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PubMed1998

Effects of antidepressant drugs on rats bred for low activity in the swim test.

To determine responsivity to antidepressant medication of Sprague-Dawley rats bred for low activity in the swim test [Swim Low-Active (SwLo) rats], these animals were given different antidepressant drugs via subcutaneously implanted minipumps for 1, 12, or 26 days, and then were tested for activity in the swim test and 2 days later in the open field. Antidepressant drugs given were amitriptyline, imipramine, desipramine (tricyclics), phenelzine (monoamine oxidase inhibitor (MAOI)], fluoxetine [selective serotonin reuptake inhibitor (SSRI)], venlafaxine, and bupropion (atypical). To assess specificity of response, the nonantidepressant drugs amphetamine, caffeine, and haloperidol were also tested. For comparison, several drugs were also tested in rats bred for high activity in the swim test [Swim High-Active (SwHi) rats]. When administered for 14 and/or 28 days (but not for 1 day), imipramine, desipramine, venlafaxine, phenelzine, and bupropion significantly increased struggling behavior of SwLo rats in swim test. No nonantidepressant drug significantly elevated struggling activity. Long-term administration of phenelzine and bupropion also significantly decreased floating behavior in the swim test, although amphetamine also had this effect at all times of administration. No significant effects of antidepressants were seen in SwHi rats. Amitriptyline and fluoxetine were ineffective in altering either struggling or floating in SwLo rats; however, a high dose of an SSRI (sertraline) did reduce floating, but this type of effect is probably not indicative of antidepressant action. Behavior in the open field was not consistently affected by any drug type. It is concluded that, based on pharmacological response profile in the swim test, SwLo rats represent depression that is responsive to potent norepinephrine reuptake-blocking antidepressants and also MAOIs; atypical depression may fit this profile.

Animals↗
PubMed2002

In the rat forced swimming test, chronic but not subacute administration of dual 5-HT/NA antidepressant treatments may produce greater effects than selective drugs.

UNLABELLED: The rat forced swimming test (FST) distinguishes selective serotonin (5-HT) and selective noradrenaline (NA) reuptake-inhibitors, which respectively increase swimming and climbing behaviours. However, NA-system-mediated inhibition of 5-HT-induced swimming prevents dual 5-HT/NA reuptake-inhibition to produce concurrently climbing with swimming. Since adaptative neurochemical processes occur in the treatment of depression, we examined the influence of long-term antidepressant treatment on these interactions. METHODS: (1) Selective [fluoxetine: 10 mg/kg; desipramine: 10 mg/kg] and non-selective [milnacipran: 40 mg/kg; mirtazapine: 20 mg/kg] antidepressants were administered subacutely (3inj) and chronically (17inj) over 16 days. (2) A subacute fluoxetine-desipramine combination (10-10 mg/kg) was administered in rats that were pre-treated with chronic-desipramine (10 mg/kg per day, 14 days). (3) NA-system-mediated interactions were further examined by combining the alpha(2)-receptor agonist clonidine (5, 10, 20, 200 microg/kg) with 10 mg/kg fluoxetine. RESULTS: (1) Long-term treatment with either fluoxetine or desipramine does not modify the behavioural response produced by their subacute administration. (2) In contrast, whereas subacute-milnacipran increases climbing solely, chronic-milnacipran produces greater anti-immobility effects and increases both climbing and swimming behaviours. Similarly, the fluoxetine-desipramine combination produces climbing solely, but increases both climbing and swimming behaviours in animals pre-treated with chronic-desipramine. Chronic but not subacute-mirtazapine increases swimming behaviour. (3) clonidine dose-dependently antagonizes fluoxetine-induced anti-immobility effects and swimming behaviour. CONCLUSIONS: Chronic enhancement of NA-transmission alters NA-system-mediated inhibition of 5-HT-induced behaviour in the FST, which may involve alpha(2)-receptors.

Adrenergic Uptake Inhibitors↗
PubMed2001

Nucleus accumbens muscarinic receptors in the control of behavioral depression: antidepressant-like effects of local M1 antagonist in the Porsolt swim test.

