Untrained Rats Research Articles

Biomarkers of oxidative stress and tissue damage released by muscle and liver after a single bout of swimming exercise

Both acute exercise and excessive training can cause oxidative stress. The resulting increase in free radicals and the inadequate response from antioxidant systems can lead to a framework of cellular damage. An association between affected tissue and the biomarkers of oxidative stress that appear in plasma has not been clearly established. The aim of this study was to evaluate the source of oxidative stress biomarkers found in the plasma of untrained rats after a single bout of swimming exercise at 2 different intensities: low intensity (SBLIE) or high intensity (SBHIE). Immediately after the exercise, aspartate transaminase (AST), alanine transaminase (ALT), γ-glutamyltransferase (GGT), and lactate dehydrogenase (LDH) were measured in plasma to characterize cell damage. Oxidative stress was assessed using protein carbonylation (PC), total antioxidant capacity (TAC), and thiobarbituric acid reactive substances (TBARS) quantified by malondialdehyde concentration. SBHIE raised levels of plasma AST (93%) and ALT (17%), and both exercise regimens produced an increase in GGT (7%) and LDH (∼55%). Plasma levels of PC and TBARS were greater in the SBHIE group; there were no changes in TAC. SBLIE caused only a modest increase in TBARS. In muscle, there were no changes in TAC, PC, or TBARS, regardless of exercise intensity, In the liver, TAC and TBARS increased significantly in both the SBLIE and SBHIE groups. This indicates that the oxidative stress biomarkers measured in the plasma immediately after a single bout of swimming exercise were generated primarily in the liver, not in muscle.

Effects of treadmill training on functional recovery following peripheral nerve injury in rats

Exercise, in the form of moderate daily treadmill training following nerve transection and repair leads to enhanced axon regeneration, but its effect on functional recovery is less well known. Female rats were exercised by walking continuously, at a slow speed (10 m/min), for 1 h/day on a level treadmill, beginning 3 days after unilateral transection and surgical repair of the sciatic nerve, and conducted 5 days/wk for 2 wk. In Trained rats, both direct muscle responses to tibial nerve stimulation and H reflexes in soleus reappeared earlier and increased in amplitude more rapidly over time than in Untrained rats. The efficacy of the restored H reflex was greater in Trained rats than in Untrained controls. The reinnervated tibialis anterior and soleus were coactivated during treadmill locomotion in Untrained rats. In Trained animals, the pattern of activation of soleus, but not tibialis anterior, was not significantly different from that found in Intact rats. The overall length of the hindlimb during level and up- and downslope locomotion was conserved after nerve injury in both groups. This conservation was achieved by changes in limb orientation. Limb length was conserved effectively in all rats during downslope walking but only in Trained rats during level and upslope walking. Moderate daily exercise applied immediately after sciatic nerve transection is sufficient to promote axon regeneration, to restore muscle reflexes, and to improve the ability of rats to cope with different biomechanical demands of slope walking.

Exercise Differentially Regulates Renalase Expression in Skeletal Muscle and Kidney

Renalase is a newly discovered amine oxidase and may lower blood pressure by metabolizing catecholamines. We have hypothesized that exercise and training may regulate renalase expression to control blood pressure. In this study, we investigated changes in renalase expression after exercise and training in white and red portion of the gastrocnemius muscle, kidney, and serum in rats. Rats were either untrained or subjected to six weeks of endurance training, which predominantly recruits red fibers. Rats from each group were sacrificed before (n = 10), immediately after (n = 10), or three hours (n = 10) following exercise. Renalase mRNA and protein levels were measured by RT-PCR and ELISA, respectively. There were no significant changes in renalase expression after prolonged training or acute exercise in the serum or red muscle of rats. However, in white muscle, renalase mRNA and protein levels decreased after acute exercise in untrained rats, whereas, in trained rats, its protein level remained unchanged, despite a decrease in mRNA. Thus, exercise influenced renalase expression only in white muscle fibers that are not predominantly recruited during exercise. The reduction of renalase protein in white muscle suggests that renalase may contribute to blood redistribution between contracting and non-contracting fibers during exercise. In the kidney, renalase protein levels decreased after training, while mRNA levels increased. The reduction in renalase protein levels may contribute to functional kidney hypoperfusion, which has been observed after training. In conclusion, exercise differentially regulates renalase expression in skeletal muscle and kidney.

