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PubMed1985

Effect of endurance swimming on rat cardiac myofibrillar ATPase with experimental diabetes.

Diabetes is characterized by depressed cardiac functional properties attributed to Ca2+-activated ATPase activity. In contrast, endurance swimming enhances the cardiac functional properties and Ca2+-activated myofibril ATPase. Thus, the purpose of this study was to observe if the changes associated with experimental diabetes can be ameliorated with training. Diabetes was induced with a single i.v. injection of streptozotocin (60 mg/kg). Blood and urine glucose concentrations were 802 +/- 44 and 6965 +/- 617 mg/dL, respectively. The training control and training diabetic animals were made to swim (+/- 2% body weight) 4 days/week for 8 weeks. Cardiac myofibril, at 10 microM free Ca2+ concentration was reduced by 54% in the sedentary diabetics compared with sedentary control animals (p less than 0.05). Swim training enhanced the Ca2+-activated myofibril ATPase activities for the normal animals. The diabetic animals, which swam for 8 weeks, had further reduced their Ca2+-activated myofibril ATPase activity when compared with sedentary diabetics (p less than 0.05). Similarly, the Mg2+-stimulated myofibril ATPase activity was depressed by 31% in diabetics following endurance swimming. It is concluded that the depressed Ca2+-activated myofibril ATPase activity of diabetic hearts is not reversible with endurance swimming.

Animals↗
PubMed2006

Swimming stress in DN 14-3-3 mice triggers maladaptive cardiac remodeling: role of p38 MAPK.

It is generally believed that a mechanical signal initiates a cascade of biological events leading to coordinated cardiac remodeling. 14-3-3 family members are dimeric phosphoserine-binding proteins that regulate signal transduction, apoptotic, and checkpoint control pathways. To evaluate the molecular mechanism underlying swimming stress-induced cardiac remodeling, we examined the role of 14-3-3 protein and MAPK pathway by pharmacological and genetic means using transgenic mice with cardiac-specific expression of dominant-negative (DN) mutants of 14-3-3 (DN 14-3-3/TG) and p38alpha/beta MAPK (DNp38alpha and DNp38beta) mice. p38 MAPK activation was earlier, more marked, and longer in the myocardium of the TG group compared with that of the nontransgenic (NTG) group after swimming stress, whereas JNK activation was detected on day 5 and decreased afterward. In contrast, ERK1/2 was not activated after swimming stress in either group. Cardiomyocyte apoptosis, cardiac hypertrophy, and fibrosis were greatly increased in the TG group compared with those in the NTG group. Moreover, we found a significant correlation between p38 MAPK activation and apoptosis in the TG group. Furthermore, DN 14-3-3 hearts showed enhanced atrial natriuretic peptide expression. In contrast, DNp38alpha and DNp38beta mice exhibited reduced mortality and increased resistance to cardiac remodeling after 28 days of swimming stress compared with TG and NTG mice. Besides, treatment with a p38 MAPK inhibitor, FR-167653, resulted in regression of cardiac hypertrophy and fibrosis and improvement in the survival rate in the TG group. These results indicate for the first time that 14-3-3 protein along with p38 MAPK plays a crucial role in left ventricular remodeling associated with swimming stress.

14-3-3 Proteins↗
PubMed1992

Swimming changes vascular fatty acid composition and prostanoid generation of rats.

To define the effects of physical activity on vascular fatty acid composition and prostanoid generation, spontaneously hypertensive and normotensive rats were made to swim at 34-35 degrees C for 5-7 wk. Fatty acids were determined by gas chromatography and prostanoids by high-performance liquid chromatography and electrochemical detection. A characteristic feature of swimming rats was a markedly reduced linoleic acid content in the iliac artery and the aorta; in normotensive swimming rats stearic acid and arachidonic acid contents were increased. These changes could not be attributed to a heat loss during swimming or to depressed growth characteristics. A chemical sympathectomy using guanethidine (60 mg/kg body wt daily) did not prevent the alterations in fatty acid composition. A higher arachidonic acid content was correlated with an increased generation of 6-ketoprostaglandin F1 alpha in the aorta of untreated rats and sympathectomized rats. It is concluded that swimming can alter the vascular fatty acid composition in a manner which results in an increased potential for prostacyclin production.

