运动对糖尿病大鼠骨骼肌细胞葡萄糖运载体4转位机制的影响

目的　研究运动对链脲佐菌素 (STZ)引起的糖尿病大鼠骨骼肌细胞葡萄糖运载体 4(Glucosetransporter 4,GLUT4)转位机制的影响。 方法　将实验大鼠分为 3组 :正常对照组、糖尿病组和糖尿病运动组。糖尿病运动组大鼠进行 6周游泳训练。实验到期分离各组大鼠大腿股四头肌 ,制备细胞内、外膜 ,以Western印迹法检测GLUT4蛋白含量 ,同时检测大鼠血清胰岛素和血糖浓度。结果　糖尿病大鼠骨骼肌细胞GLUT4蛋白含量明显减少 ,与正常对照组相比 ,细胞内膜GLUT4蛋白含量减少 2 4.1% (P <0 .0 1) ,细胞外膜减少 48.1% ,(P <0 .0 1)。糖尿病大鼠经过 6周运动训练 ,与糖尿病组大鼠相比 ,骨骼肌细胞内膜GLUT4蛋白含量无明显变化 ,而细胞外膜GLUT4蛋白含量增加 10 8.7% (P <0 .0 1) ,血糖由18.5± 1.9mmol/L降至 14 .0± 3 .3mmol/L(P <0 .0 1)。结论　糖尿病状态下骨骼肌细胞GLUT4蛋白含量明显减少 ,其中以细胞外膜GLUT4蛋白含量的减少更为显著 ,即在糖尿病状态下骨骼肌细胞GLUT4蛋白转位机制出现障碍 ,使肌细胞对葡萄糖的转运发生障碍 ,血糖升高。糖尿病大鼠经过运动训练可增加骨骼肌细胞GLUT4蛋白含量 ,并改善GLUT4蛋白转位机制 ,从而增加肌细胞对葡萄糖的转运和利用 ,降低血糖 ,改善糖尿病大鼠糖代谢紊乱的状况。     

运动疗法应用于ICU困难撤机患者的效果评价

目的评价困难撤机患者在治疗期间采用运动疗法的干预效果。方法将63例困难撤机患者随机分为实验组33例和对照组30例。实验组在常规呼吸道护理基础上根据患者病情及体力进行循序渐进的4步运动疗法;对照组按常规进行呼吸道护理。比较2组不同时点的潮气量、呼吸频率、氧合指数等指标情况。结果机械通气第21天和第28天,实验组潮气量、呼吸频率、氧合指数（PaO2／FiO2）、急性生理与慢性健康评分（APACHEII评分）指标均显著优于对照组;机械通气第28天,实验组心率显著优于对照组;实验组患者机械通气日及ICU住院日均明显少于对照组;2组的并发症发生率比较差异无统计学意义。结论运动疗法对困难撤机患者具有积极的作用。     

Autologous Skeletal Muscle, an Alternative for Cardiac Assistance

Original attempts to use skeletal muscle for cardiac assistance were soon abandoned when the problem of muscle fatigue could not be solved. In the last 2 decades, better understanding of muscle physiology and the development of successful protocols of electrical muscle conditioning have given new impetus to researchers around the world to proceed in the effort to identify useful applications of skeletal muscle to support the heart. More than 100 patients around the world have undergone cardiomyoplasty, mostly for cardiac failure. While subjective improvement in symptoms was noticed in the majority of the patients, only recently favorable hemodynamic changes have been documented. The other alternative that has been pursued in the laboratory is the construction of skeletal muscle ventricles that, after conditioning and vascular delay, have been shown to provide significant cardiac support when used for diastolic counterpulsation or for right heart bypass in animal models.     

