Effects of allicin supplementation on plasma markers of exercise-induced muscle damage, IL-6 and antioxidant capacity

To investigate the effects of allicin supplementation on exercise-induced muscle damage (EIMD), interleukin-6 (IL-6), and antioxidative capacity, a double-blinded, placebo-controlled study was conducted in well-trained athletes. Subjects were randomly assigned to an allicin supplementation group (AS group) and a control group, and received either allicin or placebo for 14 days before and 2 days after a downhill treadmill run. Plasma creatine kinase (CK), muscle-specific creatine kinase (CK-MM), lactate dehydrogenase (LDH), IL-6, superoxide dismutase (SOD), total antioxidative capacity (TAC), and perceived muscle soreness were measured pre and post exercise. AS group had significantly lower plasma levels of CK, CK-MM and IL-6, and reduced perceived muscle soreness after exercise, when compared with the control group. AS group also demonstrated a trend toward reducing plasma concentration of LDH after exercise (P = 0.08), although not statistically significant. Allicin supplementation induced a higher value of TAC at rest, and this higher value was maintained 48 h after exercise, however, there was no difference in SOD values after exercise between the two groups. The results suggested that allicin might be a potential agent to reduce EIMD. Further studies concerning anti-inflammatory and anti-oxidative effects of allicin on EIMD are needed.     

Reliability of maximal muscle force and voluntary activation as markers of exercise-induced muscle damage

The loss of the ability of skeletal muscle to generate force is one of the most appropriate and valid means to quantify muscle damage. Routine measurements of maximal muscle force, however, include many potential sources of error, the most important of which may be a possible lack of central drive to the muscles. The aim of the present study was to determine the reliability of maximal isometric quadriceps muscle force and voluntary activation over a timescale that is typically employed to examine the aetiology of exercise-induced muscle damage. We also attempted to characterise the reliability of several twitch interpolation variables including the size of the interpolated twitch and the state (i.e. unpotentiated vs potentiated) and size of the resting twitch. Over a 7-day period, eight healthy active males performed repeated maximal voluntary isometric contractions (MVC) of the quadriceps (baseline and 2 h, 6 h, 24 h, 48 h, 72 h and 7 days post). Systematic variations in maximal muscle force, voluntary activation, interpolated twitch, unpotentiated twitch and potentiated twitch were not statistically significant (P>0.05) and 95% repeatability coefficients of ±76.03 N, ±4.42%, ± 8.44 N, ±25.92 N and ±43.58 N were observed, respectively. These data indicate that young healthy well-familiarised male subjects can reproduce their perceived maximal efforts both within and between days where activation levels of >90% are routinely achieved. Providing activation remains within these limits in the 7 days following an acute bout of exercise, the researcher would be 95% certain that exercise-induced muscle damage is present in individual subjects (taken from similar subject populations) if MVC force falls outside these limits.     

The effect of severe eccentric exercise-induced muscle damage on plasma elastase, glutamine and zinc concentrations

The aim of this study was to determine if severe exercise-induced muscle damage alters the plasma concentrations of glutamine and zinc. Changes in plasma concentrations of glutamine, zinc and polymorphonuclear elastase (an index of phagocytic cell activation) were examined for up to 10 days following eccentric exercise of the knee extensors of one leg in eight untrained subjects. The exercise bout consisted of 20 repetitions of electrically stimulated eccentric muscle actions on an isokinetic dynamometer. Subjects experienced severe muscle soreness and large increases in plasma creatine kinase activity indicative of muscle fibre damage. Peak soreness occurred at 2 days post-exercise and peak creatine kinase activity [21714 (6416) U · l⁻¹, mean (SEM)] occurred at 3 days post-exercise (P < 0.01 compared with pre-exercise). Plasma elastase concentration was increased at 3 days post-exercise compared with pre-exercise (P < 0.05), and is presumably indicative of ongoing phagocytic leucocyte infiltration and activation in the damaged muscles. There were no significant changes in plasma zinc and glutamine concentrations in the days following eccentric exercise. We conclude that exercise-induced muscle damage does not produce changes in plasma glutamine or zinc concentrations despite evidence of phagocytic neutrophil activation. Accepted: 3 November 1997     

Disruptions of muscle fiber plasma membranes. Role in exercise-induced damage.

