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.     

Commentary on the reduced urinary noradrenaline excretion following cold stress and exercise in physically trained rats

Urinary catecholamine excretions of rats trained by swimming or running were compared with those of cold-acclimated rats and controls i.e. sedentary warm-acclimated rats. During cold stress the trained rats excreted less noradrenaline (NA) than did controls. In fact rats trained by swimming excreted less NA than did cold-acclimated rats. while rats trained by running excreted about the same amount as did cold-acclimated rats. 2 h of swimming increased the urinary catecholamine (CA) exretions of all groups but trained rats excreted less NA than did controls and cold-acclimated rats. which had excretions of similar magnitude. The NA excretions of the two trained groups never deviated statistically from each other. It is concluded that concerning NA requirement in order to maintain homeostasis, training produces “cross tolerance” to cold stress but cold-acclimation does not produce “cross tolerance” to acute exercise. Furthermore the positive effect of training on NA excretion during the stress of cold or that of acute exercise seems essentially to be an effect of increased locomotor activity as such regardless of the type of training. It is also suggested that increased levels of locomotor activity of the rat may be of importance for seasonal acclimation of the species by increasing its tolerance to cold.     

Skeletal muscle and heart antioxidant defences in response to sprint training

Although endurance training enhances the antioxidant defence of different tissues, information on the effect of sprint training is scanty. We examined the effect of sprint training on rat skeletal muscle and heart antioxidant defences. Male Wistar rats, 16–17 weeks old, were sprint trained on a treadmill for 6 weeks. Total glutathione levels and activities of glutathione peroxidase, glutathione reductase, glutathione S-transferase and superoxide dismutase in heart and various skeletal muscles were compared in trained and control sedentary animals. Lactate dehydrogenase and citrate synthase enzyme activities were measured in muscle to test the effects of training on glycolytic and oxidative metabolism. Sprint training significantly increased lactate dehydrogenase activity in predominantly fast glycolytic muscles and enhanced total glutathione contents of the superficial white quadriceps femoris, mixed gastrocnemius and fast-glycolytic extensor digitorum longus muscles. Oxidative metabolic capacity increased in plantaris muscle only. Compared with the control group, glutathione peroxidase activities in gastrocnemius, extensor digitorum longus muscles and heart also increased in sprint trained rats. Glutathione reductase activities increased significantly in the extensor digitorum longus muscle and heart. Glutathione S-transferase activity was also higher in the sprint trained extensor digitorum longus muscle. Sprint training did not influence glutathione levels or glutathione-related enzymes in the soleus muscle. Superoxide dismutase activity remained unchanged in skeletal muscle and heart. Sprint training selectively enhanced tissue antioxidant defences by increasing skeletal muscle glutathione content and upregulating glutathione redox cycle enzyme activities in fast and mixed fibre leg muscles and heart.     

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.     

Dissociation of the effects of training on oxidative metabolism,glucose utilisation and GLUT4 levels in skeletal muscle of streptozotocin-diabetic rats

The effects of long-term, moderate physical exercise on in vivo glucose uptake, levels of two glucose transporter proteins (GLUT1 and GLUT4) and activities of various key enzymes of energy metabolism were measured in skeletal muscle from streptozotocin-diabetic rats. Diabetes (12–16 weeks) reduced the in vivo glucose uptake (glucose metabolic index, GMI) in muscle containing mainly type I fibres by 55% but had no effect in muscles containing mainly type IIa and IIb fibres. GMI was increased in the diabetic white skeletal muscle (mainly type IIb fibres) by more than 120%. In contrast to the complex changes in GMI, GLUT4 levels were reduced in all types of skeletal muscle from diabetic rats with no change in GLUT1 levels. Exercise training had no effects on GMI or the glucose transporter levels. Streptozotocin induced diabetes significantly reduced the oxidative capacity of skeletal muscle assayed as the activities of citrate synthase, succinate dehydrogenase and cytochrome c oxidase. Training increased the activities of oxidative enzymes, with this increase being more prominent in the diabetic animals. The present data indicate that long-term streptozotocin-induced diabetes decreases oxidative metabolic capacity and GLUT4 protein levels in skeletal muscle, but that the changes of glucose transport largely depend on the fibre type composition. Moderate training fully reverses the effect of insulinopenia and hyperglycaemia on muscle oxidative metabolism. In contrast to the previous suggestions, the expression of GLUT4 is not correlated with the capacity of oxidative metabolism in skeletal muscle of streptozotocin-diabetic rats.     