Age dependent differences in the regulation of hippocampal steroid hormones and receptor genes: Relations to motivation and cognition in male rats

Estrogen and estrogenic functions are age-dependently involved in the modulation of learning, memory and mood in female humans and animals. However, the investigation of estrogenic effects in males has been largely neglected. Therefore, we investigated the hippocampal gene expression of estrogen receptors α and β (ERα, β) in 8-week-old, 12-week-old and 24-week-old male rats. To control for possible interactions between the expression of the estrogen receptor genes and other learning-related steroid receptors, androgen receptors (AR), corticosterone-binding glucocorticoid receptors (GR) and mineralocorticoid receptors (MR) were also measured. Furthermore, the concentrations of the ligands 17β-estradiol, testosterone and corticosterone were measured. The spatial training was conducted in a hole-board. The 8-week-old rats exhibited higher levels of general activity and exploration during the training and performed best with respect to spatial learning and memory, whereas no difference was found between the 12-week-old and 24-week-old rats. The trained 8-week-old rats exhibited increased gene expression of ERα compared with the untrained rats in this age group as well as the trained 12-week-old and 24-week-old rats. The concentrations of estradiol and testosterone, however, were generally higher in the 24-week-old rats than in the 8-week-old and 12-week-old rats. The ERα mRNA concentrations correlated positively with behavior that indicate general learning motivation. These results suggest a specific role of ERα in the age-related differences in motivation and subsequent success in the task. Thus, estrogen and estrogenic functions may play a more prominent role in young male behavior and development than has been previously assumed.

Ventricular and autonomic benefits of exercise training persist after detraining in infarcted rats

We evaluate the effects of detraining (DT, for 1 month) on the left ventricular (LV) remodeling and function, hemodynamic and baroreflex sensitivity (BRS), as well as on mortality rate of infarcted (MI) rats after 3 months of exercise training (ET, 50-70 % of VO₂max). Male Wistar rats were divided into five groups: control (C, n = 10), untrained-infarcted (UI, n = 15), trained-infarcted (TI, n = 12), untrained-infarcted plus 1 month (UI-1, n = 15) and detrained-infarcted 1 month (DI-1, n = 15). LV function was evaluated by echocardiography at the initial and final of the protocols. After following, ET and/or DT protocols, hemodynamic and BRS [by tachycardic (TR) and bradycardic (BR) responses] were assessed. TI group displayed increased VO2max in comparison with UI and DI-1 groups; however, DI-1 values remained increased compared to UI-1 group. MI area was reduced by ET and maintained after DT. Ejection fraction (TI = 60 ± 2 and DI-1 = 61 ± 2 % vs. UI = 41 ± 1 and UI-1 = 37 ± 3 %), E/A ratio (TI = 1.6 ± 0.1 and DI-1 = 1.9 ± 0.1 vs. UI = 2.9 ± 0.2 and UI-1 = 2.9 ± 0.3), TR (TI = 3.3 ± 0.3 and DI-1 = 3.3 ± 0.4 vs. UI = 1.7 ± 0.1 and UI-1 = 1.6 ± 0.1 bpm/mmHg) and BR (TI = -2.2 ± 0.1 and DI-1 = -2.0 ± 0.1 vs. UI = -1.3 ± 0.09 and UI-1 = -1.2 ± 0.09 bpm/mmHg) were improved by ET and maintained after DT in comparison with untrained rats. These changes resulted in mortality reduction in the TI (8 %) and DI-1 groups (13 %) compared with the UI (46 %) and UI-1 (53 %) groups. These findings indicate that ET is not only an effective tool in the management of cardiovascular and autonomic MI derangements, but also that these positive changes were maintained even after 1 month of DT in rats.

Eccentric training improves tendon biomechanical properties: A rat model

The treatment of choice for tendinopathies is eccentric reeducation. Although the clinical results appear favorable, the biomechanical changes to the tissue are not yet clear. Even if the mechanotransduction theory is commonly accepted, the physiology of tendons is not clearly understood. We aimed to better define the biomechanical and histological changes that affect healthy tendon after eccentric and concentric training. This study compared the effects of two methods of training (eccentric [E] training and concentric [C] training) with untrained (U) rats. The animals were trained over a period of 5 weeks. The tricipital, patellar, and Achilles tendons were removed, measured and a tensile test until failure was performed. A histological analysis (hematoxylin and eosin and Masson's trichrome stains) was also realized. There was a significant increase in the rupture force of the patellar and tricipital tendons between the U and E groups. The tricipital tendons in the control group presented a significantly smaller cross-sectional area than the E- and C-trained groups, but none was constated between E and C groups. No significant difference was observed for the mechanical stress between the three groups for all three tendons. Histological studies demonstrated the development of a greater number of blood vessels and a larger quantity of collagen in the E group. The mechanical properties of tendons in rats improve after specific training, especially following eccentric training. Our results partly explained how mechanical loading, especially in eccentric mode, could improve the healing of tendon.