Influence of physical exercise on polyamine synthesis in the rat skeletal muscle

BACKGROUND: Physical exercise and testosterone administration result in a series of adaptive anabolic phenomena in the skeletal muscle. The role of polyamines in these processes has been poorly explored. DESIGN: We measured the activities of polyamine-synthesising enzymes, ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAMDC) and polyamine content in skeletal muscle of male rats exposed to endurance or resistance exercise, or a single testosterone treatment. Soleus muscle (consisting mainly of slow-twitching oxidative fibres-STO) and extensor digitorum longus (mainly fast-twitching glycolytic muscle fibres-FTG) were analysed for polyamine content by HPLC, and ODC and SAMDC activity. RESULTS: Both endurance and resistance exercise induced a threefold increase in endogenous testosterone production. Two hours after exercise, ODC was increased in STO fibres, returning to baseline after 24 h; in FTG fibres the increase was less prominent. An increase in SAMDC activity occurred in a more sustained manner, with its peak 8 h after exercise. Polyamines were subsequently accumulated in both skeletal muscle fibres, with a rise in putrescine concentration after 2 h, and a fall corresponding to conversion of putrescine to spermidine and spermine by SAMDC. Single dose of 17alpha-methyltestosterone resulted in a similar increase in polyamine-synthesising enzyme activities and polyamine concentrations in the skeletal muscle. CONCLUSION: Polyamine accumulation in the skeletal muscle after physical exercise is likely to occur secondary to testosterone production. Polyamines are apparently involved in the oxidative, but not in glycolytic processes related to muscle adaptation to exercise.     

运动对大鼠骨骼肌废用性萎缩的恢复及血清雄激素水平的影响

目的探讨在肌肉萎缩和恢复中血清睾酮(ST)水平的变化及不同的锻炼方式对肌萎缩恢复的作用.方法将30只雄性SD大鼠随机分为5组①正常对照组;②外固定3周后即刻宰杀组;③外固定3周后自然恢复3周组;④外固定3周后跑台训练3周组;⑤外固定3周后游泳训练3周组.以放免法测定ST水平.结果固定3周后,即刻宰杀组大鼠ST水平为(0.58±0.24)nmol/L,较正常对照组(6.21±3.51)nmol/L显著下降,两组比较差别有非常显著性意义(P＜0.01);自然恢复组(1.93±0.77)nmol/L和运动组[跑台组(3.01±1.82)nmol/L,游泳组(3.71±2.84)nmol/L]的ST水平均显著高于固定即杀组(0.58±0.24)nmol/L,差别有显著或非常显著性意义(P＜0.05或P＜0.01),但自然恢复组和跑台组仍显著低于对照组水平,差别有显著或非常显著性意义(P＜0.05或P＜0.01),而游泳组已恢复到对照组水平,两组比较差别无显著性意义(P＞0.05);两个运动组之间比较差别无显著性意义(P＞0.05).结论外固定可造成骨骼肌废用性萎缩;解除固定后,萎缩的肌肉可以逐渐恢复,而运动对萎缩肌肉的恢复过程有促进作用,这可能与运动提高机体ST水平有关;游泳锻炼较跑台运动能更有效地提高ST水平.     

Metabolic Activity in Rat Skeletal Muscle:Effect of Intermittent Hypoxia

Abstract. In order to determine whether hypoxia is a trigger for changed metabolic activity in muscle tissue, rats were exposed to intermittent hypoxia of varying degree (5% 0₂, 8% 0₂, 10% 0₂, 12% 0₂, 15% 0₂ in N₂) 3 h per day for 1–4 weeks. The effects of hypoxia on the rate of incorporation of glucose-carbon into glycogen, lipids, carbon dioxide and lactate and on succinic oxidase activity in skeletal muscle tissue were determined. Rats intermittently exposed to 5% oxygen in nitrogen for one week showed a significant decrease of the rate of incorporation of glucose-carbon into lipids and carbon dioxide and a significant decrease in succinic oxidase activity. In rats exposed to 8 and 10% 0₂ a significant increase of the incorporation rate of glucose-carbon into glycogen, lipids and carbon dioxide was found after 1 and 4 weeks and succinic oxidase activity increased after 4 weeks. The phospholipid concentration in muscle tissue decreased after 8 and 10% 0₂ exposure for 4 weeks. In the rats exposed to 8% oxygen for 4 weeks the protein concentration of muscle tissue increased significantly.–Based on these results it is suggested that the change of the glycolytic activity and succinic oxidase activity in muscle tissue after physical training and in arterial insufficiency are induced by hypoxia in the muscles.     