Animals↗
PubMed1992

Morphological and physiological correlates with swimming performance in juvenile largemouth bass.

Winter- and summer-acclimatized largemouth bass (Micropterus salmoides) were collected from hatchery ponds in eastern Colorado during late winter and midsummer, then challenged with two prolonged swimming performances (step test and constant-velocity endurance). Variation in the step test performances was significantly correlated with variation in the endurance performances in the winter-acclimatized but not in the summer-acclimatized fish. Fourteen physiological and morphological traits were measured on each fish, and correlations among these traits and swimming performance were tested. None of the traits measured were correlated with performance variation in both the winter- and summer-acclimatized fish. The only significant correlate with swimming performance in the summer-acclimatized fish was white muscle lactate dehydrogenase activity (n = 19). Six of the seven factors correlating with winter swimming performance (n = 18-19) could be divided into two categories: traits associated with fasting (condition factor and liver enzymatic activity) and those associated with oxygen delivery (heart mass, heart and red muscle cytochrome oxidase activity). The results of this study suggest that morphological and physiological correlates of swimming performance in juvenile largemouth bass are profoundly influenced by seasonal variation.

Acclimatization↗
PubMed1994

Modeling red muscle power output during steady and unsteady swimming in largemouth bass.

We recorded electromyograms of slow-twitch (red) muscle fibers and videotaped swimming in the largemouth bass (Micropterus salmoides) during cruise, burst-and-glide, and C-start maneuvers. By use of in vivo patterns of stimulation and estimates of strain, in vitro power output was measured at 20 degrees C with the oscillatory work loop technique on slow-twitch fiber bundles from the midbody area near the soft dorsal fin. Power output increased slightly with cycle frequency to a plateau of approximately 10 W/kg at 3-5 Hz, encompassing the normal range of tail-beat frequencies for steady swimming (approximately 2-4 Hz). Power output declined at cycle frequencies simulating unsteady swimming (burst-and-glide, 10 Hz; C-start, 15 Hz). However, activating the muscle at 10 Hz did significantly increase the net work done compared with the work produced by the inactive muscle (work done by the viscous and elastic components). Thus this study provides further insight into the apparently paradoxical observation that red muscle can contribute little or no power and yet continues to show some recruitment during unsteady swimming. Comparison with published values of power requirements from oxygen consumption measurements indicates a limit to steady swimming speed imposed by the maximum power available from red muscle.

Animals↗
PubMed1995

Effects of swimming and environmental hypoxia on coronary blood flow in rainbow trout.

Previous studies have suggested that trout cardiac performance is highly dependent on coronary blood flow during periods of increased activity or hypoxia. To examine the relationship between coronary perfusion and cardiac performance in swimming trout, cardiac output (Q), coronary blood flow (qcor), and dorsal aortic blood pressure were measured in rainbow trout (Oncorhynchus mykiss) during normoxia and hypoxia (PO2 approximately 9 kPa). In normoxic trout, stepwise changes in cardiovascular variables were observed as the swimming speed was incrementally increased from 0.15 body lengths (bl)/s to 1.0 bl/s. At 1.0 bl/s, qcor and cardiac power output had both increased by approximately 110%, and coronary artery resistance (Rcor) had decreased by 40%. During hypoxia, resting qcor was 35% higher, and Rcor was 20% lower, compared with normoxic values. In hypoxic swimming trout, the maximum changes in qcor (155% increase) and Rcor (50% decrease) were recorded at 0.75 bl/s. In contrast, cardiac power output and Q increased by an additional 40 and 20%, respectively, as swimming speed was increased from 0.75 to 1.0 bl/s. The results indicate that 1) increases in qcor parallel changes in cardiac power output; 2) during hypoxia there are compensatory increases in cardiac performance and coronary perfusion; and 3) the scope for increasing qcor in swimming trout is approximately 150%. In addition, results from preliminary experiments suggest that beta-adrenergic, but not cholinergic, mechanisms are involved in the regulation of coronary blood flow during exercise.