Involvment of nitric oxide and MPTP in heart adaptation to physical training

After physical training of rats (4 weeks swimming) we observed in myocardium and aorta the activation of both salvage and de novo nitric oxide synthesis, an increase in nitric oxide bioavailability and endothelium-dependent vasorelaxation. However, it reminds unclear how NO takes part in myocardial adaptation to workload. Using isolated rat heart by Langendorf preparation we studied myocardial response to gradually increased left ventricular volume (Frank-Starling low) and increasing concentration of Ca2+ in perfusion solution (from 1.7 mM to 12,5 mM) in trained and untrained rats. It was shown that swimming improved heart function: heart rate was decreased, contractile activity and coronary flow were increased by 20% and 33%, respectively. Equal volume stretching of balloon in left ventricle provoked greater contraction in trained comparing to untrained hearts, demonstrating extended functional reserves after swimming course. Furthermore, trainingsignificantly increased mitochondrial membrane potential in isolatedmitochondria (−176.5 ± 8.4 mV vs −56 ± 3.5 mV in control), that points to improved efficiency of oxidative phosphorylation. The opening of mitochondrial permeability transition pore (MPTP) in trained heart was detected at higher concentration of calcium that reveals extended calcium capacity of mitochondria and lesser sensitivity of MPTP to its inductor - calcium. Blockade of NO synthesis with L-NAME application of (10–4 M for 15 min) abolished reaction of trained heart during Frank-Starling and calcium upload. NOS inhibition prevented the increased functional hyperaemia of the hearts from trained rats. Thus, heart adaptation to physical training and extend of functional reserves of heart are provided by increased endogenous NO production.

Influence of 5-HT2 Receptor Agonist on Cardiac Pumping Function of Trained Offspring of Trained Rats

We studied cardiac pumping function in the offspring of rats subjected to swimming exercise and the offspring of untrained rats. The rat pups were adapted for swimming with stepwise increasing load from day 21 to 70 life. At the age of 21 and 70 days, offspring of trained rats showed lower HR and significantly higher stroke volume and cardiac output than offspring of untrained rats. Agonist of 5-HT(2)-receptors α-methyl-5-hydroxytryptamine maleate (30 μg/kg) reduced enhanced stroke volume in trained offspring born by trained mothers. In trained offspring of untrained rats, the agonist had more pronounced effect on HR.

GABA, glutamate, dopamine and serotonin transporters expression on forgetting

Notwithstanding several neurotransmission systems are frequently related to memory formation; forgetting process and neurotransmission systems or their transporters; the role of γ-aminobutyric acid (GAT1), glutamate (EACC1), dopamine (DAT) and serotonin (SERT) is poorly understood. Hence, in this paper western-blot analysis was used to evaluate expression of GAT1, EAAC1, DAT and SERT during forgetting in trained and untrained rats treated with the selective serotonin transporter inhibitor fluoxetine, the amnesic drug d-methamphetamine (METH) and fluoxetine plus METH. Transporters expression was determined in the hippocampus (HIP), prefrontal cortex (PFC) and striatum (STR). Results indicated that forgetting of Pavlovian/instrumental autoshaping was associated to up-regulation of GAT1 (PFC and HIP) and DAT (PFC) while SERT (HIP) was down-regulated; no-changes were observed in striatum. Methamphetamine administration did not affect forgetting at 216h post-training but up-regulated hippocampal DAT and EACC, prefrontal cortex DAT and striatal GAT1 or EACC1. Fluoxetine alone prevented forgetting, which was associated to striatal GAT1 and hippocampal DAT up-regulation, but prefrontal cortex GAT1 down-regulation. Fluoxetine plus METH administration was also able to prevent forgetting, which was associated to hippocampal DAT, prefrontal cortex SERT and striatal GAT1, DAT or SERT up-regulation, but prefrontal cortex GAT1 down-regulation. Together these data show that forgetting provokes primarily hippocampal and prefrontal cortex transporters changes; forgetting represent a behavioral process hardly modifiable and its prevention could causes different transporters expression patterns.

