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PubMed1982

Physiological basis for swimming endurance differences between LDH-B genotypes of Fundulus heteroclitus.

Adenosine triphosphate levels in erythrocytes are correlated with LDH-B genotype in Fundulus heteroclitus. Adenosine triphosphate is the fish's allosteric modifier of hemoglobin oxygen affinity. Since oxygen delivery to muscle affects swimming performance, fish of each homozygous LDH-B phenotype were swum to exhaustion at 10 degrees or 25 degrees C to determine whether in vitro differences attributed to the LDH-B allelic isozymes were manifest in vivo. At 10 degrees C, the critical swimming speed of the LDH-BaBa phenotype was 3.6 body lengths per second, whereas that of the LDH-BbBb phenotype was 4.3 body lengths per second. At 25 degrees C there were no differences between LDH-B phenotypes in erythrocyte adenosine triphosphate levels, blood oxygen affinity, or swimming performance.

Adenosine Triphosphate↗

PubMed1993

How fish power swimming.

It is thought that fish generate the power needed for steady swimming with their anterior musculature, whereas the posterior musculature only transmits forces to the tail and does negative work. Isolated red muscle bundles driven through the length changes and stimulation pattern that muscles normally undergo during steady swimming showed the opposite pattern. Most of the power for swimming came from muscle in the posterior region of the fish, and relatively little came from the anterior musculature. In addition, the contractile properties of the muscle along the length of the fish are significantly adapted to enhance power generation.

Animals↗

PubMed1983

Comparison of Vogel-Johnson and Baird-Parker media for membrane filtration recovery of staphylococci in swimming pool water.

Previous studies have indicated that the coagulase-positive Staphylococcus (Staphylococcus aureus) has potential as a useful indicator of the infection hazard associated with the use of swimming pools and other recreational waters. However, before this indicator system can be used effectively, a recovery system that is sufficiently selective, accurate, and reliable for the enumeration of S. aureus must be developed. In this study, Vogel-Johnson (VJ) and Baird-Parker (BP) agars were compared for efficacy in the primary isolation and recovery of S. aureus from swimming pool water. For equal sample volumes of pool water containing adequate free chlorine residual, VJ agar was found to be more selective for staphylococcal species and less inhibitory to general cell growth than was BP agar. However, neither medium was found to be sufficiently differential to permit the accurate identification of S. aureus. In contrast, water samples obtained from a swimming pool containing very low levels of chlorine (none of which was in the free form) showed abundant growth of staphylococci on both test media, with both VJ and BP agars showing increased sensitivity for the detection of S. aureus. Thus, VJ and BP agars show increased sensitivity for the detection of coagulase-positive staphylococci from unchlorinated versus chlorinated waters.

Agar↗

PubMed2001

Assessing the risk of primary amoebic meningoencephalitis from swimming in the presence of environmental Naegleria fowleri.

Free-living Naegleria fowleri amoebae cause primary amoebic meningoencephalitis (PAM). Because of the apparent conflict between their ubiquity and the rarity of cases observed, we sought to develop a model characterizing the risk of PAM after swimming as a function of the concentration of N. fowleri. The probability of death from PAM as a function of the number of amoebae inhaled is modeled according to results obtained from animals infected with amoeba strains. The calculation of the probability of inhaling one or more amoebae while swimming is based on a double hypothesis: that the distribution of amoebae in the water follows a Poisson distribution and that the mean quantity of water inhaled while swimming is 10 ml. The risk of PAM for a given concentration of amoebae is then obtained by summing the following products: the probability of inhaling n amoebae x the probability of PAM associated with inhaling these n amoebae. We chose the lognormal model to assess the risk of PAM because it yielded the best analysis of the studentized residuals. Nonetheless, the levels of risk thereby obtained cannot be applied to humans without correction, because they are substantially greater than those indicated by available epidemiologic data. The curve was thus adjusted by a factor calculated with the least-squares method. This provides the PAM risk in humans as a function of the N. fowleri concentration in the river. For example, the risk is 8.5 x 10(-8) at a concentration of 10 N. fowleri amoebae per liter.

Amebiasis↗

PubMed1967

Factors influencing the effectiveness of swimming pool bactericides.

