Swimming Training In Rats Research Articles

Swimming training improves cardiovascular autonomic dysfunctions and prevents renal damage in rats fed a high-sodium diet from weaning.

What is the central question of this study? How does swimming exercise training impact hydro-electrolytic balance, renal function, sympathetic contribution to resting blood pressure and cerebrospinal fluid (CSF) [Na+ ] in rats fed a high-sodium diet from weaning? What is the main finding and its importance? An exercise-dependent reduction in blood pressure was associated with decreased CSF [Na+ ], sympathetically driven vasomotor tonus and renal fibrosis indicating that the anti-hypertensive effects of swimming training in rats fed a high-sodium diet might involve neurogenic mechanisms regulated by sodium levels in the CSF rather than changes in blood volume. High sodium intake is an important factor associated with hypertension. High-sodium intake with exercise training can modify homeostatic hydro-electrolytic balance, but the effects of this association are mostly unknown. In this study, we sought to investigate the effects of swimming training (ST) on cerebrospinal fluid (CSF) Na+ concentration, sympathetic drive, blood pressure (BP) and renal function of rats fed a 0.9% Na+ (equivalent to 2% NaCl) diet with free access to water for 22weeks after weaning. Male Wistar rats were assigned to two cohorts: (1) fed standard diet (SD) and (2) fed high-sodium (HS) diet. Each cohort was further divided into trained and sedentary groups. ST normalised BP levels of HS rats as well as the higher sympathetically related pressor activity assessed by pharmacological blockade of ganglionic transmission (hexamethonium). ST preserved the renal function and attenuated the glomerular shrinkage elicited by HS. No change in blood volume was found among the groups. CSF [Na+ ] levels were higher in sedentary HS rats but were reduced by ST. Our findings showed that ST effectively normalised BP of HS rats, independent of its effects on hydro-electrolytic balance, which might involve neurogenic mechanisms regulated by Na+ levels in the CSF as well as renal protection.

Moxibustion Reduces Inflammatory Response in the Hippocampus of a Chronic Exercise-Induced Fatigue Rat.

Accumulating data indicates that brain inflammation plays an important role in the pathophysiology of chronic exercise-induced fatigue. Moxibustion in traditional Chinese medicine has been found to alleviate exercise-induced fatigue. However, it remains unclear whether the effect of moxibustion is related to its anti-inflammatory properties. In this study, rats were exposed to 3-week exhaustive swimming to induce chronic exercise-induced fatigue. The body weight, exhaustive swimming time, tail suspension test and open-field test were observed. Real-time polymerase chain reaction (RT-PCR) was used to determine the mRNA expression of proinflammatory cytokines (interleukin-1β [IL-1β], interleukin-6 [IL-6], and tumor necrosis factor-α[TNF-α]), and enzyme-linked immunosorbent assay (ELISA) was used to detect IL-1β, IL-6, and TNF-α concentrations. Chronic exhaustive exercise significantly reduced the body weight and exhaustive swimming time, and increased tail suspension immobility time, which were reversed by moxibustion treatment. Compared with control rats, the mRNA and protein expression of IL-1β, IL-6, and TNF-α in the hippocampus was significantly increased in exhaustive swimming trained rats. Moxibustion significantly decreased the level of IL-6 in the hippocampus, but not affected IL-1β and TNF-α level significantly. Our results suggested that a potential inflammatory damage in the brain may be involved during chronic exhaustive exercise-induced fatigue. Moxibustion could attenuate the inflammatory impairment in exercise-induced fatigue, which might be mediated by inhibition of the proinflammatory cytokine IL-6 levels in the brain region.

Combined effects of exercise training and high doses of anabolic steroids on cardiac autonomic modulation and ventricular repolarization properties in rats.