Systemically administered cholinomimetics or cholinesterase inhibitors can depress behavior in humans and animals, whereas antimuscarinic agents reverse this effect or even produce euphoria. Although these effects have been well documented, the specific brain regions that mediate them remain largely unknown. In the present experiments, muscarinic agonists and antagonists were locally injected into the nucleus accumbens of female Sprague-Dawley rats to test for their effects on behavioral depression in the Porsolt swim test and locomotor activity. Local, microinjections of the drugs in the accumbens elicited behaviors that were similar to the systemic effects reported in other studies. Injection of the non-specific agonist arecoline (40 and 80 microg) dose-dependently inhibited swimming and escape behavior. This may be mediated in part by accumbens M1 receptors because blocking these receptors with the specific antagonist pirenzepine (17.5 and 35.0 microg) did the opposite by increasing swimming. Gallamine (0.13, 0.44, and 0.88 microg), an antagonist at M2 receptors, dose-dependently decreased swimming. Two-way microdialysis suggested that this was in part due to the release of ACh by blocking M2 autoreceptors. Scopolamine, a mixed M1/M2 receptor antagonist, also released ACh but did not decrease swimming, probably because the M1 receptors were blocked; the drug (1.0 microg) increased swimming time, much like pirenzepine. With the exception of arecoline, none of the drugs significantly affected locomotor activity in a photocell cage. Arecoline (40 microg), which had decreased swimming, reduced activity. The present study suggests that muscarinic receptors in the nucleus accumbens can control immobility in the Porsolt swim test. The onset of immobility may depend on the activation of post-synaptic M1 receptors.

Acetylcholine↗
PubMed1999

Molluscum contagiosum, swimming and bathing: a clinical analysis.

The link between swimming and bathing behaviour, and molluscum contagiosum (MC), in a sample of 198 patients with clinically confirmed MC was investigated. Results show that of all the swimming behaviour variables tested, only one (swimming in a school swimming pool) was significant. In relation to the bathing variables tested, only two (sharing a bath sponge with a MC-infected person, and sharing a bath towel with a MC-infected person), were significant. No relationship was found between MC and swimming in a private (home) pool, swimming in a public pool, swimming at the beach, sharing a bath tub with a MC-infected person, and using a private (home) spa. The Relative Risk (RR) ratio of a person sharing a bath sponge with an infected person is three times more at risk of procuring a severe case of MC infection (i.e. > 26 lesions) than a person who does not share a bath sponge with an infected person (r = 0.5; P < 0.01). There was a correlation found between the mode of MC acquisition by site location (r = 0.63; P < 0.05). The anatomical position of MC lesions was shown to be highly dependent on the way the patient was primarily infected. There was also an additive effect with the mode of transmission in that patients who were in the upper extremes in terms of the total number of lesions (average, 124 lesions; mean diameter size, 4.2 mm; n = 42), were those patients who shared a number of fomites (bath sponge, bath towel) with a known MC-infected person, and also swam at the school swimming pool.

Adolescent↗
PubMed2004

Sustained swimming increases erythrocyte MCT1 during erythropoiesis and ability to regulate pH homeostasis in rat.

We investigated the effect of sustained swimming exercise on the increase in monocarboxylate transporter 1 (MCT1) concentration and its ability to regulate pH homeostasis in rat erythrocytes. Male Sprague-Dawley rats aged 9 weeks were divided into sedentary and swimming groups for both 1- and 3-week experiments. The exercise group swam for 30 - 60 min/day, 5 days/week. Before and 1 and 3 weeks after initiation of the exercise, blood was collected for lactate concentration measurement during pre-exercise rest and post-exercise recovery periods. On the last day of each experiment, venous blood and erythroid cells in bone marrow were collected to assay the capacity for erythropoiesis and MCT1 concentration. In the swimming group at 0 weeks (p < 0.05), 1 week (p < 0.01) and 3 weeks (p < 0.001), the blood lactate concentration post-exercise was significantly higher than at rest. The ratio of young erythrocytes to total erythrocytes was significantly higher in the 3-week swimming group than in the sedentary group (p < 0.05). The MCT1 concentration in erythrocytes was higher in the 3-week swimming group than in the sedentary group (18 %, p < 0.05), which was found in young erythrocytes (22 %, p < 0.05) when total erythrocytes were separated into young and old fractions. The MCT1 concentration in erythroid cells was higher in both the 1-week and 3-week swimming groups than in either of the sedentary groups (27 and 28 %, respectively, p < 0.05). The pH recovery of erythrocyte suspensions at 10, 15 and 20 seconds after addition of lactate to the suspension medium was significantly faster in the 3-week swimming group than in the sedentary group (p < 0.001). These findings suggest that erythrocyte MCT1 is increased during erythropoiesis in bone marrow and that the increase of the transporter facilitates, at least partly, lactate/proton co-transport due to sustained swimming exercise in rats.

