Effect of high-intensity intermittent swimming training on fatty acid oxidation enzyme activity in rat skeletal muscle

We previously reported that high-intensity exercise training significantly increased citrate synthase (CS) activity, a marker of oxidative enzyme, in rat skeletal muscle to a level equaling that attained after low-intensity prolonged exercise training (Terada et al., J Appl Physiol 90: 2019-2024, 2001). Since mitochondrial oxidative enzymes and fatty acid oxidation (FAO) enzymes are often increased simultaneously, we assessed the effect of high-intensity intermittent swimming training on FAO enzyme activity in rat skeletal muscle. Male Sprague-Dawley rats (3 to 4 weeks old) were assigned to a 10-day period of high-intensity intermittent exercise training (HIT), low-intensity prolonged exercise training (LIT), or sedentary control conditions. In the HIT group, the rats repeated fourteen 20 s swimming sessions with a weight equivalent to 14-16% of their body weight. Between the exercise sessions, a 10 s pause was allowed. Rats in the LIT group swam 6 h/day in two 3 h sessions separated by 45 min of rest. CS activity in the triceps muscle of rats in the HIT and LIT groups was significantly higher than that in the control rats by 36 and 39%, respectively. Furthermore, 3-beta hydroxyacyl-CoA dehydrogenase (HAD) activity, an important enzyme in the FAO pathway in skeletal muscle, was higher in the two training groups than in the control rats (HIT: 100%, LIT: 88%). No significant difference in HAD activity was observed between the two training groups. In conclusion, the present investigation demonstrated that high-intensity intermittent swimming training elevated FAO enzyme activity in rat skeletal muscle to a level similar to that attained after 6 h of low-intensity prolonged swimming exercise training.     

Effects of nonexhaustive bouts of high-intensity intermittent swimming training on GLUT-4 expression in rat skeletal muscle

We previously reported that 14 bouts of exhaustive high-intensity intermittent training [20 s periods of swimming while carrying a weight (14% of body weight), separated by pauses of 10 s] is the highest stimuli in terms of exercise training-induced glucose transporter 4 (GLUT-4) expression in rat epitrochlearis (EPI) muscles. In the present study, we found that the GLUT-4 protein content in the skeletal muscle of male Sprague-Dawley rats (age 5 weeks old; body weight 90–110 g) that underwent intermittent exercise training of 3 and 14 bouts of 20 s swimming for 5 days was increased over age-matched sedentary control rats by 75 and 71%, respectively, 18 h after the last bout of exercise. These results suggest that GLUT-4 content in rat EPI muscle increases dramatically after very short (60 s) and nonexhaustive high-intensity intermittent exercise training.     

Skeletal muscle and hormonal adaptation to physical training in the rat: role of the sympatho-adrenal system

The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training-induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague-Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham-operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h X day-1, 4 days X week-1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochrome c oxidase, and 3-hydroxyacyl-CoA dehydrogenase. In sham-operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training-induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham-operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training-induced increase in muscle mitochondrial enzymes. The training-induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.     