Animals↗
PubMed1997

Age and gender interactions in physiological functional capacity: insight from swimming performance.

One experimental approach to studying the effects of aging on physiological functional capacity in humans is to analyze the peak exercise performance of highly trained athletes with increasing age. To gain insight into the relationships among age, gender, and exercise task duration with use of this model, we performed a 5-yr (1991-1995) retrospective analysis of top freestyle performance times from the US Masters Swimming Championships. Regression analysis showed that in both men and women endurance swimming performance (i.e., 1,500 m) declined linearly from peak levels at age 35-40 yr until approximately 70 yr of age, whereupon performance declined exponentially thereafter. In both genders, the variability among the top 10 winning times in each 5-yr age interval increased markedly with advancing age. Compared with the 1,500-m freestyle, performance in the 50-m freestyle (short-duration task) showed only a modest decline until ages 75 and 80 yr in women and men, respectively. The rate and magnitude of the declines in both short- and long-duration swimming performance with age were significantly (P < 0.05) greater in women than in men. In the women, the percent decline in swimming performance over a 50-yr age period from the 19- to 24-yr to the 69- to 74-yr age groups became progressively greater from the shortest distance (50 m) to the two longest distances (800 and 1,500 m), whereas in men, no differences were observed in the magnitude of performance decline with age among the five longest distance events (i.e., 100-1,500 m). The percent gender difference in performance throughout the age range studied became progressively smaller (P < 0.05) with increasing distance from 50 m (19 +/- 1%) to 1,500 m (11 +/- 1%). The findings in this cross-sectional study indicate that from peak levels at age 35-40 yr, physiological functional capacity, as assessed by swimming performance, decreases linearly until approximately 70-80 yr of age, whereupon the decline becomes exponential. Moreover, the rate of decline with advancing age appears to be associated with event duration and gender.

Adolescent↗
PubMed2006

Circadian variation in swim performance.

Previous findings of time-of-day differences in athletic performance could be confounded by diurnal fluctuations in environmental and behavioral "masking" factors (e.g., sleep, ambient temperature, and energy intake). The purpose of this study was to examine whether there is a circadian rhythm in swim performance that is independent of these masking factors. Experienced swimmers (n = 25) were assessed for 50-55 consecutive hours in the laboratory. The swimmers followed a 3-h "ultra-short" sleep-wake cycle, involving 1 h of sleep in darkness and 2 h of wakefulness in dim light, that was repeated throughout the observation. The protocol distributes behavioral and environmental masking factors equally across the 24-h period. Each swimmer was scheduled to perform six maximal-effort 200-m swim trials that were distributed equally across eight times of day (n = 147 trials). Each trial was separated by 9 h. A cosine fit of intra-aural temperature data established the time of the lowest body temperature (Tmin). Swim performances were z-transformed and compared across the eight times of day and across twelve 2-h intervals relative to Tmin. Analysis of covariance, controlling for trial number, revealed a significant (P < 0.001) pattern in swim performance relative to environmental and circadian times of day. Performance peaked 5-7 h before Tmin (approximately 2300) and was worst from 1 h before to 1 h after Tmin (approximately 0500). Mean swim performance was 169.5 s; circadian variation from peak to worst performance was 5.8 s. These data suggest a circadian rhythm in athletic performance independent of environmental and behavioral masking effects.

Adult↗
PubMed1977

Swimming movements elicited by electrical stimulation of turtle spinal cord. I. Low-spinal and intact preparations.