Acid-Base Equilibrium↗
PubMed1993

Adaptations to six months of aerobic swim training. Changes in velocity, stroke rate, stroke length and blood lactate.

The purpose of this investigation was to determine how swimming velocity (SV), stroke rate (SR), stroke length (SL) and blood lactate concentration change as adaptations to six months of aerobic swim training. Subjects were trained male college swimmers (n = 8). Measurements were obtained following specially designed 400m freestyle swim tests, pre- and post-intervention. The swim test consisted of 4 x 400 m freestyle over two days. On day 1, subjects performed a maximal effort 400 m freestyle swimming trial; maximal mean velocity (Vmax) for each swimmer was calculated from this effort. On the next day, subjects were instructed to perform three 400 m freestyle swims at constant velocities equal to 85%, 90% and 95% of Vmax, respectively. Subjects rested one hour between swims. During each 400 m trial, lap time and time to complete 10 mid-pool strokes (50 m) were measured to determine SV (m.s-1), SR (stroke.min-1) and SL (m.stroke-1). Mixed arterial blood samples were taken at the end of each 400 m trial to evaluate blood lactate concentration. Results indicated that post-maximal swimming velocity (Vpostmax) increased significantly from pre-intervention measures (p < 0.05). Blood lactate concentration decreased significantly relative to SV and absolute lactate concentration following Vpostmax was significantly lower than that at Vpremax (p < 0.05). Six of seven subjects increased Vmax due to increases in SL. Mean SL during the second test was significantly higher (p < 0.05). Also, during the 400 m maximal test, SL increased significantly after sixth lap (p < 0.05). There was no significant difference between SRs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1984

Effects of NaHCO3, alpha-, and beta-adrenergic blockade on albuminuria after swimming in splenectomized dogs.

The albuminuria occurring after swimming in splenectomized dogs was investigated. Swimming in splenectomized dogs induces metabolic acidosis, a decrease in renal vascular conductance, and an increase in plasma renin activity, all three factors possibly implicated in the occurrence of albuminuria. The administration of sodium bicarbonate prior to swimming reduced the magnitude of the acidosis and eliminated the increase in albuminuria after swimming. Phenoxybenzamine, an alpha-adrenergic blocking agent that maintains the renal blood flow during exercise also blocked the increase in albuminuria despite a decrease of blood pH during swimming. However, after metoprolol, a beta 1-adrenergic blocking agent that blocks the rise in plasma renin activity during exercise, swimming causes a threefold increase in albuminuria (P less than 0.01). The albuminuric response to swimming preceded by saline was also significant (P less than 0.05). It is likely that post-swimming albuminuria in splenectomized dogs is linked to the decrease of renal vascular conductance or to the decrease in blood pH rather than to the rise in plasma renin activity.

Acidosis↗
PubMed1990

Dietary carbohydrate and intensity of interval swim training.

We tested the effects of 9 d of a high-carbohydrate diet (80% of calories as CHO, 80% CHO diet) vs. a moderate-CHO diet (43% of calories as CHO, 43% CHO diet) on the abilities of collegiate swimmers to maintain a high intensity of interval swim training. Interval swim times and other physiological indices were recorded the last 5 d of each diet. Swim-interval distances ranged from 50-m interval sets to continuous 3000-m swims. There were no diet effects on mean swim velocities for any interval distance, and mean (+/- SEM) velocities for all swims were identical for both diets. There were no diet effects on the physiological indices; however, postswim blood lactate concentrations were higher after the 80% CHO diet. When mean +/- SEM daily caloric intake is 19.56 +/- 2.16 MJ (4675 +/- 516 kcal) for swimmers undertaking swim training to develop aerobic capacity, an 80% CHO diet provides no advantage over a 43% CHO diet for maintaining interval-swim-training intensity.

