Chronic Swimming Research Articles

Exercise-induced cardiac mitochondrial reorganization and enhancement in spontaneously hypertensive rats.

The myocardium is a highly oxidative tissue in which mitochondria are essential to supply the energy required to maintain pump function. When pathological hypertrophy develops, energy consumption augments and jeopardizes mitochondrial capacity. We explored the cardiac consequences of chronic swimming training, focusing on the mitochondrial network, in spontaneously hypertensive rats (SHR). Male adult SHR were randomized to sedentary or trained (T: 8-week swimming protocol). Blood pressure and echocardiograms were recorded, and hearts were removed at the end of the training period to perform molecular, imaging, or isolated mitochondria studies. Swimming improved cardiac midventricular shortening and decreased the pathological hypertrophic marker atrial natriuretic peptide. Oxidative stress was reduced, and even more interesting, mitochondrial spatial distribution, dynamics, function, and ATP were significantly improved in the myocardium of T rats. In the signaling pathway triggered by training, we detected an increase in the phosphorylation level of both AKT and glycogen synthase kinase-3 β, key downstream targets of insulin-like growth factor 1 signaling that are crucially involved in mitochondria biogenesis and integrity. Aerobic exercise training emerges as an effective approach to improve pathological cardiac hypertrophy and bioenergetics in hypertension-induced cardiac hypertrophy.

Reducing sugar intake through chronic swimming training: Exploring palatability changes and central vasopressin mechanisms

Excessive sugar intake has been associated with the onset of several non-communicable chronic diseases seen in humans. Physical activity could affect sweet taste perception which may affect sugar intake. Therefore, it was investigated the chronic effects of swimming training on sucrose intake/preference, reactivity to sucrose taste, self-care in neurobehavioral stress, and the possible involvement of the vasopressin type V1 receptor in sucrose solution intake. Male Wistar rats, of from different cohorts were used, subjected to a sedentary lifestyle (SED) or swimming training (TR - 1 h/day, 5×/week, for 8 weeks, with no added load). Weekly intake was verified in SED and TR rats after access to a sucrose solution 1×/week, 2 h/day, for eight weeks. Chronic effects of swimming and/or a sedentary lifestyle were carried out three days after the end of the physical exercise protocol. Swimming training reduced the intake of sucrose solution from the third week onwards in the two-bottle test measured once a week for 8 weeks. After the ending of the swimming protocol, sucrose intake was also reduced as per its preference. This reduced intake is probably correlated with the carbohydrate aspect of sucrose since saccharin intake was not affected. In addition, chronic swimming training was shown to reduce ingestive responses, increase neutral responses, without interfering with aversive, in the sucrose solution taste reactivity test. In addition, these results are not related to a depressive-like behavior, nor to neurobehavioral stress. Furthermore, treatment with vasopressin V1 receptor antagonist abolished the reduced sucrose intake in trained rats. The results suggest that swimming performed chronically is capable of reducing intake and preference for sucrose by decreasing the palatability of sucrose without causing depressive-type behavior or stress. In addition, the results also suggest that central V1 vasopressin receptors are part of the mechanisms activated to reduce sucrose intake in trained rats.

The Effect of Chronic Swimming Exercise and Vitamin E Supplementation on Bone Element Metabolism in Epileptic Rats.

This study aimed to investigate the effects of chronic swimming exercise and vitamin E administration on elemental levels in the bone tissue of epileptic rats. Forty-eight rats were divided into six groups: Control, Swimming, Swimming + vitamin E, Swimming + Epilepsy, Swimming + Epilepsy + vitamin E, and Epilepsy. Vitamin E was administered to the animals chronically by gavage at a dose of 500 mg/kg every other day for 3 months. Epileptiform activity was induced with penicillin in animals 24 hours after the last vitamin E intake. The exercise program consisted of daily 30-minute swimming sessions. At the end of the treatment period, the levels of calcium, chromium, copper, iron, magnesium, manganese, lead, and zinc (µg/gram tissue) in bone tissue samples were measured using an atomic emission device. The results showed that all epileptic groups had significantly lower bone chromium levels compared to the control groups (p<0.05). The epileptic, and epileptic swimming groups had the lowest levels of bone calcium, magnesium, and zinc (p<0.05). Vitamin E administration resulted in a significant increase in bone calcium, magnesium, and zinc levels in the epileptic swimming group with vitamin E compared to the epileptic and epileptic swimming groups. (p<0.05). The findings of the study show that the administration of vitamin E improves calcium, magnesium, and zinc metabolism in the deteriorated bone tissue of the epileptic rat model.