Effects of treatment with coenzyme Q10on exercised rat aorta

In this study, the effect of long-term supplementation of coenzyme Q10 (CoQ10) on the responses of swim-trained rat aorta was investigated. Twenty-four adult male Wistar rats were divided into four groups: untrained, trained, untrained+CoQ10, and trained+CoQ10 group. In the trained groups rats swam for 60 min/day, five days/week for six weeks. The CoQ10 supplements were administered by intraperitoneal injection at a daily dose of 10 mg·kg-1 of body weight five days/week for six weeks. Swimming of the rats was performed in a container containing tap water. Rats were sacrificed and thoracic aortas were removed for ex vivo analysis after the last swimming session. The aortas were cut into rings 2.5 mm in length. Concentration-response curves for phenylephrine (PHE, 10-9-3×10-4 M) and potassium chloride (KCl, 5-100 mM) were isometrically recorded. The sensitivity and maximal responses to PHE and KCl of aortic rings obtained from trained rats were lower than those of untrained rats. CoQ10 supplementation decreased the responses to both vasoconstrictors in untrained and especially in trained groups. Although neither CoQ10 nor training did affect malondialdehyde (MDA) and protein carbonyl (PC) levels, creatine kinase (CK) activity decreased and superoxide dismutase (SOD) activity increased only with exercise training. Glutathione (GSH) levels increased in CoQ10 supplemented-untrained rats. In conclusion, our results suggest that CoQ10 supplementation may have beneficial effects during exercise.

Maternal Prolactin Inhibition during Lactation Affects Physical Performance Evaluated by Acute Exhaustive Swimming Exercise in Adult Rat Offspring

Maternal prolactin inhibition at the end of lactation programs for metabolic syndrome and hypothyroidism in adult offspring, which could negatively affect exercise performance. We evaluated the effects of maternal hypoprolactinemia in late lactation on physical performance in adult progeny. Lactating Wistar rats were treated with bromocriptine (BRO, 1 mg per day) or saline on days 19, 20, and 21 of lactation and offspring were followed until 180 days old. Physical performance was recorded in untrained rats at 90 and 180 days by an acute exhaustive swimming test (exercise group-Ex). At day 90, BRO offspring showed higher visceral fat mass, higher plasma thiobarbituric acid reactive substances, lower total antioxidant capacity, higher liver glycogen, lower glycemia, and normal insulinemia. Although thyroid hormones (TH) levels were unchanged, mitochondrial glycerol phosphate dehydrogenase (mGPD) activity was lower in muscle and in brown adipose tissue (BAT). At this age, BRO-Ex offspring showed higher exercise capacity, lower blood lactate, higher serum T3, and higher muscle and BAT mGPD activities. At day 180, BRO offspring showed central obesity, hypothyroidism, insulin resistance, and lower EDL (extensor digitorum longus) muscle glycogen with unaltered plasma oxidative stress markers. This group showed no alteration of exercise capacity or blood lactate. After exercise, EDL and liver glycogen were lower, while T3 levels, BAT and muscle mGPD activities were normalized. Liver glycogen seem to be related with higher exercise capacity in younger BRO offspring, while the loss of this temporary advantage maybe related to the hypothyroidism and insulin resistance developed with age.

Effects of Gender, Endurance Training and Acute Exhaustive Exercise on Oxidative Stress in the Heart and Skeletal Muscle of the Rat