Vasovagal Syncope and Skeletal Muscle Vasodilatation: The Continuing Conundrum

During vasovagal syncope, profound bradycardia and hypotension occur. Atropine administration can prevent the bradycardia but not the hypotension, suggesting that marked peripheral vasodilation is a major cause of the fall in arterial pressure. This concept has been confirmed since vasovagal syncope can be seen in patients who have undergone heart transplantation and also in patients subject to cardiac pacing. In both cases, there is no bradycardia but hypotension during the syncopal attacks. The major site of the vasodilation is in skeletal muscle and muscle sympathetic nerve activity is suppressed just prior to and during vasovagal attacks, indicating that sympathetic withdrawal contributes to the dilation. However, the skeletal muscle vasodilation seen during syncope is greater than that caused by sympathetic withdrawal alone, and it is absent in limbs that have undergone surgical sympathectomy, or local anesthetic nerve block. These observations suggest a role for neurally mediated "active" vasodilation during syncope. The afferent neural pathways that evoke the profound vasodilation during vasovagal attacks remain the subject of debate. The neural pathways responsible for the active component of the dilation are also unknown. Recent evidence has demonstrated that cholinergic, β-adrenergic, and nitroxidergic (nitric oxide) vasodilator mechanisms are not essential to observe the dilation, demonstrating that the mechanisms responsible for it remain a continuing conundrum.     

Androgens and the control of skeletal muscle protein synthesis

Athletes have long supported the concept that anabolic steroids increase skeletal muscle mass. However, it was only recently that both testosterone and its synthetic analogue, oxandrolone, were proven capable of inducing myotrophic effects in postabsorptive human skeletal muscle. These findings have provided the physiological evidence that anabolic steroids deserve attention in the clinical arena as a pharmacological intervention against losses in lean body mass associated with age, disease, trauma and burn injury. However, we are lacking in vivo molecular evidence that would directly or indirectly link androgens and the androgen receptor with increases in skeletal muscle mass. Clearly, a need exists to link in vivo and in vitro studies from both the physiological and molecular arena as they relate to androgens and the control and regulation of skeletal muscle mass. In this brief review, newly discovered information and emerging theories relating to the direct, indirect, priming and antiglucocorticoid action of androgens on skeletal muscle will be presented.     

Long-Term Neurostimulation of Skeletal Muscle: Its Potential for a Tether-Free Biologic Cardiac Assist Device

Skeletal muscle has a tremendous capacity to adapt. This adaptive phenomenon is seen perhaps to the greatest extent when skeletal muscle is subjected to chronic low frequency stimulation via the motor nerve. There is a decrease in glycolytic enzymes and an increase in oxidotive enzymes, as well as a change in the contractile proteins and an increase in the mitochondrial volume fraction of the muscle fiber. These adaptive changes result in a muscle that is considerably more fatigue-resistant. Specifically herein, we report on a pneumatic aortic counterpulsator device powered by skeletal muscle. These muscle pumps functioned continuously and pumped blood effectively in tether-free animals for several weeks.     