Adropin increases with swimming exercise and exerts a protective effect on the brain of aged rats

Adropin is a protein in the brain that decreases with age. Exercise has a protective effect on the endothelium by increasing the level of adropin in circulation. In this study, whether adropin, whose level in the brain decreases with age, may increase with swimming exercise, and exhibit a protective effect was investigated. Young and aged male Sprague Dawley rats were submitted to 1 h of swimming exercise every day for 8 weeks. Motor activity parameters were recorded at the end of the exercise or waiting periods before the animals were euthanized. Increased motor functions were observed in only the young rats that exercised regularly. Adropin levels in the plasma, and the adropin and VEGFR2 immunoreactivities and p-Akt (Ser473) levels in the frontal cortex were significantly increased in the aged rats that exercised regularly. It was also observed that the BAX/Bcl2 ratio and ROS-RNS levels decreased, while the TAC levels increased in the aged rats that exercised regularly. The results of the study indicated that low-moderate chronic swimming exercise had protective effects by increasing the level of adropin in the frontal cortex tissues of the aged rats. Adropin is thought to achieve this effect by increasing the VEGFR2 expression level and causing Akt (Ser473) phosphorylation. These results indicated that an exercise-mediated increase in endogenous adropin may be effective in preventing the destructive effects of aging on the brain.

IL-6 and HSPA1A Gene Polymorphisms May Influence the Levels of the Inflammatory and Oxidative Stress Parameters and Their Response to a Chronic Swimming Training.

The aim of the study was to evaluate whether the most common polymorphisms in the IL-6 and HSP70 genes affect the circulating heat shock protein 70 (HSP70), as well as inflammatory and prooxidant-antioxidant parameters in healthy men undergoing chronic endurance training. The subjects were randomly assigned to a 12-week swimming training (ST group) or control group (CON). Fasting blood samples were collected pre- and post-study period to assessment: superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, serum levels of lipid hydroperoxides (LHs), tumor necrosis factor α (TNFα), and HSP70. Subjects were genotyped for IL-6-174G/C, HSPA1A + 190 G/C and HSPA1B + 1538 A/G single nucleotide polymorphisms (SNPs) by real-time PCR. After a 12-week study period, a decrease in TNFα, HSP70, and GPx was observed in the ST group, but not the CON group. IL-6 SNP affected serum TNFα levels (main effect of genotype). Higher TNFα levels (pre- and post-study period) was observed in CC CON than in other IL-6 genotypes of CON and ST groups. However, a post-training decrease in TNFα was observed in both GG and CC IL-6 genotypes of ST group. In turn, only GG IL-6 genotype of the ST group was related to a post-training decrease in HSP70 (main time and genotype interaction). Moreover, pre- and post-training LHs were lower in GG than GC/CC HSPA1A genotypes of the ST group (main genotype effect). In conclusion, polymorphisms within the IL-6 and HSPA1A genes seem to affect baseline levels of some inflammatory parameters and prooxidant-antioxidant status and/or their changes after chronic swimming training. However, the results should be confirmed in a study with a larger sample size, one that includes individuals with sedentary lifestyles.

Comparison of ANP and BNP Granular Density in Atria of Rats After Physiological and Pathological Hypertrophy.