The authors have tested the hypothesis that plasma membrane disruptions are an early form of structural damage to the fibers of eccentrically exercised muscle. Rat serum albumin (RSA) was used as a marker for muscle-fiber wounding in the rat tricep (medial head) exercised eccentrically by downhill running. In all muscles examined, strong staining with a horseradish peroxidase (HRP)-conjugated anti-RSA antibody was observed between fibers (intercellular staining) and also within certain fibers (intracellular staining). This intracellular staining was interpreted as identifying muscle fibers wounded at their plasma membranes and hence rendered transiently or permanently permeable to extracellular RSA. The most striking finding of this study was a 6.9-fold increase relative to unexercised controls in the number of wounded cells in the medial head immediately after eccentric exercise. The authors also reproducibly observed, albeit less frequently, myocytes that stained with anti-RSA in the medial head and several other muscles of the "unexercised," caged laboratory rat. The extreme vulnerability of muscle plasma membranes to mechanically induced stress was revealed in this study by HRP injections into the triceps long head. A single injection of 200 microliters HRP through a 26-gauge needle resulted in extensive labeling of the muscle fibers present in the long head cross-sectioned at the injection site. The authors propose that initially resealable and/or highly localized, unsealable membrane wounds are an early form of exercise-induced damage that could progress along the length of the fiber until, 1 to 4 days after eccentric exercise, it becomes sufficiently severe that it can be readily recognized as the frank fiber necrosis and cellular infiltration described in numerous previous studies. In possessing cells wounded at their plasma membranes, normal, undisturbed rat muscle and eccentrically exercised muscle appears to resemble gut and skin, two additional tissues routinely exposed to mechanical forces in vivo. The authors propose that membrane disruptions provide a route into and out of myofiber cytoplasm distinct from the conventional, membrane-bounded routes of endo- and exocytosis, and therefore may be of importance both technically, as a route for introducing foreign genes into muscle cells, and biologically, as a route for release of the growth factor, basic fibroblast growth factor.     

运动诱导骨骼肌损伤对结蛋白聚集体的影响

文题释义： 蛋白聚物：在某些生理或是病理生理情况下,蛋白质折叠异常,暴露出本应包裹在蛋白中心的疏水核团,暴露在外的疏水核团之间容易相互吸引,形成的大分子、具有细胞毒性的蛋白聚集物。 蛋白聚集体：蛋白聚集物被泛素标记,并通过组蛋白去乙酰化酶6经微管dynein蛋白运输至微管组织中心,被波形蛋白和角蛋白构成的笼状结构包裹,形成蛋白聚集体。蛋白聚集体的形成是对细胞的保护,一方面隔离储存了毒性的蛋白聚集物,以免攻击其他细胞器;另一方面是自噬降解的前提步骤,有助于毒性蛋白的降解。 背景：蛋白降解是运动诱导骨骼肌损伤的重要原因,大强度的运动会导致蛋白错误折叠,易形成蛋白聚集体,损害骨骼肌超微结构。 目的：初步探索运动诱导骨骼肌损伤中蛋白聚集尤其是结蛋白聚集体的发生,以期明确结蛋白聚集在运动诱导骨骼肌损伤中的作用。 方法：将64只成年雄性SD大鼠(购自北京维通利华实验技术有限公司)随机分为安静对照组(n=8)和运动组(n=56),运动组又按运动后时相分为0,3,6,12,24,48,72 h组,每组8只。运动组大鼠进行一次跑台下坡跑运动(-16°,16 m/min,90 min),分别在运动后的相应时刻取比目鱼肌,使用透视电子显微镜观察损伤发生程度,采用 Western Blot方法检测比目鱼肌难溶蛋白中泛素蛋白的表达,免疫荧光双标观察结蛋白聚集体的表达。实验获得北京体育大学运动科学实验伦理委员会批准(2016030A)。 结果与结论：①透射电镜显示一次大负荷离心运动后,大鼠比目鱼肌部分位置肌节变宽,Z线断裂,肌原纤维断裂、扭曲,其中运动后12 h损伤最为严重,于运动后72 h完全恢复;②Western Blot方法检测显示一次大负荷离心运动后,骨骼肌中泛素蛋白表达总体呈先升高后降低的趋势,于运动后12 h达峰值,于运动后72 h恢复至安静对照组水平;③免疫荧光双标染色显示一次大负荷离心运动后,骨骼肌结蛋白聚集体表达总体上呈现先升高后降低的趋势,运动后12 h达到峰值,运动后24,48 h有所降低,72 h完全恢复安静对照组水平;④结果表明,结蛋白聚集可能是运动诱导骨骼肌损伤的原因之一。 ORCID: 0000-0002-6365-7822(高扬) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Effects of eccentric exercise-induced muscle damage on intramyocellular lipid concentration and high energy phosphates

