Prevent Muscle Damage Research Articles

The effects of pre-exercise vibration stimulation on the exercise-induced muscle damage

[Purpose] To investigate the effects of pre-induced muscle damage vibration stimulation on the pressure-pain threshold and muscle-fatigue-related metabolites of exercise-induced muscle damage. [Subjects and Methods] Thirty healthy, adult male subjects were randomly assigned to the pre-induced muscle damage vibration stimulation group, post-induced muscle damage vibration stimulation group, or control group (n=10 per group). To investigate the effects of pre-induced muscle damage vibration stimulation, changes in the pressure-pain threshold (lb), creatine kinase level (U/L), and lactate dehydrogenase level (U/L) were measured and analyzed at baseline and at 24 hours, 48 hours, and 72 hours after exercise. [Results] The pressure-pain thresholds and concentrations of creatine kinase and lactate dehydrogenase varied significantly in each group and during each measurement period. There were interactions between the measurement periods and groups, and results of the post-hoc test showed that the pre-induced muscle damage vibration stimulation group had the highest efficacy among the groups. [Conclusion] Pre-induced muscle damage vibration stimulation is more effective than post-induced muscle damage vibration stimulation for preventing muscle damage.

Effect of Oral Branched-Chain Amino Acid Supplementation Prior to Resistance Exercise on Metabolic Hormones, Plasma Amino Acids, and Serum Indices of Muscle Damage in the Recovery Period

The purpose of this study was to examine the effects of oral branched-chain amino acid (BCAA) supplementation before resistance exercise on plasma levels of amino acids, cortisol, insulin, and serum creatine kinase and lactate dehydrogenase. Ten active female students in a double-blind crossover design randomly were assigned to a BCAA supplement or a placebo group. Both groups performed 5 sets of 12 to 15 repetitions at 50% of the 1-repetition maximum. Plasma leucine and isoleucine levels were increased whereas glutamine and phenylalanine were decreased at the end of exercise in the S group. BCAA supplementation did not affect plasma insulin, cortisol, serum creatine kinase and lactate dehydrogenase levels. These results suggest that in resistance exercise, BCAAs may support an insulin-independent anabolic state, but it cannot prevent muscle damage.

Amelioration of energy metabolism by melatonin in skeletal muscle of rats with LPS induced endotoxemia.

In the literature, few studies have investigated the effects of melatonin on energy metabolism in skeletal muscle in endotoxemia. We investigated the effects of melatonin on tissue structure, energy metabolism in skeletal muscle, and antioxidant level of rats with endotoxemia. We divided rats into 4 groups, control, lipopolysaccharide (LPS) (20 mg/kg, i.p., single dose), melatonin (10 mg/kg, i.p., three times), and melatonin + LPS. Melatonin was injected i.p. 30 min before and after the 2nd and 4th hours of LPS injection. Antioxidant status was determined by glutathione (GSH) measurement in the blood. Muscle tissue was stained using modified Gomori trichrome (MGT), succinic dehydrogenase (SDH), and cytochrome oxidase (COX) and histological scored. Also the sections were then stained with hematoxylin and eosin. The stained sections were visualized and photographed. Creatine, creatine phosphate, adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) levels were investigated using high performance liquid chromatography (HPLC) in muscle tissue. In the Melatonin + LPS group, blood GSH levels were increased compared with the LPS group (P<0.01). Melatonin reduced myopathic changes in the LPS group according to the histopathologic findings. In addition, ATP values were increased compared with the LPS group (P<0.05). Our findings showed melatonin treatment prevented muscle damage by increasing ATP and GSH levels in rats with LPS induced endotoxemia.

Curcumin prevents muscle damage by regulating NF-κB and Nrf2 pathways and improves performance: an in vivo model.