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are cardiac hormones located in atria granules. Both peptides respond to cardiac pressure and volume dynamics and accordingly serve as translation biomarkers for the clinical treatment of heart failure. Serum ANP and BNP play central secretary roles in blood pressure and cardiac output regulation and have proven utility as differential biomarkers of cardiovascular proficiency and drug-induced maladaptation, yet both peptides are impervious to exercise-induced hypertrophy. We employed immunoelectron microscopy to examine the effects of 28 days of chronic swim exercise or administration of a PPARγ agonist on atrial granules and their stored natriuretic peptides in Sprague Dawley rats. Chronic swimming and drug treatment both resulted in a 15% increase in heart weight compared with controls, with no treatment effects on perinuclear granule area in the left atria (LAs). Drug treatment resulted in larger size granules with greater BNP density in the right atria. Comparing swimming and PPARγ agonist treatment effects on ANP:BNP granule density ratios between atrial chambers revealed a shift toward a greater proportion of ANP than BNP in LAs of swim-trained rats. These data suggest a distinction in the population of ANP and BNP after chronic swim or PPARγ that makes it a novel metric for the differentiation of pathological and physiological hypertrophy.

Exercise ameliorates high-fat diet-induced insulin resistance accompanied by changes in protein levels of hepatic ATF3-related signaling in rats

PurposeExercise is an effective way to alleviate insulin resistance (IR). However, the underlying mechanisms remain to be elucidated. Previous studies demonstrated that cardiolipin synthase 1 (CRLS1)/interferon-regulatory factor-2 binding protein 2 (IRF2bp2)-activating transcription factor 3 (ATF3)-adiponectin receptor 2 (AdipoR2)-adaptor protein containing pH domain, PTB domain and leucine zipper motif 1 (APPL1)-protein kinase B (AKT/PKB)-related signaling was closely associated with obesity-induced IR-related diseases, but the correlation between exercise training alleviating obesity-induced IR and the protein levels of hepatic CRLS1/IRF2bp2-ATF3-AdipoR2-APPL1-AKT-related signaling in rats is unknown. Therefore, We want to investigate the effect of exercise training on IR and the protein levels of hepatic CRLS1/IRF2bp2-ATF3-AdipoR2-APPL1-AKT-related signaling in rat. MethodsThe male healthy Sprague-Dawley rats were divided into four groups: normal control group (NCG, n = 10), diet-induced obesity-sedentary group (DIO-SG, n = 10), diet-induced obesity-chronic exercise group (DIOCEG, n = 10) received chronic swim exercise training and diet-induced obesity-acute exercise group (DIO-AEG, n = 10) received acute swim exercise training. We measured the levels of IR-related indicators and the protein levels of hepatic CRLS1/IRF2bp2-ATF3-AdipoR2-APPL1-AKT-related signaling in NCG, DIO-SG, DIOCEG and DIO-AEG. ResultsWe found that high-fat diet (HFD)-induced obesity decreased insulin sensitivity in rats accompanied by decreased protein levels of hepatic CRLS1, IRF2bp2, AdipoR2, APPL1, p-AKT and increased protein level of hepatic ATF3. The acute exercise and the chronic exercise both increased insulin sensitivity in rats. The chronic exercise decreased hepatic ATF3 protein level and increased CRLS1, IRF2bp2, AdipoR2, APPL1, p-AKT protein levels in HFD-fed rats. The acute exercise decreased hepatic ATF3 protein level and increased hepatic IRF2bp2, APPL1 and p-AKT protein levels in HFD-fed rats. The acute exercise had no significant effect on hepatic CRLS1 and AdipoR2 protein levels in HFD-fed rats. ConclusionOur current findings indicated that exercise alleviated obesity-induced IR accompanied by changes in protein levels of hepatic ATF3-related signaling in rats. Our results are meaningful for exploring the molecular mechanism of exercise alleviating IR symptoms.

Evaluation of muscle-specific and metabolism regulating microRNAs in a chronic swimming rat model

Making benefit from the epigenetic effects of environmental factors such as physical activity may result in a considerable improvement in the prevention of chronic civilization diseases. In our chronic swimming rat model, the expression levels of such microRNAs were characterized, that are involved in skeletal muscle differentiation, hypertrophy and fine-tuning of metabolism, which processes are influenced by chronic endurance training, contributing to the metabolic adaptation of skeletal muscle during physical activity. After chronic swimming, the level of miR-128a increased significantly in EDL muscles, which may influence metabolic adaptation and stress response as well. In SOL, the expression level of miR-15b and miR-451 decreased significantly after chronic swimming, which changes are opposite to their previously described increment in insulin resistant skeletal muscle. MiR-451 also targets PGC-1α mRNA, whiches expression level significantly increased in SOL muscles, resulting in enhanced biogenesis and oxidative capacity of mitochondria. In summary, the microRNA expression changes that were observed during our experiments suggest that chronic swim training contributes to a beneficial metabolic profile of skeletal muscle.

