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.     

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.     

The effects of exercise training of different intensities on neuromuscular junction morphology

Summary Little is known about the effects of exercise training on neuromuscular junction morphology in skeletal muscle. The objectives of this investigation were: 1) to determine if exercise training would elicit changes in neuromuscular junction morphology, 2) to determine if exercise training of different intensities would evoke specific changes in neuromuscular junction morphology, and 3) to determine whether changes in neuromuscular junction structure occur independently of changes in muscle fibre type and size. Twenty-four age and size matched male Sprague-Dawley rats were randomly assigned to three groups: high-intensity trained (HIT), low-intensity trained (LIT), or untrained. Neuromuscular junction morphology of the soleus muscle was determined via immunofluorescent staining. Presynaptic acetylcholine vesicles were visualized with SV-2 antibody in conjunction with fluorescein isothiocyanate labelled secondary antibody. Postsynaptic acetylcholine receptors were identified with rhodamine labelled -bungarotoxin. Laser scanning microscopy was used to produce images of synapses, which were used to quantitate the following: total area of SV-2 and -bungarotoxin staining, density of acetylcholine vesicles and receptors, structural complexity, and synaptic coupling. To visualize nerve terminal branching, a smaller number of neuromuscular junctions were stained with C-2 antibody, which reacts with a neurofilament epitope, in conjunction with fluorescein isothiocyanate labelled secondary antibody. Total length of branching, number of branches, average length of branches, and ratio of secondary to primary branches per neuromuscular junction were determined. Citrate synthase activity, fibre type composition and fibre cross-sectional areas of the soleus muscle were assessed to determine the presence of a training effect in that muscle. Results indicate that training did induce hypertrophy of the neuromuscular junction that was independent of muscle hypertorphy. Although the HIT and LIT groups exhibited similar hypertrophic responses of the neuromuscular junction, the HIT group displayed more dispersed synapses than the LIT group. Neither exercise training program, however, resulted in altered densities of acetylcholine vesicles or receptors, nor did training significantly change synaptic coupling. Nerve terminal branching was also affected by exercise training. Neuromuscular junctions from the HIT group demonstrated a greater total length of branching, average length per branch, and number of finer, or secondary, branches than those of the LIT group.     

The effect of high-intensity intermittent swimming on post-exercise glycogen supercompensation in rat skeletal muscle

A single bout of prolonged endurance exercise stimulates glucose transport in skeletal muscles, leading to post-exercise muscle glycogen supercompensation if sufficient carbohydrate is provided after the cessation of exercise. Although we recently found that short-term sprint interval exercise also stimulates muscle glucose transport, the effect of this type of exercise on glycogen supercompensation is uncertain. Therefore, we compared the extent of muscle glycogen accumulation in response to carbohydrate feeding following sprint interval exercise with that following endurance exercise. In this study, 16-h-fasted rats underwent a bout of high-intensity intermittent swimming (HIS) as a model of sprint interval exercise or low-intensity prolonged swimming (LIS) as a model of endurance exercise. During HIS, the rats swam for eight 20-s sessions while burdened with a weight equal to 18% of their body weight. The LIS rats swam with no load for 3 h. The exercised rats were then refed for 4, 8, 12, or 16 h. Glycogen levels were almost depleted in the epitrochlearis muscles of HIS- or LIS-exercised rats immediately after the cessation of exercise. A rapid increase in muscle glycogen levels occurred during 4 h of refeeding, and glycogen levels had peaked at the end of 8 h of refeeding in each group of exercised refed rats. The peak glycogen levels during refeeding were not different between HIS- and LIS-exercised refed rats. Furthermore, although a large accumulation of muscle glycogen in response to carbohydrate refeeding is known to be associated with decreased insulin responsiveness of glucose transport, and despite the fact that muscle glycogen supercompensation was observed in the muscles of our exercised rats at the end of 4 h of refeeding, insulin responsiveness was not decreased in the muscles of either HIS- or LIS-exercised refed rats compared with non-exercised fasted control rats at this time point. These results suggest that sprint interval exercise enhances muscle glycogen supercompensation in response to carbohydrate refeeding as well as prolonged endurance exercise does. Furthermore, in this study, both HIS and LIS exercise prevented insulin resistance of glucose transport in glycogen supercompensated muscle during the early phase of carbohydrate refeeding. This probably led to the enhanced muscle glycogen supercompensation after exercise.     