PurposeExercise (Ex) increases reactive oxygen species and impairs antioxidant defense systems. Recent data suggest that curcumin (CW) possesses peroxisome proliferator-activated receptor gamma activity and anti-inflammatory properties. Therefore, this study was designed to investigate the effects of CW supplementation on Ex performance, endurance, and changes in serum and muscle proteins in rats after exhaustive Ex.Materials and methodsTwenty-eight (28) male Wistar rats (age: 8 weeks and body weight: 180±20 g) were divided into four treatment groups: 1) control (C; no Ex), 2) C + CW (no Ex + CW), 3) C + Ex, and 4) C + Ex + CW (Ex + CW). CW was administered as 100 mg/kg CurcuWin®, providing 20 mg of curcuminoids daily for 6 weeks. A motor-driven rodent treadmill was used to carry out the Ex protocols. During a 5-day period, animals in chronic Ex groups were put through different regimens: day 1, 10 m/min for 10 minutes; day 2, 20 m/min for 10 minutes; day 3, 25 m/min for 10 minutes; day 4, 25 m/min for 20 minutes; and day 5, 25 m/min for 30 minutes. Animals were exercised at 25 m/min for 45 min/d for 5 d/wk for 6 weeks. Blood and muscle samples were analyzed for muscle markers, oxidative stress, and antioxidant markers.ResultsLactate and muscle malondialdehyde levels decreased in the CW-treated groups (P<0.0001). However, activities of antioxidant enzyme levels increased in the CW-treated groups. Run to exhaustion (minutes) improved in the CW-treated groups. Muscle nuclear factor-κB (P<0.05) and heat shock protein 70 (P<0.05) levels were much lowered in the CW treated group followed by Ex group. In addition, muscle inhibitors of kappa B, peroxisome proliferator-activated receptor gamma coactivator 1-alpha, thioredoxin-1, sirtuin 1, nuclear factor (erythroid-derived 2)-like 2, and glucose transporter 4 protein levels in the Ex + CW group were higher than those in the control and Ex groups (P<0.05).ConclusionThis study suggests that novel CW has the potential to help prevent muscle damage by regulating the nuclear factor-κB and nuclear factor (erythroid-derived 2)-like 2 pathways and improve the performance and nutritional values of CW.

Muscle damage, physiological changes, and energy balance in ultra-endurance mountain-event athletes.

The biological response to ultra-endurance mountain race events is not yet well understood. The aim of this study was to determine the biochemical and physiological changes after performing an ultra-endurance mountain race in runners. We recruited 11 amateur runners (age: 29.7 ± 10.2 years; height: 179.7 ± 5.4 cm; body mass: 76.7 ± 10.3 kg). Muscle damage, lactate concentration, energy balance, rating of perceived exertion (RPE), heart rate (HR), heart rate variability (HRV), body composition changes, and jump performance were analyzed before, during (only lactate, HR, and HRV), and after the race. Athletes completed 54 km in 6 h, 44 min (±28 min). After the race, myoglobin and creatine kinase concentration increased from 14.9 ± 5.2 to 1419.9 ± 1292.1 μg/L and from 820.0 ± 2087.3 to 2421.1 ± 2336.2 UI/L, respectively (p < 0.01). In addition, lactate dehydrogenase and troponin I significantly increased after the race (p < 0.01). Leukocyte and platelet count increased by 180.6% ± 68.9% and 23.7% ± 11.2%, respectively (p < 0.001). Moreover, after the competition, athletes presented a 3704 kcal negative energy balance; a significant increase in RPE values; a decrease in countermovement and squat jump height; and a decrease in body mass and lower limb girths. During the event, lactate concentration did not change and subjects presented a mean HR of 158.8 ± 17.7 beats/min, a significant decrement in vagal modulation, and a significant increase in sympathetic modulation. Despite the relative "low" intensity achieved, ultra-endurance mountain race is a stressful stimulus that produces a high level of muscle damage in the athletes. These findings may help coaches to design specific training programs that may improve nutritional intake strategies and prevent muscle damage.

Blood flow restriction prevents muscle damage but not protein synthesis signaling following eccentric contractions.