Ilex paraguariensisA. St.-Hil. (Yerba Mate) Differently Regulates the Lipid Mobilization and, Irisin and Lactate Levels in Sedentary and Chronic Swimming Mice

Healthy mice were submitted or not to daily chronic swimming and/or daily yerba mate (YM) infusion intake and had their bloods analyzed after four weeks. We hypothesized that daily intake of YM may act differently on lipid mobilization and, on the creatine, lactate and irisin levels in sedentary mice and those submitted to chronic exercise. The groups were (n=48): YM-non-treated control (NTC), YM-non-treated swimming control (NSC), non-roasted YM (NRY), roasted YM (RY), swimming plus non-roasted YM (SNRY), swimming plus roasted YM (SRY). No significant (P&gt;0.05) difference was observed concerning creatine phosphoskinase (CPK) value. Lactate level decreased significantly (P&lt;0.05) for SNRY and SRY, suggesting accelerated lipid mobilization and glycogen sparing potential. There was significant (P&lt;0.05) body weight loss in all, except for NTC. Higher weight loss in NRY, RY, SNR and SRY indicated greater lipid mobilization. Thiobarbituric acid reactive substances (TBARS) and irisin had significantly (P&lt;0.05) higher values for RY. This is first report that deals with the effect of YM consumption on serum irisin level. Major amounts of caffeic acid derivatives, slightly increased caffeine and less amount of rutin may be responsible by accelerated lipoperoxidation in sedentary healthy mices chronically treated with roasted YM. Chronically consumed YM plus swimming aid in healthy weight loss. Sedentary lifestyle plus roasted YM chronic consumption may cause accelerated lipid mobilization and increased TBARS production via irisin overexpression leading to an increase in lipoperoxidation.

Determination of the pathways of potential muscle damage and regeneration in response to acute and long-term swimming exercise in mice

The objective of the current study was examining early and late (3, 24 h) responses to acute, chronic swimming exercise as muscle damage and regeneration in gastrocnemius-soleus muscle complexes. We also aimed to reveal the signaling pathways involved. 8–12 weeks old mice were grouped as control, exercise. Exercising groups were firstly divided into two as acute and chronic, later every group was again divided in terms of time (3, 24 h) passed from the last exercise session until exsanguination. Acute exercise groups swam 30 min, while chronic swimming groups exercised 30 min/day, 5 days/week, 6 weeks. Histological investigations were performed to determine muscle damage and regeneration. Whole-genome expression analysis was applied to total RNA samples. Microarray data was confirmed by quantitative real-time PCR. Exercising mice muscle revealed enhanced damage, leukocyte infiltration. Increments in acute and chronic 3 h groups were statistically significant. Car3, Neb, Obscn, Ttn, Igfbp5, Igfbp7, Gsk3β, and Usp2 were down-regulated in muscles of swimming mice. The exercise-induced signaling pathways involved in muscle damage and regeneration were drawn. Our findings demonstrate that swimming induces muscle damage. Samples were obtained at 3 and 24 h following exercise, this time duration seems not sufficient for the development of myofibrillogenesis.

Exercise ameliorates insulin resistance and improves SIRT6-mediated insulin signaling transduction in liver of obese rats.