运动训练对慢性心力衰竭患者运动耐量的影响

目的　探讨运动训练对慢性心力衰竭患者运动耐量的影响。方法　 70例患者随机分为 2组 ,A组 (n =3 4)运动培训 3周 ,B组 (n =3 6)限制活动 3周 ,然后比较 2组 6min内步行的距离、左室射血分数(超声心动图测定 )、血白介素 6(双抗体夹心法 )及去甲肾上腺素浓度 (荧光法测定 )的变化。结果　运动训练组患者试验后 6min步行距离 ( 3 85± 3 0 .12 )m ,血IL 6( 0 .86± 0 .2 5 ) pmol/L ,NE( 2 .0 5± 0 .48)nmol/L ,LVEF( 43± 5 .2 3 ) % ,上述各指标与对照组相比 ,差异均有显著性意义 (P <0 .0 5 ) ,而且运动试验组试验前、后各指标的差异也有显著性意义 (P <0 .0 5 ) ,但对照组试验前、后差异无显著性意义 (P >0 .0 5 )。结论　运动训练能改善慢性心力衰竭患者的运动能力及心功能 ,对慢性心力衰竭患者的康复治疗是有益的。     

离心跑台运动对小鼠骨骼肌炎性因子、肌再生因子及血管再生因子表达的影响

目的:观察小鼠离心运动后骨骼肌炎性因子、肌再生因子以及血管再生因子的表达变化,探讨其在离心运动骨骼肌损伤修复中可能发挥的作用。方法:32只雄性C57BL/6小鼠随机分为对照组(C组,n=8)和离心运动组(D组,n=24)。根据取材时间,离心运动组又分为3个小组(运动后1d,3d和7d组)。离心运动后不同时间点取双侧腓肠肌。HE染色观察骨骼肌形态学变化,比色法检测血浆肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,荧光定量PCR检测炎性因子、肌再生因子及血管再生因子基因表达的变化。结果:小鼠下坡跑后骨骼肌纤维结构无明显破坏,无显著炎性细胞浸润。与对照相比,血浆CK和LDH活性在运动后各时间点均无显著变化(P0.05)。从基因层面看,炎性细胞标志物(MPO—嗜中性粒细胞标志物;F4/80—巨噬细胞标志物)在下坡跑后显著上升。部分炎症因子(如肿瘤坏死因子-α、白介素-1β、白介素-6)在下坡跑后显著上调。而肌再生调节因子中,只有机械生长因子和白血病抑制因子在运动后出现显著上调。而肌再生关键细胞——肌卫星细胞的特异性标记分子(分子标志—Pax7,增殖标记—Myo D,分化标记—myogenin)在离心运动后未出现显著变化(P0.05)。此外,其他与肌肉和血管再生密切相关的再生因子(如:胰岛素样生长因子1、肝细胞生长因子、尿激酶型纤溶酶原激活物、环氧合酶2、低氧诱导因子-1α、血管内皮生长因子、血管生成素1等)在离心运动后均未见显著变化(P0.05)。结论:从形态学表现、血清指标和基因表达综合来看,离心跑台运动并非小鼠骨骼肌损伤建模的理想方式。     

ATP and IMP in single human muscle fibres after high intensity exercise

Summary. Within a muscle there is large variation in the activity of various enzymes among single fibres. It is reasonable, therefore, to expect a corresponding variation in their metabolic response to exercise. This was examined by obtaining muscle biopsies from five men at rest and after intense short-term exercise consisting of three bouts of 30 knee extensions each and intervened by 60 s rest. Freeze-dried dissected single fibres identified as type 1 or type 2 were analysed for ATP and IMP contents by liquid chromatography. Rest. Average ATP tended to be higher in type 2 than in type 1 fibres. The ATP range was 14–30 and 14–32 mmol × kg^-1 dry muscle (dm) in type 1 and 2 fibres, respectively. IMP was less than 1 mmol × kg^-1 dm in most fibres and similar in types 1 and 2. Exercise. Muscle force decreased 70% during exercise. The average decrease in ATP content was significant for both fibre types with somewhat larger response for type 2 (20%) than type 1 (10%) fibres. The ATP range was 10–28 and 10–30 mmol × kg^-1 dm in type 1 and 2 fibres, respectively. Average IMP content increased substantially in both fibre types, more so for type 2, and the range for individual fibres was 0–13 (type 1) and 0–21 (type 2) mmol × kg^-1 dm. Conclusion. After exhaustive short-term exercise, a large variation in ATP and IMP contents was evident among single type 1 and type 2 fibres. None of the fibres, however, showed an ATP content lower than 10 mmol × kg^-1 dm. It is suggested that the muscle force loss, demonstrated in the present study, is not attributed to a lowered ATP content per se.     