There is a growing body of evidence to suggest that resistance training exercise combined with blood flow restriction (BFR) increases muscle size and strength in humans. Eccentric contraction (ECC) frequently induces severe muscle damage. However, it is not known whether and to what extent muscle damage occurs following ECC + BFR due to the difficulty of conducting definitive invasive studies. The purpose of this study was to examine muscle fiber damage following ECC + BFR at the cellular level. High-intensity ECC was purposefully selected to maximize the opportunity for muscle damage and hypertrophic signaling in our novel in vivo animal model. Male Wistar rats were assigned randomly to the following groups: ECC and ECC + BFR at varying levels of occlusion pressure (140, 160, and 200 Torr). In all conditions, electrical stimulation was applied to the dorsiflexor muscles simultaneously with electromotor-induced plantar flexion. We observed severe histochemical muscle fiber damage (area of damaged fibers/total fiber area analyzed) following ECC (26.4 ± 4.0%). Surprisingly, however, muscle damage was negligible following ECC + BFR140 (2.6 ± 1.2%), ECC+BFR160 (3.0 ± 0.5%), and ECC + BFR200 (0.2 ± 0.1%). Ribosomal S6 kinase 1 (S6K1) phosphorylation, a downstream target of rapamycin (mTOR)-phosphorylation kinase, increased following ECC + BFR200 as well as ECC. In contrast, S6K1 phosphorylation was not altered by BFR alone. The present findings suggest that ECC combined with BFR, even at high exercise intensities, may enhance muscle protein synthesis without appreciable muscle fiber damage.

The use of compression stockings during a marathon competition to reduce exercise-induced muscle damage: are they really useful?

Case-control study; ecological study. To examine the efficacy of wearing compression stockings to prevent muscle damage and to maintain running performance during a marathon competition. Exercise-induced muscle damage has been identified as one of the main causes of the progressive decrease in running and muscular performance found during marathon races. Thirty-four experienced runners were pair-matched for age, anthropometric data, and best race time in the marathon, and randomly assigned to a control group (n = 17) of runners who wore conventional socks or to a group of runners who wore foot-to-knee graduated compression stockings (n = 17). Before and after the race, a sample of venous blood was obtained, and jump height and leg muscle power were measured during a countermovement jump. Serum myoglobin and creatine kinase concentrations were determined as blood markers of muscle fiber damage. Total race time was not different between the control group and the compression stockings group (210 ± 23 and 214 ± 22 minutes, respectively; P = .58). Between the control group and the compression stockings group, postrace reductions in leg muscle power (-19.8% ± 17.7% versus -24.8% ± 18.4%, respectively; P = .37) and jump height (-25.3% ± 14.1% versus -32.5% . 20.4%, respectively; P = .27) were similar. At the end of the race, there were no differences between the control group and the compression stockings group in serum myoglobin (568 ± 347 ng·mL(-1) versus 573 ± 270 ng·mL(-1), respectively; P = .97) and creatine kinase concentration (390 ± 166 U·L(-1) versus 487 ± 227 U·L(-1), respectively; P = .16). The use of compression stockings did not improve running pace and did not prevent exercise-induced muscle damage during the marathon. Wearing compression stockings during long-distance running events is an ineffective strategy to avoid the deleterious effects of muscle damage on running performance. Therapy, level 2b.

Effect of dantrolene premedication on various cardiovascular and biochemical variables and the recovery in healthy isoflurane-anesthetized horses.

To determine the effect of dantrolene premedication on various cardiovascular and biochemical variables and recovery in isoflurane-anesthetized horses. 6 healthy horses. Each horse was anesthetized twice with a 21- to 28-day washout period between anesthetic sessions. Food was not withheld from horses before either session. During each session, dantrolene (6 mg/kg in 2 L of water) or water (2 L) was administered via a nasogastric tube 1 hour before anesthesia was induced. Anesthesia was maintained with isoflurane for 90 minutes, during which blood gas analyses and lithium-dilution cardiac output (CO) measurements were obtained every 10 minutes. Serum creatine kinase activity was measured before and at 4, 8, and 12 hours after anesthesia. When horses were premedicated with dantrolene, CO at 25, 35, and 45 minutes after induction of anesthesia was significantly lower than that when horses were premedicated with water after which time difficulty in obtaining valid measurements suggested a continued decrease in CO; plasma potassium concentration progressively increased during anesthesia, whereas serum creatine kinase activity remained fairly stable and within reference limits through 12 hours after anesthesia; and 2 of 6 horses developed cardiac arrhythmias that required medical intervention. The quality of anesthetic recovery was slightly better when horses were premedicated with dantrolene versus water, although the time required for recovery did not differ significantly between treatments. Results suggested that dantrolene premedication prevented muscle damage without affecting anesthetic recovery but impaired CO and precipitated hyperkalemia and cardiac arrhythmias in healthy isoflurane-anesthetized horses.