Is swimming exercise or cold exposure for rats?

Rats were trained by daily swimming sessions (up to 3 h per day) for at least 6 weeks in water at 30, 36 and 38 degrees C. After this training, the adaptive changes obtained were compared with those typical of cold-acclimated (cold-specific changes) and running-trained (training-specific changes) rats. The most typical training-specific change, an increased activity of oxidative muscle enzymes was negligible for swimming-trained rats, while the lowered activity of muscle lactate dehydrogenase was evident for all trained groups. Cold-specific changes, such as increased food intake, increased calorigenic response to injected noradrenaline, an increase both in mass and metabolic capacity of brown adipose tissue, and maintenance of the stores of ascorbic acid and muscle glycogen during cold exposure, were observed for rats trained at 36 and 30 degrees C. The cold tolerance test in cold air did not make any distinct difference between the rats trained at different water temperatures, while in cool water the 30 degrees C -swimmers were clearly superior to other groups, that is, their cooling rate was slowest. Other adaptive changes were found, to a variable extent, for all trained groups. These included loss of body fat, cardiac hypertrophy, reduced urinary catecholamine excretion after test swimmings either in cold or warm water, increased tail-skin temperature response to isoprenaline, and a higher tail-skin temperature in response to cold. Generally, however, the adaptive changes observed for 30- and 36 degrees C-swimmers were similar, while the changes observed for 38 degrees C-swimmers were different. The latter group neither displayed any cardiac enlargement nor any cold-specific changes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of 8 weeks' endurance training on skeletal muscle metabolism in 56–70-year-old sedentary men

Summary The effects of 8 weeks' endurance training on muscle metabolism at rest and after a submaximal bicycle ergometer exercise were studied in 31 previously sedentary men, aged 56–70. Training consisted of 3–5 one hour exercise bouts per week including walking-jogging, swimming, gymnastics and ball games. The effects of training were similar to those previously reported for younger men. Mean maximal oxygen uptake increased (11%), as did the resting values for muscle glycogen concentration, the enzymes representing aerobic energy metabolism (malate dehydrogenase, succinate dehydrogenase), and also some of the anaerobic enzymes (creatine phosphokinase, lactate dehydrogenase). Lactate production during submaximal work decreased. The enzyme activities were lower following acute exercise both before and after training.     

Differential effect of oestrogen on post‐exercise cardiac muscle myeloperoxidase and calpain activities in female rats

The effects of oestrogen administration on 1 h post‐exercise cardiac muscle myeloperoxidase (MPO) and calpain activities were determined in female rats. Rats were ovariectomized and implanted for 2 weeks with either oestrogen (25 mg 17‐oestradiol) or placebo pellets or left with ovaries intact. Rats were then run for 1 h at 21 m min^–1, 12% grade, killed 1 h post‐exercise and cardiac muscle and blood samples were removed. Control animals from each group were killed without prior exercise. Serum oestrogen levels in the order of the highest to lowest were; ovariectomized oestrogen replaced rats > intact ovaries rats > ovariectomized placebo rats. Oestrogen induced significant (P < 0.05) elevations in cardiac MPO activity at rest and at 1 h post‐exercise in ovariectomized rats. No significant elevations in cardiac MPO activity were evident in placebo ovariectomized or normal ovary rats at rest or post‐exercise. Cardiac calpain activities were similar in all unexercised groups. Ovariectomized placebo and intact ovary rats had significantly (P < 0.05) elevated cardiac calpain activities 1 h post‐exercise while calpain activity was not significantly elevated in hearts from ovariectomized oestrogen rats. These results demonstrate that oestrogen supplementation in ovariectomized rats induces elevations in cardiac muscle MPO activities at rest and at 1 h post‐exercise. This is opposite to the effect of oestrogen in post‐exercise skeletal muscle and implies a greater neutrophil infiltration into cardiac muscle caused by oestrogen. This effect cannot be explained by changes in 1 h post‐exercise cardiac muscle calpain activity, the elevation of which was suppressed by oestrogen administration. Oestrogen influences cardiac calpain activity similarly to its effect in skeletal muscle. Thus, oestrogen administration to ovariectomized rats induces elevations in cardiac MPO activity while suppressing cardiac calpain activity.     