Vitamin C supplementation does not alter high-intensity endurance training-induced mitochondrial biogenesis in rat epitrochlearis muscle

The purpose of this study was to investigate whether vitamin C supplementation prevents high-intensity intermittent endurance training-induced mitochondrial biogenesis in the skeletal muscle. Male Wistar-strain rats were assigned to one of five groups: a control group, training group, small dose vitamin C supplemented training group, middle dose vitamin C supplemented training group, and large dose vitamin C supplemented training group. The rats of the trained groups were subjected to intense intermittent swimming training. The vitamin C supplemented groups were administrated vitamin C for the pretraining and training periods. High-intensity intermittent swimming training without vitamin C supplementation significantly increased peroxisome proliferator-activated receptor-γ coactivator-1α protein content and citrate synthase activity in the epitrochlearis muscle. The vitamin C supplementation did not alter the training-induced increase of these regardless of the dose of vitamin C supplementation. The results demonstrate that vitamin C supplementation does not prevent high-intensity intermittent training-induced mitochondrial biogenesis in the skeletal muscle.     

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.     

Comparison of the Effects of Physical Exercise,Cold Acclimation and Repeated Injections of Isoprenaline on Rat Muscle Enzymes

The metabolic effects on rat cardiac and skeletal muscle of a strenuous program of swimming, of cold acclimation and of isoprenaline treatment (0.3 mg/kg daily for 5 five-day weeks) were compared. Exercised and cold-exposed rats gained less body weight than did controls or isoprenaline-treated rats. In all treated groups the heart and the interscapular brown adipose tissue hypertrophied. The size of the adrenals increased only in isoprenaline-treated animals. Cold-acclimation and physical training increased and isoprenaline treatment reduced or did not affect the activities of succinate dehydrogenase, rnalate dehydrogenase and citrate synthase of cardiac muscle. In skeletal muscle all treatments resulted in increased activities of these enzymes. Of the anaerobic enzymes analysed, only the activity of hexokinase increased in response to the treatments used. This increase was the same in cardiac as in skeletal muscle, but it was significantly greater with isoprenaline-treatment than with training or with cold-acclimation. The activities of lactate dehydrogenase and phosphofructokinase did not differ significantly. All treatments improved cold resistance, but only swimming exercise and cold acclimation significantly increased tolerance to exercise. It is concluded that prolonged stimulation of adrenergic β-receptors by catecholamines is responsible for the metabolic changes observed.     

中药复方补剂对运动大鼠骨骼肌酶活性的影响

目的研究中药复方补剂对运动大鼠骨骼肌酶活性的影响。方法将40只SD大鼠分为补剂组和对照组,进行游泳运动后每组再分别分为即刻处死组和休息24h再行处死组,用酶组织化学方法染色观察骨骼肌中多种酶活性的变化。结果方剂组的运动鼠骨骼肌酶活性较对照组高（P〈0．05）。结论中药复方补剂能通过提高运动大鼠骨骼肌酶活性来改善骨骼肌细胞的能量供给,从而减缓大鼠体力性疲劳产生和促进大鼠体力性疲劳恢复。     

Comparison of the effects of physical exercise, cold acclimation and repeated injections of isoprenaline on rat muscle enzymes.

The metabolic effects on rat cardiac and skeletal muscle of a strenous program of swimming, of cold acclimation and of isoprenaline treatment (0.3 mg/kg daily for 5 five-day weeks) were compared. Exercised and cold-exposed rats gained less body weight than did controls or isoprenaline-treated rats. In all treated groups the heart and the intercapular brown adipose tissue hypertrophied. The size of the adrenals increased only in isoprenaline-treated animals. Cold-acclimation and physical training increased and isoprenaline treatment reduced or did not affect the activities of succinate dehydrogenase, malate dehydrogenase and citrate synthase of cardiac muscle. In the skeletal muscle all treatments resulted in increased activities of these enzymes. Of the anaerobic enzymes analysed, only the activity of hexokinase increased in response to the treatements used. This increase was the same in cardiac as in skeletal muscle, but it was significantly greater with isoprenaline-treatment than with training or with cold-acclimation. The activities of lactate dehydrogenase and phosphofructokinase did not differ significantly. All treatments improved cold resistance, but only swimming exercise and cold acclimation significantly increased tolerance to exercise. It is concluded that prolonged stimulation of adrenergic beta-receptors by catecholamines is responsible for the metabolic changes observed.     

Effects of high‐intensity intermittent swimming on PGC‐1α 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 γ coactivator‐1α (PGC‐1α) protein in rat skeletal muscle. Methods: We measured PGC‐1α 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‐1α 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‐1α protein content in the muscle was significantly elevated by 84, 95 and 67% respectively. The PGC‐1α 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‐1α 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‐1αprotein, which may induce mitochondrial biogenesis in exercise‐activated skeletal muscle.     