Effects of gender differences and endurance training on exhaustive exercise induced-oxidative stress have been a question that has not been clarified in the literature. The aim of this study was to determine the effects of sex, acute exhaustive exercise and chronic aerobic exercise training on oxidative stress in the heart and the skeletal muscle. The study was carried out with 12 week-old male (n = 24) and female (n = 24) young adult Wistar rats. They were randomly divided into four groups: untrained, trained, untrained exhausted and trained exhausted. The rats in the trained group swam for 60 min/day, five days per week for eight weeks. Thereafter, one-half of the trained and one-half of the untrained rats were randomly selected into the trained and untrained exhaustive exercise groups, respectively. They were killed immediately after one last exhaustive swimming exercise. In the heart, endurance training decreased malondialdehyde (MDA) levels in the female rats at rest, but did not change in the male rats in the heart; MDA levels were also increased in female rats at rest in the gastrocnemius tissues. [corrected]. In the trained female rats, exhaustive exercise decreased MDA levels in the heart and gastrocnemius tissues. The nitric oxide (NO) levels in the heart in the untrained female rats were higher than in the male rats after exhaustive exercise. Training decreased the NO levels in both sexes in the gastrocnemius tissue at rest. In the heart, the untrained female rats had higher total glutathione (GSH) levels than in the male rats at rest. Also, exhaustive exercise decreased the GSH levels in the trained female rats. In the gastrocnemius, untrained female rats showed higher GSH levels than in the male after exhaustive exercise. The superoxide dismutase activities in the gastrocnemius were similar between the female and male rats. The results suggested that gender was a major determinant of changes in MDA, NO and GSH levels in the heart and gastrocnemius tissues after the exhaustive exercise or endurance training. Also, the responses to oxidative stress induced by acute exercise or training in the heart and gastrocnemius muscle tissues are different.

Adaptations in Glutamate and Glycine Content within the Lumbar Spinal Cord Are Associated with the Generation of Novel Gait Patterns in Rats following Neonatal Spinal Cord Transection

After spinal cord transection, the generation of stepping depends on neurotransmitter systems entirely contained within the local lumbar spinal cord. Glutamate and glycine likely play important roles, but surprisingly little is known about how the content of these two key neurotransmitters changes to achieve weight-bearing stepping after spinal cord injury. We studied the levels of glutamate and glycine in the lumbar spinal cord of spinally transected rats. Rats (n = 48) received spinal cord transection at 5 days of age, and 4 weeks later half were trained to step using a robotic treadmill system and the remaining half were untrained controls. Analyses of glutamate and glycine content via high-performance liquid chromatography showed training significantly raised the levels of both neurotransmitters in the lumbar spinal cord beyond normal. The levels of both neurotransmitters were significantly correlated with the ability to perform independent stepping during training. Glutamate and glycine levels were not significantly different between Untrained and Normal rats or between Trained and Untrained rats. There was a trend for higher expression of VGLUT1 and GLYT2 around motor neurons in Trained versus Untrained rats based on immunohistochemical analyses. Training improved the ability to generate stepping at a range of weight support levels, but normal stepping characteristics were not restored. These findings suggested that the remodeling of the lumbar spinal circuitry in Trained spinally transected rats involved adaptations in the glutamatergic and glycinergic neurotransmitter systems. These adaptations may contribute to the generation of novel gait patterns following complete spinal cord transection.

GABA, glutamate, dopamine and serotonin transporters expression on memory formation and amnesia

Notwithstanding several neurotransmission systems are frequently related to memory formation, amnesia and/or therapeutic targets for memory alterations, the role of transporters γ-aminobutyric acid (GABA, GAT1), glutamate (neuronal glutamate transporter excitatory amino acid carrier; EACC1), dopamine (DAT) and serotonin (SERT) is poorly understood. Hence, in this paper Western-blot analysis was used to evaluate expression changes on them during memory formation in trained and untrained rats treated with the selective serotonin transporter inhibitor fluoxetine, the amnesic drug d-methamphetamine (METH) and fluoxetine plus METH. Transporters expression was evaluated in the hippocampus, prefrontal cortex and striatum. Data indicated that in addition of memory performance other behavioral parameters (e.g., explorative behavior, food-intake, etc.) that memory formation was recorded. Thus, memory formation in a Pavlovian/instrumental autoshaping was associated to up-regulation of prefrontal cortex GAT1 and EAAC1, striatal SERT, DAT and EACC1; while, hippocampal EACC1, GAT1 and SERT were down-regulated. METH impaired short (STM) and long-term memory (LTM), at 24 or 48h. The METH-induced amnesia down-regulated SERT, DAT, EACC1 and GAT1 in hippocampus and the GAT1 in striatum; no-changes were observed in prefrontal cortex. Post-training administration of fluoxetine improved LTM (48h), which was associated to DAT, GAT1 (prefrontal cortex) up-regulation, but GAT1 (striatum) and SERT (hippocampus) down-regulation. Fluoxetine plus METH administration was able to prevent amnesia, which was associated to DAT, EACC1 and GAT1 (prefrontal cortex), SERT and DAT (hippocampus) and EACC1 or DAT (striatal) up-regulation. Together these data show that memory formation, amnesia and anti-amnesic effects are associated to specific patters of transporters expression.