Physical training under the influence of beta-blockade in rats

Summary Rats were trained by daily running exercises for 7 weeks. In addition, one group of rats was trained under the influence of propranolol, while another group received daily injections of propranolol only. None of the treatments used had influence on the activities of myocardial enzymes: 3-hydroxyacyl-CoA dehydrogenase (HADH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and citrate synthase (CS) which were assayed for estimating oxidative capacity, or lactate dehydrogenase (LDH) which was used as a measure of anaerobic capacity. Training without propranolol resulted in elevated activities of the oxidative enzymes in M. extensor digitorum and in M. soleus. The corresponding changes in the rat group trained with propranolol always were much smaller, despite an equal amount of training. Only the trend for lowered activity of LDH was observable in skeletal muscle of the rat groups trained both with and without propranolol. Long-term beta-blockade alone did not induce enzymatic changes. It is concluded that a functioning sympathetic nervous system is necessary for the adaptive responses of muscular metabolism to training. Blockade of the sympathetic influence during exercise periods also hampers the training-induced responses.This research was supported by grants from the Ministry of Education, Finland (Nos. 8731/78/77 and 8224/78/78)     

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.     

耐力训练模型大鼠骨骼肌代谢酶与自由基变化

背景：骨骼肌代谢酶与自由基的变化与不同的运动方式和运动强度有关。 目的：观察递增大强度耐力训练下大鼠骨骼肌代谢酶活性和自由基代谢的变化。 方法：健康雄性SD大鼠,随机分为安静组和运动组,后者建立8周的递增大强度耐力训练模型,训练结束后取骨骼肌样本测试肌酸激酶、乳酸脱氢酶、谷草转氨酶、谷丙转氨酶、丙二醛、总抗氧化酶、过氧化氢酶水平。 结果与结论：8周训练后,运动组大鼠肌酸激酶、乳酸脱氢酶、谷草转氨酶、谷丙转氨酶酶活性及丙二醛水平均高于安静组(P < 0.01或0.05),而总抗氧化酶、过氧化氢酶、谷胱甘肽过氧化物酶活性低于安静组(P < 0.05)。说明8周的递增大强度的耐力训练能使骨骼肌受到一定的损伤,并且提示抗氧化酶活性的下降和部分代谢酶活性以升高之间有一定的关系。     

Effects of aerobic exercise training on antioxidant enzyme activities and mRNA levels in soleus muscle from young and aged rats

The aim of this study was to investigate the effect of aerobic exercise training on activities and mRNA levels of catalase (CAT), glutathione peroxidase (GPX), Cu,Zn- and Mn-superoxide dismutases (SOD), TBARS content, and xanthine oxidase (XO) activity, in soleus muscle from young and aged rats. The antioxidant enzyme activities and mRNA levels were markedly increased in soleus muscle with aging. TBARS content of soleus muscle from the aged group was 8.3-fold higher as compared with that of young rats. In young rats, exercise training induced an increase of all antioxidant enzyme activities, except for Cu,Zn-SOD. XO also did not change. The TBARS content was also increased (2.9-fold) due to exercise training in soleus muscle from young rats. In aged rats, the activities of CAT, GPX and Cu,Zn-SOD in the soleus muscle did not change with the exercise training, whereas the activities of Mn-SOD (40%) and XO (27%) were decreased. The mRNA levels of Mn-SOD and CAT were decreased by 42% and 24%, respectively, in the trained group. Exercise training induced a significant decrease of TBARS content (81%) in the soleus muscle from aged rats. These findings support the proposition that exercise training presents an antioxidant stress effect on skeletal muscle from both young and aged rats.     