Physical exercise is essential for the amelioration of insulin resistance (IR). The mechanisms in charge of improved IR, regulated by exercise, are insufficiently studied. Previous research revealed that Sirtuin 6 (SIRT6) - mediated insulin signaling acts a crucial element in hepatic IR. The objective of our research was to determine the effects of exercise on SIRT6-mediated insulin signaling in liver of IR rats. Forty male Sprague Dawley rats were randomly assigned to four groups (n = 10 rats each): control rats fed with standard chow (Lean group); sedentary rats fed with a high-fat diet (HFD-SED); rats fed with HFD and submitted to 8 week chronic swimming exercise training (HFD-CE); and rats fed HFD and submitted to one acute swimming exercise training (HFD-AE). HFD feeding lead to increased body weight, accumulation of hepatic triglyceride and serum free fatty acids, and enhanced gluconeogenesis. Besides, HFD feeding decreased body insulin sensitivity. Hepatic USP10 and SIRT6 protein levels decreased under obese status. Both chronic and acute exercise intervention alleviated physiological and metabolic status, increased hepatic USP10 and SIRT6 levels, improved insulin signaling transduction, and inhibited gluconeogenesis. These results showed that exercise intervention regulated SIRT6-mediated insulin signaling, which contributes to our understanding of the molecular mechanisms behind IR, in that a regular exercise can mitigate the effects of IR.

Stress-induced alterations of social behavior are reversible by antagonism of steroid hormones in C57/BL6 mice

Various disturbances of social behavior, such as autism, depression, or posttraumatic stress disorder, have been associated with an altered steroid hormone homeostasis and a dysregulation of the hypothalamus–pituitary–adrenal axis. A link between steroid hormone antagonists and the treatment of stress-related conditions has been suggested. We evaluated the effects of stress induction on social behavior in the three chambers and its potential reversibility upon specific steroid hormone antagonism in mice. C57BL/6 mice were stressed twice daily for 8 days by chronic swim testing. Social behavior was evaluated by measuring, first, the preference for sociability and, second, the preference for social novelty in the three-chamber approach before and after the chronic swim test. The reversibility of behavior upon stress induction was analyzed after applying steroid hormone antagonists targeting glucocorticoids with etomidate, mineralocorticoids with potassium canrenoate, and androgens with cyproterone acetate and metformin. In the chronic swim test, increased floating time from 0.8 ± 0.2 min up to 4.8 ± 0.25 min was detected (p < 0.01). In the three-chamber approach, increased preference for sociability and decreased preference for social novelty was detected pre- versus post-stress induction. These alterations of social behavior were barely affected by etomidate and potassium canrenoate, whereas the two androgen antagonists metformin and cyproterone acetate restored social behavior even beyond baseline conditions. The alteration of social behavior was better reversed by the androgen as compared with the glucocorticoid and mineralocorticoid antagonists. This suggests that social behavior is primarily controlled by androgen rather than by glucocorticoid or mineralocorticoid action. The stress-induced changes in preference for sociability are incompletely explained by steroid hormone action alone. As the best response was related to metformin, an effect via glucose levels might confound the results and should be subject to future research.

Chronic swimming training resulted in more relaxed coronary arterioles in male and enhanced vasoconstrictor ability in female rats.

Exercise training is associated with hypertrophy of left ventricle (LV). The aim of the present study is to evaluate sex differences in the adaptation of the coronary contractile function in physiological left ventricular hypertrophy induced by long-term swim training. Thirty-two Wistar rats were randomly divided into 4 groups: exercised male (ExM), exercised female (ExF), untrained control male (CoM), and untrained control female (CoF). The trained animals underwent a 12-week-long swim training program. After finishing the training program, LV morphology and function were checked by echocardiography. The spontaneous tone, thromboxane (TxA<inf>2</inf>) agonist-induced vascular contractility and non-endothelial dilatation of the isolated intramural coronary resistance artery were examined by pressure microangiometry. The thromboxane receptor (TxA<inf>2</inf>R) protein expression in the wall of coronary arteries was examined using immunohistochemistry. The LV mass index was significantly higher in the ExM and ExF groups, furthermore the LV mass index was significantly higher in female than in male animals. ExM animals had lower spontaneous tone than ExF. TxA<inf>2</inf> agonist-induced tone was raised only in ExF animals. The resistance coronary artery of exercised male animals had a significantly lower level of TxA<inf>2</inf>R positivity compared to exercised females. Both sexes broaden their range of contractility following chronic swimming, but the vessel tone shifted toward contraction in exercised female rats, while these values shifted toward relaxation in males. These observations underline the significance of identifying potential gender differences in the chronic exercise-induced coronary vascular remodeling in human athletes.

Relationships Between Dry-land Resistance Training and Swim Start Performance and Effects of Such Training on the Swim Start: A Systematic Review.