大强度耐力运动抑制骨骼肌线粒体的生物合成

背景：耐力运动对骨骼肌线粒体生成影响的研究多采用中小强度,长期大强度对其有何影响还不清楚,这种影响是否涉及5’-一磷酸腺苷激活的蛋白激酶(AMPK)、沉默信息调节因子2相关酶1(SIRT1)等调节线粒体生成的信号分子也未见报道。 目的：观察AMPK/SIRT1信号级联在7周不同强度耐力运动中对骨骼肌线粒体生物合成的影响。 方法：42只雄性SD大鼠分为安静组、中等强度运动组和大强度运动组。运动负荷为中等强度组28 m/min,60 min/d、大强度组38 m/min,60 min/d,每周运动5 d,休息2 d,共7周。运动组动物分别在运动后即刻、6 h和24 h取材。荧光定量PCR检测骨骼肌PGC-1α 、SIRT1基因表达,Western blot测定P-AMPK、SIRT1蛋白表达。 结果与结论：①中等强度运动后即刻、6 h、24 h,骨骼肌PGC-1α mRNA表达分别为安静组的362%(P < 0.01)、657%(P < 0.01)、116%,P-AMPK蛋白表达分别为安静组的112%、163%(P < 0.05)、129%(P < 0.05),SIRT1蛋白和mRNA表达分别为安静组的55%(P < 0.05)、86%、103%和109%、155%(P < 0.05)、132%(P < 0.05)。②大强度运动后即刻、6 h、24 h,骨骼肌PGC-1α mRNA表达分别为安静组的274%(P < 0.01)、130%(P < 0.05)、68%(P < 0.05),P-AMPK蛋白表达分别为安静组的235%(P < 0.01)、166%(P < 0.05)、160%(P < 0.05),SIRT1蛋白和mRNA表达分别为安静组的199%(P < 0.01)、166%(P < 0.05)、164%(P < 0.05)和255%(P < 0.01)、292%(P < 0.01)、122%。结果表明：①7周中等强度耐力运动显著增加骨骼肌PGC-1α基因表达,其机制可能涉及AMPK/SIRT1信号级联。②7周大强度耐力运动造成骨骼肌PGC-1α基因表达在运动后24 h时被抑制,这一过程是以非AMPK/SIRT1信号级联依赖性方式进行的。 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     

运动性过氧化物酶体增殖物受体γ共激活因子1α的变化机制

背景：研究发现,过氧化物酶体增殖物受体γ共激活因子1α可能在运动诱导骨骼肌的适应机制起着重要的作用,参与调节运动诱导多种生物学反应过程。 目的：综述过氧化物酶体增殖物受体γ共激活因子1α与运动性骨骼肌的适应机制相关方面的研究。 方法：以PGC1α,skeletal muscle,exercise,mitochondrial biogenesis,adaptations为检索词,检索Pubmed数据库(1995年1月至2010年10月)。文献检索语种限制为英文。纳入过氧化物酶体增殖物受体γ共激活因子1α与运动性骨骼肌适应的相关的内容,排除重复性研究。计算机初检得到59篇文献,根据纳入排除标准,对37篇进行分析。 结果与结论：耐力训练可增加骨骼肌膜的转运蛋白的表达、线粒体代谢酶的活性和毛细血管的密度等,从而增加骨骼肌氧化能力,提高碳水化合物和脂肪酸的氧化能力。氧化物酶体增殖物受体γ共激活因子1α基因敲除或过表达转基因小鼠研究表明在维持骨骼肌线粒体代谢和抗氧化酶表达,氧化物酶体增殖物受体γ共激活因子1α起着重要的作用。氧化物酶体增殖物受体γ共激活因子1α影响运动性线粒体蛋白的适应。但是,氧化物酶体增殖物受体γ共激活因子1α不是惟一的因素,其他的一些因素同样涉及到基础的表达和运动性骨骼肌的适应机制。运动诱导氧化物酶体增殖物受体γ共激活因子1α表达和活性的提高可能是运动性线粒体的适应一个机制,合理体力活动可获得健康的效果。 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;组织工程全文链接：     

Stimulation of HSP72 expression following ATP depletion and short-term exercise training in fast-twitch muscle

AIM: Previous data have reported increases in HSP72 expression in skeletal muscles after endurance training but the physiological and biochemical signals that induce HSP72 accumulation remain largely unknown. In this study, we tested the hypothesis that energy status is a key regulatory event for HSP72 accumulation in skeletal muscles. METHODS: Reduction of high-energy phosphate levels was induced by supplementation with a creatine analogue, beta-guanidinopropionic acid (GPA) for 3 weeks while control rats received distilled water in the same conditions. Half of the animals were kept sedentary while the others were submitted to a short-term (2 weeks) training program on a treadmill (30 m min-1, 0% slope; 50-70 min day-1). RESULTS: GPA supplementation resulted in a large drop ( approximately 50%) in adenosine triphosphate (ATP) level in both fast and slow muscles whether the animals were trained or remained sedentary. HSP72 level did not change with GPA alone, but the training-induced increase in HSP72 level was strongly enhanced by superimposition of GPA diet in fast but not in slow skeletal muscles. The changes in HSP72 level were not linked to changes in fibre typology and/or mitochondrial capacities. CONCLUSIONS: The results of the present investigation indicate that levels of high-energy phosphate per se do not play a direct role in determining HSP72 level in skeletal muscles. However, during superimposition of training to GPA, then the adaptive strategy of fast-twitch muscle (e.g. plantaris) seems to be directed towards appearance of some properties of red, oxidative fibres (increase in oxidative capacities and HSP72 level).     

