The role of insulin in the control of triacyglycerol (TG) in the rat skeletal muscles

The role of insulin in the control of triacyglycerol (TG) in different types of skeletal muscle has not been fully recognized so the aim of the present study was to fill this gap. The experiments were carried out on control rats, those fed with olive oil or fed with the oil and treated with insulin and on streptozotocin diabetic animals at rest and there after exercise till exhaustion. The level of TG was measured in the white and red layers of the vastus lateralis, the soleus and the diaphragm. It was found that acute feeding with olive oil had no effect on TG level in either muscle type examined. Insulin administered to rats fed with oil increased TG level in the red vastus. Streptozotocin diabetes caused an increase in TG level in muscles with high oxidative potential. Exercise lowered the level of TG only in the red vastus of the diabetic rats. It is concluded that insulin may increase muscle TG level. Accumulation of TG in muscles of rats with acute diabetes is likely to be a result of the high plasma free fatty acid concentration. Acute insulin deficiency did not affect the muscle TG response to exercise.     

有氧运动对2型糖尿病大鼠骨骼肌ERK1/2活性的影响

目的：观察有氧运动对2型糖尿病大鼠骨骼肌细胞外信号调节激酶（ERK1/2）活性的影响,探讨有氧运动对2型糖尿病的预防和调控机制。方法：将75只SD大鼠随机分为正常对照组（CON）、糖尿病对照1组（DC1）、糖尿病运动1组（DE1）、糖尿病对照2组（DC2）、糖尿病运动2组（DE2）5组（n=15）。正常对照组用普通饲料喂养,糖尿病组用高脂高糖配方饲料喂养。经过8周高脂高糖喂养后,糖尿病2组大鼠腹腔内注射链脲佐菌素（STZ）,诱发2型糖尿病;糖尿病运动1组游泳的最后1周初和糖尿病对照1组同时注射STZ,注射剂量为35 mg/kg,3 d后尾部取血测血糖≥ 16.7 mmol/L为造模成功。运动干预8周后,测定大鼠血清胰岛素、骨骼肌中ERK1/2蛋白表达等指标。结果：①与正常对照组比较,糖尿病各对照组血液中总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL-C）、游离脂肪酸（FFA）显著升高（P<0.05,P<0.01）,空腹血糖（FBG）、胰岛素（FIN）含量和胰岛素抵抗指数（HOMA-IR）显著升高（P<0.01）,ERK1/2磷酸化的蛋白表达显著下降（P<0.05）,糖尿病对照2组ERK1/2蛋白含量显著下降（P<0.05）;②8周游泳运动后,与糖尿病对照组比较,糖尿病运动组血液中TC、TG、FFA、LDL-C显著下降（P<0.05）,FBG、FIN、HOMA-IR显著下降（P<0.05,P<0.01）,ERK1/2磷酸化蛋白表达显著升高（P<0.05）。结论：长时间有氧运动,增加了骨骼肌ERK1/2磷酸化水平,改善了2型糖尿病大鼠胰岛素抵抗的状况,降低血糖。这可能是改善糖代谢紊乱,提高胰岛素敏感性的机制之一。     

The effect of exercise and zinc supplement on the hematological parameters in rats

This study evaluates the consequences of a session of intensive short-duration exercise and Zn supplementation on different hematological variables. Forty male Wistar rats were divided into four groups (n=10): the first nonsupplemented, maintained at rest (R); the second nonsupplemented, undergoing exercise (E); the third supplemented with Zn, kept at rest (ZnR); and the fourth supplemented with Zn, undergoing exercise (ZnE). Zinc supplements (200 ppm) were given in drinking water. The exercise consisted of a single session of swimming until exhaustion. At rest, RBC, Hb, and Hto fell (p<0.05), whereas red cell indices, MCV, and MCH rose (p<0.05) in +ZnR compared with R; MCHC remained unchanged (ZnR vs R). After exercise, RBC, Hb, and Hto increased significantly in E and in ZnE compared with R and ZnR, respectively. In addition, RBC and Hb were lower (p<0.01) in ZnE compared with E; however, MCV and MCH were higher (p<0.05) in the group ZnE vs E. With respect to white blood cells—leukocytes (WBC), limphocytes (LYMPH), and neutrophiles (NEUT)—no significant differences were observed between groups at rest (ZnR vs R). WBC and LYMPH increased significantly in E with respect to the rest situation (E vs R), but this did not happen in supplemented animals (ZnE vs ZnR). Level of pH decreased after exercise both in E and in ZnE, but the fall was lower in the latter. We believe that a single session of swimming until exhaustion leads to an increase in RBC, Hb, and Hto without causing changes in MCV, MCH, and MCHC. On the other hand, Zn supplementation leads to an increase of MCV and MCH, although they remain within normal levels. Furthermore, this supplementation produces lower metabolic acidoses after exercise that leads to leukocyte stability.     