Several studies have reported that high doses of synthetic anabolic androgenic steroids (AAS) can have serious negative effects on health, including the cardiovascular system. The aim of this study was to evaluate the combined effects of AAS and exercise training on ventricular repolarization and cardiac autonomic modulation in rats. Male Wistar rats were allocated into 4 groups: sedentary rats treated with vehicle, sedentary rats treated with nandrolone decanoate, swimming-trained rats treated with vehicle, and swimming-trained rats treated with nandrolone decanoate. Ventricular repolarization was evaluated by electrocardiographic analysis of QT interval and QT dispersion. Cardiac autonomic modulation was assessed by heart rate variability. Our results show that AAS increased QT interval and QT dispersion in sedentary rats treated with nandrolone decanoate as compared to sedentary rats treated with vehicle, indicating AAS-induced ventricular repolarization abnormalities. When rats treated with nandrolone decanoate were subjected to concomitant exercise training, ventricular repolarization was normalized. On the other hand, AAS-induced reduction in cardiac parasympathetic modulation was not prevented by exercise training. In conclusion, AAS produced cardiac autonomic dysfunction and ventricular repolarization disturbances in rats. Combining an exercise training protocol during the AAS treatment attenuated the ventricular repolarization abnormalities and did not prevent cardiac autonomic dysfunction.

Swimming exercise in combination with garlic extract administration as a therapy against doxorubicin-induced hepatic, heart and renal toxicity to rats

Effect of swimming training is considered on doxorubicin-induced toxicity in the liver, heart, and kidney of rats. Histopathological degeneration could partially be prevented in swimming-trained rats pretreated with garlic extract. Exercise combined with garlic extract reduced the malondialdehyde value and improved the activities of antioxidant enzymes. Doxorubicin treatment enhanced the mean values of blood ALT, AST, and ALP enzymes, as well as hepatic, cardiac, and renal TNF-α and HSP70 (p < .05). Swimming alone or supplemented with garlic extract can protect liver, heart, and kidney against doxorubicin toxicity by increasing antioxidants and reducing oxidative stress and inflammation.

Effect of a 12-week submaximal swimming training in rats exposed to tobacco- derived nitrosamine ketone.

Background:Tobacco contains carcinogens such as NNK (nicotine-derived nitrosamine ketone) that makes induction of lung cancer by changing the stimulation of IL-10 expression. The aim of this study was to investigate changes in resting levels of IL-10 in lung tissues of rats exposed to NNK after a 12-week aerobic submaximal swimming training.Methods:For this purpose, 46 Wistar rats were randomly divided into five groups consisting training, training + NNK, NNK, saline and control. NNK-induced groups received NNK subcutaneously one day per week at a rate of 12/5 mg per kg body weight and the training groups performed submaximal swimming training for 12 weeks. The levels of IL-10 in homogenized lung tissue were measured by ELISA.Results:Findings indicated that a period of swimming training increased the IL-10 levels significantly in lung tissue of training group when compared to control (P=0.00) and NNK groups (P=0.00). Also, a significant increase of IL-10 level was observed in exercise + NNK group when compared to NNK group (p≤0/02). Furthermore, it was observed that IL-10 levels of NNK group had a significant decrease when compared to training group (P=0/00), training + NNK group (p≤0/02), but had insignificant increase when compared to saline group (p≤0/85).Conclusions:Generally, it could be confirmed that regular submaximal aerobic training plays an important role in the inhibition of the effects of lung inflammation induced by NNK via increasing IL-10 activity.

Ibuprofen intake increases exercise time to exhaustion: A possible role for preventing exercise-induced fatigue.

Although the intake of nonsteroidal anti-inflammatory drugs (NSAIDs) intake by athletes prevents soreness, little is known concerning their role in exercise performance. This study assessed the effects of ibuprofen intake on an exhaustive protocol test after 6 weeks of swimming training in rats. Animals were divided into sedentary and training groups. After training, animals were subdivided into two subsets: saline or ibuprofen. Afterwards, three repeated swimming bouts were performed by the groups. Ibuprofen (15 mg/kg) was administered once a day. Pain measurements were performed and inflammatory and oxidative stress parameters were assayed in cerebral cortex and gastrocnemius muscle. Training, ibuprofen administration, or both combined (P < 0.05; 211 ± 18s, 200 ± 31s, and 279 ± 23s) increased exercise time to exhaustion. Training decreased the acetylcholinesterase (AChE) activity (P < 0.05; 149 ± 11) in cerebral cortex. Ibuprofen intake decreased the AChE activity after exhaustive protocol test in trained and sedentary rats (P < 0.05; 270 ± 60; 171 ± 38; and 273 ± 29). It also prevented neuronal tumor necrosis factor-α (TNF-α) and interleukin (IL 1β) increase. Fatigue elicited by this exhaustive protocol may involve disturbances of the central nervous system. Additive anti-inflammatory effects of exercise and ibuprofen intake support the hypothesis that this combination may constitute a more effective approach. In addition, ergogenic aids may be a useful means to prevent exercise-induced fatigue.