Techniques for culturing, harvesting, and testing bacteria to evaluate bactericidal chemicals for swimming pools are described. Concentrations of 25, 50, and 100 mg of the chlorine stabilizer cyanuric acid per liter increased the time required for a 99% kill of Streptococcus faecalis by 0.5 mg of chlorine per liter at pH 7.4 and 20 C from less than 0.25 min without cyanuric acid to 4, 6, and 12 min, respectively. The effect of concentrations of ammonia nitrogen in the range found in swimming pools on the rate of kill of 0.5 mg of chlorine per liter and of chlorine plus cyanuric acid was tested. At concentrations of ammonia nitrogen greater than 0.05 mg per liter, faster rates of kill of S. faecalis were obtained with 100 mg of cyanuric acid per liter plus 0.5 mg of chlorine per liter than with 0.5 mg of chlorine per liter alone. When water samples from four swimming pools with low ammonia levels were used as test media, 0.5 mg of added chlorine per liter killed 99.9% of the added S. faecalis in less than 2 min, but water from a pool with a large number of children required 60 to 180 min of treatment.

Ammonia↗

PubMed1993

Plasma TSH, T3, T4 and cortisol responses to swimming at varying water temperatures.

The acute effect of 30-min swimming at a moderate speed, at three water temperatures (20, 26 and 32 degrees C) on plasma thyroid stimulating hormone (TSH), free thyroxine (F.T4), triiodothyronine (T3) and cortisol concentrations was studied in 15 élite male swimmers. Blood was sampled before and immediately after the events. The heart rate, which was continuously monitored during exercise, had the highest response at 32 degrees C and the lowest at 20 degrees C. Blood lactate concentrations were found to be similar after the three tests. Plasma TSH and F.T4 were found to be significantly increased (by 90.4% and 45.7% respectively) after swimming at 20 degrees C, decreased at 32 degrees C (by 22.3% and 10.1% respectively) and unchanged at 26 degrees C. Exercise at these three water temperatures did not significantly affect T3. Finally, plasma cortisol was found to be increased after swimming at 32 degrees C (by 82.8%) and 26 degrees C (by 46.9%), but decreased at 20 degrees C (by 6.1%).

Adolescent↗

PubMed1995

Do the competition rules of synchronized swimming encourage undesirable levels of hypoxia?

Recent anecdotal reports that some synchronized swimmers have become dizzy or disorientated towards the end of their performance, and in the worst cases fainted underwater, have caused concern. However, the rules of synchronized swimming encourage slow performance of compulsory figures, and an analysis of the competition placings and duration of underwater sequences showed that the highest rankings were gained by slowly performed compulsory figures and free programmes containing a long underwater sequence. The combination of breath-holding and the vigorous exercise involved suggests that some of the symptoms complained of by the swimmers might be due to hypoxia. We therefore studied the alveolar gas tensions in nine members of the Great Britain National Squad immediately following the performance of set figures and the initial underwater sequence of their free routine in a swimming-bath. All were cyanosed after the underwater sequences of the free routine and reported being mildly confused. The mean(s.d.) alveolar PO2 at this stage was 5.07(1.1) KPa, while three girls had an alveolar PO2 below 4 KPa, the lowest being 3.67 KPa. These gas tensions suggest that potentially dangerous levels of hypoxia may develop during competitive synchronized swimming and that prolonged underwent sequences should not be encouraged.

Adolescent↗

PubMed2003

Benefits of swimming pools in two remote Aboriginal communities in Western Australia: intervention study.

OBJECTIVE: To determine the health impact of swimming pools built with the aim of improving quality of life and reducing high rates of pyoderma and otitis media. DESIGN: Intervention study assessing prevalence of ear disease and skin infections before and at six monthly intervals after opening of swimming pools. SETTING: Two remote Aboriginal communities in Western Australia. PARTICIPANTS: 84 boys and 78 girls aged < 17 years. MAIN OUTCOME MEASURES: Changes in prevalence and severity of pyoderma and perforation of tympanic membranes with or without otorrhoea over 18 months after opening of pools. RESULTS: In community A, 61 children were seen before the pool was opened, and 41, 46, and 33 children were seen at the second, third, and fourth surveys. Equivalent figures for community B were 60, 35, 39, and 45. Prevalence of pyoderma declined significantly from 62% to 18% in community A and from 70% to 20% in community B during the 18 months after the pools opened. Over the same period, prevalence of severe pyoderma fell from 30% to 15% in community A and from 48% to 0% in community B. Prevalence of perforations of the tympanic membrane fell from 32% in both communities to 13% in community A and 18% in community B. School attendance improved in community A. CONCLUSION: Swimming pools in remote communities were associated with reduction in prevalence of pyoderma and tympanic membrane perforations, which could result in long term benefits through reduction in chronic disease burden and improved educational and social outcomes.