1. Electrical stimulation applied within the dorsolateral funiculus of the spinal cord of an intact, unanesthetized turtle can elicit rhythmic limb movements similar to those observed during swimming. 2. A spontaneous display of hindlimb swimming movements is not observed in adult turtles whose spinal cord is transected at D2. Such swimming movements are observed in these "low-spinal" turtles in response to electrical stimulation applied within the dorsolateral funiculus caudad to the transection. 3. The repetition rate of these swimming movements can be altered by changing stimulus parameters, such as the frequency of electrical pulses. 4. The present results indicate that, in the turtle, a neural pattern generator contributing to the production of hindlimb movements during swimming is located mainly in structures caudad to the cervical enlargement of the spinal cord. These data support the hypothesis that a pattern generator for locomotion is largely resident within the spinal cord.

Animals↗
PubMed1991

Neural control of swimming in Aplysia brasiliana. I. Innervation of parapodial muscle by pedal ganglion motoneurons.

1. Swimming is an oscillatory locomotor behavior in Aplysia accomplished by rhythmic undulating movements of the parapodia, winglike flaps that cover the dorsum of the body. As part of an analysis of the neural basis of this behavior, we have identified and characterized motoneurons in the pedal ganglia that directly innervate parapodial muscle and fire phasically during fictive swimming. 2. Parapodial musculature is organized into at least eight discrete layers. Fibers of adjacent layers are directed orthogonally. 3. Motoneurons were localized to the middle and rostral portions of the dorsal surface of each pedal ganglion by the use of backfill staining and intracellular dyes. These neurons were defined as motoneurons on the basis of additional physiological evidence for peripheral axons and their ability to cause excitatory junction potentials (EJPs; average amplitude, 2-5 mV) in muscle fibers and discrete contractions of parapodial muscles. Muscle fibers are polyneuronally innervated. Fibers had an average resting potential of -79 mV and no over-shooting action potentials. 4. There are probably at least 50 motoneurons. Their average resting potential was -48 mV, and they do not appear to be directly connected synaptically to one another. One identifiable motoneuron is described in detail. It participates in the opener (downstroke) phase of swimming and causes contraction of one of the described muscle layers. 5. Divalent ion concentrations were altered centrally and peripherally during motoneuron activity to demonstrate that the motoneurons directly innervate muscle fibers. Blockage of EJPs by hexamethonium and the presence of specific anticholinesterase staining in parapodial nerves and muscle fibers strongly suggest that many of the motoneurons are cholinergic. 6. Studies of excitation-contraction coupling showed that single or a few spikes in motoneurons rarely cause an EJP. Bursts of motoneuron spikes produced facilitating EJPs. With approximately 10 spikes in a 1-s motoneuron burst, adequate depolarization occurred in muscle fibers to initiate a small, slow contraction. Increased spike frequency led to greater depolarization, because of EJP summation, and larger contractions. Contraction requires depolarization of the muscle above a threshold, beyond which the force of contraction depends on both the duration and degree of depolarization. 7. Although dozens of motoneurons appear to be involved in the complex control of parapodial movements during swimming, preliminary evidence indicates that these neurons are probably not participating directly in the circuitry of the central pattern generator for swimming, which has been shown by others also to reside in the pedal ganglia.

Acetylcholinesterase↗
PubMed1997

Spinal cord coordination of hindlimb movements in the turtle: interlimb temporal relationships during bilateral scratching and swimming.