Physiological adaptations during endurance training below anaerobic threshold in rats

To assess the effects of continuous exercise training at intensities corresponding to 80 and 90 % of the lactate minimum test (LM), we evaluated antioxidant activity, hormone concentration, biochemical analyses and aerobic and anaerobic performance, as well as glycogen stores, during 12 weeks of swimming training in rats. One-hundred rats were separated into three groups: control (CG, n = 40), exercise at 80 (EG80, n = 30) and 90% (EG90, n = 30) of LM. The training lasted 12 weeks, with sessions of 60 min/day, 6 days/week. The intensity was based at 80 and 90% of the LM. The volume did not differ between training groups (X of EG80 = 52 ± 4 min; X of EG90 = 56 ± 2 min). The glycogen concentration (mg/100 mg) in the gastrocnemius increased after the training in EG80 (0.788 ± 0.118) and EG90 (0.795 ± 0.157) in comparison to the control (0.390 ± 0.132). The glycogen stores in the soleus enhanced after the training in EG90 (0.677 ± 0.230) in comparison to the control (0.343 ± 0.142). The aerobic performance increased by 43 and 34% for EG80 and EG90, respectively, in relation to baseline. The antioxidant enzymes remain unchanged during the training. Creatine kinase (U/L) increased after 8 weeks in both groups (EG80 = 427.2 ± 97.4; EG90 = 641.1 ± 90.2) in relation to the control (246.9 ± 66.8), and corticosterone (ng/mL) increased after 12 weeks in EG90 (539 ± 54) in comparison to the control (362 ± 44). The continuous exercise at 80 and 90% of the LM has a marked aerobic impact on endurance performance without significantly biomarkers changes compared to control.

Swimming Training in Rats Increases Cardiac MicroRNA-126 Expression and Angiogenesis

MicroRNA (miRNA)-126 is angiogenic and has two validated targets: Sprouty-related protein 1 (Spred-1) and phosphoinositol-3 kinase regulatory subunit 2 (PI3KR2), negative regulators of angiogenesis by VEGF pathway inhibition. We investigated the role of swimming training on cardiac miRNA-126 expression related to angiogenesis. Female Wistar rats were assigned to three groups: sedentary (S), training 1 (T1, moderate volume), and training 2 (T2, high volume). T1 consisted of 60 min·d of swimming, five times per week for 10 wk with 5% body overload. T2 consisted of the same protocol of T1 until the eighth week; in the ninth week, rats trained for two times a day, and in the 10th week, rats trained for three times a day. MiRNA and PI3KR2 gene expression analysis was performed by real-time polymerase chain reaction in heart muscle. We assessed markers of training, the cardiac capillary-fiber ratio, cardiac protein expression of VEGF, Spred-1, Raf-1/ERK 1/2, and PI3K/Akt/eNOS. The cardiac capillary-fiber ratio increased in T1 (58%) and T2 (101%) compared with S. VEGF protein expression was increased 42% in T1 and 108% in T2. Cardiac miRNA-126 expression increased 26% (T1) and 42% (T2) compared with S, correlated with angiogenesis. The miRNA-126 target Spred-1 protein level decreased 41% (T1) and 39% (T2), which consequently favored an increase in angiogenic signaling pathway Raf-1/ERK 1/2. On the other hand, the gene expression of PI3KR2, the other miRNA-126 target, was reduced 39% (T1) and 78% (T2), and there was an increase in protein expression of components of the PI3K/Akt/eNOS signaling pathway in the trained groups. This study showed that aerobic training promotes an increase in the expression of miRNA-126 and that this may be related to exercise-induced cardiac angiogenesis, by indirect regulation of the VEGF pathway and direct regulation of its targets that converged in an increase in angiogenic pathways, such as MAPK and PI3K/Akt/eNOS.