Adult↗
PubMed2000

Swimming training prevents generation of suppressor macrophages during acute cold stress.

PURPOSE: Acute cold stress induces suppressor macrophages expressing large numbers of receptors to Fc portion of immunoglobulin G (MAC-1+ Fc gammaRII/IIIbright cells), resulting in suppression of splenocyte mitogenesis. The generation of MAC-1+ Fc gammaRII/IIIbright cells is partly mediated by increased glucocorticoid levels during acute cold stress. The aim of the current study was to investigate the effect of swimming training on the generation of the MAC-1+ Fc gammaRII/IIIbright suppressor macrophages by acute cold stress. METHODS: The trained mice underwent a 6-wk endurance swimming training (5 times/wk) in water at 35-36 degrees C for 90 min. The swimming training significantly increased brown adipose tissue mass, suggesting improved cold tolerance. Actually, when the swimming-trained mice were exposed to 5 degrees C for 3 h (acute cold stress), the rectal temperature was not decreased. The proportion of MAC-1+ Fc gammaRII/IIIbright cells in peritoneal exudate cells from swimming-trained mice was significantly lower than that from control mice. In addition, the proportion of MAC-1+ Fc gammaRII/IIIbright cells in peritoneal exudate cell population from swimming-trained mice was unaffected by the acute cold stress. The swimming training significantly attenuated the increases in serum corticosterone levels in response to acute cold stress. These results suggested that swimming training not only improves cold tolerance but also inhibits the generation of suppressor macrophages under acute cold stress as well as under normal conditions.

Acclimatization↗
PubMed2005

Cross-tolerance between antinociception induced by swim-stress and morphine in formalin test.

The present study investigated cross-tolerance between antinociception induced by water swim-stress and morphine in the formalin test. Intraperitoneal administration of morphine (3, 6 and 9 mg/kg) induced dose-dependent antinociception in both phases of the formalin test. Mice treated with a lower dose of morphine (25 mg/kg), once daily for 3 days, showed tolerance to antinociception induced by a lower test dose of morphine (3 mg/kg). Similar repeated treatments with a higher dose of morphine (50 mg/kg) produced tolerance to antinociception induced by different test doses of morphine (3, 6 and 9 mg/kg). Exposure to water swim-stress, once daily for 2 or 3 days in order to induce tolerance, also decreased morphine-induced antinociception. Swim-stress exposure for 2 or 3 days also tends to potentiate tolerance induced by a lower dose of morphine. Acute swim-stress of different durations (0.5, 1 and 3 min) induced antinociception in both phases of the formalin test, which was not reduced by naloxone, but showed even more antinociception in the second phase. The response to swim stress was decreased in mice treated with higher doses of morphine, but not those animals that received swimming stress (3 min) once daily for 2-3 days, in order to induce habituation to swim-stress-induced antinociception. The results may indicate a possible cross-tolerance between antinociception induced by morphine and by swim stress.

Analgesia↗
PubMed1996

Injuries in female collegiate swimmers due to swimming and cross training.