Attenuating the decline in ATP arrests the exercise training-induced increases in muscle GLUT4 protein and citrate synthase activity

Thirty-two female Sprague-Dawley rats were assigned to one of four groups: control (CON); exercise training (TR); exercise training + clenbuterol treatment (0.8 mg kg body wt(-1) d(-1)) (TR + CL) or exercise training + clenbuterol treatment + 2% beta-guanidinoproprionic acid diet (TR + CL + beta) to examine whether alterations in the high energy phosphate state of the muscle mediates exercise training-induced increases in skeletal muscle GLUT4 protein concentration and citrate synthase activity. Exercise training consisted of running the rats 5 d week(-1) for 8 weeks on a motor-driven treadmill (32 m min(-1), 15% grade). Gastrocnemius GLUT4 protein concentration and citrate synthase activity were significantly elevated in the TR animals, but these adaptations were attenuated in the TR + CL animals. Providing beta-GPA in combination with clenbuterol enabled training to elevate GLUT4 protein concentration and citrate synthase activity, with the increase in GLUT4 being greater than that observed for the TR animals. Skeletal muscle ATP levels were reduced in the TR + CL + beta animals while ATP levels in the TR + CL animals were significantly elevated compared with CON. An acute 40-min bout of electrical stimulation of the sciatic nerve was found to lower skeletal muscle ATP levels by approximately 50% and elevate cAMP levels in all groups. No difference in post-contraction cAMP levels were observed among groups. However, post-contraction ATP levels in the TR + CL animals were significantly greater than the other groups. Collectively, these findings suggest that exercise training-induced increases in skeletal muscle GLUT4 protein concentration and citrate synthase activity are initiated in response to a reduction in the skeletal muscle ATP concentration.     

骨骼肌细胞线粒体通透性转换孔及bcl-2和bax mRNA表达与运动

背景：运动影响骨骼肌细胞的凋亡,而线粒体途径是介导细胞凋亡的一个重要途径。 目的：研究运动对大鼠骨骼肌线粒体通透性转换孔、凋亡调控基因bcl-2和bax表达的影响。 方法：将24只成年雄性SD大鼠随机分为3组：对照组正常饲养,6周游泳训练组进行6周的游泳训练,每周6次,一次性游泳力竭组于第6周进行一次力竭性游泳运动。应用紫外分光光度仪检测各组大鼠骨骼肌线粒体通透性转换孔的开放情况,应用RT-PCR测定大鼠骨骼肌bcl-2和bax mRNA的表达。 结果与结论：与对照组比较,6周游泳训练组大鼠骨骼肌线粒体通透性转换孔的开放程度变化不明显,bcl-2 mRNA的表达显著增加,bax mRNA的表达显著减少,bcl-2/bax mRNA比值显著增大(P < 0.01)。与对照组比较,一次性游泳力竭组大鼠骨骼肌线粒体通透性转换孔开放程度明显增加(P< 0.01),bcl-2 mRNA的表达显著减少,bax mRNA的表达显著增加,bcl-2/bax mRNA比值显著减小(P< 0.01)。说明运动训练可通过改变线粒体通透性转换孔的开放、调节bcl-2/bax表达,调控骨骼肌细胞凋亡。     

Effects of high-intensity intermittent swimming on PGC-1alpha protein expression in rat skeletal muscle