Impact of Swimming Exercise Training on the Effects of Modulation of Mitochondrial Permeability Transition and NOS-1 Activation in Medullary Cardiovascular Neurons of Rats

Physical inactivity can be considered one of the major risk factors related to cardiovascular diseases. There are reasons to believe that the positive effect of exercise training is, to a large extent, mediated by modulation of the nervous control of the circulation system. In our previous studies, we showed that modulation of mitochondrial permeability transition in medullary cardiovascular neurons significantly contributes to the hemodynamic reactions in both the norm and a number of pathological states. In this study, we examined in acute experiments on urethane-anesthetized rats the hemodynamic effects mediated by either modulation of mitochondrial permeability transition in medullary neurons, or activation of neuronal NO synthase (NOS-1) in these neuronal populations after preliminary moderate exercise training (everyday swimming sessions of increased duration carried out for four weeks). It was shown that, after exercise training had been completed, the effects of injections of an inductor of mitochondrial permeability transition pore (MPTP) opening, phenylarsine oxide (PAO, 0.5 to 1.5 nmol), into populations of cardiovascular neurons in the medullary autonomic nuclei (nucl. tractus solitarius and paramedian and lateral reticular nuclei) were less expressed, as compared with those in control (untrained) animals. The data obtained suggest that exercise training can exert a protective action on functional activity of medullary neurons due to the decreased sensitivity of MPTPs to their opening. Injections of an inhibitor of MPTP opening, melatonin (0.7 to 2.1 nmol), into populations of medullary neurons under study in trained rats induced a decrease in the systemic arterial pressure (SAP), in contrast to untrained animals demonstrating mostly hypertensive responses following injections of melatonin into the above nuclei. Injections of an activator of neuronal NO synthase (NOS-1), L-arginine, into the medullary nuclei of swimming-trained rats resulted in more expressed hemodynamic shifts than in control animals, which suggests an increase in the activity of neuronal NO synthase in medullary neurons of such animals.

The cardiac hypertrophy induced by anabolic steroid associated with the swimming training in rats: Involvement of the Renin Angiotensin Aldosterone System

Experimental groups (n=56): Control (C), Anabolic Steroid (AS), AS+Losartan (AS+L), AS+Spironolactone (AS+S), Trained (T), Trained AS (TAS), Trained AS+Losartan (TAS+L) and Trained AS+Spironolactone (TAS+S). The AS was administered twice a week (10mg/kg/wk). The swimming training (ST) was performed for 10 weeks (5x/wk). The Losartan and Spironolactone were administered in drink water. AS induced cardiac hypertrophy (CH) in AS group compared to C group and it was increased in TAS group. AS treatment increased collagen volumetric fraction and collagen type III expression. The Losartan treatment inhibited the CH, but not Spironolactone. However, both treatments prevented cardiac collagen formation. AS groups increased the angiotensin converting enzyme (ACE) activity, AT1 and AT2 receptors expression. Treatment with Losartan or Spironolactone prevented the increase in ACE activity, but not AT1 and AT2 receptors expression. CYP11B2 expression was increased in TAS group and 11 βHSD2, TGFβ and osteopontin expression were increased in AS and TAS group. Both antagonists inhibited the AS effects and its association with ST. The results show the important participation of RAAS on CH induced by the association of AS and ST. For the first time we are showing the aldosterone (aldosterone synthase and 11β‐HSD2 expression) participation in these association.