Curcumin (CurcuWINTM) Improves Antioxidant Capacity and Reduces Inflammation Following Downhill Running‐Induced Muscle Damage

Exercise (Ex) increases ROS and impairs antioxidant defense systems. Recent data suggest curcumin [CurcuWINTM Turmeric Extract, minimum 20% curcuminoids] possesses PPAR gamma activity and anti‐inflammatory properties. Therefore, the present study was undertaken to investigate the effects of curcumin (Cur) supplementation on Ex performance, changes in serum and muscle proteins in rats after exhaustive Ex. Twenty‐eight (28) male Wistar rats (8 wk. old, BW:180 ± 20 g) were divided into four treatment groups (i) control [no Ex, Group I (C)] (ii) C + Cur [no Ex, Group II] (iii) C + Ex [Group III] and (iv) C + Ex+ Cur [Group IV]. Cur [100 mg/ kg, contains approximately 20 mg of curcuminoids] was administered daily for 6 wks. The Ex protocols were performed on a motor‐driven rodent treadmill. The animals in the chronic Ex groups were habituated by treadmill Ex over a 5‐d period such as: 1st day 10 m/min, 10 min, 2nd day 20 m/min; 10 min, 3rd day 25 m/min, 10 min, 4th day 25 m/min, 20 min and 5th day 25 m/min, 30 min. Animals were exercised at 25 m/min, 45 min/d, 5 d/ week for 6 wks. Blood and muscle samples were analyzed. Running time was improved in Cur groups. Lactate and MDA significantly decreased, lipid profile, SOD, GPx and GSH were improved significantly in Cur treated groups. Significant decrease in NF‐kB and increase in I‐kB, HSP70 and PGC‐1 α in Cur treated rats were observed. These results suggest Curcumin (CurcuWINTM) is a potential ingredient of preventing muscle damage and improved exercise performance.

Light-emitting diode therapy (LEDT) before matches prevents increase in creatine kinase with a light dose response in volleyball players.

Low-level laser (light) therapy (LLLT) has been applied over skeletal muscles before intense exercise (muscular pre-conditioning) in order to reduce fatigue and muscle damage (measured by creatine kinase, CK) in clinical trials. However, previous exercise protocols do not exactly simulate the real muscle demand required in sports. For this reason, the aim of this randomized and double-blind placebo-controlled trial was to investigate whether light-emitting diode therapy (LEDT) applied over the quadriceps femoris muscles, hamstrings, and triceps surae of volleyball players before official matches could prevent muscle damage (CK) with a dose response, establishing a therapeutic window. A professional male volleyball team (12 athletes) was enrolled in this study, and LEDT was applied before 4 matches during a national championship. LEDT used an array of 200 light-emitting diodes (LEDs) arranged in 25 clusters of 4 infrared LEDs (850 ± 20 nm; 130 mW) and 25 clusters of 4 red LEDs (630 ± 10 nm; 80 mW). Athletes were randomized to receive one of four different total doses over each muscle group in a double-blind protocol: 105 J (20 s), 210 J (40 s), 315 J (60 s), and placebo (no light for 30 s). CK in blood was assessed 1 h before and 24 h after each match. LEDT at 210 J avoided significant increases in CK (+10 %; P = 0.993) as well as 315 J (+31 %, P = 0.407). Placebo (0 J) allowed a significant increase in CK (+53 %; P = 0.012) as well as LEDT at 105 J (+59 %; P = 0.001). LEDT prevented significant increases of CK in blood in athletes when applied before official matches with a light dose response of 210-315 J, suggesting athletes might consider applying LEDT before competition.

Occurrence of sulfated fucose branches in fucosylated chondroitin sulfate are essential for the polysaccharide effect preventing muscle damage induced by toxins and crude venom from Bothrops jararacussu snake.