Absenteeism↗

PubMed1994

Changes in blood lactate and heart rate in thoroughbred horses during swimming and running according to their stage of training.

The purpose of this study was to investigate whether the change in the performance capacity of horses trained by running could be evaluated with a standardised swimming exercise test as well as by a standardised running exercise test. Seven two-year-old thoroughbred horses were trained by running for four months and were subjected to a standardised swimming exercise tolerance test before the training began and after two and four months of training in addition to the standardised running tolerance test after two and four months of training. The running training brought about a significant change in the correlation between the swimming speed of the horses and their blood lactate concentration, and the correlation between the blood lactate concentration and maximum heart rate and running speed also changed significantly after two months of training.

Animals↗

PubMed2005

Does prior 1500-m swimming affect cycling energy expenditure in well-trained triathletes?

The purpose of this study was to determine the effects of a 1,500-m swim on energy expenditure during a subsequent cycle task. Eight well-trained male triathletes (age 26.0 +/- 5.0 yrs; height 179.6 +/- 4.5 cm; mass 71.3 +/- 5.8 kg; VO(2)max 71.9 +/- 7.8 ml.kg(-1).min(-1)) underwent two testing sessions in counterbalanced order. The sessions consisted of a 30-min ride on the cycle ergometer at 75% of maximal aerobic power (MAP), and at a pedaling frequency of 95 rev.min(-1), preceded either by a 1,500-m swim at 1.20 m.s(-1) (SC trial) or by a cycling warm-up at 30% of MAP (C trial). Respiratory and metabolic data were collected between the 3rd and the 5th min, and between the 28th and 30th min of cycling. The main results indicated a significantly lower gross efficiency (13.0%) and significantly higher blood lactate concentration (56.4%), VO(2) (5.0%), HR (9.3%), VE (15.7%), and RF (19.9%) in the SC compared to the C trial after 5 min, p < 0.05. After 30 min, only VE (7.9%) and blood lactate concentration (43.9%) were significantly higher in the SC compared to the C trial, p < 0.05. These results confirm the increase in energy cost previously observed during sprint-distance triathlons and point to the importance of the relative intensity of swimming on energy demand during subsequent cycling.

Adult↗

PubMed2006

Non-exhaustive test for aerobic capacity determination in swimming rats.

The aim of this study was to describe a double-bout exercise test for non-exhaustive aerobic capacity determination in swimming rats. Adult rats were submitted to 4 swimming tests at different intensities (4%, 6%, 7%, and 8% of body mass), with intervals of 48 h between them. Two exercise bouts of equal intensity lasting 5 min were performed, separated by 2 min with blood collection for lactate analysis. For each intensity, delta lactate was determined by subtracting lactate concentration at the end of the first effort from the lactate at the end of the second effort. Individual linear interpolation of delta lactate concentration enabled determination of a "null" delta, equivalent to the critical load (CL). Maximal lactate steady state (MLSS) was also determined. The estimated CL was of 4.8% body mass and the MLSS was observed at 100% of CL, with blood lactate of 5.20 mmol/L. At 90%, blood lactate stabilized, with a progressive increase to 110% CL. These results offer a potential determination of aerobic capacity in swimming rats.

Animals↗

PubMed1995

Swim training alters sympathoadrenal and endocrine responses to hemorrhage in borderline hypertensive rats.

Swim training alters cardiovascular, sympathoadrenal, and endocrine responses to hemorrhage in borderline hypertensive rats (BHR). The effects of 10, 20, and 30% blood volume hemorrhages on cardiovascular, sympathoadrenal, and endocrine function in swim-trained (T; 2 h/day, 5 day/wk for 10-12 wk) and age-matched, untrained, sedentary, control (UT) borderline hypertensive rats (BHR) were assessed. Heart rate (HR) in UT BHR was significantly greater during the baseline (rest) period than T BHR. HR increased slightly from baseline in both groups after 10% hemorrhage but was significantly decreased in both groups after 20 and 30% hemorrhages. The decrease was eliminated by atropine (1 mg/kg iv). Systolic (SBP) and diastolic (DBP) blood pressures decreased significantly after 20 and 30% hemorrhages in both T and UT BHR but were not different between the groups at these times. Plasma norepinephrine levels were significantly increased above baseline after 20 and 30% hemorrhages in UT BHR and were significantly greater in UT BHR than T BHR after 30% hemorrhage. Plasma glucose levels increased significantly after 30% hemorrhage in both groups but were significantly greater in UT BHR than T BHR. Both plasma norepinephrine and plasma epinephrine levels showed strong positive correlations with plasma glucose. After 20 and 30% hemorrhages, plasma insulin levels were unchanged in T BHR but were significantly decreased in UT BHR. Plasma insulin levels were significantly less in UT than T BHR after 30% hemorrhage. These results suggest that swim training alters the effect that hemorrhage exerts on endocrine and sympathoadrenal function in BHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

PubMed1984

Biochemical alterations in heart after exhaustive swimming in rats.