Swimming Training Increases the Post-Yield Energy of Bone in Young Male Rats

The purpose of this study is to investigate the effects of non-weight-bearing exercise on growing bone. Male Wistar rats (7 week-old) were assigned to one baseline control group, one control group and two swimming training groups, which were trained with 2 and 4% body-weight mass added, respectively. After an 8-week training period, three groups showed significant development compared to the baseline control group. Among the three 15-week-old groups, swimming-trained rats were lower in body weight (BW), densitometry and size-related measurements. In femoral biomechanical testing, swimming training groups were significantly lower in yield moment and ultimate moment, which may be due to a significantly lower long bone cross-sectional moment of inertia. However, the two swimming groups were higher in post-yield energy absorption and displacement. Further, in estimated tissue-level biomaterial properties, no differences were shown in yield stress, strain or toughness among the three groups. Using BW as a covariate, results of ANCOVA showed no differences in size-related parameters among the three groups, and some parameters were even higher in the two swimming groups. Regarding Pearson's correlation, size-related parameters correlated well to BW and whole bone strength but not to tissue post-yield behaviors. In conclusion, when compared to age-matched control group, swimming rats showed lower bone strength and lower yield energy absolutely at the structural level, but similar yield stress and yield toughness at the tissue level. Moreover, swimming training benefited growing bone in post-yield behaviors. Further studies should investigate the parameters that contribute to this exercise-induced post-yield behavior.

Effect of arginine, ornithine and citrulline supplementation upon performance and metabolism of trained rats.

During intense exercise there is an augmented production of ammonia and IMP in the exercised muscle that could be related to the establishment of peripheral fatigue. In order to prevent this accumulation, the urea cycle in the liver eliminates ammonia in the form of urea and the skeletal muscle buffers the increase of ammonia via transamination reactions. In the present study we evaluated the effect of arginine, citrulline and ornithine supplementation, intermediates of the urea cycle, on the performance of sedentary and swimming-trained rats submitted to a single bout of exhaustive exercise. We also measured the glycogen content of the soleus and gastrocnemius muscles and of the liver, as well as the plasma concentrations of ammonia, urea, glutamine, glucose and lactate. The results indicate that arginine, citrulline and ornithine supplementation increased the flux of substrate through the reaction catalysed by glutamine synthetase, leading to increased glutamine production after an exhaustive bout of exercise, and of the mechanism involved in ammonia buffering.

Regular Training Modulates the Accumulation of Reactive Carbonyl Derivatives in Mitochondrial and Cytosolic Fractions of Rat Skeletal Muscle

The oxygen flux into the mitochondria of skeletal muscle increases with exercise. However, the extent of oxidative damage to mitochondrial proteins of skeletal muscle has only been estimated. We studied the alteration of reactive carbonyl derivatives (RCD) in mitochondrial and cytosolic fractions of skeletal muscle following 9 weeks of swimming training in rats. The RCD content of mitochondria was significantly elevated compared with the cytosolic fraction of both control and exercised animals. Accumulation of RCD in muscle mitochondria of the exercised group was also significantly elevated (P < 0.05). On the other hand, alteration of the accumulation of RCD was not apparent in the cytosolic fraction of skeletal muscle. The activity of proteasome complex, however, was increased in the cytosolic fraction of exercised muscle (P < 0.05). The data suggest that mitochondria of skeletal muscle accumulate significantly larger amounts of RCD than the cytosolic fraction and the tendency of the accumulation varies in cell fractions. Exercise training increases the accumulation of protein damage in mitochondria of skeletal muscle but cytosolic proteins are protected by increased activity of proteasome complex and possibly by other antioxidant enzymes.

Iron distribution in different tissues in rats following exercise.

Iron plays an essential role in blood oxygen transport and in muscle physiology. No conclusive data exist in the literature concerning its tissue distribution and behavior following exercise and training. The aim of the present work was to analyze the Fe content in different tissues following a single session of swimming to exhaustion and after swimming training in rats in order to more extensively describe the changes of Fe distribution provoked by exercise. Animals were divided into four groups (n=10): control group at rest, trained group at rest, control group after exercise, and trained group after exercise. First, rats swam until exhaustion and the maximal swimming time was noted. The training protocol consisted of swimming (5 d/week for 3 wk), limiting the time to 60% of the maximum obtained during the first session to exhaustion of each rat. The variables measured were erythrocytes, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, and, Fe in liver, kidney, erythrocytes, heart, muscle, bone, and serum. Variations in plasma volume were also calculated. Tissues presented two different profiles with regard to the changes of Fe concentration provoked by training: those displaying higher values of Fe after training, such as liver, heart, muscle, and serum, and those displaying lower values, such as bone, kidney, and red blood cells. These changes in the distribution of Fe in different tissues could be the result of an increase in the needs and use of Fe, shown by active tissues at exercise, and it is possible that the hormonal changes provoked by stress lead to a different behavior of Fe proteins.