Eccentric exercise is known to cause changes to the ultrastructure of skeletal muscle and, in turn, may alter the ability of the muscle to store and utilise intracellular substrates such as intramyocellular lipid (IMCL). The purpose of this study was to test the hypothesis that exercise-induced muscle damage (EIMD) results in IMCL accumulation. Six males (31 ± 6 years; mean ± SD, and 72.3 ± 9.7 kg body mass) performed 300 unilateral, maximal, isokinetic, eccentric contractions (Ecc) (30° s⁻¹) of the quadriceps on an isokinetic dynamometer, followed immediately by an equal amount of work by the contralateral leg but with concentric action (Con). Phosphate compounds and IMCL content of the vastus lateralis of both legs were measured using ³¹P and ¹H magnetic resonance spectroscopy. IMCL content was higher in Ecc than Con 24 h post but the reverse was evident 48 h post-exercise (P = 0.046). A significant time × trial interaction for resting [P_i] (P = 0.045), showed increases in Ecc across time but no change in Con. A significant main effect of trial (P = 0.002) was apparent indicating the Ecc leg had marked metabolic dysfunction. The P_i/PCr ratio showed a significant effect of trial (P = 0.001) with an increase evident in Ecc leg, primarily due to increases in [P_i]. The present study highlights changes in IMCL content of skeletal muscle following EIMD.     

肌肉组织工程研究现状及对运动性肌肉损伤的作用

背景：高水平快节奏的体育运动比赛中容易造成肌肉运动损伤,肌肉组织工程为其修复带来希望。 目的：综述肌肉组织工程研究的现状,为运动性肌肉损伤组织工程学研究提供理论基础。 方法：以“tissue engineering, anterior cruciate ligament repair, biological material scaffold, cytokines, seed cells”为关键词,采用计算机检索Pubmed数据库中1994-01/2010-12的相关文章。纳入与运动性肌肉损伤及肌肉组织工程相关的文章;排除重复研究或Meta分析类文章。 结果与结论：共纳入15篇文献,目前的研究重点包括肌肉组织工程重建、细胞外基质复合材料、肌肉组织工程种子细胞的来源、基质支架4个方面。目前的研究表明肌肉组织工程对运动性肌肉损伤的治疗有良好的应用前景。但在实际应用中,肌肉组织工程的种子细胞的选择、支架材料的构建、细胞外基质复合材料研究和组织的相容性等仍是肌肉组织工程学方面的难点问题。     

针刺对运动性骨骼肌损伤大鼠骨骼肌线粒体自噬的影响

目的:通过观察针刺对大负荷运动大鼠骨骼肌线粒体自噬相关蛋白表达的影响,探讨针刺在运动性骨骼肌损伤修复中的作用及其机制。方法:将128只成年雄性Sprague-Dawley大鼠随机分为4组:空白对照(control,C;n=8)组、单纯运动(exercise,E;n=40)组、单纯针刺(acupuncture,A;n=40)组和运动针刺(exercise and acupuncture,EA;n=40)组。其中,E和EA组进行1次下坡跑运动,A组和EA组(运动后即刻)施加针刺处理。后3组根据干预后不同时相又分为0 h、12 h、24 h、48 h和72 h亚组(n=8),分别于对应时点分离比目鱼肌进行检测,使用透射电子显微镜观察骨骼肌线粒体超微结构变化;采用ELISA法检测比目鱼肌线粒体定量酶柠檬酸合成酶(CS)的含量变化;应用Western blot法检测骨骼肌PTEN诱导假定激酶1(PINK1)、parkin和微管相关蛋白1轻链3(LC3)的蛋白表达变化。结果:1次大负荷运动后大鼠比目鱼肌线粒体出现明显肿胀和肌膜下积聚等超微结构异常变化,伴有大量自噬体形成;同时CS的含量明显减少(P0.05);线粒体自噬蛋白PINK1、parkin和LC3均出现一过性的表达升高(P0.05)。运动后针刺明显改善了线粒体超微结构的异常变化,减少自噬溶酶体的出现,同时抑制CS的含量减少,下调PINK1、parkin和LC3在线粒体上的表达(P0.05)。结论:1次大负荷运动后骨骼肌线粒体结构和数量受损,通过激活PINK1/parkin途径诱发线粒体自噬的过度发生。大负荷运动后针刺可以缓解骨骼肌线粒体的损伤,其作用机制可能是通过下调线粒体外膜蛋白PINK1表达,抑制其对下游胞浆蛋白parkin的招募,进而影响LC3与线粒体的结合以抑制线粒体自噬过度激活。     