Iron distribution in different tissues in rats following exercise

Iron plays an essential role in blood oxygen transport and in muscle physiology. No conclusive data exist in the literature concerning its tissue distribution and behavior following exercise and training. The aim of the present work was to analyze the Fe content in different tissues following a single session of swimming to exhaustion and after swimming training in rats in order to more extensively describe the changes of Fe distribution provoked by exercise. Animals were divided into four groups (n=10): control group at rest, trained group at rest, control group after exercise, and trained group after exercise. First, rats swam until exhaustion and the maximal swimming time was noted. The training protocol consisted of swimming (5 d/week for 3 wk), limiting the time to 60% of the maximum obtained during the first session to exhaustion of each rat. The variables measured were erythrocytes, hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, and, Fe in liver, kidney, erythrocytes, heart, muscle, bone, and serum. Variations in plasma volume were also calculated. Tissues presented two different profiles with regard to the changes of Fe concentration provoked by training: those displaying higher values of Fe after training, such as liver, heart, muscle, and serum, and those displaying lower values, such as bone, kidney, and red blood cells. These changes in the distribution of Fe in different tissues could be the result of an increase in the needs and use of Fe, shown by active tissues at exercise, and it is possible that the hormonal changes provoked by stress lead to a different behavior of Fe proteins.     

Exercise-induced muscle glycogen depletion and repletion in diabetic rats.

The purpose of this experiment was to examine glycogen depletion in muscles of chronic diabetic rats during treadmill running of moderate intensity and glycogen repletion following the exercise bouts. Diabetes was induced with a single intravenous injection of streptozotocin (70 mg × kg^?1). Glycogen concentrations in muscles from diabetic and normal animals were determined at rest, after running either 10 or 30 min at 23 m × min^?1 (5% incline), or 2, 4, or 8 hr following 30 min of running at the same speed and incline. With the exception of soleus muscle after 30 min of running, there were no differences in muscle glycogen contents between normal and diabetic rats before exercise, immediately after exercise, or during the recovery period. All muscles showed a significant loss of glycogen during exercise, and most muscles had completely restored their glycogen by 2 hr following exercise. Blood lactate concentrations were also similar for normal and diabetic rats at rest and after exercise. It is concluded that the diabetic condition studied in this experiment did not significantly alter muscle glycogen metabolism during exercise of moderate intensity or during recovery from the activity.     

Effect of streptozotocin-induced diabetes on glycogen resynthesis in fasted rats post-high-intensity exercise

It has recently been shown that food intake is not essential for the resynthesis of the stores of muscle glycogen in fasted animals recovering from high-intensity exercise. Because the effect of diabetes on this process has never been examined before, we undertook to explore this issue. To this end, groups of rats were treated with streptozotocin (60 mg/kg body mass ip) to induce mild diabetes. After 11 days, each animal was fasted for 24 h before swimming with a lead weight equivalent to 9% body mass attached to the tail. After exercise, the rate and the extent of glycogen repletion in muscles were not affected by diabetes, irrespective of muscle fiber composition. Consistent with these findings, the effect of exercise on the phosphorylation state of glycogen synthase in muscles was only minimally affected by diabetes. In contrast to its effects on nondiabetic animals, exercise in fasted diabetic rats was accompanied by a marked fall in hepatic glycogen levels, which, surprisingly, increased to preexercise levels during recovery despite the absence of food intake.     