Effects of exercise of different intensities on the angiogenesis, infarct healing, and function of the left ventricle in postmyocardial infarction rats

Lifestyle interventions, including physical exercise, are feasible options for the prevention and treatment of cardiovascular diseases. In this study, the effects of exercise of different intensities on the infarct region, function, and angiogenesis of the left ventricle (LV) in postmyocardial infarction (MI) rats were investigated and the levels of vascular endothelial growth factor (VEGF) proteins in the LV and plasma were examined. Male Sprague-Dawley rats were randomly assigned to six groups. The exercise-trained rats observed a daily 60-min treadmill routine 5 days/weeks for 6 weeks. Different treadmill speeds were used in the high-intensity exercise (HIE), moderate-intensity exercise (MIE), and low-intensity exercise (LIE) groups, whereas the untrained rats remained sedentary (Sed). At 6 weeks, all rats underwent either an acute MI operation or a sham (Sh) MI operation 24 h after their last treadmill exercise or the corresponding Sed protocol. They were then killed 7 days after recovery. Echocardiographic and hemodynamic measurements were taken at the end of the experimental protocol. The infarct regions were analyzed using Masson's trichrome staining, whereas intramyocardial microvessels were detected using Factor VIII-related antigen staining. The cardiac VEGF protein levels were determined by western blotting analysis, and plasma VEGF concentrations were examined by enzyme-linked immunosorbent assay. Compared with the corresponding parameters in the Sed-Sh group, LV function did not significantly ameliorate and microvessel density did not increase in the MIE-Sh group. Compared with the Sed-MI group, the MIE-MI and HIE-MI groups had significantly reduced LV infarct size, improved hemodynamic parameters, and increased fractional shortening, scar thickness, and microvessel density, these parameters did not significantly change in the LIE-MI group. In addition, the MIE-MI and HIE-MI rats had significant differences in hemodynamic parameters and microvessel density. Compared with those of the Sed-MI group, the heart and plasma of the exercise-trained rats in the MIE-MI and HIE-MI groups displayed higher levels of VEGF protein, but the difference between the MIE-MI and HIE-MI groups was not significant. Moderate-intensity running before acute MI improved LV function, reduced scar size, and increased scar thickness and microvessel density in post-MI rats. Exercise at a higher intensity could have further small effects. LIE may be beneficial, but it would not be sufficient to improve MI. Moderate-intensity and high-intensity running upregulated the expression of VEGF protein and increased microvessels, which may have partly improved cardiac function after MI in this study.

Proteomic analysis and protein carbonylation profile in trained and untrained rat muscles

Understanding the relationship between physical exercise, reactive oxygen species and skeletal muscle modification is important in order to better identify the benefits or the damages that appropriate or inappropriate exercise can induce. Unbalanced ROS levels can lead to oxidation of cellular macromolecules and a major class of protein oxidative modification is carbonylation. The aim of this investigation was to study muscle protein expression and carbonylation patterns in trained and untrained animal models. We analyzed two muscles characterized by different metabolisms: tibialis anterior and soleus. Whilst tibialis anterior is mostly composed of fast-twitch fibers, the soleus muscle is mostly composed of slow-twitch fibers. By a proteomic approach we identified 15 protein spots whose expression is influenced by training. Among them in tibialis anterior we observed a down-regulation of several glycolitic enzymes. Concerning carbonylation, we observed the existence of a high basal level of protein carbonylation. Although this level shows some variation among individual animals, several proteins (mostly involved in energy metabolism, muscle contraction, and stress response) appear carbonylated in all animals and in both types of skeletal muscle. Moreover we identified 13 spots whose carbonylation increases after training.

Effects of selenium supplementation on the muscle contractile properties, fatigue and antioxidant enzymes activities of gastrocnemius muscles in trained and untrained rats