The effect of exercise-induced muscle damage on perceived exertion and cycling endurance performance

This study evaluated the effects of exercise-induced muscle damage (EIMD) on fixed-load cycling and 5-min time-trial performance. Seven recreational athletes performed two submaximal fixed-load exercise bouts followed by a 5-min time-trial before, 48 and 168 h following 100 counter-movement jumps. Measurements of heart rate, RER and blood lactate concentration remained unchanged during the fixed-load bouts following jumping exercise. However, and increased (P < 0.05) at 48 h. RPE values were higher at 48 h as were the ratio of RPE:HR and RPE: (P < 0.05). In the time-trial, mean peak power output, mean power output, distance covered and post exercise blood lactate were lower at 48 h (P < 0.05). RPE remained unchanged between trials. These findings indicate that the ventilatory equivalent for oxygen and perceived exertion at submaximal work rates are increased 48 h following eccentric exercise. Furthermore, EIMD increases perceived exertion and impairs performance during a 5-min all-out effort.     

The effects of exercise-induced muscle damage on maximal intensity intermittent exercise performance

Exercise-induced muscle damage (EIMD) is a common occurrence following activities with a high eccentric component. Alterations to the torque–velocity relationship following EIMD would appear to have serious implications for athletic performance, particularly as they relate to impairment of maximal intensity exercise. However, this has been studied infrequently. The purpose of this study was to assess the effects of EIMD on maximal intermittent sprint performance. Ten male participants (age 22.4±3.2 years, height 178.6±5.2 cm, mass 80.6±10.7 kg) performed 10×6 s cycle ergometer sprints, interspersed with 24 s recovery against a load corresponding to 0.10 kp/kg and 10×10 m sprints from a standing start, each with 12 s active (walking) recovery. All variables were measured immediately before and at 30 min, 24, 48 and 72 h following a plyometric exercise protocol comprising of 10×10 maximal counter movement jumps. Repeated measures ANOVA showed significant changes over time (all P<0.05) for perceived soreness, plasma creatine kinase activity (CK), peak power output (PPO), sprint time and rate of fatigue. Soreness was significantly higher (P<0.01) than baseline values at all time intervals (3.1, 4.9, 5.5 and 3.2 at 30 min, 24, 48 and 72 h, respectively). CK was significantly elevated (P<0.05) at 24 h (239 IU/l) and 48 h (245 IU/l) compared to baseline (151 IU/l). PPO was significantly lower (P<0.05) than baseline (1,054 W) at all time intervals (888, 946, 852 and 895 W, at 30 min, 24, 48 and 72 h, respectively). The rate of fatigue over the ten cycling sprints was reduced compared to baseline, with the greatest reduction of 48% occurring at 48 h (P<0.01). This was largely attributed to the lower PPO in the initial repetitions, resulting in a lower starting point for the rate of fatigue. Values returned to normal at 72 h. Sprint times over 10 m were higher (P<0.05) at 30 min, 24 h and 48 h compared to baseline (1.96 s) with values corresponding to 2.01, 2.02 and 2.01 at 30 min, 24 h and 48 h, respectively. Values returned to baseline by 72 h. The results provide further evidence that, following a plyometric, muscle-damaging exercise protocol, the ability of the muscle to generate power is reduced for at least 3 days. This is also manifested by a small, but statistically significant reduction in very short-term (2 s) intermittent sprint running performance. These findings have implications for appropriate training strategies in multiple sprint sports.     