Snake envenoming is an important public health problem around the world, particularly in tropics. Beyond deaths, morbidity induced by snake venoms, such as myotoxicity, is of pivotal consequence to population. Bothrops jararacussu is the main venomous snake in southeast region of Brazil, and particularly presents strong myotoxic effect. The only available therapy, antibothropic antivenom, poorly affects venom-induced myotoxicity. The aim of this study is to assess the ability of fucosylated chondroitin sulfate (fucCS), a glycosaminoglycan with anticoagulant and antithrombotic properties, and its derivatives to inhibit toxic activities of B. jararacussu crude venom and its isolated toxins, named bothropstoxins (BthTX-I and BthTX-II). The in vitro myotoxic activities induced by crude venom, by BthTX-I alone and by toxins together were abolished by fucCS. Carboxyl reduction (fucCS-CR) kept this ability whereas defucosilation (defucCS) abrogates myoprotection. We observed the same pattern in the response of these polysaccharides in antagonizing the increase in plasma creatine kinase (CK) levels, the reduction of skeletal muscle CK content and the rise of myeloperoxidase (MPO) activity induced by crude venom and isolated toxins. FucCS inhibited edematogenic activity and partially prevented the reduction of total leukocytes in blood when pre-incubated with crude venom. Furthermore, the venom procoagulant effect was completely antagonized by increasing concentrations of fucCS, although this polyanion could stop neither the tail bleeding nor the skin hemorrhage induced by Bothrops jararaca venom. The B. jararacussu phospholipase, hyaluronidase, proteolytic and collagenase activities were inhibited in vitro. The results suggest that fucCS could be able to interact with both toxins, and it is able to inhibit BthTX-II phospholipase activity. Light microscopy of extensor digitorum longus muscle (EDL) muscle showed myoprotection by fucCS, once necrotic areas, edema and inflammatory cells were all decreased as compared to venom injection alone. Altogether, data show that fucCS was able to inhibit myotoxicity and inflammation induced by B. jararacussu venom and its phospholipase toxins, BthTX-I and BthTX-II. Thus, fucosylated chondroitin sulfate is a new polyanion with potential to be used as an adjuvant in the treatment of snakebites in the future.

Therapeutic option by synergistic administration of the β-hydroxy-β-methyl butyrate and R(+) Lipoic Acid in a cellular model of dexamethasone-dependent sarcopenia

The decline of muscle mass and strength, known as sarcopenia, is a clinical problem associated with osteo-articular diseases, muscle disuse, cancer, renal failure, postmemenopause, age and corticosteroid treatments [1,2]. In this scenario, alterations in mitochondrial function [3] and accelerated apoptosis in skeletal muscle [4] are considered a major factor underlying sarcopenia and muscle atrophy. These evidences suggests that targeting myonuclear apoptosis as well as reducing the oxidative stress might provide novel and effective therapeutic tools to combat sarcopenia. Alpha-lipoic acid (1,2-dithiolane- 3-pentanoic acid), is a natural antioxidant with two optical isomers of which the (+)- possess a more pronounced effect (R (+) LA) [7]. Beta-hydroxy-beta-methylbutyrate (HMB), a leucine catabolite, has been shown to prevent muscle damage directly enhancing myogenic cells (satellite cells) proliferation and attenuating apoptosis [8]. Aim of the present research was the evaluation of the pharmacological profile of the HMB associated with the natural R(+)LA in a cellular model of muscle wasting. Material and Methods. C2C12 cell line was used as myoblasts or differentiated in miotubes by 7 day culture with 2% horse serum. Cell damage was induced by dexamethasone. Results. Dexamethasone toxicity was evaluated measuring cell viability (MTT assay) and apoptosis induction (caspase 3 activity) after 24h and 48h incubation of myoblasts with the glucocorticoid (0.01–300 μM concentration range). One μM dexamethasone (48h) decreased cell viability by about 50% and increased caspase 3 activity by 80%. R(+)LA (100 and 300 μM) or HMB (1 and 3 mM) significantly prevented dexamethasone-induced cell mortality; the efficacy was improved when 100 μM R(+)LA was combined with 1mM HMB, demonstrating the synergistic effect of R(+)LA and HMB in preventing cell mortality and caspase 3 activation. Similarly, the evaluation of dexamethasone evoked O2-. production and protein carbonylation demonstrated the efficacy of the combination of R(+)LA with HMB. In the early phase of myotube differentiation (72h) the combination of R(+)LA and HMB preserved the number of myogenin-positive cells as well as in the later (7 days) phase of differentiation the dexamethasone-dependent damage (evaluated as cell diameter and percentage of multinucleated cells). These data offer a rational to candidate the mixture as a therapeutic option for sarcopenia treatment.