The swim start requires an explosive muscular response of the lower body musculature to effectively initiate movement off the starting blocks. There are currently key gaps in the literature evaluating the relationship between dry-land resistance training and swim start performance and the effects of this training on swim start performance, as assessed by the time to 5, 10 or 15m. The aims of this systematic review were to critically appraise the current literature on (1) the acute relationship between dry-land resistance training and swim start performance and (2) the acute and chronic effects of dry-land resistance training on swim start performance. An electronic search using AusportMed, Embase, Medline (Ovid), SPORTDiscus and Web of Science was performed. The methodological quality of the studies was evaluated using the Newcastle-Ottawa quality assessment scale (NOS) (cross-sectional studies) and the Physiotherapy Evidence Database (PEDro) scale (intervention studies). Sixteen studies met the eligibility criteria, although the majority did not utilise the starting blocks or technique currently used in elite swimming. Swim start performance was near perfectly related (r > 0.90) to vertical bodyweight jumps and jump height. Post-activation potentiation and plyometrics were found to produce significant improvements in acute and chronic swim start performance, respectively. While there appears to be strong evidence supporting the use of plyometric exercises such as vertical jumps for monitoring and improving swim start performance, future studies need to replicate these findings using current starting blocks and techniques and compare the chronic effects of a variety of resistance training programmes.

Piracetam potentiates neuronal and behavioral effects of ketamine

Introduction: Ketamine has a fast, but short-term antidepressant effect. To support the therapeutic effect, repeated administrations of the drug are needed, which causes cognitive disorders. The drugs with cerebroprotective action can potentially intensify the main and weaken the side effects of drugs. Materials and methods: The impact of ketamine (5 and 20 μM), piracetam (100 μM), and their combinations on the synaptic transmission was studied on hippocampal slices in the CA1 area of rat hippocampus by means of electrophysiological methods. In behavioral experiments were aimed at studying an impact of the used drugs on the predictors which mark depressant behavior of rats: the duration of immobilization in a forced swimming test and preference for the consumption of sucrose solution (comparably with water). The behavioral experiments were performed on intact rats and rats with behavioral depression induced by chronic swimming stress. Results and discussion: Ketamine (5 and 20 μM) potentiates synaptic transmission in the radial layer of the CA1 hippocampal area. At a smaller concentration, ketamine potentiates synaptic transmission only due to the postsynaptic action, and at a greater concentration – with help of post- and presynaptic action. Piracetam (100 µM), like ketamine at a concentration of 5 μM stimulated synaptic transmission, but to a lesser degree. Ketamine at a concentration 5 μM under combined effect with piracetam induced the same effect as that at a concentration of 20 μM without piracetam, only due to a postsynaptic action. Ketamine at doses of 5 and 20 mg/kg one hour after a single systemic administration resulted in the reduced immobilization duration, but not predictors of preference for consuming a sweet solution; piracetam at a dose of 100 mg/kg under these conditions had no impact on the parameters of the rats’ behavior. The studied behavior parameters in cases of behavioral depression also changed after a single administration of ketamine at the doses of 5 and 20 mg/kg. Piracetam significantly stimulated an antidepressant action of ketamine under these circumstances. Conclusion: Piracetam potentiates a ketamine-induced enhancement of the synaptic transmission at the radial layer of the CA1 hippocampal area when investigating at the brain slices. Piracetam stimulates an antidepressant action of a single dose of ketamine in cases of behavioral depression, though it has no antidepressant effect when administered at a single dose.

Potential inhibitory effect of swimming exercise on the Kisspeptin–GnRH signaling pathway in male rats