Muscle enzyme adaptation to training and tapering-off in spinal-cord-injured humans

The activity of muscle metabolic enzymes depends on the amount and type of physical training. We examined muscle enzyme adaptation to prolonged training followed by a period of lowered activity in spinal-cord-injured individuals (SCI). Ten SCI [mean age 35 (SEM 2) years , mean body mass 78 (SEM 4) kg, mean time post-injury 12 (SEM 2) years and range of lesion C5–T4] were given 12 months of functional electrical stimulation of an upright cycling motion for 30 min a day, three times a week, followed by 6 months of training once a week. Activities of glycolytic (hexokinase HK, lactate dehydrogenase LDH) and oxidative (citrate synthase CS, 3-hydroxyacyl-CoA dehydrogenase HAD) enzymes were determined in biopsies of the vastus lateralis muscle taken at 0, 3, 6, 12, and 18 months of training. The degree of sympathoadrenergic activity was evaluated from arterial concentrations of catecholamines in response to acute exercise. Training three times a week induced increases (P<0.05) in HK (150%), LDH (40%), CS (100%), and HAD (70%) activities that reached a plateau after 3 months. Peak oxygen uptake and power output during exercise by electrical stimulation rose continuously over the first 12 months. After reducing the amount of training by two-thirds, HK, LDH and CS activities remained elevated above basal levels (P<0.05), whereas HAD, power output and maximal oxygen uptake returned to pretraining levels (P>0.05). It is concluded that most improvements in glycolytic and mitochondrial oxidative enzyme activities induced by long-term training can be maintained in spinal-cord-injured individuals despite a marked reduction in training frequency unrelated to performance or to the degree of sympathoadrenergic impairment. Electronic Publication     

Effects of high-intensity and blood flow-restricted low-intensity resistance training on carotid arterial compliance: role of blood pressure during training sessions

We examined the effects of high-intensity resistance training (HIT) and low-intensity blood flow-restricted (LI-BFR) resistance training on carotid arterial compliance. Nineteen young men were randomly divided into HIT (n = 9) or LI-BFR (n = 10) groups. The HIT and LI-BFR groups performed 75 and 30 %, respectively, of one-repetition maximum (1-RM) bench press exercise, 3 days per week for 6 weeks. During the training sessions, the LI-BFR group wore elastic cuffs around the most proximal region of both arms. Muscle cross-sectional area (CSA), 1-RM strength, and carotid arterial compliance were measured before and 3 days after the final training session. Acute changes in systolic arterial pressure (SAP), plasma endothelin-1 (ET-1), nitrite/nitrate (NOx), and noradrenalin concentrations were also measured during and after a bout of training session. The training led to significant increases (P < 0.01) in bench press 1-RM and arm and chest muscle CSA in the two training groups. Carotid arterial compliance decreased significantly (P < 0.05) in the HIT group, but not in the LI-BFR group. There was a significant correlation (r = ?0.533, P < 0.05) between the change in carotid arterial compliance and the acute change in SAP during training sessions; however, ET-1 and NOx did not correlate with carotid arterial compliance. Our results suggest that muscle CSA and strength increased following 6 weeks of both HIT and LI-BFR training. However, carotid arterial compliance decreased in only the HIT group, and the changes were correlated with SAP elevations during exercise sessions.     

Different metabolic adaptation of heart and skeletal muscles to moderate-intensity treadmill training in the rat

The effect was investigated of treadmill training of moderate intensity on the fatty acid-binding protein (FABP) content in relation to parameters of oxidative and glycolytic metabolism. To this end, the cytoplasmic FABP content and the activity of β-hydroxyacyl-coenzyme A dehydrogenase (HAD), citrate synthase (CS), and 6-phosphofructokinase (PFK) were measured in heart, fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus muscles (SOL) of male Wistar rats. To investigate the influence of the amount of training (defined as the product of exercise duration, intensity and frequency), two training groups were created that differed in training frequency (HF, high frequency 5 days?·?week^?1, n=9; LF, low frequency 2 days?·?week^?1, n?=?9; the exercise being 20?m?·?min^?1 for 2?h with no gradient, over 6 weeks) and compared with SC, sedentary controls (n?=?7). In heart muscle, the cytoplasmic FABP content was 34% higher in HF than in SC but was the same as in LF. The CS and HAD activities were no different in the three groups, suggesting that the capacity to oxidize fatty acids (FA) was not affected by training. The PFK activity was higher (43%) in HF, suggesting a shift towards carbohydrate utilization. The FABP content and HAD activity did not change in SOL and EDL after training whereas the CS activity increased (27%) in SOL and decreased (21%) in EDL in both training groups. In addition, PFK activity in EDL was much higher (113%) in the HF than in SC group. The HF training was associated with a fine-tuning of FA availability and use in heart muscle, and with a more efficient energy production. It is suggested therefore that cytoplasmic FABP could be an early marker of muscle adaptation to training in heart but not in skeletal muscle. The training reinforced the metabolic profile of the skeletal muscles, in particular that of the fast-twitch glycolytic muscle. We concluded that a large amount of training is needed when the effect on both oxidative and glycolytic parameters is to be studied.     