Do sex and BMI predict or does stem design prevent muscle damage in anterior supine minimally invasive THA?

Cadaveric and clinical studies have suggested that, despite being touted as muscle-sparing, the direct anterior approach is still associated with muscle damage, particularly to the tensor fascia lata (TFL). Patient body mass index (BMI) and/or sex may also influence this parameter. The purposes of the study were to determine if using a shorter femoral component reduces TFL damage or if patient sex or increasing BMI increases intraoperative TFL damage in direct anterior THA. Over a 1-year period, 599 direct anterior THAs were performed by three experienced anterior hip surgeons; of those, 421 direct anterior hips had complete data (70%) and were included in the study. The amount of visible damage to the TFL was recorded before closure. Two stem types were used, a standard-length flat-wedge taper (standard) or a 3-cm shortened version of the same stem (short). Stem selection was based on timeframe of the surgery, surgeon preference, or matching a previous implant type. During the study period, the three surgeons performed an additional 225 primary THAs with other approaches such that the direct anterior approach represented 73% of the THAs performed. A member of the operating team, either a fellow or physician assistant, graded the extent of damage based on a 0 to 3 scale. On this scale, 0 represented no muscle fiber damage, 1 superficial tearing, 2 deep tearing or maceration, and 3 complete tear or severe damage. Patient sex and BMI were recorded and compared with stem type and muscle damage scores. An ordinal logistic regression model was used for statistical analysis. After controlling for relevant confounding variables using logistic regression, we found that mean muscle damage was associated with male sex (0.93, SD 0.76 versus 0.70, SD 0.68; p<0.001) and increasing BMI levels (p<0.001). As BMI increased, more muscle damage also was found in men compared with women (p=0.05; odds ratio [OR], 1.029; 95% confidence interval [CI], 1.000-1.060). There was no overall difference in mean muscle damage between short and standard-length stems (0.78, SD 0.77 versus 0.85, SD 0.69, p=0.32); however, as BMI increased, less damage was seen with a short stem (p=0.04; OR, 0.968; 95% CI, 0.931-0.997). Visible muscle damage occurred in most hips during anterior supine intermuscular hip arthroplasty. The clinical importance of this muscle damage requires further study, because some evidence suggests earlier restoration of gait and cessation of walking aids with direct anterior THA despite this damage; however, this was not studied here. Surgeons performing this approach can expect more difficulty and as a result possibly more damage to the TFL in patients with male sex and increased BMI. The use of a short stem can be considered for patients with increased BMI to limit damage to the TFL. Level III, therapeutic study.

A 7-day oral supplementation with branched-chain amino acids was ineffective to prevent muscle damage during a marathon

The aim of this study was to determine the effectiveness of a 7-day oral supplementation with branched-chain amino acids (BCAA) to prevent muscle damage during a marathon. Forty-six experienced runners were randomly divided into two groups, one with BCAA supplementation (n = 25, supplemented with 5 g day(-1) of powdered 1:0.5:0.5 leucine:isoleucine:valine, during the 7 days prior to the competition) and the other as a control group (n = 21, supplemented with an isocaloric placebo). Before the marathon race and within 3 min of finishing, leg muscle power was measured with a maximal countermovement jump and a urine sample was obtained. During the race, running pace was measured by means of a time-chip. Myoglobin concentration was determined in the urine samples as an indirect marker of muscle damage. A visual analog scale (0-10 points) was used to assess leg muscle pain during the race. In the BCAA group, the mean running pace during the marathon was similar to the control group (3.3 ± 0.4 vs. 3.3 ± 0.5 m s(-1), respectively, 0.98). The pre- to post-race reduction in muscle power was similar in both BCAA and control groups (-23.0 ± 16.1 vs. -17.3 ± 13.8 %, P = 0.13). Post-race urine myoglobin concentration was similar in both BCAA and control groups (5.4 ± 7.5 vs. 4.5 ± 8.6 μg mL(-1), P = 0.70). Finally, there were no differences between groups in the perceived muscle pain during the race (6 ± 1 vs. 5 ± 1 points, P = 0.80). A 7-day supplementation of BCAA (5 g day(-1)) did not increase the running performance during a marathon. Furthermore, BCAA supplementation was ineffective to prevent muscle power loss, muscle damage or perceived muscle pain during a marathon race.