Selenium (Se) is an important component of cellular seleno ‐compounds andan integral component of glutathione Peroxidase (GPx), which catalyzes thereduction of harmful radicals produced during muscular exercise. The currentstudy was carried out to evaluate the muscle contractile properties andfatigue resistance of gastrocnemius muscle under selenium supplementationschemes in sedentary and exercise protocols as well as measure the antioxidantenzymes activity and lipid peroxidation. Rats were divided into fourgroups; sedentary Selenium supplementation (S), exercise Selenium (SE)groups, sedentary control (SC) and exercise control (EC) groups. The ratswere fed with 80 μg/kg body weights selenium for six weeks. The exerciseprotocol consisted the 40 jumps up to the height of 40 cm for 6 ‐week. Themuscle fatigue protocol consisted the trains of pulses of 40 Hz at every secondfor at least 2 min. Significant (P<0.05) increase was observed in treatedgroups than control in the muscle contractile properties like twitch tension(Pt), contraction time (CT) and twitch/tetanic tension Ratio (Pt/Po Ratio),tetanic tension (Po) and EMG amplitude. Decreased EMG failure and increasedfatigue index were observed in ES group. Moreover, a significant(P<0.05) increase and decrease in the GPx activity and lipid peroxidation respectivelywas also reported than SC and EC group. While there were nochanges reported in the activity of CAT and SOD enzymes. This study revealedthat the Se with jumping exercise induces muscle contractile propertiesand decreases the muscular fatigue.

Differential Effects of Low versus High Amounts of Weight Supported Treadmill Training in Spinally Transected Rats

Intensive weight-supported treadmill training (WSTT) improves locomotor function following spinal cord injury. Because of a number of factors, undergoing intensive sessions of training may not be feasible. Whether reduced amounts of training are sufficient to enhance spinal plasticity to a level that is necessary for improving function is not known. The focus of the present study was to assess differences in recovery of locomotor function and spinal plasticity as a function of the amount of steps taken during WSTT in a rodent model of spinal cord injury. Rats were spinally transected at 5 days of age. When they reached 28 days of age, a robotic system was used to implement a weight-supported treadmill training program of either 100 or 1000 steps/training session daily for 4 weeks. Antibodies for brain-derived neurotrophic factor (BDNF), TrkB, and the pre-synaptic marker, synaptophysin, were used to examine the expression of these proteins in the ventral horn of the lumbar spinal cord. Rats that received weight-supported treadmill training performed better stepping relative to untrained rats, but only the rats that received 1000 steps/training session recovered locomotor function that resembled normal patterns. Only the rats that received 1000 steps/training session recovered normal levels of synaptophysin immunoreactivity around motor neurons. Weight-supported treadmill training consisting of either 100 or 1000 steps/training session increased BDNF immunoreactivity in the ventral horn of the lumbar spinal cord. TrkB expression in the ventral horn was not affected by spinal cord transection or weight-supported treadmill training. Synaptophysin expression, but not BDNF or TrkB expression was correlated with the recovery of stepping function. These findings suggested that a large amount of weight-supported treadmill training was necessary for restoring synaptic connections to motor neurons within the locomotor generating circuitry. Although a large amount of training was best for recovery, small amounts of training were associated with incremental gains in function and increased BDNF levels.

Comfortable at just below your critical speed: how is blood flow distribution coupled to muscle fibre recruitment during exercise?

Comfortable at just below your critical speed: how is blood flow distribution coupled to muscle fibre recruitment during exercise?

Effect of Nandrolone Decanoate Treatment on Contractile Responses of Male Rats Skeletal Muscles

This study examine if the administration of different doses of an anabolic-androgenic steroids, nandrolone decanoate (ND), could produce changes in contractile responses of untrained rat fast- (edl) and slow- (soleus) twitch skeletal muscles. Male adult rats received weekly an intramuscular injection of sterile peanut oil (control; C), 0.75 mg/kg (Therapeutical-dose; TD), 1.5 mg/kg (low-dose; LD), 6 mg/kg (Intermediate-dose; ID) or 15 mg/kg (High-dose; HD) of ND during 8 weeks. Compared with respective C, although no significant effect was observed in slow and fast- twitch characteristics for TD, LD and ID rats, an increasing by 103% in the amplitude of fast- twitch of HD animals and no significant effect was observed in the time constant of relaxation. A prolongation in the time constant of relaxation was observed in slow- twitch fibers of HD rats and no significant modification was observed at the level of amplitude of contraction generated. Moreover, no significant effect was observed in K-contracture characteristics of slow- muscles of TD, LD, ID and HD rats, a progressive increase in the amplitude of K-contracture was observed in ID (17%) and HD (57%) of ND treated rats and no significant modification was observed in the kinetic of the contracture. These results suggest that the effect of ND treatment of male rats is muscle types and dose dependent and the edl muscles are more sensitive than soleus muscles to treatment.