Hindlimb interlimb coordination was examined in turtles during symmetrical "same-form" behaviors in which both hindlimbs utilized the same movement strategy ("form") and during asymmetric "mixed-form" behaviors in which the form exhibited by one hindlimb differed from that of its contralateral partner. In spinal turtles, three forms of scratching were examined: rostral, pocket, and caudal. Bilateral symmetrical same-form scratching was studied for each of the forms. Asymmetric mixed-form scratching (rostral scratching of a hindlimb and pocket scratching of the other hindlimb) was also examined. In intact turtles, two forms of swimming were examined: forward swimming and back-paddling. The symmetrical behavior of bilateral forward same-form swimming and the asymmetric behavior of turning mixed-form swimming (forward swimming of 1 hindlimb and back-paddling of the other hindlimb) were studied. For all behaviors examined, most episodes displayed absolute or 1:1 coordination; in this type of coordination, during each movement cycle that began and ended with the onset of ipsilateral hip flexion, there was a single onset of contralateral hip flexion. For most of these episodes there was out-of-phase coordination between hip movements; the onset of contralateral hip flexion occurred near the onset of ipsilateral hip extension midway through the ipsilateral movement cycle. Bilateral caudal/caudal same-form scratching displayed out-of-phase 1:1 coordination during some episodes and in-phase 1:1 coordination during other episodes. During in-phase coordination, the onset of contralateral hip flexion occurred near the onset of ipsilateral hip flexion close to the start of the ipsilateral movement cycle. In a few cases of bilateral same-form scratching there were episodes of relative or 2:1 coordination; in this type of coordination, during each movement cycle of the slowly moving limb that began and ended with ipsilateral hip flexion, there were two distinct occurrences of the onset of contralateral hip flexion. The observation that out-of-phase movements of the hip occurred during symmetrical as well as asymmetric behaviors is consistent with the hypothesis that timing signals related to hip movement play a major role in interlimb phase control. The neural mechanisms responsible for interlimb phase control are not well understood in vertebrates. The present demonstration of bilateral scratching in spinal turtles suggests that this preparation may be suitable for additional experiments to examine mechanisms of vertebrate interlimb phase control.

Animals↗
PubMed2000

Step, swim, and scratch motor patterns in the turtle.

The turtle generates a variety of coordinated hindlimb movements, including different forms of locomotion and scratching. The intact turtle produces forward step, forward swim, and backpaddle. Following spinal cord transection, rostral, pocket, and caudal scratches can be evoked by mechanical stimulation of the shell. Comparisons of the kinematics and motor patterns of these six behaviors provide insights regarding neuronal mechanisms underlying their production. All six behaviors were characterized by alternating hip flexion and extension and by an event during which force was exerted against a substrate. The portion of the cycle occupied by hip flexion or extension movement varied across behaviors. Hip extension occupied well over half the cycle period in the forward step and the caudal scratch. The cycle was split into approximately half hip flexion and half hip extension for the forward swim, the backpaddle, and the rostral scratch. Hip flexion occupied over half the cycle in the pocket scratch. The swim and scratch forms had curvilinear, crescent-shaped toe trajectories and a single burst of monoarticular knee extensor activity during each cycle. The forward step had a linear toe trajectory and two bursts of knee extensor activity during each cycle, one during swing and one during stance. Timing of monoarticular knee extensor onset was similar for: the forward swim, the rostral scratch, and the swing phase burst of forward step; the pocket scratch and the stance phase burst of forward step; and the backpaddle and the caudal scratch. Amplitudes of muscle activity varied among the six behaviors; high amplitudes of activity were associated with events during which force was exerted against a substrate. These times of force exertion were: stance phase in the forward step, powerstroke in the forward swim and the backpaddle, and rubs of the limb against the shell in the scratch forms. The six behaviors studied represent a range of parameter values, as evidenced by relative durations of hip flexion to hip extension, knee extensor phasing, and electromyogram (EMG) amplitudes. This range of behaviors could be produced by assembling different combinations of neurons from a common pool, with all six behaviors likely sharing some basic circuitry. The extent of shared circuitry may be greater between behaviors with similar timing, e.g., backpaddle and caudal scratch.

Animals↗
PubMed2002

Model for intersegmental coordination of leech swimming: central and sensory mechanisms.