Aerobic exercises are considered as an effective method of improving several undesirable health outcomes; however, their implications in the male reproductive axis have remained controversial. The present study evaluated the impact of physical exercise on the male reproductive system in rats and investigated the potential central and peripheral mechanisms involved in it. Twenty male Sprague–Dawley rats were randomly divided into control and exercise groups, with 10 rats per group. The rats were subjected to a swimming exercise for 60 min/day for five days a week and the protocol was followed for six constitutive weeks. We found that the swimming exercise significantly decreased the testicular weight and the testicular somatic index. Furthermore, there was a marked reduction in several sperm characteristics, including sperm count, motility, morphology, and viability in the exercised rats. The serum levels of reproductive hormones, i.e., testosterone (T), luteinizing hormone (LH), and follicle stimulating hormone (FSH) were significantly decreased. A histological examination of testes and epididymis revealed defective spermatogenesis. Molecular analysis revealed the downregulation of the expression of mRNAs of the hypothalamic kisspeptin (Kiss1), Kiss1 receptor (Kiss1r), gonadotropin-releasing hormone (GnRH1), GnRH1 receptor (GnRHr), and testicular Kiss1r along with an upregulation in the gene expression of GnRHr in the pituitary. We also observed a significant reduction in the activity and the expression of mRNAs of testicular superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and a marked elevation in the levelsof malondialdehyde (MDA). These findings implied that chronic swimming exercise suppressed the Kisspeptin–GnRH signaling pathway, consequently reducing the production of male reproductive hormones. A simultaneous increase in the oxidative stress could contribute to exercise-induced inhibition of male reproductive functions. To conclude, an appropriate training program is important to maximize the benefits and minimize the side effects of physical exercises on the male reproductive system.

Characterization of the relaxin family peptide receptor 3 system in the mouse bed nucleus of the stria terminalis

The bed nucleus of the stria terminalis (BNST) is a critical node involved in stress and reward-related behaviors. Relaxin family peptide receptor 3 (RXFP3) signaling in the BNST has been implicated in stress-induced alcohol seeking behavior. However, the neurochemical phenotype and connectivity of BNST RXFP3-expressing (RXFP3+) cells have yet to be elucidated. We interrogated the molecular signature and electrophysiological properties of BNST RXFP3+ neurons using a RXFP3-Cre reporter mouse line. BNST RXFP3+ cells are circumscribed to the dorsal BNST (dBNST) and are neurochemically heterogeneous, comprising a mix of inhibitory and excitatory neurons. Immunohistochemistry revealed that ~48% of BNST RXFP3+ neurons are GABAergic, and a quarter of these co-express the calcium-binding protein, calbindin. A subset of BNST RXFP3+ cells (~41%) co-express CaMKIIα, suggesting this subpopulation of BNST RXFP3+ neurons are excitatory. Corroborating this, RNAscope® revealed that ~35% of BNST RXFP3+ cells express vVGluT2 mRNA, indicating a subpopulation of RXFP3+ neurons are glutamatergic. RXFP3+ neurons show direct hyperpolarization to bath application of a selective RXFP3 agonist, RXFP3-A2, while around 50% of cells were depolarised by exogenous corticotrophin releasing factor. In behaviorally naive mice the majority of RXFP3+ neurons were Type II cells exhibiting Ih and T type calcium mediated currents. However, chronic swim stress caused persistent plasticity, decreasing the proportion of neurons that express these channels. These studies are the first to characterize the BNST RXFP3 system in mouse and lay the foundation for future functional studies appraising the role of the murine BNST RXFP3 system in more complex behaviors.

Physical exercise prevents memory impairment in an animal model of hypertension through modulation of CD39 and CD73 activities and A2A receptor expression.

Herein, we investigated the effect of chronic swimming training on the purinergic system in cortex and hippocampus of L-NAME-induced hypertensive rats. Male Wistar rats were divided into four groups: Control, Exercise, L-NAME and Exercise L-NAME. Inhibitory avoidance test was used to assess memory status. NTPDase, CD73 and adenosine deaminase activities and expression, and P2 receptors expression were analyzed. Data were analyzed using two-way ANOVA and Kruskal-Wallis tests, considering P less than 0.05. Physical exercise reduced the blood pressure and prevented memory impairment induced by L-NAME model of hypertension. L-NAME treatment promoted an increase in NTPDase1, NTPDase3 and CD73 expression and activity in the cortex. A2A expression is increased in hippocampus and cortex in the hypertension group and exercise prevented this overexpression. These changes suggest that hypertension increases adenosine generation, which acts through A2A receptors, and exercise prevents these effects. These data may indicate a possible mechanism by which exercise may prevent memory impairment induced by L-NAME.