AIM: The aim of the present investigation was to elucidate the effects of exercise intensity on exercise-induced expression of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) protein in rat skeletal muscle. METHODS: We measured PGC-1alpha content in the skeletal muscles of male Sprague-Dawley rats (age: 5-6 weeks old; body weight: 150-170 g) after a single session of high-intensity intermittent exercise (HIE) or low-intensity prolonged swimming exercise (LIE). During HIE, the rats swam for fourteen 20-s periods carrying a weight (14% of body weight), and the periods of swimming were separated by a 10-s pause. LIE rats swam with no load for 6 h in two 3-h sessions, separated by 45 min of rest. RESULTS: After HIE, the PGC-1alpha protein content in rat epitrochlearis muscle had increased by 126, 140 and 126% at 2, 6 and 18 h, respectively, compared with that of the age-matched sedentary control rats' muscle. Immediately, 6 and 18-h after LIE, the PGC-1alpha protein content in the muscle was significantly elevated by 84, 95 and 67% respectively. The PGC-1alpha protein content observed 6 h after HIE tended to be higher than that observed after LIE. However, there was no statistically significant difference between the two values (P = 0.12). CONCLUSION: The present investigation suggests that irrespective of the intensity of the exercise, PGC-1alpha protein content in rat skeletal muscle increases to a comparable level when stimuli induced by different protocols are saturated. Further, HIE is a potent stimulus for enhancing the expression of PGC-1alpha protein, which may induce mitochondrial biogenesis in exercise-activated skeletal muscle.     

Effect of Vitamin C Supplements on Antioxidant Defence and Stress Proteins in Human Lymphocytes and Skeletal Muscle

Oxidative stress induces adaptations in the expression of protective enzymes and heat shock proteins (HSPs) in a variety of tissues. We have examined the possibility that supplementation of subjects with the nutritional antioxidant, vitamin C, influences the ability of lymphocytes to express protective enzymes and HSPs following exposure to an exogenous oxidant and the response of skeletal muscle to the physiological oxidative stress that occurs during exercise in vivo . Our hypothesis was that an elevation of tissue vitamin C content would reduce oxidant-induced expression of protective enzymes and HSP content. Lymphocytes from non-supplemented subjects responded to hydrogen peroxide with increased activity of superoxide dismutase (SOD) and catalase, and HSP60 and HSP70 content over 48 h. Vitamin C supplementation at a dose of 500 mg day⁻¹ for 8 weeks was found to increase the serum vitamin C concentration by ∼50 %. Lymphocytes from vitamin C-supplemented subjects had increased baseline SOD and catalase activities and an elevated HSP60 content. The SOD and catalase activities and the HSP60 and HSP70 content of lymphocytes from supplemented subjects did not increase significantly in response to hydrogen peroxide. In non-supplemented subjects, a single period of cycle ergometry was found to significantly increase the HSP70 content of the vastus lateralis. Following vitamin C supplementation, the HSP70 content of the muscle was increased at baseline with no further increase following exercise. We conclude that, in vitamin C-supplemented subjects, adaptive responses to oxidants are attenuated, but that this may reflect an increased baseline expression of potential protective systems against oxidative stress (SOD, catalase and HSPs).     

Exercise training in late middle-aged male Fischer 344 x Brown Norway F1-hybrid rats improves skeletal muscle aerobic function.

The Fischer 344 x Brown Norway F1-hybrid (F344BN) rat has become an increasingly popular and useful strain for studying age-related declines in skeletal muscle function because this strain lives long enough to experience significant declines in muscle mass. Since exercise is often considered a mechanism to combat age-related declines in muscle function, determining the utility of this strain of rat for studying the effects of exercise on the ageing process is necessary. The purpose of this study was to evaluate the plasticity of skeletal muscle aerobic function in late middle-aged male rats following 7 weeks of treadmill exercise training. Training consisted of 60 min per day, 5 days per week with velocity gradually increasing over the training period according to the capabilities of individual rats. The final 3 weeks involved 2 min high-intensity intervals to increase the training stimulus. We used in situ skeletal muscle aerobic metabolic responses and in vitro assessment of muscle mitochondrial oxidative capacity to describe the adaptations of aerobic function from the training. Training increased running endurance from 11.3 +/- 0.6 to 15.5 +/- 0.8 min, an improvement of approximately 60%. Similarly, distal hindlimb muscles from trained rats exhibited a higher maximal oxygen consumption in situ (23.2 +/- 1.3 versus 19.7 +/- 0.8 mumol min(-1) for trained versus sedentary rats, respectively) and greater citrate synthase and complex IV enzyme activities in gastrocnemius (29 and 19%, respectively) and plantaris muscles (24 and 28%, respectively) compared with age-matched sedentary control animals. Our results demonstrate that skeletal muscles from late middle-aged rats adapt to treadmill exercise by improving skeletal muscle aerobic function and mitochondrial enzyme activities. This rat strain seems suitable for further investigations using exercise as an intervention to combat ageing-related declines of skeletal muscle aerobic function.     

