutaneous fat quantity was 13.40 kcal/min, requiring a fat weight gain of 6,363.03 g (13.88 lbs) to resist heat loss. CONCLUSIONS: Finally, the data from the cold water immersions suggested that acclimatization occurred following two weeks of immersions. There results were provided to the swimmer and utilized in making decisions in preparation for the swim.

Acclimatization↗
PubMed1988

Analgesia induced by continuous versus intermittent cold water swim in the rat: differential effects of intrathecal administration of phentolamine and methysergide.

Continuous cold water swim produces analgesia that is partially mediated by a noradrenergic mechanism, but is independent of both serotonergic and opioid systems. On the other hand, intermittent cold water swim elicits analgesia which is partly mediated by an opioid mechanism; the contribution of the monoamines to the production of this analgesia is not known. Therefore, the present study was done to determine whether intermittent cold water swim is also mediated by noradrenergic and/or serotonergic substrates. Prior to either continuous (3.5 min) or intermittent (10 sec in, 10 sec out for 6 min) cold water (4 degrees C) swim, male Sprague-Dawley rats (225-250 g) were administered either the noradrenergic receptor blocker phentolamine (30 micrograms), the serotonergic blocker methysergide (30 micrograms) or artificial cerebrospinal fluid to the fifth lumbar vertebral spinal level via chronic intrathecal catheters. Phentolamine significantly attenuated the analgesia resulting from both continuous and intermittent cold water swim. Methysergide attenuated intermittent cold water swim analgesia, but was without effect on continuous cold water swim analgesia. Phentolamine, but not methysergide, also attenuated continuous footshock- (2.5 mA for 3 min) induced analgesia. The similarity between the effects of phentolamine and methysergide on continuous footshock and continuous cold water swim analgesia suggests that the effects of these drugs on cold water swim analgesia are not attributable to changes in thermoregulation. These results suggest that a spinal noradrenergic mechanism is involved in the mediation of both forms of cold water swim analgesia, whereas a spinal serotonergic mechanism is involved in only intermittent cold water swim analgesia.

Animals↗
PubMed1997

Kinematics and efficiency of steady swimming in adult axolotls (Ambystoma mexicanum)

The kinematics of steady swimming at a wide range of velocities was analysed using high-speed video recordings (500 frames s-1) of eight individuals of Ambystoma mexicanum swimming through a tunnel containing stationary water. Animals in the observed size range (0.135­0.238 m total body length) prefer to swim at similar absolute speeds, irrespective of their body size. The swimming mechanism is of the anguilliform type. The measured kinematic variables ­ the speed, length, frequency and amplitude (along the entire body) of the propulsive wave ­ are more similar to those of anguilliform swimming fish than to those of tadpoles, in spite of common morphological features with the latter, such as limbs, external gills and a tapering tail. The swimming speed for a given animal size correlates linearly with the tailbeat frequency (r2=0.71), whereas the wavelength and tail-tip amplitude do not correlate with this variable. The shape of the amplitude profile along the body, however, is very variable between the different swimming bouts, even at similar speeds. It is suggested that, for a given frequency, the amplitude profile along the body is adjusted in a variable way to yield the resulting swimming speed rather than maintaining a fixed-amplitude profile. The swimming efficiency was estimated by calculating two kinematic variables (the stride length and the propeller efficiency) and by applying two hydrodynamic theories, the elongated-body theory and an extension of this theory accounting for the slope at the tail tip. The latter theory was found to be the most appropriate for the axolotl's swimming mode and yields a hydromechanical efficiency of 0.75±0.04 (mean ± s.d.), indicating that Ambystoma mexicanum swims less efficiently than do anuran tadpoles and most fishes. This can be understood given its natural habitat in vegetation at the bottom of lakes, which would favour manoeuvrability and fast escape.