OBJECTIVE: To identify and compare the nature and frequency of training and cross-training injuries incurred by members of a women's collegiate swim team. DESIGN: A longitudinal survey of training-room and medical records for 7 years, classifying injuries by diagnosis and time lost from participation. SETTING: Division I women's collegiate swimming program, United States. PARTICIPANTS: All swimmers in a Division I women's collegiate swimming program over 7 years, for a total of 68 swimmers. ASSESSMENT OF RISK FACTOR: Not applicable. INTERVENTION: Not applicable. MAIN OUTCOME MEASURES: "Injury" was defined as any contact with a trainer or physician that resulted in evaluation or treatment. Each injury was categorized with respect to (a) activity during which injury was incurred; (b) diagnosis, including body part injured; (c) time lost from participation in practice or competition; and (d) severity, i.e., minor (< or = 7 days), moderate (7-21 days), and major (> 21 days). An "Exposure" was defined as participation in one practice session or competition. MAIN RESULTS: The overall injury rate per 1,000 exposures per athlete was 2.12; 44% of injuries were due to swimming, 44% to cross training, and 11% to activities unrelated to athletics. Cross-training injuries occurred primarily in the lower extremities, while swimming injuries occurred more commonly in the upper extremities. The ratio of upper to lower extremity injuries due to swimming was 3:1, whereas the ratio for cross training was 1:4. CONCLUSIONS: Injuries to swimmers occur at a lower rate per exposure than to other collegiate athletic populations. Swimming injuries occurred primarily in the upper extremities, especially the shoulder. Lower extremity injuries occurred primarily due to cross training. We conclude that swimming is relatively safe compared to other collegiate sports, but special care should be used in designing injury-avoiding cross-training programs.

Athletic Injuries↗
PubMed1989

Swim-stress-induced antinociception in young rats.

1. Opioid and non-opioid mechanisms have been implicated in the phenomenon of stress-induced antinociception in adult rodents. We have studied stress-induced antinociception in developing rats and characterized differences in the neurochemical basis of this effect in pre- and post-weanling animals. 2. Twenty and 25 day old rats were stressed using warm water (20 degrees C) swimming for 3 or 10 min periods and antinociception was assessed by the tail immersion test (50 degrees C). 3. A 3 min swim in 20 and 25 day old rats produced marked antinociception which was blocked by naloxone, Mr 1452, 16-methyl cyprenorphine and levallorphan but not Mr 1453 or N-methyl levallorphan. The delta-opioid receptor antagonist ICI 174,864 attenuated stress-induced antinociception in 25 day old rats but was without effect in 20 day old animals. 4. A 10 min swim in 25 day old rats produced antinociception which was non-opioid in nature. In contrast, antinociception was not observed in 20 day old rats after a 10 min swim-stress. 5. Pretreatment of animals with dexamethasone blocked 3 min swim-stress antinociception in 20 and 25 day old animals but had no effect on antinociception induced by a 10 min swim. 6. Swim-stress-induced antinociception can be observed in young rats and dissociated into opioid and non-opioid types dependent on the duration of swimming stress. The non-opioid type appears to develop more slowly and cannot be observed in preweanling rats. The opioid type is a predominantly mu-receptor phenomenon in preweanling animals but delta-receptor components are observable in postweanling rats.

Aging↗
PubMed1993

Effect of delayed weaning on opioid receptor control of swim stress-induced antinociception in the developing rat.

1. The opioid type of swim-stress induced antinociception (SIA) is mediated via mu-sites in preweanling rats and predominantly by delta-sites in postweanling animals. We have studied the effect of delay of weaning on the receptor transition of this behaviour in the developing rat. 2. Litters were weaned normally at day 21 or allowed to remain with their mothers until assessment of swim SIA. Animals were stressed by warm water (20 degrees C) swimming for 3 min periods and antinociception assessed by the tail immersion test (50 degrees C). 3. Naloxone (10 mg kg-1) partially reversed swim SIA in both 25 day old weaned and non-weaned rats. 4. Naltrindole (1 mg kg-1) partially reversed swim SIA in 25 day old weaned rats but had no effect in non-weaned animals. Naltrindole (5 mg kg-1) completely abolished swim SIA in weaned rats but was without effect in non-weaned groups. Antinociceptive responses to the mu-agonist, alfentanil (60 micrograms kg-1) were unaffected by naltrindole at 1 mg kg-1 but were partially reversed at 5 mg kg-1. 5. In 30 day old non-weaned rats, naltrindole (5 mg kg-1) abolished the swim SIA. 6. In conclusion, transition from mu to delta-receptor control of swim SIA in rat pups can be delayed by between 5 and 10 days by delay of weaning. The environmental stimulus of weaning can activate opioid receptor subtype operation of biological responses in the developing animal.