CARDIAC HYPERTROPHY INDUCED BY SWIMMING TRAINING IS ASSOCIATED WITH ACTIVATION OF RENIN-ANGIOTENSIN SYSTEM

635 Cardiac hypertrophy is one of the compensatories cardiovascular adaptations induced by exercise training (ET). Angiotensin II is a throphic factor which is involved in many cardiac hypertrophy models. In this study we evaluated the plasmatic and cardiac reninangiotensin system (RAS) components, during the cardiac hypertrophy development associated with swimming training in rats. We studied 16 male normotensive Wistar rats. Eigth were trained using a low-intensity swimming protocol for 8 weeks and 8 were kept sedentary. After ET arterial blood pressure (BP) was measured directly and tissue samples were extracted for morphometric and biochemical analysis. ACE activity was determined by fluorometric method using Hip-His-Leu as the substrate. Plasma renin activity (PRA) was evaluated by radioimunoassay (RIA). Results showed no changes in BP among the groups. The swimming training produced 13% hypertrophy of the left ventricle (LV) (1.95 vs. 2.2) and an increase in myocytes transversal diameter of 21% (10-13μm). Cardiac ACE activity increased 25% (1.7 vs. 2.2 nMol His-Leu/min/mg of protein) without changes in plasma (104.5 vs 111.5 nMol His-Leu/min/ml). The RPA increased 196% (0.4 vs. 1.3 ng Ang I/ml/h) in trained rats. These results suggested that swimming training induced cardiac hypertrophy and increased plasma renin and cardiac ACE activities indicating that systemic and local RAS may contribute to the development of this hypertrophy.

Compartmental shifts of calcium and magnesium as a result of swimming and swimming training in rats.

To describe accurately the mineral changes (Ca and Mg) provoked by swimming, the aims of this study were to analyze those tissues that, with regard to their mineral content, can better classify individuals performing both swimming until exhaustion and swimming as training and to know the shifts of these minerals between different tissues after a single session of swimming until exhaustion and after training. Wistar rats were distributed into 12 groups, six male and six female (N = 10): 1) control rest group (CR); 2) trained rest group (TR); 3) control exercise group (CE); 4) trained exercise group (TE); 5) control recovery group (CER) and 6) trained recovery group (TER). The most informative tissues of Ca and Mg compartmental shifts during exercise have been determined. Discriminant analysis selected heart Ca, muscle Ca and bone Ca, bone Mg, erythrocyte Mg, and serum Mg as the most significant variables. The animals were classified by means of two canonical axes: the first one relates to training situation and sex, and the second one shows the special characteristics of trained male rats. Another independent discriminant analysis applied to male and female groups separately showed that the first canonical axis (control/trained) is basically defined by heart Ca, bone Ca, and erythrocyte Mg (male), and by heart Ca, bone Ca, and bone Mg (female), while the second axis, related to the exercise situations, is defined by the serum Mg levels in both sexes. We think that discriminant analysis is a statistical method capable of explaining physiological processes and classifying individuals performing exercises of different length. It suggests that the homeostasis of Ca and Mg is somewhat different for males and females. Serum magnesium must be considered to distinguish exercise situations. The analysis of these tissues could inform us about the mineral status of the rats and then we could correct possible deficiencies in our research. In this work we have only found different mineral redistributions among tissues. The trained animals have a better mineral recovery capacity than the untrained ones. Training has a different physiological repercussion in male and female rats on the basis of their respective maximal swimming times after training and their mineral behavior.

Effects of chronic swimming training on cardiac sarcolemmal function and composition.