Journal Article↗
PubMed1998

Initial recruitment of anaerobic metabolism during sub-maximal swimming in rainbow trout (Oncorhynchus mykiss)

Lactate and phosphocreatine concentrations were monitored in the white muscle of rainbow trout Oncorhynchus mykiss following swimming at 70, 80 and 100 % of critical swimming speed (Ucrit) using 31P-nuclear magnetic resonance (NMR) spectroscopy. Lactate was detected following swimming at all speeds, but its concentration was greatest following swimming at 80 and 100 %Ucrit. Phosphocreatine stores were reduced following swimming at 70 and 80 %Ucrit, but were further depleted following swimming at 100 %Ucrit. Following swimming at 70 and 80 %Ucrit, lactate concentrations were higher in the rostral, relative to the caudal, musculature, whereas phosphocreatine stores were least depleted in the mid, relative to the rostral and caudal, musculature. There were no differences among muscle locations in concentrations of lactate and phosphocreatine following swimming to 100 %Ucrit. Our results indicate that anaerobic metabolism is required to support swimming at speeds equal to and greater than 70 %Ucrit. Estimates of the relative cost of anaerobic metabolism during sub-maximal swimming are presented for swimming at 70 %, 80 % and 100 %Ucrit, and the implications of these results to energy budgets are discussed.

Journal Article↗
PubMed1985

Central generation of swimming activity in the hydrozoan jellyfish Aequorea aequorea.

Swimming in Aequorea is controlled by a network of electrically coupled neurons (swim motorneurons) located in the inner nerve ring. The network is made up of the largest neurons in the ring, up to 22 microns in diameter. Intracellular recordings from swim motorneurons reveal slow membrane potential oscillations and a superimposed barrage of synaptic "noise." The synaptic noise, but not the slow oscillations, is eliminated in seawater containing an elevated Mg++ concentration. The swim motorneurons produce a rapid burst of two to eight action potentials preceding each contraction of the subumbrella. Spontaneous bursting persists in high-Mg++ seawater. Injected ramp currents indicated a "bursty" character of the swim motorneurons as suprathreshold depolarizations produced repetitive bursting with an increasing burst frequency with increased depolarization. Hyperpolarizing currents locally blocked spiking in swim motorneurons. Intercellular coupling was demonstrated with Lucifer Yellow injection and dual electrode recordings. In dye fills, only the large neurons of the inner nerve ring were dye-coupled. Two pieces of evidence suggest that swim motorneurons activate the overlying epithelial cells via chemical synapses. First, direct synaptic connections have been noted in ultrastructural examination of the inner nerve ring region. Second, dual recordings from a swim motorneuron and an epithelial cell reveal a 1:1 correspondence between neuron spikes and epithelial synaptic potentials. The synaptic potentials occur with a latency as short as 3 ms which is constant in any one recording session. The results suggest that the swim motorneuron network of Aequorea not only performs a motorneuron function, but also serves as the pattern generator for swimming activity.

Animals↗
PubMed2005

Changes in in vivo [(3)H]-Ro15-4513 binding induced by forced swimming in mice.

Mice were forced to swim for 5 min in water at a temperature of 12 degrees C (cold water swim stress) or 32 degrees C (warm water swim stress), and stress-induced analgesia (SIA) was measured using the tail-flick test. The cold water swim stress induced non-opioid SIA as well as hypothermia, whereas the warm water swim stress caused opioid SIA. The in vivo binding of [(3)H]-Ro15-4513 was measured in the stressed mice and compared with that in control mice. The specific binding of [(3)H]-Ro15-4513 in the cerebral cortex, hippocampus, and cerebellum was significantly altered by forced swimming in cold water. Apparent association and dissociation rate of [(3)H]-Ro15-4513 binding were decreased, and the change in the dissociation rate was most pronounced in the hippocampus. In contrast, no significant alterations were observed in in vitro binding. The hypothermia induced by the cold water swim stress seems to be the main reason for alterations in the specific binding of [(3)H]-Ro15-4513. The kinetics of a saturable amount of [(3)H]-Ro15-4513 in the blood and brain were also measured. The relative ratio of the radioactivity concentration in the brain to that in the blood was significantly decreased by forced swimming in cold water, indicating that the cold water swim stress induced changes in the nonspecific binding of [(3)H]-Ro15-4513 in the brain. These results together with previous reports suggested that non-opioid SIA induced by the cold water swim stress might be related to alterations in the rates of general ligand-receptor interactions including GABA(A)/benzodiazepine system. Changes in the nonspecific binding might be also involved in non-opioid SIA.