Effect of alpha-lipoic acid supplementation on trace element levels in serum and in postmitotic tissue in aged rats

Redistribution of redox-active divalent metal ions (e.g. copper, zinc, and iron) in postmitotic tissues of lipoic acid supplemented aging rats has been proposed to contribute to metal-catalyzed protein oxidation. DL-alpha lipoic acid (LA) (100 mg/kg body wt/day) was administered intraperitoneally to the Sprague-Dawley rats for 14 days. Serum copper levels lowered in the aged rats with LA supplementation compared to the rats without LA supplementation. On the other hand, serum zinc and iron levels increased in the aged rats with LA supplementation compared to the rats without LA supplementation. Copper levels of the postmitotic tissues were not changed in the aged rats with LA supplementation compared to the controls. The heart zinc levels detected in LA supplemented rats were significantly lower than controls. Similarly, the iron levels of the heart were found to be significantly lower in LA supplemented rats when compared to control rats. LA supplementation did not affect brain and muscle iron levels. The brain and muscle zinc levels remained the same in both group of rats. Based on the findings of our study, we have concluded that LA may exhibit prooxidant effect depending on the altered trace element homeostasis. Therefore, our results emphasize the importance of monitoring the dose of LA supplementation, duration of treatment and its potential harmful effects in the postmitotic tissues of aged rats.     

AT1 receptors are necessary for eccentric training-induced hypertrophy and strength gains in rat skeletal muscle

This study was undertaken to measure the response of skeletal muscle to eccentric contractions (EC) in the presence of the angiotensin type 1 (AT1) receptor blocker, losartan. It was hypothesized that blocking AT1 receptors prior to an initial bout of EC would prevent the muscle from developing the normal adaptation to EC as demonstrated by the repeated bout effect. It was also hypothesized that continuous AT1 receptor blockade during EC training would significantly reduce muscle hypertrophy and strength gains that occur with repeated EC. Rats received losartan in their drinking water at either a low dose (20 mg (kg body weight)-1 day-1) or a high dose (40 mg (kg body weight)-1 day-1). Each bout of EC consisted of a total of 24 contractions. Rats were assigned to four groups: a single acute bout of EC (n=6); two bouts of EC separated by 14 days (n=8); and 4 weeks of training twice a week on the low dose (n=5) or the high dose (n=9). There was no effect of AT1 receptor blockade on the initial loss of function following a single acute bout of EC, or on the repeated bout effect following a second exposure to EC. AT1 receptor blockade did alter the results of EC training, in both the low and high dose groups. Losartan treatments prevented EC training-induced increases in muscle wet and dry weights compared to untreated rats. Finally, the low and high dose losartan treatments also prevented an increase in muscle contractile force following EC training compared to the untreated group. Functional AT1 receptors are therefore not necessary for an acute adaptation to EC as demonstrated by the repeated bout effect, but are necessary for muscle hypertrophy and increased contractile force associated with EC training.     