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。     

人参二醇组皂甙及游泳训练对大鼠股四头肌α-肌动蛋白mRNA表达的影响

目的:观察大鼠7周大负荷游泳训练及人参二醇组皂甙(PDS)对大鼠股四头肌α-肌动蛋白mRNA表达的影响。方法:采用Northernblot分析7周大负荷游泳训练后恢复期大鼠股四头肌α-肌动蛋白mRNA表达水平及PDS对其影响。结果:α-肌动蛋白mRNA杂交信号的扫描积分光密度值(A),运动·盐水组较安静组略强;运动·PDS,扫描积分光密度值(A)显著强于运动·盐水组和安静组,运动·甲睾组与运动·盐水组表达无明显差异。结论:PDS可提高长期耐力运动大鼠股四头肌α-肌动蛋白mRNA表达,从而提高耐力运动能力;长期应用外源性雄激素对耐力训练大鼠股四头肌α-肌动蛋白无明显提高,这可能与外源睾酮对内源性睾酮分泌的抑制有关。     

The effects of high-intensity exercise on skeletal muscle neutrophil myeloperoxidase in untrained and trained rats

The primary purpose of this study was to examine the effects of high-intensity acute exercise on neutrophil infiltration in different muscle fiber types of untrained rats and to compare postexercise neutrophil accumulation in muscles of untrained and trained animals. The effect of high-intensity acute exercise on blood neutrophil degranulation reaction in trained animals was also elucidated. Neutrophil enzyme myeloperoxidase (MPO) was determined as a measure of neutrophil migration into muscles and blood neutrophil degranulation. Male albino rats were subjected to acute exercise and 5 weeks of training. The used model of intensive acute exercise consisted of 5, 15, and 25 intermittent swimming bouts with the addition of weight (8% of total body mass) for 1-min each, followed by 1.5-min rest intervals. MPO was analyzed in quadriceps muscle (white and red portion) and in soleus muscle 24 h after acute exercise. MPO content in resting blood plasma and neutrophils was determined 48-h following the completion of a training process. In addition, MPO content in the trained rats was measured immediately (in blood plasma and neutrophils) after and 24 h (in muscles) following a single-bout of exercise to exhaustion. The remaining two-third of the trained animals were exposed to a single-bout of nonstop swimming with the addition of 6% body mass until exhaustion. These animals were sacrificed immediately and 24 h after loaded swimming to analyze leukocyte count, MPO content in blood plasma and neutrophils and in muscles, respectively. About 24 h after exercise MPO concentrations in the red portion of quadriceps muscle and in soleus muscle were 4–7-fold higher as compared to the white portion of m. quadriceps. There was an association between the quantity of repetitive bouts of swimming and MPO content in the muscles. The duration of swimming to exhaustion of trained rats was 3.8-fold longer than untrained sedentary control. At rest, plasma MPO concentration was found to be 40% higher in trained rats compared to untrained controls (P < 0.05). Postexercise plasma MPO concentrations were significantly higher both in untrained (+137%; P < 0.05) and trained (+81%; P < 0.05) rats compared to resting values. At rest neutrophil MPO concentration was found to be 33% lower in trained rats compared to untrained controls (P < 0.05). There were no significant differences in muscle MPO concentrations between untrained and trained rats at rest. A single-bout of exercise to exhaustion produced a greater increase in MPO content in untrained compared to trained rats. The data suggest that postexercise neutrophil infiltration is more intensive in red fibers types compared to white fiber types. A smaller neutrophil infiltration in muscles of trained animals after exhaustive exercise suggests a protective effect of previous training to muscle injury.Portions of this paper were presented by V. Morozov in 2003 at the 6th ISEI Symposium on Exercise Muscle Metabolism and Immune Function, Copenhagen.