Analysis of Variance↗
PubMed1998

Sensitization of the Tritonia escape swim.

When repeatedly elicited, the oscillatory escape swim of the marine mollusc Tritonia diomedea undergoes habituation of the number of cycles per swim. Previous work has shown that this habituation is accompanied by sensitization of another feature of the behavior: latency to swim onset. Here we focused on the behavioral features of sensitization itself. Test swims elicited 5 min after a strong sensitizing head stimulus differed in several ways from control swims: sensitized animals had shorter latencies for gill and rhinophore withdrawal, a shorter latency for swim onset, a lower threshold for swim initiation, and an increased number of cycles per swim. Sensitized animals did not, however, swim any faster (no change in cycle period). A separate experiment found that swim onset latency also sensitized when Tritonia came into contact with one of their natural predators, the seastar Pycnopodia helianthoides, demonstrating the ecological relevance of this form of nonassociative learning. These results define the set of behavioral changes to be explained by cellular studies of sensitization in Tritonia.

Animals↗
PubMed1993

Does critical swimming velocity represent exercise intensity at maximal lactate steady state?

The purpose of this investigation was to determine whether the critical swimming velocity (vcrit), which is employed in competitive swimming, corresponds to the exercise intensity at maximal lactate steady state. vcrit is defined as the swimming velocity which could theoretically be maintained forever without exhaustion and expression as the slope of a regression line between swimming distances covered and the corresponding times. A total of eight swimmers were instructed to swim two different distances (200 m and 400 m) at maximal effort and the time taken to swim each distance was measured. In the present study, vcrit is calculated as the slope of the line connecting the two times required to swim 200 m and 400 m. vcrit determined by this new simple method was correlated significantly with swimming velocity at 4 mmol.l-1 of blood lactate concentration (r = 0.914, P < 0.01) and mean velocity in the 400 m freestyle (r = 0.977, P < 0.01). In the maximal lactate steady-state test, the subjects were instructed to swim 1600 m (4 x 400 m) freestyle at three constant velocities (98%, 100% and 102% of vcrit). At 100% vcrit blood lactate concentration showed a steady-state level of approximately 3.2 mmol.l-1 from the first to the third stage and at 98% of vcrit lactate concentration had a tendency to decrease significantly at the fourth stage. On the other hand, at 102% of vcrit, blood lactate concentration increased progressively and those of the third and fourth stages were significantly higher than those at 100% of vcrit (P < 0.05). These data suggest that vcrit, which can be calculated by performing two timed, maximal effort swimming tests, may correspond to the exercise intensity at maximal lactate steady state.

Adolescent↗
PubMed1981

VO2 peak during free swimming using the backward extrapolation of the O2 recovery curve.

The purpose of this study was to evaluate the accuracy and feasibility of estimating oxygen consumption (VO2) during maximal swimming by using the backward extrapolation (BE) of the VO2 recovery curve to time zero. Two series of experiments were conducted. In the first, the validity of the BE method was ascertained by comparing the VO2 peak values obtained during free swimming (Douglas bag technique) with those estimated by the BE method during recovery after the same tests. These results were also compared with VO2 peak measured during uphill treadmill running. VO2 peak measured during maximal free swimming and estimated by the BE method during the recovery period of that test, were not significantly different. No significant difference was found between VO2 peak uphill treadmill running and free swimming. In the second series of experiments, VO2 peak was measured in each of 28 swimmers during uphill running (conventional method) and during unimpeded swimming using the BE method. The mean value was significantly higher during swimming (mean = 3.37) than during running (mean = 3.23). Seventy-five percent of the subjects had higher VO2 peak during swimming. The swimming speed during maximal swimming effort was 10% higher when the BE method was used then when the same subjects were tested by the conventional Douglas bag technique. The BE method is reliable and valid way to measure VO2 peak in maximal swimming and allows the swimmer to use his specifically trained musculature fully.

Adolescent↗
PubMed1996

Susceptibility and resistance of rats to stress-induced decreases in swim-test activity: a selective breeding study.