骨骼肌细胞αB-晶状体蛋白基因在大强度离心运动后的表达

背景：骨骼肌含有被称为“分子伴侣”的小热休克蛋白αB-晶状体蛋白,有可能在肌肉运动中具有重要的生理功能。 目的：观察离心运动后骨骼肌细胞αB-晶状体蛋白基因表达。 方法：将成年雄性Wistar大鼠随机分为安静对照组和运动后即刻组,运动后24 h组。安静对照组正常喂养,两个运动组进行一次性大负荷离心运动,分别取对照组腓肠肌和运动组运动后0和24 h的腓肠肌,使用冰冻切片原位杂交法检测αB-晶状体蛋白基因表达情况。 结果与结论：骨骼肌细胞αB-晶状体蛋白基因在对照组呈低水平表达,在运动后即刻和运动后24 h组均呈较高表达 (P < 0.05),αB-晶状体蛋白基因表达杂交信号主要位于肌细胞膜下。结果证实,大强度离心运动可诱导骨骼肌细胞αB-晶状体蛋白基因表达增高。     

Hypoxia preconditioning by cobalt chloride enhances endurance performance and protects skeletal muscles from exercise-induced oxidative damage in rats

Aim: Training under hypoxia has several advantages over normoxic training in terms of enhancing the physical performance. Therefore, we tested the protective effect of hypoxia preconditioning by hypoxia mimetic cobalt chloride against exercise-induced oxidative damage in the skeletal muscles and improvement of physical performance. Method: Male Sprague–Dawley rats were randomly divided into four groups (n = 8), namely control, cobalt-supplemented, training and cobalt with training. The red gastrocnemius muscle was examined for all measurements, viz. free radical generation, lipid peroxidation, muscle damage and antioxidative capacity. Results: Hypoxic preconditioning with cobalt along with training significantly increased physical performance (33%, P < 0.01) in rats compared with training-only rats. Cobalt supplementation activated cellular oxygen sensing system in rat skeletal muscle. It also protected against training-induced oxidative damage as observed by an increase in the GSH/GSSG ratio (36%, P < 0.001; 28%, P < 0.01 respectively) and reduced lipid peroxidation (15%, P < 0.01; 31%, P < 0.01 respectively) in both trained and untrained rats compared with their respective controls. Cobalt supplementation along with training enhanced the expression of antioxidant proteins haem oxygenase-1 (HO-1; 1.2-fold, P < 0.05) and metallothionein (MT; 4.8-fold, P < 0.001) compared with training only. A marked reduction was observed in exercise-induced muscle fibre damage as indicated by decreased necrotic muscle fibre, decreased lipofuscin content of muscle and plasma creatine kinase level (16%, P < 0.01) in rats preconditioned with cobalt. Conclusion: Our study provides strong evidence that hypoxic preconditioning with cobalt chloride enhances physical performance and protects muscle from exercise-induced oxidative damage via GSH, HO-1 and MT-mediated antioxidative capacity.     

Effects of thyroid hormone administration on skeletal muscle mitochondria.

The effects of thyroid hormone administration on the levels of a number of mitochondrial markers were measured in skeletal muscle and liver of normal rats. Injection of 18 mug of L-thyroxine (T4) per 100 g body wt every 4th day for 3 wk had no effect on the concentrations of cytochrome c, on citrate synthase activity, or on respiratory capacity of skeletal muscle. Injection of 200 mug of L-triiodothyronine (T3) daily for 5 days, or feeding 23 mg T4 and 7 mg T3/kg of diet for 2 wk, resulted in thyrotoxicosis and large increases in the activity of hepatic alpha-glycerophosphate dehydrogenase and other mitochondrial markers; however, the levels of activity of mitochondrial marker enzymes in gastrocnemius and quadriceps muscles were not significantly changed. Only when rats were fed 3 mg T4 and 1 mg T3/kg diet for a 6-wk period did we observe an increase in skeletal muscle mitochondrial markers. Thus, thyroxine treatment must be sufficiently prolonged if it is to be used as a tool for studying skeletal muscle mitochondrial biogenesis.     