Alfentanil↗
PubMed1991

Contribution of galanin to stress-induced impairment of insulin secretion in swimming mice.

This study examines the potential role of the neuropeptide, galanin, in stress-induced inhibition of insulin secretion in swimming mice. Firstly, the pancreatic and adrenal content of galanin-like immunoreactivity was determined in mice after swimming stress. It was found that pancreatic content was significantly lower in stressed mice than in resting controls, both after 2 (P less than 0.05) and 6 (P less than 0.025) minutes of swimming, suggesting partial release of pancreatic galanin during stress. In contrast, the adrenal content of galanin-like immunoreactivity did not change during the swimming stress. Gel filtration of tissue extracts indicated that (1) mouse pancreas contains two forms of galanin-like immunoreactivity; one co-eluting with synthetic porcine galanin (centered on Kav of 0.70) and another with a larger molecular weight (centered on Kav of 0.30), and (2) mouse adrenal contains a small void volume-peak and a larger peak of immunoreactivity, the latter co-eluting with synthetic galanin. Secondly, the effects of swimming stress on plasma glucose and insulin levels were compared in mice that received high titre rabbit anti-galanin serum with those in mice receiving normal rabbit serum. In normal rabbit serum-pretreated swimming mice, glucose-induced insulin levels were only 50% of resting controls (P less than 0.01). Immunoneutralization of galanin with specific antiserum abolished this swimming stress-induced inhibition of glucose-stimulated insulin levels. This was accompanied by a modestly enhanced rate of glucose disappearance. These findings suggest that pancreatic galanin is released during swimming stress in mice and that endogenous galanin makes a major contribution to stress-induced impairment of insulin secretion.

Adrenal Glands↗
PubMed2005

Long-term effects of microgravity on the swimming behaviour of young rats.

The postnatal development of sensory systems has been shown in studies over the last four decades to be influenced by experience during critical periods of development. We report here that similar experience-dependent development can be observed in the swimming behaviour of young rats reared from postnatal day 14 (P14) to P30 in the reduced gravitational field of low earth orbit. Animals flown in space when placed in the water on the day of landing maintained their head and forelimbs in a balanced posture. However, until the animals began to swim, their hindquarters showed little lateral postural control resulting in rotation about the longitudinal axis (60 degrees+/-4 deg). Such results suggest an 'unlinking' of postural control of the forequarters from the hindquarters in the early hours after landing. Similar instability seen in animals age-matched to the day of launch (97+/-7 deg) and in ground control animals (9+/-3 deg) was corrected within one or two rotations, even in the absence of swimming. Animals flown in space began to swim sooner after being placed in the water, and the duration of swimming strokes was shorter than in control animals. Motion analysis revealed a difference in the swimming style on landing day. In flight animals, the knee joint was more flexed throughout the stroke, there was a narrower range of movement, and the linear velocity of the tip of the foot was faster throughout most of the stroke than in age-matched control animals. Thus, posture in the water as well as swimming speed and style were altered in the animals flown in space. Some of these characteristics persisted for as long as the animals were followed (30 days). These included the short pre-swimming interval and short stroke duration in flight animals. These findings clearly show that an altered gravitational field influences the postnatal development of motor function. The nature of the differences between animals reared in space for 16 days and those remaining on the ground reflects an adaptation of the flight animals to the microgravity environment. The data suggest that the most fundamental of these adaptations is a resetting of the basic motor rhythm to a higher frequency.

Adaptation, Physiological↗
PubMed1999

Creatine supplementation and swimming performance.

The purpose of this study was to determine if oral creatine (CR) ingestion, compared to a placebo (PL), would enable swimmers to maintain a higher swimming velocity across repeated interval sets over 2 weeks of supplementation. Fourteen female and 18 male university swimmers consumed a PL during a 2-week baseline period. Using a randomized, double-blind design, during the next 2 weeks subjects consumed either CR or PL. Swimming velocity was assessed twice weekly during 6 X 50-m swims and once weekly during 10 X 25-yd swims. There was no effect of CR on the 10 X 25-yd interval sets for men and women and no effect on the 6 X 50-m interval sets for women. In contrast, for men, CR significantly improved mean overall swimming velocity in the 6 X 50-m interval after 2 weeks of supplementation, whereas PL had no effect. Although ineffective in women, CR supplementation apparently enables men to maintain a faster mean overall swimming velocity during repeated swims each lasting about 30 s; however, CR was not effective for men in repeated swims each lasting about 10 - 15 s.