Physical training under the influence of beta blockade in rats: Effect on adrenergic responses

Summary Rats were trained by daily swimming or running exercises with and without daily propranolol injections. Both training methods resulted in cardiac enlargement, but only swimming exercise caused hypertrophy of the brown adipose tissue. These changes were antagonized by beta blockade. The size of the adrenals reflected the stress of the treatments, but other known stress parameters, such as the size of the thymus or sexual organs dit not. Only swimming training without beta blockade sensitized the rats to the calorigenic action of noradrenaline. The cooling rate of the rats in water, when taking into account the insulative capacity of the body, was decreased in swimming-trained as well as in propranolol-treated rats but increased in running-trained rats. The latter two changes may be due to circulatory alterations, while the delayed body cooling in swimming-trained rats probably results from increased heat production capacity. Training-induced resting bradycardia and enhanced tachycardic response to isoprenaline were observable only in the animal groups trained without beta blockade. The pressor response to noradrenaline tended to be higher in the trained groups and the propranolol-treated group than in the controls and was smaller in the animal groups trained under the influence of beta blockade. On the other hand, the hypotonic response to isoprenaline was smaller in the propranolol-treated and running-trained animals. The results emphasize the importance of the sympathetic nervous system in the adaptation of an organism to physical training.     

Different metabolic responses to exercise training programmes in single rat muscle fibres

Summary The aim of this report is to elucidate the effects of exercise training on metabolic properties of different muscle fibre types of the rat hindlimb. Single muscle fibres were dissected from soleus (SOL) or extensor digitorum longus (EDL) muscles of Wistar strain male rats trained on a treadmill for 16 weeks. Each fibre was typed histochemically (SO, slow-twitch oxidative; FOG, fast-twitch oxidative glycolytic; FG, fast-twitch glycolytic). Then glycolytic and oxidative enzymes (CK, LDH, PFK, PK, SDH, and MDH) activities were measured biochemically. Slow,-type fibres (SO) were hypertrophied following endurance training and fast-twitch fibres (FOG and FG) were hypertrophied following sprint training. In EDL muscles the distribution of the slow-type fibres was reduced following the sprint training. The activity of glycolytic enzymes increased significantly in the fast-type fibres (FOG and FG) following sprint training, while oxidative enzymes activities increased in both fast (FOG and FG) and slow (SO) muscle fibres following the endurance training. Neither glycolytic nor oxidative enzymes' activities always increased equally in all types of fibre following exercise training. Consequently, the metabolic profiles in each type of single muscle fibre were affected differently by different intensities of exercise training. These results suggest that the functional (enzymes activity) and structural (muscle fibre hypertrophy) changes of skeletal muscle fibre following exercise training appeared gradually, and would be controlled by different factors.     

Quantitative assessment of nitric oxide in rat skeletal muscle and plasma after exercise

Nitric oxide (NO), a short-lived vasoactive substance that has multiple physiological functions, is also involved in skeletal muscle physiology. This work examines the levels of nitrate (the metabolic end-product of NO) in muscle and plasma after different exercise protocols: namely acute, eccentric, cardiac stress and training. Plasma nitrate levels were augmented after strenuous exercise and did not change after training. The vastus intermedius and the gastrocnemius, both oxidative muscles, showed the highest concentrations of cytosolic nitrate after strenuous exercise. NO levels varied, depending on the fibre type, and this may correlate well with the specific contractile function performed. Electronic Publication     