This study investigated alterations in glycogen, catecholamines, and the function of various subcellular membranes of the heart after exhaustive swimming in rats. The rats were exhausted by daily exercise over 1, 3, or 7 consecutive days. Glycogen content of the heart and three selected skeletal muscles was depleted after a single bout of exhaustive exercise. Repeated bouts of exhaustive swimming elicited a depletion of glycogen in only the plantaris and gastrocnemius skeletal muscles. Plasma norepinephrine and epinephrine levels were highly elevated, and cardiac concentrations of these hormones were significantly depleted immediately after all exercise sessions. Cardiac sarcoplasmic reticulum (SR) Ca2+ transport was depressed after a single exhaustive exercise period. After three exercise bouts SR Ca2+ accumulation remained depressed; however, mitochondrial Ca2+ transport was found to be augmented. If the exhaustive exercise protocol was continued up to seven days, only mitochondrial Ca2+ accumulation was depressed. Various parameters of sarcolemmal membrane function were observed to be unaltered after exhaustive exercise. These findings demonstrate that exhaustive swimming exercise in rats is capable of producing significant alterations in the Ca2+ transport capacity of the SR and mitochondrial membrane systems of the heart but is without apparent effect on the sarcolemmal membrane.

Animals↗

PubMed1986

Chronic swimming reverses cardiac dysfunction and myosin abnormalities in hypertensive rats.

The purpose of this study was to determine whether a chronic swimming program could reverse the decreased cardiac function and altered myosin biochemistry found in hearts of rats with established renal hypertension. Ten wk after the onset of hypertension [midpoint (m)], hearts from normotensive controls (C) and hypertensives (H) were studied in an isolated working heart apparatus, and myosin biochemistry was analyzed. Half of the control and hypertensive animals were then subjected to a 10-wk swimming program (Sw) and their hearts were compared with those from age-matched sedentary rats. Body weight was no different at the midpoint of the study between Cm and Hm or at the end point (e) of the study among Ce, Swe, He, or H-Swe. Swimming had no effect on blood pressure in either normotensive or hypertensive rats. Dry heart weight was increased by 46% in Hm compared with Cm and by 36% in He, 21% in Swe, and 61% in H-Swe when compared with Ce. Hypertension was associated in both the mid- and end-point studies, with decreases in coronary flow, stroke work (both per gram left ventricle), ejection fraction, and midwall fractional shortening. In addition, actin-activated myosin adenosinetriphosphatase (ATPase) activity was decreased in Hm and He associated with an increase in the content of the V3 myosin isoenzyme. Although the coronary deficit was not corrected in H-Swe, stroke work, ejection fraction, and fractional midwall shortening were normalized compared with control hearts. Myosin ATPase activity and the myosin isoenzyme distribution were similarly restored in H-Swe.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗

PubMed1987

Effects of swim training on lung volumes and inspiratory muscle conditioning.

Lung volumes and inspiratory muscle (IM) function tests were measured in 16 competitive female swimmers (age 19 +/- 1 yr) before and after 12 wk of swim training. Eight underwent additional IM training; the remaining eight were controls. Vital capacity (VC) increased 0.25 +/- 0.25 liters (P less than 0.01), functional residual capacity (FRC) increased 0.39 +/- 0.29 liters (P less than 0.001), and total lung capacity (TLC) increased 0.35 +/- 0.47 (P less than 0.025) in swimmers, irrespective of IM training. Residual volume (RV) did not change. Maximum inspiratory mouth pressure (PImax) measured at FRC changed -43 +/- 18 cmH2O (P less than 0.005) in swimmers undergoing IM conditioning and -29 +/- 25 (P less than 0.05) in controls. The time that 65% of prestudy PImax could be endured increased in IM trainers (P less than 0.001) and controls (P less than 0.05). All results were compared with similar IM training in normal females (age 21.1 +/- 0.8 yr) in which significant increases in PImax and endurance were observed in IM trainers only with no changes in VC, FRC, or TLC (Clanton et al., Chest 87: 62-66, 1985). We conclude that 1) swim training in mature females increases VC, TLC, and FRC with no effect on RV, and 2) swim training increases IM strength and endurance measured near FRC.