Skeletal muscle mitochondrial ATP production rate and walking performance in peripheral arterial disease

This study tested the hypotheses that skeletal muscle mitochondrial ATP production rate (MAPR) is impaired in patients with peripheral arterial disease (PAD) and that it relates positively to their walking performances. Seven untrained patients, eight exercise-trained patients and 11 healthy controls completed a maximal walking test and had muscle sampled from the gastrocnemius medialis muscle. Muscle was analysed for its MAPR in the presence of pyruvate, palmitoyl-L-carnitine or both, as well as citrate synthase (CS) activity. MAPRs were not different between untrained PAD and controls. In contrast, MAPRs (pyruvate) were significantly higher in trained PAD vs. controls. MAPR (pyruvate combinations) was also significantly higher in trained than untrained PAD muscle. MAPR and CS activity were highly correlated with walking performance in patients, but not in controls. These data do not support the hypothesis that isolated mitochondria are functionally impaired in PAD and demonstrate that the muscle mitochondrial capacity to oxidize carbohydrate is positively related to walking performance in these patients.     

Metabolic Activity of Skeletal Muscle in Patients with Peripheral Arterial Insufficiency

Abstract. 18 patients with intermittent claudication were studied to find some explanation for the beneficial effect of physical training on their symptoms. The patients were randomly allocated to a training group and a placebo-treated control group. The effect of treatment on serum lipids, muscle lipids and glycogen, walking tolerance, calf blood flow, muscle succinic oxidase activity and the in vitro incorporation rate of glucose-carbon into various metabolites were studied.
In the control group none of these parameters were changed.
In the trained group the following significant changes were found: Walking tolerance improved; muscle contents of cholesterol and phospholipids increased, as did succinic oxidase activity and the incorporation rate of glucose-carbon into glycogen, lipids and carbon dioxide. Incorporation of glucose-carbon into lactate decreased.
The improvement in walking tolerance was correlated with the altered pattern of metabolic activity but was not associated with increased calf blood flow. It is concluded that metabolic changes in skeletal muscles may be important in explaining the beneficial effects of physical training in patients with peripheral arterial insufficiency.     

The Use of Electrically Stimulated Skeletal Muscle to Pump Blood

Electrically stimulated skeletal muscle can be used in many ways to pump blood. The important physiological characteristics of skeletal muscle for use in a cardiac assist role are presented. The force developed by a twitch and tetanic contraction are quantitated and the considerations in the choice of the stimulus applied to the innervating motor nerve are discussed. The importance of stimulus frequency and duration of the stimulus train are presented in terms of the stroke volume produced by skeletal muscle contracting around a pouch. The effect that preload has on pouch stroke volume and muscle blood flow are demonstrated. Finally an example is given in which cardiac output is augmented by an untrained, electrically stimulated, canine rectus abdominis muscle wrapped around a pouch connected between the apex of the left ventricle and the aorta. In this study, the augmentation in cardiac output was measured when the skeletal muscle was contracted after each second, third, and fourth ventricular contraction. The augmentation was 46% +/- 4, 31% +/- 7, and 25% +/- 4, respectively, for the three contraction regimens. Although electrically stimulated skeletal muscle can be used as a power source to assist the failing heart, the optimum application is yet to be discovered. Important considerations in selecting the optimal application are preload, stimulus train duration, train rate, and muscle blood flow.     