Sensory feedback as well as the coupling signals within the CNS are essential for leeches to produce intersegmental phase relationships in body movements appropriate for swimming behavior. To study the interactions between the central pattern generator (CPG) and peripheral feedback in controlling intersegmental coordination, we have constructed a computational model for the leech swimming system with physiologically realistic parameters. First, the leech swimming CPG is simulated by a chain of phase oscillators coupled by three channels of coordinating signals. The activity phase, the projection direction, and the phase response curve (PRC) of each channel are based on the identified intersegmental interneuron network. Output of this largely constrained model produces stable coordination in the simulated CPG with average phase lags of 8-10 degrees/segment in the period range from 0.5 to 1.5 s, similar to those observed in isolated nerve cords. The model also replicates the experimental finding that shorter chains of leech nerve cords have larger phase lags per segment. Sensory inputs, represented by stretch receptors, were subsequently incorporated into the CPG model. Each stretch receptor with its associated PRC, which was defined to mimic the experimental results of phase-dependent phase shifts of the central oscillator by the ventral stretch receptor, can alter the phase of the local central oscillator. Finally, mechanical interactions between the muscles from neighboring segments were simulated by PRCs linking adjacent stretch receptors. This model shows that interactions between neighboring muscles could globally increase the phase lags to the larger value required for the one-wavelength body form observed in freely swimming leeches. The full model also replicates the experimental observation that leeches with severed nerve cords have larger intersegmental phase lags than intact animals. The similarities between physiological and simulation results demonstrate that we have established a realistic model for the central and peripheral control of intersegmental coordination of leech swimming.

Animals↗
PubMed1999

A possible pathway connecting the photosensitive pineal eye to the swimming central pattern generator in young Xenopus laevis tadpoles.

The pineal eye of young Xenopus laevis tadpoles mediates a swimming response to dimming. Our aim was to define pathways that allow pineal photoreceptors to influence the swimming central pattern generator (CPG) in the hindbrain and spinal cord. Retrograde filling with horseradish peroxidase (HRP) and carboxyfluorescein showed that: (1) pineal ganglion cells do not project to the hindbrain, and (2) diencephalic/mesencephalic descending (D/MD) neurons, which could be contacted by pineal ganglion cell axons, do project to the hindbrain. Lesion experiments demonstrated that ganglion cell axons form ipsilateral and contralateral connections, either of which is sufficient to mediate a swimming response. Latency measurements suggest that the contralateral pathway is stronger than the ipsilateral one. Multiple unit recordings from the midbrain in the region of the D/MD neurons showed short latency activity in response to dimming or a brief current pulse to pineal axons. This activity could last for many seconds after the stimulus. Pharmacological experiments showed that it depended on synaptic excitation and suggested that the ganglion cell transmitter is glutamate. If pineal ganglion cells excite midbrain D/MD neurons on both sides of the brain, the D/MD neuron projections to the hindbrain could excite the swimming CPG and initiate swimming.

Animals↗
PubMed2002

Forced swimming differentially affects male and female brain corticosteroid receptors.

Corticosteroid receptors are key mediators of the neuroendocrine response to stress. Previously, we have determined the effects of restraint stress on the regulation of corticosteroid receptor genes in the brain and pituitary of male and female rats. Significant gender- and regional-specific regulation of receptor mRNAs was observed. To further investigate the stressor specificity in the same context, we have determined glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) mRNAs following exposure to swimming stress paradigms applied alone, or in combination with restraint stress. Our data revealed stressor-specific alterations in GR or MR mRNA levels, which were more pronounced in males, the gender most affected by swimming stress. No alterations in GR or MR mRNA levels were detected in the female hippocampus and hypothalamus upon exposure to swimming paradigms, while in males the same stressors down-regulated GR mRNA in the hippocampus (chronic exposure) and up-regulated both genes in the hypothalamus (acute exposure). In the frontal cortex, acute swimming stress caused a reciprocal change in GR mRNA levels in the two sexes. The above difference is not due to circulating ovarian steroids, since ovariectomy did not change the female pattern of GR gene expression following acute stress. Our results further showed a hypothalamic-pituitary-adrenal axis facilitation to a novel superimposed stressor expressed at the level of limbic corticosteroid receptors: When chronically restrained rats of both sexes were exposed to acute swimming stress, a reduced GR/MR mRNA ratio, implying reduced feedback axis sensitivity, was detected in both the hippocampus and the hypothalamus. In conclusion, our work provides additional evidence on stressor, gender and region specificity in the regulation of brain corticosteroid receptors.

Adrenal Glands↗
PubMed1988

Swimming depresses nighttime melatonin content without changing N-acetyltransferase activity in the rat pineal gland.