Chronic Swimming Exercise Ameliorates Low-Soybean-Oil Diet-Induced Spatial Memory Impairment by Enhancing BDNF-Mediated Synaptic Potentiation in Developing Spontaneously Hypertensive Rats.

Exercise and low-fat diets are common lifestyle modifications used for the treatment of hypertension besides drug therapy. However, unrestrained low-fat diets may result in deficiencies of low-unsaturated fatty acids and carry contingent risks of delaying neurodevelopment. While aerobic exercise shows positive neuroprotective effects, it is still unclear whether exercise could alleviate the impairment of neurodevelopment that may be induced by certain low-fat diets. In this research, developing spontaneously hypertensive rats (SHR) were treated with chronic swimming exercise and/or a low-soybean-oil diet for 6weeks. We found that performance in the Morris water maze was reduced and long-term potentiation in the hippocampus was suppressed by the diet, while a combination treatment of exercise and diet alleviated the impairment induced by the specific low-fat diet. Moreover, the combination treatment effectively increased the expression of brain-derived neurotrophic factor (BDNF) and N-methyl-D-aspartic acid receptor (NMDAR), which were both down-regulated by the low-soybean-oil diet in the hippocampus of developing SHR. These findings suggest that chronic swimming exercise can ameliorate the low-soybean-oil diet-induced learning and memory impairment in developing SHR through the up-regulation of BDNF and NMDAR expression.

Effect of Exercise Training on Metabolic Homeostasis and Some Hemodynamics (Some Hepatic and Cardiovascular Functions) in Experimentally Induced Obesity

Background: Obesity is associated with many chronic disorders such as type-2 diabetes mellitus, essential hypertension and non-alcoholic fatty liver disease (NAFLD). High fat diet (HFD) induced obesity in rats is associated with altered adipocytes release of several adipocytokines. Physical exercise has also been shown to have positive effects in the prevention and attenuation of many of the obesity-related disorders, however; the mechanisms have not been fully elucidated. Objective: The present study was designed to examine the effect of moderate intensity exercise training on existing cardio metabolic and hepatic complications linked to obesity including dyslipidemia, insulin resistance, hypertension and NAFLD. Materials and methods: Thirty healthy adult male albino rats of initial body weight 151-190 gm were included. Rats were randomly and equally divided into 3 groups: group (1): normal diet fed group, group (II): HFD induced obesity group in which obesity was induced by HFD for 12 weeks and group (III): HFD induced obesity group fed on high fat diet for 12 weeks then followed by moderate intensity swimming exercise training for 8 weeks. Rats were examined for the body weight, length, abdominal circumference (AC) and body mass index (BMI), Systolic, diastolic & mean arterial blood pressures, heart rate, serum glucose, insulin & HOMA-IR, serum total cholesterol (TC), triglyceride (TG), very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), high-density lipoprotein (HDL) & atherogenic index (AI), serum adiponectin, leptin, irisin, , tumor necrosis factor alpha (TNF- α), Interleukin-6 (IL-6) malondialdehyde (MDA), superoxide dismutase (SOD), alanine aminotransferase (ALT), aspartate aminotransferase (AST), Alkaline Phosphatase (ALP), lactate dehydrogenase (LDH) and albumin. Histopathological examination for hepatic tissue was also evaluated. Results: The present study revealed that HFD significantly increased final body weight, BMI, AC, Systolic, diastolic & mean arterial blood pressures, heart rate, serum levels of glucose, insulin, TC, TG, LDL, VLDL, ALT, AST, ALP, LDH, TNF- α, IL-6, MDA and leptin levels, in addition to HOMA-IR and atherogenic index in HFD-induced obesity group. However, there were significant decreases in serum levels of HDL, SOD, albumin, adiponectin and irisin levels in the same group. Histopathological changes in hepatic tissue that indicate the development of NASH were also observed in HFD-induced obesity group. On the other hand, chronic moderate intensity swimming exercise training significantly reversed all these manifestations even in the absence of caloric restriction. Conclusion: moderate exercise training seems to be an effective strategy to reverse almost all risk factors of cardiovascular diseases and NAFLD associated with metabolic syndrome.