有氧训练对衰老小鼠快缩型骨骼肌蛋白质降解的抑制作用研究

目的:探讨规律有氧训练对衰老小鼠骨骼肌蛋白质降解的影响。方法:17月龄雄性C57BL/6小鼠18只据体重随机纳入对照组(C组)与有氧训练组(AE组)。训练组小鼠以自身体重2.5%的负荷进行8周游泳训练,每周训练6天,每天1次,每次45min。末次训练24h后处死全部小鼠,禁食6h。酶联免疫吸附测定血清TNF-α、IL-1β和IL-6含量,荧光法检测类糜蛋白酶与钙蛋白酶活性,对硝基苯磷酸底物法检测酸性磷酸酶活性,免疫印迹法检测泛素蛋白酶体系统关键蛋白Atrogin-1、MuRF-1、Ubquitin及钙蛋白酶系μ-Calpain表达,色谱法检测腓肠白肌内3-MH含量。结果:8周有氧训练可致衰老小鼠腓肠白肌促炎细胞因子含量、类糜蛋白酶与钙蛋白酶活性、3-MH含量以及Atrogin-1、MuRF-1、Ubquitin与μ-Calpain蛋白表达显著下降,且变化具有显著性意义(P=0.000)。但溶酶体酶活性未见组间差异。结论:有氧训练可削弱衰老小鼠快缩型骨骼肌蛋白质降解,可能具有防治衰老性肌肉萎缩发生发展的潜力,其作用机制可能与其削弱炎性细胞因子生成集聚,进而抑制泛素蛋白酶体与钙蛋白酶系统的活性有关。     

有氧运动促进老年前期小鼠快缩型骨骼肌蛋白质合成代谢的研究

目的:探讨中等强度有氧运动对老年前期小鼠快缩型骨骼肌蛋白质合成代谢的保护作用及其可能性机制。方法:20只13月龄雄性CD-1小鼠根据体重随机纳入对照组(C组)与有氧运动干预组(E组),运动组以自体重3%的负荷进行8周游泳训练,每日训练1次,每次45min,每周训练6天。末次运动后24h处死小鼠(禁食17h),采用便携式血糖仪检测血糖,氨基酸分析仪检测血浆游离氨基酸谱,酶联免疫法检测血清胰岛素,BCA法进行蛋白定量,免疫印迹法检测mTOR~(Ser2448)、4E-BP1~(Thr37/46)与p70S6K~(Thr389)磷酸化表达以及MHCⅡ蛋白表达。结果:与对照组(C组)小鼠相比,有氧运动干预组(E组)小鼠血浆游离氨基酸水平表现出下降趋势,其中亮氨酸、谷氨酸与甘氨酸含量下降显著(P0.01)。腓肠白肌蛋白质总量、mTOR~(Ser2448)、4E-BP1~(Thr37/46)、p70S6K~(Thr389)磷酸化表达与MHCⅡ蛋白表达均明显升高,有显著性意义(P0.01)。结论:中等强度有氧运动可以促进老年前期小鼠快缩型骨骼肌蛋白质合成,可能具有削弱衰老性肌肉萎缩发生发展的潜力,其作用机制可能涉及肌细胞内mTOR/p70S6K信号通路的活化。     

Effects of endurance exercise training on risk components for metabolic syndrome,interleukin-6, and the exercise capacity of postmenopausal women

We conducted this study to investigate how an exercise program affects the risk components of metabolic syndrome (MS), serum interleukin (IL)-6 levels, and exercise capacity in postmenopausal women. A randomized clinical trial design was used. Women in an exercise group participated in a treadmill-exercise program for 12 weeks, whereas women in a control group maintained their customary lifestyle. Data on variables were collected at baseline and after 12 weeks of the study, which was completed by 46 women (mean age, 56.0 ± 7.0 y). Our results indicate endurance exercise exerted significant beneficial effects on waist circumference, serum high-density lipoprotein cholesterol (HDL-C) and IL-6 levels, and exercise capacity (all P < 0.05). The beneficial effects on IL-6 and exercise capacity were correlated with improvements in HDL-C levels (r = −0.33, P = 0.03 and r = 0.31, P = 0.04, respectively). Our results suggest that health-care providers can incorporate an exercise program in treatments to improve the health of postmenopausal women.     