Cardiac contractile function is dependent on the integrity and function of the sarcolemmal membrane. Swimming exercise training is known to increase cardiac contractile performance. The purpose of the present study was to examine whether a swimming exercise program would alter sarcolemmal enzyme activity, ion flux, and composition in rat hearts. After approximately 11 wk of exercise training, cardiac myosin and actomyosin Ca2+-adenosinetriphosphatase (ATPase) activity was significantly higher in exercised rat hearts than in sedentary control rat hearts. Glycogen content was increased in plantaris and gastrocnemius muscles from exercised animals as was succinic dehydrogenase activity in gastrocnemius muscle of exercised rats in comparison to sedentary rat preparations. Sarcolemmal vesicles were isolated from hearts of exercise-trained and control rats. Sarcolemmal Na+-K+-ATPase and K+-p-nitrophenylphosphatase activities, Na+-Ca2+ exchange, and passive Ca2+ binding did not differ between the two groups. ATP-dependent Ca2+ uptake and 5'-nucleotidase activity were elevated in the cardiac sarcolemmal vesicles isolated from exercised animals compared with sedentary control rats. Sarcolemmal phospholipid composition was not altered by the exercise training. Our results demonstrate that swimming training in rats does not affect most parameters of cardiac sarcolemmal function or composition. However, the elevated sarcolemmal Ca2+ pump activity in exercised rats may help to reduce intracellular Ca2+ and augment cardiac relaxation rates. The enhanced 5'-nucleotidase activity may stimulate adenosine production, which could affect myocardial blood flow. The present results further our knowledge on the subcellular response of the heart to swimming training in the rat.

Is swimming exercise or cold exposure for rats?

Rats were trained by daily swimming sessions (up to 3 h per day) for at least 6 weeks in water at 30, 36 and 38 degrees C. After this training, the adaptive changes obtained were compared with those typical of cold-acclimated (cold-specific changes) and running-trained (training-specific changes) rats. The most typical training-specific change, an increased activity of oxidative muscle enzymes was negligible for swimming-trained rats, while the lowered activity of muscle lactate dehydrogenase was evident for all trained groups. Cold-specific changes, such as increased food intake, increased calorigenic response to injected noradrenaline, an increase both in mass and metabolic capacity of brown adipose tissue, and maintenance of the stores of ascorbic acid and muscle glycogen during cold exposure, were observed for rats trained at 36 and 30 degrees C. The cold tolerance test in cold air did not make any distinct difference between the rats trained at different water temperatures, while in cool water the 30 degrees C -swimmers were clearly superior to other groups, that is, their cooling rate was slowest. Other adaptive changes were found, to a variable extent, for all trained groups. These included loss of body fat, cardiac hypertrophy, reduced urinary catecholamine excretion after test swimmings either in cold or warm water, increased tail-skin temperature response to isoprenaline, and a higher tail-skin temperature in response to cold. Generally, however, the adaptive changes observed for 30- and 36 degrees C-swimmers were similar, while the changes observed for 38 degrees C-swimmers were different. The latter group neither displayed any cardiac enlargement nor any cold-specific changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Physical training under the influence of beta blockade in rats: effect on adrenergic responses.

Rats were trained by daily swimming or running exercises with and without daily propranolol injections. Both training methods resulted in cardiac enlargement, but only swimming exercise caused hypertrophy of the brown adipose tissue. These changes were antagonized by beta blockade. The size of the adrenals reflected the stress of the treatments, but other known stress parameters, such as the size of the thymus or sexual organs dit not. Only swimming training without beta blockade sensitized the rats to the calorigenic action of noradrenaline. The cooling rate of the rats in water, when taking into account the insulative capacity of the body, was decreased in swimming-trained as well as in propranolol-treated rats but increased in running-trained rats. The latter two changes may be due to circulatory alterations, while the delayed body cooling in swimming-trained rats probably results from increased heat production capacity. Training-induced resting bradycardia and enhanced tachycardic response to isoprenaline were observable only in the animal groups trained without beta blockade. The pressor response to noradrenaline tended to be higher in the trained groups and the propranolol-treated group than in the controls and was smaller in the animal groups trained under the influence of beta blockade. On the other hand, the hypotonic response to isoprenaline was smaller in the propranolol-treated and running-trained animals. The results emphasize the importance of the sympathetic nervous system in the adaptation of an organism to physical training.