Effect of dehydroepiandrosterone administration on recovery from mix-type exercise training-induced muscle damage

This study aimed to determine the role of DHEA-S in coping against the exercise training mixing aerobic and resistance components. During 5-day successive exercise training, 16 young male participants (19.2 ± 1.2 years) received either a placebo (flour capsule) or DHEA (100 mg/day) in a double-blinded and placebo-controlled design. Oral DHEA supplementation significantly increased circulating DHEA-S by 2.5-fold, but a protracted drop (~35 %) was observed from Day 3 during training. In the Placebo group, only a minimal DHEA-S reduction (~17 %) was observed. Changes in testosterone followed a similar pattern as DHEA-S. Muscle soreness was elevated significantly on Day 2 for both groups to a similar extent. Lower muscle soreness was observed in the DHEA-supplemented group on Day 3 and Day 6. In the Placebo group, training increased circulating creatine kinase (CK) levels by approximately ninefold, while only a threefold increase was observed in the DHEA-supplemented group. This mix-type exercise training improved glucose tolerance in both groups, while lowering the insulin response to the glucose challenge, but no difference between treatments was observed. Our results suggest that DHEA-S may play a role in protecting skeletal muscle from exercise training-induced muscle damage.     

中等强度训练干预大鼠骨骼肌抗增殖蛋白PHB1表达及线粒体呼吸功能的变化

背景:研究显示长期中等强度规律运动可以改善骨骼肌细胞线粒体电子呼吸链复合体酶的活性,从而提高其做功能力和抵抗疲劳能力。目的:探讨中等强度训练对大鼠骨骼肌内抗增殖蛋白及线粒体呼吸功能的影响。方法:32只健康雄性SD大鼠随机分为2组:安静对照组、中等强度训练组,每组16只。中等强度训练组的训练方案:第1周以10 m/min速度跑,每周6 d,每天10 min,坡度10°;第2周以15 m/min速度跑,每周6 d,每天增加10 min至60 min结束,坡度10°;第3-8周以15 m/min速度跑,每周6 d,每天60 min,坡度10°。末次实验后48 h处死大鼠,提取骨骼肌以及线粒体,检测线粒体呼吸控制率、ATP含量、活性氧水平、复合体V活性及PHB1蛋白表达。结果与结论:①与安静对照组相比,中等强度训练组骨骼肌线粒体呼吸控制率显著性升高(P<0.001)、ATP含量显著性升高(P<0.05)、活性氧水平显著降低(P<0.001)、复合体V活性显著升高(P<0.05)、PHB1表达显著升高(P<0.01);②通过相关性分析得出:经过8周中等强度训练后大鼠骨骼肌内PHB1的表达分别与ATP含量、复合体V活性呈正相关,与活性氧水平呈负相关;③结果表明,中等强度训练通过促进PHB1表达提高线粒体氧化磷酸化功能,维持线粒体膜结构,增强线粒体呼吸功能。     

Resveratrol and/or exercise training counteract aging-associated decline of physical endurance in aged mice; targeting mitochondrial biogenesis and function

Mitochondrial dysfunction and decreased mitochondrial content are hallmarks of aging that leads to decreased physical endurance. Our aim was to explore the anti-aging effect of resveratrol (RSVT) supplementation, a polyphenol, and/or exercise training, started at an older age, on improving physical activity, therefore, help in frailty avoidance and promotion of healthy aging in elderly. Eighteen-month-old aged mice received RSVT (15 mg/kg/day) and/or exercise trained for 4 weeks showed significant longer time to exhaustion with decreased blood lactate and free fatty acids levels associated with improved oxidative stress evidenced by decreased gastrocnemius muscle lipid peroxidation and increased antioxidant enzymes activities, catalase and superoxide dismutase, when compared to aged mice control group. These changes were accompanied by over-expression of skeletal muscle peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) mRNA, the master regulator of mitochondrial biogenesis, and increased muscle citrate synthase activity, a marker for mitochondrial function. These findings may provide evidence for improved physical endurance by RSVT supplementation or exercise training with better results of their combination, even at an older age, through increasing mitochondrial biogenesis and function. Increased muscle PGC-1α mRNA expression and citrate synthase enzyme activity in addition to improved aging-associated oxidative damage were among the mechanisms involved in this protection.