Vinho Tinto melhora o Perfil Lipídico, mas não Atenua o Estresse Oxidativo provocado pelo Treinamento resistido até a Falha Concêntrica

Objective: To analyze the effects of red wine on muscle damage, oxidative stress and lipid profile in individuals practicing resistance exercise performed until concentric failure, for three weeks. Material and Methods: eleven young individuals were randomly distributed into experimental group (EG) (n = 6; 25 ± 3 years) and control group (CG) (n = 5; 27 ± 5 years), and then consumed 120 mL (females) or 180 mL (men) of red wine before workout. The individuals had three weeks of intense resistance training and another week of regenerative training, with three weekly sessions; each session was preceded by consumption of red wine or water. Measurements of lipoprotein, glucose, triglycerides, creatine kinase, malondialdehyde and psychometric testing of fatigue were taken at baseline, during and at the end of the study. The data were submitted to one-way ANOVA at p 0.05). However, the activity of malondialdehyde increased from baseline to the end of the treatment in both groups (p<0.05). Conclusion: moderate consumption of red wine before workout with high intensity resistance exercise improves lipid profile in young individuals, but does not prevent muscle damage and oxidative stress induced by this type of training. DESCRIPTORS Wine. Oxidative Stress. Lipoproteins. Resistance Training.

FATSOLUBLE VITAMINS AND SPORT

Vitamins are the cell biocatalysts, indispensable factors in performing the basic body functions. Fat-soluble vitamins are not involved in processes related to musscle contractions and energy expenditure, but they can affect physical performance indirectly because they are important for immune function (vitamin A, vitamin D, vitamin E), antioxidant function (vitamin A, vitamin E) or bone methabolism (vitamin D, vitamin K). Currently there are no clear recommendations for increase of fat-solubile vitamins intake in athletes, as well as evidence that athletic performance may be improved due to fatsolubile vitamins supplementation. In a small number of studies, it was shown that an antioxidant effect of beta carotene and vitamin E can prevent muscle damage and facilitate recovery after exercise. Also, athletes who perform the exercises in the halls should be informed about the necessity of sun exposure, as vitamin D is synthesised in the skin. Most athletes are not familiar with their needs for vitamins and trace elements, and take these compounds as supplements without consulting a nutritionist. It is important to emphasize that liposulubile vitamins are deposited in the body and can cause hypervitaminosis and toxic effects if taken in excess. It is indisputable that the lack of any fat-soluble vitamin cause problems in normal physiological processes, but supplementation is generally not required in athlets who have a well-balanced diet. Acta Medica Medianae 2013;52(4):63-68.

M.I.4 Progress in gene therapy for muscular dystrophy using vascular delivery of GALGT2

The myomatrix present at the neuromuscular junction, as well as the transmembrane receptor complexes linking it to the F-actin cytoskeleton, are distinct from those present along the rest of the skeletal myofiber sarcolemmal membrane. Covalent protein modifications, including glycosylation, also differ between these two muscle regions. We have shown that overexpression of GALGT2, a glycosyltransferase normally confined to the neuromuscular synapse, in mouse or macaque skeletal muscle leads to ectopic glycosylation of alpha dystroglycan and the overexpression of normally synaptic dystroglycan-binding proteins, including utrophin, laminin alpha5 and agrin. As a likely result of these and related changes, GALGT2 overexpression can inhibit the development of muscle disease in the mdx model of Duchenne muscular dystrophy, the dyW model of Congenital Muscular Dystrophy 1A, and the Sgca−/− model of Limb Girdle Muscular Dystrophy 2D. In addition, GALGT2 overexpression can increase binding of myomatrix proteins to alpha dystroglycan and prevent muscle damage induced by eccentric contractions. Moreover, elimination of endogenous GALGT2 upregulation in mdx muscles leads to more severe disease. These proof of concept studies suggest that GALGT2 is a surrogate gene therapy with potentially broad applications in muscle disease. With help from a team of investigators in the Center for Gene Therapy at Nationwide Children's Hospital, we are developing methods for vascular delivery of gene therapies, using both gene replacement and surrogate gene strategies, with the goal of performing clinical trials in multiple forms of muscular dystrophy. This work was supported by grants from the NIH U54 NS055958 and R01 AR060949.