高强度间歇游泳训练对衰老小鼠骨骼肌蛋白质合成的影响研究

目的:探讨高强度间歇训练对衰老小鼠快缩骨骼肌蛋白质合成的影响。方法:16月龄雄性C57BL/6小鼠,20只据体重随机纳入对照组(C组)与高强度间歇运动干预组(CE组)。CE组小鼠每周一至五晚七点进行高强度间歇训练,为期8周。训练时小鼠在尾根绑缚相当于10%体重的负荷,游泳20s后休息10s,重复4组。每周增加1组训练,第8周时每次训练12组。实验前及训练后第2、4、6、8周的周日采用抓握力计测定肌力。末次训练24h后处死全部小鼠,同位素示踪法测定腓肠肌蛋白质合成率,Bradford法测定总蛋白、肌原纤维与肌浆蛋白浓度,Western blotting法检测mTOR~(Ser2448)、4E-BP1~(Thr37/46)与p70S6K~(Thr389)磷酸化率及MHCⅡ蛋白表达。结果:8周高强度间歇训练导致腓肠肌蛋白质合成率、肌原纤维、肌浆蛋白质含量及蛋白质总量增加,mTOR~(Ser2448)、p70S6K~(Thr389)及4E-BP1~(Thr37/46)磷酸化率与MHCⅡ蛋白表达均升高,后肢抓握力亦有增长,且变化均具有显著性意义(P=0.000)。结论:高强度间歇训练能够显著促进衰老小鼠腓肠肌骨骼肌蛋白质合成,并最终导致肌力增长,具有干预衰老性肌肉萎缩的潜力,其作用机理涉及骨骼肌内mTOR~(-p70S6K)/4E-BP1的活化。     

Skeletal muscle ischemia–reperfusion injury and cyclosporine A in the aging rat

Old patients exhibit muscle impairments and increased perioperative risk during vascular surgery procedures. Although aging generally impairs protective mechanisms, data are lacking concerning skeletal muscle in elderly. We tested whether cyclosporine A (CsA), which protects skeletal muscle from ischemia–reperfusion (IR) in young rats, might reduce skeletal muscle mitochondrial dysfunction and oxidative stress in aging rats submitted to hindlimb IR. Wistar rats aged 71–73 weeks were randomized to IR (3 h unilateral tourniquet application and 2 h reperfusion) or IR + CsA (10 mg/kg cyclosporine IV before reperfusion). Maximal oxidative capacity (V_Max), acceptor control ratio (ACR), and relative contribution of the mitochondrial respiratory chain complexes II, III, IV (V_Succ), and IV (V_TMPD/Asc), together with calcium retention capacity (CRC) a marker of apoptosis, and tissue reactive oxygen species (ROS) production were determined in gastrocnemius muscles from both hindlimbs. Compared to the nonischemic hindlimb, IR significantly reduced mitochondrial coupling, V_Max (from 7.34 ± 1.50 to 2.87 ± 1.22 μMO₂/min/g; P < 0.05; ?70%), and V_Succ (from 6.14 ± 1.07 to 3.82 ± 0.83 μMO₂/min/g; P < 0.05; ?42%) but not V_TMPD/_Asc. IR also decreased the CRC from 15.58 ± 3.85 to 6.19 ± 0.86 μMCa²⁺/min/g; P < 0.05; ?42%). These alterations were not corrected by CsA (?77%, ?49%, and ?32% after IR for V_Max, V_Succ, and CRC, respectively). Further, CsA significantly increased ROS production in both hindlimbs (P < 0.05; +73%). In old rats, hindlimb IR impairs skeletal muscle mitochondrial function and increases oxidative stress. Cyclosporine A did not show protective effects.