Recently, it was shown that a 1.5-ml subcutaneous saline injection depressed N-acetyltransferase (NAT) activity and melatonin content in the rat pineal gland at night. The present studies were undertaken to determine if another perturbation, swimming, could duplicate this response. Rats swam at 23.10 h (lights out at 20.00 h) for 10 min and were killed 15 and 30 min after the unset of swimming. Pineal NAT activity was found to be unaffected while melatonin content was depressed dramatically. Hydroxyindole-O-methyltransferase (HIOMT) activity as well as the content of serotonin (5HT), 5-hydroxytryptophan (5HTP) and 5-hydroxyindoleacetic acid (5HIAA) were not changed by this treatment. In a second study, pineal melatonin again was depressed without a concomitant drop in NAT activity. Mean serum melatonin at 15 min after onset of swimming was increased although the rise was not statistically significant. In the final study, it was found that NAT activity was slightly increased in intact rats and unchanged in adrenalectomized rats at 7 min after swimming onset. At 15 min both intact and adrenalectomized animals had NAT activity values similar to those of controls. Pineal melatonin content in intact and adrenalectomized rats plummeted to 50% of control values at 7 min and fell further to 25% at 15 min. While the rate of melatonin synthesis was not directly measured, lack of change in the activities of the enzymes involved in melatonin synthesis and the contents of two melatonin precursors suggests that swimming depresses pineal melatonin content by enhancing melatonin efflux from the gland.

Acetyltransferases↗
PubMed1979

Hydrolase activities in the rat aorta. III. Effects of regular swimming activity and its cessation.

It is possible that one of the consequences of regular physical activity could be a change of vascular metabolism. We studied the effects of regular swimming activity on specific activities of aortic hydrolases of male rats. Enzymes included: neutral alpha-glucosidase and lysosomal beta-galactosidase, N-acetyl-beta-glucosaminidase, cathepsin C, acid alpha-glucosidase, and acid cholesteryl esterase. After 8 or 16 weeks of a 1-hour/day swimming protocol, specific activities of four of the six aortic enzymes studied were increased over control levels, increases ranging from 7 to more than 42%. Acid cholesteryl esterase was one of the enzymes most affected by the exercise, increasing 25-30% above control levels. An 8-week sedentary period, after 8 weeks of a swimming regimen, resulted in return of the activity of acid cholesteryl esterase, but not those of the other hydrolases, to control levels. Decreases in body weight, blood pressure, and serum lipid levels also occurred in the swimming rats. Weight reduction per se was excluded as an explanation for the increases in aortic enzymes or decrease in serum cholesterol found with swimming. These findings show that regular physical activity is yet another factor with discrete and significant effects on the catabolic activity of vascular tissue.

Acetylglucosaminidase↗
PubMed2002

Occupational asthma caused by chloramines in indoor swimming-pool air.

The first series of three workers who developed occupational asthma following exposure to airborne chloramines in indoor chlorinated swimming pools is reported. Health problems of swimmers in indoor pools have traditionally been attributed to the chlorine in the water. Chlorine reacts with bodily proteins to form chloramines; the most volatile and prevalent in the air above swimming pools is nitrogen trichloride. Two lifeguards and one swimming teacher with symptoms suggestive of occupational asthma kept 2-hourly measurements of peak expiratory flow at home and at work, analysed using the occupational asthma system (OASYS) plotter, and/or had specific bronchial challenge testing to nitrogen trichloride, or a workplace challenge. Air measurement in one of the pools showed the nitrogen trichloride levels to be 0.1-0.57 mg x m(-3), which was similar to other studies. Two workers had peak expiratory flow measurements showing occupational asthma (OASYS-2 scores 2.88 and 3.8), both had a positive specific challenge to nitrogen trichloride at 0.5 mg x m(-3) with negative challenges to chlorine released from sodium hypochlorite. The third worker had a positive workplace challenge. Swimming-pool asthma due to airborne nitrogen trichloride can occur in workers who do not enter the water because of this chloramine. The air above indoor swimming pools therefore needs to be assessed and managed as carefully as the water.

Adult↗