In this study, selective breeding was used to generate two populations of rats that differed in their susceptibility to showing decreased struggling activity in a swim test after being exposed to uncontrollable electric tail-shock. After five generations of selective breeding, we obtained a population that displayed large decreases in swim-test struggling after shock (swim-test susceptible) and a population that displayed no decrease in struggling after shock (swim-test resistant). Males of this fifth generation from the two selectively-bred populations were then compared for differences in non-swim behavioral measures (home-cage 24-h spontaneous ambulatory activity and food/water intake) and several aspects of brain catecholaminergic activity, including electrophysiological activity of locus coeruleus (LC) neurons, catecholamine/metabolite concentrations in various brain regions, and in vivo tyrosine hydroxylase activity. Interestingly, swim-test resistant rats displayed larger decreases in home-cage ambulatory activity and water intake after exposure to shock than did swim-test susceptible animals. Marked differences were also seen in measures of brain noradrenergic activity. Compared to the susceptible rats, resistant rats showed higher levels of evoked activity of LC neurons, larger shock-induced depletions of norepinephrine (NE) and 3-methoxy-4-hydroxyphenylglycol (MHPG) in the LC, lower in vivo tyrosine hydroxylase (TH) activity in ventral bundle projection areas such as the hypothalamus, and larger amounts of NE in dorsal bundle projection areas. Finally, swim-test resistant rats had much higher concentrations of dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in striatum and nucleus accumbens than susceptible rats. These results appear to be explainable on the basis that differences in swim-test struggling behavior for which the two populations were selectively bred were a consequence of differences in forebrain DA whereas stress-induced differences in other behavioral measures (i.e. spontaneous ambulation and intake) occurred because swim-test resistant animals showed greater disturbance of the LC-NE system after uncontrollable shock.

Animals↗
PubMed1993

Effect of the tail ganglion on swimming activity in the leech.

In the medicinal leech, Hirudo medicinalis, isolated segmental nerve cords are capable of generating swimming activity. The role played by the head and tail ganglia in regulating the expression of swimming activity by the segmental nerve cord was evaluated by comparing swimming activity in nerve cord preparations with and without the head and tail ganglia attached. Several swim properties were examined, including length of induced swim episodes, ability to initiate swim episodes, swim cycle period, and phase. We found that, in general, the presence of the tail ganglion attached to isolated nerve cords countered the effects produced by the head ganglion on swimming activity. Moreover, we observed that the tail ganglion itself provides excitatory drive to the swim generating system. Thus, the inputs from the head and tail ganglia influence significantly the expression of swimming activity.

Animals↗
PubMed2004

The determination of drag in front crawl swimming.

The measurement of drag while swimming (i.e. active drag) is a controversial issue. Therefore, in a group of six elite swimmers two active drag measurement methods were compared to assess whether both measure the same retarding force during swimming. In method 1 push-off forces are measured directly using the system to measure active drag (MAD-system). In method 2 (the velocity perturbation method, VPM) drag is estimated from the difference in swimming speed when subjects swim twice at maximal effort (assuming equal power output and assuming a quadratic drag-speed relationship): once swimming free, and once swimming with a hydrodynamic body attached that created a known additional resistance. The average drag for the VPM tests (53.2 N) was statistically significant and different from the active drag for the MAD-test (66.9 N), paired Student's t-test: 2.484, 12 DF, p=0.029. A post hoc analysis was performed to assess whether the two methods measure a different phenomenon. Based on the drag speed curve obtained with the MAD-system, the VPM-data were re-examined. For diverging drag determinations the assumption of equal power output of the 'free' trial (swimming free) vs. the towing trial (swimming with hydrodynamic buoy) appeared to be violated. The regression of the relative difference in force (MAD vs. VPM) on the relative difference in power (swimming free vs. swimming with hydrodynamic body) was: %Deltadrag=1.898 x %Deltapower -4.498, r2=0.88. This suggests that the major part of the difference in active drag values is due to a non-equal power output in the 'free' relative towing trial during the VPM-test. The simulation of the violation of the equal power output assumption and the calculation of the effect of an other than quadratic drag-speed relationship corroborated the tentative conclusion that both methods measure essentially the same phenomenon and that active drag differences can be explained by a violation of test assumptions.