Adult↗
PubMed2005

Effect of swimming intensity on subsequent cycling and overall triathlon performance.

OBJECTIVES: To investigate the effects of different swimming intensities on subsequent cycling and overall triathlon performance. METHODS: Nine highly trained, male triathletes completed five separate laboratory sessions comprising one graded exercise test, a swim time trial (STT), and three sprint distance triathlons (TRI). The swimming velocities of the three TRI sessions were 80-85% (S80), 90-95% (S90), and 98-102% (S100) of the STT velocity. Subsequent cycling and running were performed at a perceived maximal intensity. Swimming stroke mechanics were measured during the swim. Plasma lactate concentration and ratings of perceived exertion were recorded at the conclusion of the swim and over the course of subsequent cycling and running. Oxygen consumption was recorded during the cycle. RESULTS: The S80 and S90 cycle times were faster than the S100 cycle time (p<0.05). The overall triathlon time of S80 was faster than that of S100 (p<0.05). The S100 swim was characterised by a greater stroke rate than S80 and S90 (p<0.05) and a greater plasma lactate concentration than S80 (p<0.01). CONCLUSION: A swimming intensity below that of a time trial effort significantly improves subsequent cycling and overall triathlon performance.

Adult↗
PubMed1984

Modulation of myosin isoenzyme populations and activities of monoamine oxidase and phenylethanolamine-N-methyltransferase in pressure loaded and normal rat heart by swimming exercise and stress arising from electrostimulation in pairs.

The question of whether the effects of physical exercise on the heart of 15-weeks normotensive and hypertensive rats can be modulated by additional stressors was studied. Intermittent swimming (33-35 degrees C water, maximum 2 X 1.5 h/day, 2-6 weeks) was employed as a model of exercise. Electrostimulation of rats in pairs (maximum 2 X 1.5 h/day, 6 weeks) served as a model leading predominantly to stress. When the above procedures were combined, electrostimulation in pairs was performed in one session and was followed up by swimming. The myosin isoenzyme population was used as a marker of changes in contractile performance of myofibrils. Activities of the catecholamine-degrading enzyme monoamine oxidase (MAO) and the adrenaline-synthesizing enzyme phenylethanolamine-N-methyltransferase (PNMT) served to monitor chronic alterations of catecholamine turnover in myocardium. Redistribution in favour of VM-1 (ventricular myosin isoenzyme 1) occurred as early as 2 weeks after the onset of intermittent swimming and was observed under several experimental conditions. The redirection of genetic expression of the isoenzymes was not linked to the presence of an increased ratio of right to left ventricular weight, most probably arising from intermittent hypoxia during drownproofing. The myosin isoenzyme population of swimming spontaneously hypertensive rats (SHR) resembled that of sedentary Wistar rats. The enzyme activities of MAO and PNMT were both significantly reduced following 6 weeks intermittent swimming in Wistar rats and SHR. This can most probably be attributed to the exercise component of swimming which, on average, led to reduced catecholamine turnover in heart. Electrostimulation of rats in pairs for 6 weeks, which resulted in aggressivity and aggressions, did not alter the myosin isoenzyme population in Wistar rats; in SHR, it further augmented the proportion of VM-3 (ventricular myosin isoenzyme 3), which had already increased in the sedentary state. Furthermore, electrostimulation increased PNMT activity, but did not affect MAO activity. Electrostimulation in pairs, followed by swimming, altered the myosin isoenzyme population in the same way as did swimming alone. However, the activities of PNMT and MAO seemed to be governed by the routine involving stress and not by the exercise routine. This demonstrates that stressors supplementing exercise can decisively modify or even prevent reactions of the organism in response to exercise.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