Acute effect of physical exercise on glycogen content and lipoprotein lipase activity in untrained diabetic rats

The effect of acute physical exercise on skeletal muscle glycogen content and on lipoprotein lipase activity of muscle, adipose and lung tissues was studied in streptozotocin diabetic and control rats. Rats were accustomed to treadmill running for two weeks after streptozotocin treatment. For an exercise bout of moderate intensity rats were randomly divided into two groups: one was sacrificed immediately after exercise and the other 24 hours afterwards. In addition there was a nonexercised sedentary group. No depletion of glycogen was observed after exercise in the vastus lateralis muscle of control (nondiabetic) rats. No difference in glycogen utilization was found in soleus muscle between diabetic and control rats. In diabetic rats a slight decrease occurred in the lipoprotein lipase activity in adipose tissue immediately after exercise, while in control rats there was a significant decline 24 hours after exercise. In soleus muscle a slight but significant increase of lipoprotein lipase activity occurred 24 hours after exercise in diabetic rats but not in control rats. The results suggest that nonketotic streptozotocin diabetes of short duration does not influence muscle glycogen in the resting state, but glycogen utilization is disturbed in white muscle during moderate treadmill running in untrained diabetic rats. The increase in lipoprotein lipase activity after physical exercise in red muscle of diabetic rats occurs during the recovery phase.     

Effect of Long-Term Intraperitoneal Zinc Administration on Liver Glycogen Levels in Diabetic Rats Subjected to Acute Forced Swimming

This study aims to examine the effect of zinc administration on liver glycogen levels of rats in which diabetes was induced with streptozotocin and which were subjected to acute swimming exercise. The study was conducted on 80 adult Sprague–Dawley male rats, which were equally allocated to eight groups: group 1, general control; group 2, zinc-administrated control; group 3, zinc-administrated diabetic control; group 4, swimming control; group 5, zinc-administrated swimming; group 6, zinc-administrated diabetic swimming; group 7, diabetic swimming; group 8, diabetic control group. In order to induce diabetes, animals were injected with 40 mg/kg intraperitoneal (ip) streptozotocin. The injections were repeated in the same dose after 24 h. Animals which had blood glucose at or above 300 mg/dl 6 days after the last injections were accepted as diabetic. Zinc was administrated ip for 4 weeks as 6 mg/kg/day per rat. Hepatic tissue samples taken from the animals at the end of the study were fixed in 95% ethyl alcohol. Cross sections of 5 μm thickness, taken by the help of a microtome from the tissue samples buried in paraffin, were placed on a microscope slide and stained with periodic acid–Schiff and evaluated by light microscope. All microscopic images were transferred to a PC and assessed with the help of Clemex PE3.5 image analysis software. The lowest liver glycogen levels in the study were obtained in groups 3, 4, 6, 7, and 8. Liver glycogen levels in group 5 were higher than groups 3, 4, 6, 7, and 8, but lower than groups 1 and 2 (p < 0.05). Groups 1 and 2 had the highest liver glycogen levels. The results obtained from the study indicate that liver glycogen levels which dropped in acute swimming exercise were restored by zinc administration and that diabetes induced in rats prevented the protective effect of zinc.     

Myostatin信号通路在4周离心耐力运动改善2型糖尿病大鼠骨骼肌萎缩中的作用

目的：观察4周离心耐力运动对2型糖尿病大鼠代谢障碍及肌萎缩的影响,探讨myostatin/Smad3/atrogin-1信号通路在肌萎缩中的作用。方法：9周高脂饲养联合STZ注射建立2型糖尿病大鼠模型。将普通饲料组大鼠随机分为对照组（C,n=6）和运动组（E,n=9;将2型糖尿病模型组大鼠随机分为糖尿病对照组（D,n=8）和糖尿病运动组（DE,n=12）。运动方案：坡度-5°,跑速16 m/min,每次60 min、每日一次,每周训练5 d,连续4周。最后一次运动后禁食12 h,测定空腹血糖（FBG）、空腹胰岛素（FINS）,计算稳态模式胰岛素抵抗指数（HOMA-IR）和胰岛素敏感指数（ISI）,进行葡萄糖耐量试验。取比目鱼肌观察肌萎缩现象并检测myostatin、Smad3、p-Smad3和atrogin-1表达情况。结果：①与对照组相比,糖尿病组大鼠体重、比目鱼肌质量/胫骨长和肌纤维平均横截面积、FINS和ISI显著降低（P<0.01）,FBG、HOMA-IR和血糖曲线下面积（AUC_BG）以及myostatin、Smad3、p-Smad3、atrogin-1表达均显著升高（P<0.01）。②4周离心运动后,与糖尿病组相比,糖尿病运动组大鼠肌纤维平均横截面积显著升高（P<0.01）,AUC_BG、HOMA-IR及myostatin、p-Smad3、atrogin-1表达显著降低（P<0.05,P<0.01）。结论：myostatin/Smad3/atrogin-1信号通路上调是导致2型糖尿病肌萎缩的重要原因,4周离心耐力运动可能通过下调myostatin、p-Smad3和atrogin-1表达抑制肌萎缩,进而改善2型糖尿病代谢障碍,提高胰岛素敏感性。     