Adolescent↗
PubMed2006

The effects of exercise intensity or drafting during swimming on subsequent cycling performance in triathletes.

The purpose of this study was to compare the affects of drafting or a reduction of exercise intensity during swimming on the power output sustained (P(mean)) during a subsequent cycle time trial (TT). In addition the relationship between peak power output (PPO) and P(mean) generated during the cycle TT after swimming was examined. Nine well-trained triathletes performed an incremental cycling test to exhaustion for determination of PPO. In addition, each subject performed three swim-cycle (SC) trials consisting of 20 min cycle TT preceded by a 400 m swimming trial completed as (1) "all out" and in a non-drafting situation (SC(100%)); (2) at 90% of SC(100%) in a non-drafting situation (SC(90%)); (3) in a drafting position at the same controlled velocity as SC(100%) (SC(drafting)). Swimming velocity (ms(-1)) was significantly (p<0.01) lower at each time point during the 400 m swimming trial in SC(90%) compared with SC(100%) and SC(drafting). There was no significant difference in velocity between SC(100%) and SC(drafting). Blood lactate (BLA) concentration was also significantly (p<0.01) lower after swimming in SC(90%) compared to SC(100%) and SC(drafting) (3.8+/-0.9 versus 7.3+/-2.4 and 7.9+/-2.4mM). The Pmean was also significantly (p<0.05) lower in SC(100%) relative to the SC(90%) and SC(drafting) (226+/-15 versus 253+/-33 and 249+/-36W). There was no significant correlation between PPO (W) and P(mean) for SC(100%) (r=-0.32), SC(90%) (r=0.65; p=0.058) or SC(drafting) (r=0.54). This study indicates that drafting or swimming at a lower velocity did not induce any conflicting affects on power output during a subsequent cycle TT. However, this study confirms that P(mean) during a cycle TT is reduced when prior swimming is performed. Furthermore the positive relationship typically observed between PPO and P(mean) is disrupted by swimming activity performed before a cycling TT. This factor should be considered in terms of physiological analysis of triathletes.

Adult↗
PubMed2000

Sex differences in forced-swim and open-field test behaviours after chronic administration of melatonin.

The effects of melatonin administered chronically on forced-swim test and open-field test behaviours were examined in male and female rats. The forced-swim test has been shown to be sensitive to all major classes of antidepressants and evidence indicates that melatonin possesses putative antidepressive properties. Male and female Long-Evans rats received either a regimen of chronic administration of melatonin or the control condition for 14 days via the drinking water. On day 15, each animal was individually introduced into a swim chamber, and was scored for 15 min on the duration of swimming, struggling, and immobility. After 24 h, each animal was again tested in the forced-swim test for 10 min. On day 18, all animals were tested in the open-field test apparatus for 5 min. Results revealed that females consistently showed higher activity levels than males in the forced-swim and open-field tests. Melatonin significantly increased struggling in males on day 15, but failed to do so in females. Also, whereas melatonin-treated females showed higher levels of behavioural immobility during their first exposure to the forced-swim test, this effect was prevented upon a second exposure. In both males and females, melatonin decreased swimming in the forced-swim test while increasing open-field ambulatory behaviour. Therefore, it is unlikely that melatonin's mechanism of action is a general inhibitory effect on motor activity. Taken together, the results suggest that the effects of melatonin treatment on forced-swim test behaviours are sex- and test-dependent.

Animals↗
PubMed2001

Swim stress alters the behavioural response of mice to GABA-related and some GABA-unrelated convulsants.