Effect of volume of milk consumed on the attenuation of exercise-induced muscle damage

Exercise-induced muscle damage (EIMD) leads to decrements in muscle performance, increases in intramuscular proteins and delayed-onset of muscle soreness (DOMS). Previous research demonstrated that one litre of milk-based protein-carbohydrate (CHO) consumed immediately following muscle damaging exercise can limit changes in markers of EIMD possibly due to attenuating protein degradation and/or increasing protein synthesis. If the attenuation of EIMD is derived from changes in protein metabolism then it can be hypothesised that consuming a smaller volume of CHO and protein will elicit similar effects. Three independent matched groups of 8 males consumed 500 mL of milk, 1,000 mL of milk or a placebo immediately following muscle damaging exercise. Passive and active DOMS, isokinetic muscle performance, creatine kinase (CK), myoglobin and interleukin-6 were assessed immediately before and 24, 48 and 72 h after EIMD. After 72 h 1,000 mL of milk had a likely benefit for limiting decrements in peak torque compared to the placebo. After 48 h, 1,000 mL of milk had a very likely benefit of limiting increases in CK in comparison to the placebo. There were no differences between consuming 500 or 1,000 mL of milk for changes in peak torque and CK. In conclusion, decrements in isokinetic muscle performance and increases in CK can be limited with the consumption of 500 mL of milk.     

Effects of eccentric exercise-induced muscle injury on blood levels of platelet activating factor (PAF) and other inflammatory markers

It has been reported that exercise with eccentric contractions can induce damage and inflammation in human muscle tissue, the severity of which depends on the duration and the intensity of exercise. Platelet activating factor (PAF) is a potent inflammatory mediator implicated in a series of pathophysiological conditions. We sought to investigate the relationship between PAF and eccentric exercise induced muscle damage. Thirteen healthy, recreationally active male subjects (27.5±3.78 year) performed 36 maximum voluntary eccentric contractions on a motorized muscle dynamometer using the elbow flexor muscles of the non-dominant arm. Venous blood samples were collected immediately before and after exercise at 2, 24, 48, 72 and 96 h. PAF was isolated, purified and determined by a platelet aggregation assay. Serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), C-reactive protein (CRP) and complement C3 (C3), plasma level of fibrinogen and whole blood level of leukocytes (and their subsets) were determined. Established indicators of muscle damage as maximum isometric torque (MIT), range of motion (ROM), relaxed arm angle (RANG), flexed arm angle (FANG), arm circumference (CIRC) and muscle soreness were also measured at the same time points. PAF, leukocytes, CK and LDH were elevated after exercise, while other biochemical parameters such as CRP, C3 and fibrinogen were unchanged. We also observed an inverse association between PAF and MIT and ROM, as well as a positive association with other markers of muscle injury, i.e. CK, LDH, FANG and CIRC (all P’s<0.05). Our findings may imply a role for PAF in the mechanism of eccentric exercise induced muscle damage.     

Preventive effects of Spirulina platensis on skeletal muscle damage under exercise-induced oxidative stress

The effects of spirulina supplementation on preventing skeletal muscle damage on untrained human beings were examined. Sixteen students volunteered to take Spirulina platensis in addition to their normal diet for 3-weeks. Blood samples were taken after finishing the Bruce incremental treadmill exercise before and after treatment. The results showed that plasma concentrations of malondialdehyde (MDA) were significantly decreased after supplementation with spirulina (P < 0.05). The activity of blood superoxide dismutase (SOD) was significantly raised after supplementation with spirulina or soy protein (P < 0.05). Both of the blood glutathione peroxidaes (GP _x ) and lactate dehydrogenase (LDH) levels were significantly different between spirulina and soy protein supplementation by an ANCOVA analysis (P < 0.05). In addition, the lactate (LA) concentration was higher and the time to exhaustion (TE) was significantly extended in the spirulina trail (P < 0.05). These results suggest that ingestion of S. platensis showed preventive effect of the skeletal muscle damage and that probably led to postponement of the time of exhaustion during the all-out exercise.     

Effect of two maximal isometric contractions on eccentric exercise-induced muscle damage of the elbow flexors

This study investigated the time wise protective effect conferred by two maximal voluntary isometric contractions (2MVCs) at 20° elbow flexion on muscle damage induced by 30 maximal isokinetic (60° s^?1) eccentric contractions of the elbow flexors (MaxECC). Sixty-five young untrained men were randomly assigned to a control group that did not perform 2MVCs, or one of four experimental groups (n = 13 per group) who performed 2MVCs either immediately (0d), 2 (2d), 4 (4d) or 7 days (7d) before MaxECC. Changes in maximal isokinetic (60° s^?1) concentric torque (MVC-CON), optimum angle (OA), range of motion, upper arm circumference, muscle soreness, plasma creatine kinase activity and myoglobin concentration, and ultrasound echo-intensity following MaxECC were compared among the groups by a two-way repeated measures ANOVA. No significant changes in any variables were evident following 2MVCs. The 2d and 4d groups showed 16–62 % smaller (P < 0.05) changes in all variables following MaxECC than the control, 0d and 7d groups. The 2d group showed 14–34 % smaller (P < 0.05) changes in all variables except for OA compared with the 4d group. The changes in the variables were similar among the control, 0d and 7d groups. These results show that 2MVCs that were performed between 2 and 4 days before MaxECC attenuated the magnitude of muscle damage, but no such effect was evident if the 2MVCs were performed immediately or 7 days before MaxECC. It is concluded that the protective effect conferred by 2MVCs is relatively short-lived, and there is a window for the effect to be conferred.     