Skeletal muscle training in chronic heart failure

Patients with heart failure are limited in their ability to tolerate exercise. Recent research has suggested that this limitation cannot be entirely attributed to cardiac or lung impairment but rather that changes in peripheral muscles may play an important role. There are objective similarities between heart failure and muscular deconditioning. Deficiencies in peripheral blood flow and skeletal muscle function, morphology, metabolism and function are present in both conditions. Moreover, an exaggerated activity of the receptors sensitive to exercise‐derived metabolic signals (muscle ergoreceptors and peripheral and central chemoreceptors) leads to early and profound exercise‐induced fatigue and dyspnoea. These muscle afferents contribute to the ventilatory, haemodynamic and autonomic responses to exercise both in physiological and pathological conditions, including chronic heart failure. Against this background, a skeletal muscle origin of symptoms in heart failure has been proposed. The protective effects of physical training have been described in many recent studies: training improves ventilatory control, skeletal muscle metabolism and autonomic nervous system activity. The exercise training appears to induce its beneficial effects on skeletal muscle both directly (on muscle function, histological and biochemical features) and indirectly (by reducing the activation of the muscle afferents). The metabolic mediators of these muscle afferents may become a potential target in the future therapy of heart failure symptoms.     

Regulation of dihydropyridine receptor levels in skeletal and cardiac muscle by exercise training

To examine the influence of exercise training on the expression of dihydropyridine (DHP)-sensitive Ca²⁺ channels in skeletal and cardiac muscle, we have determined DHP receptor levels by [³H]PN200-110-binding and immunoblot analysis in homogenates and microsomal fractions of slow- and fast-twitch muscles and heart from rats subjected to a 12-week programme of moderate endurance training. We found that exercise increases the amount of DHP receptor in homogenates of the slow-twitch soleus (42%) and the fast-twitch extensor digitorum longus (60%). Comparable increases in DHP receptor density with training were also observed in the microsomal fractions isolated from both skeletal muscles; these increases were not due to differences in the membrane composition of the microsomal fractions, since the relative proportion of specific enzyme markers was not affected by exercise training. Levels of DHP receptor were not modified in cardiac muscle as a result of the exercise programme. These data suggest an up-regulation of the DHP receptor in the skeletal muscle as a consequence of exercise training, which may play a role in the adaptation of skeletal muscle to increased contractile activity.     

Effects of endurance training on alkaline protease activities in rat skeletal muscles

This study aimed at comparing the effects of running and swimming training protocols and the termination of training on the activities of two proteases with alkaline pH-optima (alkaline protease and myofibrillar protease) in the tibialis anterior, soleus, and gastrocnemius muscles of male rats. The training on treadmill decreased the activities of alkaline and myofibrillar proteases by approx. 10-20% in the muscles studied. The activities of both proteases were unchanged in swimming-trained rats. Two weeks after the termination of running training the activity of alkaline protease was increased in gastrocnemius muscle but not in the other muscles. Swimming training increased the activity of citrate synthase in all muscles studied but training by running only in the soleus muscle. The running protocol increased the activity of beta-glucuronidase in the tibialis anterior muscle and decreased the activity in the gastrocnemius muscle. The swimming program did not affect beta-glucuronidase activities. These results show diverse effects of running and swimming training on alkaline proteolytic activities as well as on mitochondrial and lysosomal marker enzymes.     

Swim training does not protect mice from skeletal muscle oxidative damage following a maximum exercise test

We investigated whether swim training protects skeletal muscle from oxidative damage in response to a maximum progressive exercise. First, we investigated the effect of swim training on the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), in the gastrocnemius muscle of C57Bl/6 mice, 48 h after the last training session. Mice swam for 90 min, twice a day, for 5 weeks at 31°C (± 1°C). The activities of SOD and CAT were increased in trained mice (P < 0.05) compared to untrained group. However, no effect of training was observed in the activity of GPx. In a second experiment, trained and untrained mice were submitted to a maximum progressive swim test. Compared to control mice (untrained, not acutely exercised), malondialdehyde (MDA) levels were increased in the skeletal muscle of both trained and untrained mice after maximum swim. The activity of GPx was increased in the skeletal muscle of both trained and untrained mice, while SOD activity was increased only in trained mice after maximum swimming. CAT activity was increased only in the untrained compared to the control group. Although the trained mice showed increased activity of citrate synthase in skeletal muscle, swim performance was not different compared to untrained mice. Our results show an imbalance in the activities of SOD, CAT and GPx in response to swim training, which could account for the oxidative damage observed in the skeletal muscle of trained mice in response to maximum swim, resulting in the absence of improved exercise performance.