To elucidate the relationship between stress and seizures, the effect of a single swim stress on the convulsive signs and death produced by several GABA-related and GABA-unrelated convulsants, and the effect of repeated swim stress on picrotoxin-induced convulsions was studied. Mice were subjected to swim stress (10 min swimming at 18-19 degrees C), and the i.v. infusion of convulsants started 15 min thereafter. The latency to the onset of several convulsant signs and death was measured, and the doses of convulsants producing convulsions and death were calculated. Additional experiments included mice swimming at room temperature, and those which were stressed repeatedly (twice a day for four consecutive days, plus one stressful procedure on the fifth day). Swim stress increased the dose needed to produce convulsant signs and death after bicuculline, picrotoxin, pentylenetetrazole, strychnine and 4-aminopyridine, while kainic acid-induced convulsions were not affected. Using picrotoxin infusion, the effect of swimming in room temperature water was less than the effect of swimming in 18-19 degrees C water. In addition, the effect of repeated stress was less than the effect of acute stress on picrotoxin-induced convulsions. The results demonstrate that acute swim stress lowers the convulsive potency of GABA-related and some GABA-unrelated convulsants. Repeatedly stressed animals develop tolerance to anticonvulsive effect of swim stress.

Animals↗
PubMed2002

Alpha-adrenoreceptor activation modulates swimming via glycinergic and GABAergic inhibitory pathways in Xenopus laevis tadpoles.

This study focuses upon the network pathways underlying the adrenoreceptor-mediated modulation of fictive swimming in the immobilized Xenopus laevis tadpole. As shown recently, noradrenaline (NA) increases cycle periods while simultaneously reducing the rostrocaudal delay in head-to-tail firing and the duration of swimming episodes. Furthermore, both swimming frequency and duration are reduced by selective pharmacological activation of alpha1- and/or alpha2-adrenoreceptors, while alpha1-receptor activation also reduces rostrocaudal delays. We show that NA could still modulate aspects of swimming after blocking either glycine or GABA(A) receptors with strychnine and bicuculline, respectively. Furthermore, after prior application of NA, strychnine could counteract noradrenergic effects on cycle periods and rostrocaudal delays, while bicuculline could counteract effects on cycle periods, suggesting that these two fast inhibitory pathways are both involved in the NA modulation of swimming. In addition, blocking glycine receptors reduced the effects of alpha1-receptors on cycle periods and delays, while blocking GABA(A) receptors had no effect. Blocking either glycine or GABA(A) receptors, however, lessened the reduction in swimming frequency by alpha2-receptors. In addition, pre-application of bicuculline prevented a reduction in episode durations by NA, alpha1- and alpha2-receptors. Our findings suggest that the noradrenergic modulation of Xenopus swimming is mediated via alpha-adrenoreceptors interacting with both glycinergic and GABAergic inhibitory pathways. Both alpha1- and alpha2-receptor activation influences the GABAergic pathway controlling the duration of swimming episodes and is involved in the glycinergic modulation of the swimming rhythm and its longitudinal co-ordination, with alpha2-receptors additionally affecting swimming frequency through GABAergic pathways.

Adrenergic alpha-Agonists↗
PubMed1985

Relationship between swimming velocity and lactic concentration during continuous and intermittent training exercises.

The present study examined the relationship between lactic acid concentration in capillary blood and swimming velocity during 11 typical endurance exercises (continuous swimming for 30 and 60 min, interval swimming with distances between 50 and 400 m, and with rest periods of 10 and 30 s) and during the "two-speed test" recently described by Mader. It was expected that a better understanding of these relationships could provide evidence how to adjust training intensities from results obtained during the two-speed test. Fifty-nine male swimmers of the German national level participated in this study. After a 30-min maximal swimming test, a mean lactic acid concentration of 4.01 +/- 0.75 mmol/l was found. The corresponding mean velocity was similar to the speed (V4) calculated for the 4 mmol/l level on the basis of the results obtained during the two-speed test (2 X 400). During 30 min continuous swimming at 95% to 105% of the velocity V4, there was a significant correlation (r = 0.82, P less than 0.001) between the swimming speed and the lactic acid concentration. In the 30-min maximal test, the velocity V4 correlated significantly with both the lactic acid concentration (r = -0.58, P less than 0.005) and the swimming speed (r = 0.97, P less than 0.001). During the interval exercises with rest periods of 10 s, the swimming velocities corresponding to the same lactic acid level as during continuous swimming, increased for the 50, 100, 200, and 400 m by 11.23%, 4.21%, 2.95%, and 2.02% of V4, respectively. With rest periods of 30 s, the swimming velocity for the 100, 200, and 400 m increased by 7.34%, 4.22%, and 3.01% of V4, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