Eccentric exercise-induced muscle damage of pre-adolescent and adolescent boys in comparison to young men

Purpose

This study compared changes in indirect muscle damage markers after maximal eccentric exercise of the elbow flexors (EF) among pre-adolescent (9–10 years), adolescent (14–15 years) and post-adolescent (20–25 years) men to test the hypothesis that the magnitude of muscle damage would increase with increase in age.

Methods

Thirteen untrained men of each age group performed two bouts (ECC1, ECC2) of 30 maximal EF eccentric contractions. Several indirect muscle damage markers were measured from the exercised arm before, immediately after, and 1–5 days post-exercise. Changes in maximal voluntary concentric contraction torque of the EF (MVC), range of motion of the elbow joint, upper arm circumference (CIR), muscle passive stiffness, muscle soreness, plasma creatine kinase activity and myoglobin concentration after ECC1 and ECC2 were compared amongst groups by a mixed-design two-way ANOVA.

Results

MVC before exercise was smaller (P < 0.05) for pre-adolescent (8.9 ± 1.9 Nm) than adolescent (25.1 ± 3.9 Nm) and adult (35.3 ± 4.6 Nm), and for adolescent than adult. Changes in all variables after ECC1 were smaller (P < 0.05) for pre-adolescent and adolescent when compared with adult, and all except CIR changes were smaller (P < 0.05) for pre-adolescent than adolescent. After ECC2, changes in all variables were smaller (P < 0.05) than those after ECC1 for all groups, but the magnitude of the changes was different among groups (P < 0.05) in the same way as that after ECC1.

Conclusion

These results indicate that the magnitude of muscle damage is increased from pre-adolescent, adolescent to post-adolescent men.     

Effects of calpain inhibition on dopaminergic markers and motor function following intrastriatal 6-hydroxydopamine administration in rats

The neurotoxin 6-hydroxydopamine has been widely used to model aspects of Parkinson's disease in rodents, but the mechanisms underlying toxin-induced dopaminergic degeneration and functional impairment have not been fully elucidated. The main aim of the present study was to assess a possible role for calpains in neurochemical and behavioral deficits following unilateral infusion of intrastriatal 6-hydroxydopamine in adult rats. Toxin administration produced a profound dopaminergic denervation, as indicated by a 90–95% reduction in dopamine transporter radiolabeling measured in the caudate-putamen at 2 weeks post-lesion. Treatment with 6-hydroxydopamine also resulted in calpain activation in both caudate-putamen and substantia nigra, as measured by the appearance of calpain-specific spectrin breakdown products. Calpain activation peaked at 24 h after 6-hydroxydopamine infusion and remained elevated at later time points. In contrast, caspase-3-mediated spectrin cleavage subsided within 48 h in both brain areas. In a subsequent experiment, calpain inhibition was achieved by intrastriatal infusion of an adenovirus expressing the endogenous calpain inhibitor, calpastatin. Calpastatin delivery abolished the lesion-induced calpain-mediated spectrin cleavage and alleviated forelimb asymmetries resulting from unilateral intrastriatal 6-hydroxydopamine. Unexpectedly, dopamine transporter and tyrosine hydroxylase labeling revealed significant neuroprotection, not in the nigrostriatal pathway but rather in the ventral tegmental area. These findings support a role for calpain activation in 6-hydroxydopamine-induced degeneration of dopaminergic neurons. However, after near-total dopaminergic depletion, the primary benefit of calpain inhibition may not occur within the nigrostriatal dopaminergic pathway itself.     

Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40?min of bench stepping (knee high step; 15 steps?·?min^?1). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150?W, with increments of 50?W every 2?min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P?V˙O₂ during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P?P?相似文献