Federal committee supports adding Pompe disease to screening panel

Federal committee supports adding Pompe disease to screening panel

LED therapy or cryotherapy between exercise intervals in Wistar rats: anti-inflammatory and ergogenic effects

The aim of this study was to test, between two bouts of exercise, the effects of light-emitting diode (LED) therapy and cryotherapy regarding muscle damage, inflammation, and performance. Male Wistar rats were allocated in four groups: control, passive recovery (PR), cryotherapy (Cryo), and LED therapy. The animals were submitted to 45min of swimming exercise followed by 25min of recovery and then a second bout of either 45min of exercise (muscle damage analysis) or time to exhaustion (performance). During the rest intervals, the rats were kept in passive rest (PR), submitted to cold water immersion (10min, 10°C) or LED therapy (940nm, 4J/cm(2)) of the gastrocnemius muscle. Blood samples were collected to analyze creatine kinase activity (CK), C-reactive protein (CRP), and leukocyte counts. The soleus muscles were evaluated histologically. Time to exhaustion was recorded during the second bout of exercise. After a second bout of 45min, the results demonstrated leukocytosis in the PR and Cryo groups. Neutrophil counts were increased in all test groups. CK levels were increased in the Cryo group. CRP was increased in PR animals. The PR group presented a high frequency of necrosis, but the LED group had fewer necrotic areas. Edema formation was prevented, and fewer areas of inflammatory cells were observed in the LED group. The time to exhaustion was greater in both the LED and Cryo groups, without differences in CK levels. CRP was decreased in LED animals. We conclude that LED therapy and cryotherapy can improve performance, although LED therapy is more efficient in preventing muscle damage and local and systemic inflammation.

Exertional Rhabdomyolysis in a Collegiate American Football Player After Preventive Cold-Water Immersion: A Case Report

To describe a case of exertional rhabdomyolysis in a collegiate American football player after preventive coldwater immersion. A healthy man (19 years old) participated in full-contact football practice followed by conditioning (2.5 hours). After practice, he entered a coach-mandated postpractice cold-water immersion and had no signs of heat illness before developing leg cramps, for which he presented to the athletic training staff. After 10 minutes of repeated stretching, massage, and replacement of electrolyte-filled fluids, he was transported to the emergency room. Laboratory tests indicated a creatine kinase (CK) level of 2545 IU/L (normal range, 45-260 IU/L), CK-myoglobin fraction of 8.5 ng/mL (normal < 6.7 ng/mL), and CK-myoglobin relative index of 30% (normal range, 25%-30%). Myoglobin was measured at 499 ng/mL (normal = 80 ng/mL). The attending physician treated the athlete with intravenous fluids. Exercise-associated muscle cramps, dehydration, exertional rhabdomyolysis. The patient was treated with rest and rehydration. One week after the incident, he began biking and swimming. Eighteen days later, the patient continued to demonstrate elevated CK levels (527 IU/L) but described no other symptoms and was allowed to return to football practice as tolerated. Two months after the incident, his CK level remained high (1900 IU/L). The athlete demonstrated no signs of heat illness upon entering the cold-water immersion but experienced severe leg cramping after immersion, resulting in a diagnosis of exertional rhabdomyolysis. Previously described cases have not linked cold-water immersion with the pathogenesis of rhabdomyolysis. In this football player, CK levels appeared to be a poor indicator of rhabdomyolysis. Our patient demonstrated no other signs of the illness weeks after the incident, yet his elevated CK levels persisted. Cold-water immersion immediately after exercise should be monitored by the athletic training staff and may not be appropriate to prevent muscle damage, given the lack of supporting evidence.