Adolescent↗

PubMed1988

Effects of systolic overload and swim training on cardiac mechanics and biochemistry in rats.

We have previously shown that swim conditioning corrects the depressed mechanical function and myosin adenosinetriphosphatase (ATPase) activities associated with renovascular hypertension (HTN) in the rat. The present study was designed to assess the effects of swim conditioning on another form of systolic overload, subdiaphragmatic suprarenal aortic stenosis. Cardiac mechanics in an isolated working heart apparatus and myosin enzymology were studied in four groups of rats: controls (C), animals with chronic systolic overload secondary to aortic constriction (St), swim-conditioning animals (Sw), and animals exposed to a combined load (St-Sw). Heart weight was increased by 23% in St, 27% in Sw, and 36% in St-Sw. In contrast to HTN, cardiac pump and muscle function were not depressed in St. Sw was associated with improved cardiac output, stroke work, and velocity of circumferential fiber shortening. St-Sw showed improved mechanical cardiac performance relative to both C and St. The percent of ventricular myosin of the V1 type and Ca2+-activated myosin ATPase activity relative to C was unchanged in Sw but was depressed in St and St-Sw. These data demonstrate that the salutory mechanical effects of Sw can be superimposed on the systolic overload of St. However, the dissociation between mechanics and myosin enzymology suggests that factors in excitation-contraction coupling other than myosin isoenzyme shifts are responsible for this finding.

Animals↗

PubMed1988

Propelling efficiency of front-crawl swimming.

In this study the propelling efficiency (ep) of front-crawl swimming, by use of the arms only, was calculated in four subjects. This is the ratio of the power used to overcome drag (Pd) to the total mechanical power (Po) produced including power wasted in changing the kinetic energy of masses of water (Pk). By the use of an extended version of the system to measure active drag (MAD system), Pd was measured directly. Simultaneous measurement of O2 uptake (VO2) enabled the establishment of the relationship between the rate of the energy expenditure (PVO2) and Po (since when swimming on the MAD system Po = Pd). These individual relationships describing the mechanical efficiency (8-12%) were then used to estimate Po in free swimming from measurements of VO2. Because Pd was directly measured at each velocity studied by use of the MAD system, ep could be calculated according to the equation ep = Pd/(Pd + Pk) = Pd/Po. For the four top class swimmers studied, ep was found to range from 46 to 77%. Total efficiency, defined as the product of mechanical and propelling efficiency, ranged from 5 to 8%.

Adult↗

PubMed1989

Effect of swim exercise training on human muscle fiber function.

This study examined the effect of a typical collegiate swim-training program and an intensified 10-day training period on the peak tension (Po), negative log molar Ca2+ concentration (pCa)-force, and maximal shortening speed (Vmax) of the slow-twitch type I and fast-twitch type II fibers of the deltoid muscle. Over a 10-wk period, the swimmers averaged 4,266 +/- 264 m/day swimming intermittent bouts of front crawl, kicking, or pulling. The training program induced an almost twofold increase in the mitochondrial marker enzyme citrate synthase. Po of the single fibers was not altered by either the training or 10-day intensive training programs, and no significant differences were observed in the Po (kg/cm2) of type I compared with the type II fibers. The type II fiber diameters were significantly larger than the type I fibers (94 +/- 4 vs. 80 +/- 2 microns), and although fiber diameters were unaffected by the training, the 10-day intensive training significantly reduced the type II fiber diameter. The type I fibers from the trained swimmers showed pCa-force curves shifted to the right such that higher free Ca2+ levels were required to elicit a given percent of Po (for values less than 0.5 Po). The activation threshold (pCa) for the onset of tension and the pCa required to elicit one-half maximal tension were not altered by the training in either fiber type. Fiber Vmax (measured by the slack test) was fivefold higher in type II compared with type I fibers (4.85 +/- 0.50 vs. 0.86 +/- 0.04 fiber lengths/s). The exercise-training program significantly increased and decreased the Vmax of the slow and fast fibers, respectively. The 10 days of intensified training produced a further significant decrease in the Vmax of the type II fibers. After a period of detraining, the Vmax of both fiber types returned to the control level. The force-velocity relation was not significantly altered in either fiber type by the swim training; however, the intensified training significantly depressed the velocity of the type II fiber at all loads studied. The Vmax changes with exercise training are likely explained by an exercise-induced expression of fast myosin in slow fibers and slow myosin in fast fibers.

Adult↗