Effect of zinc supplementation on the distribution of various elements in the serum of diabetic rats subjected to an acute swimming exercise

The present study aims to examine the effect of supplementation of zinc on the distribution of various elements in the sera of diabetic rats subjected to an acute swimming exercise. A total of 80 Sprague–Dawley-type adult male rats were equally allocated to one of eight groups: Group 1, general; Group 2, zinc-supplemented; Group 3, zinc-supplemented diabetic; Group 4, swimming control; Group 5, zinc-supplemented swimming; Group 6, zinc-supplemented diabetic swimming; Group 7, diabetic swimming; and Group 8, diabetes. The rats were injected with 40 mg/kg/day subcutaneous streptozotocin (STZ) twice, with a 24-h interval between two injections. Zinc was supplemented at a dose of 6 mg/kg/day (ip) for 4 weeks. Blood samples were collected at the end of the 4-week study, and serum levels of lead, cobalt, molybdenum, chrome, sulfur, magnesium, manganese, sodium, potassium, phosphorus, copper, iron, calcium, zinc, and selenium (mg/L) were determined with atomic emission. The lowest molybdenum, chrome, copper, iron, potassium, magnesium, sodium, phosphorus, lead, selenium, and zinc values were obtained in Group 7 and 8. These same parameters were higher in the swimming exercise group (Group 4), relative to all other groups. The values in zinc-supplemented groups were found lower than the values in Group 4, but higher than those in Group 6 and 7. The results obtained from the study demonstrate that acute swimming exercise and diabetes affect the distribution of various elements in the serum, while zinc supplementation can prevent the negative conditions associated with both exercise and diabetes.     

Intensive exercise training does not improve intravenous glucose tolerance in severely diabetic rats

Several studies have recently demonstrated that exercise training improves glucose tolerance in mildly diabetic rats. To test whether some minimal levels of circulating insulin are required to observe the beneficial effects of exercise training, severe diabetes was induced by injecting female Wistar rats with streptozotocin. Half of diabetic and control rats were submitted to a strenuous program of swimming exercise. After 4 wks of training, intravenous glucose tolerance tests (IVGTT) were performed in precannulated, unrestrained and unanesthetized animals. In non-diabetic rats, exercise training significantly reduced both basal and glucose-stimulated levels of insulin (P less than 0.01) without altering glucose tolerance. On the other hand, the same training program applied to severely diabetic animals (basal plasma insulin levels less than 8 microU/ml) failed to reduce the marked hyperglycemia in the resting state (400 mg% range) as well as during the entire IVGTT (400-500 mg%). The results indicate that exercise training effectively increased the sensitivity of peripheral tissues to insulin in non-diabetic but not in diabetic animals. The data also suggest that a minimal amount of circulating insulin is required in order to observe the beneficial effects of exercise training.     

Prolactin Release during Exercise in Normal and Adrenodemedullated Untrained Rats Submitted to Central Cholinergic Blockade with Atropine

To study the role of the central cholinergic system in pituitary prolactin (PRL) release during exercise we injected atropine (5 x 10(-7) mol) into the lateral cerebral ventricle of intact or adrenodemedullated (ADM) untrained rats, at rest or submitted to exercise on a treadmill (18 m x min(-1), 5% grade) until exhaustion. The rats were implanted with chronic jugular catheters for blood sampling and with unilateral intracerebroventricular (icv) cannulas placed in the right lateral ventricle. Blood prolactin concentrations were measured before and every 10 min after the start of exercise for a period of 60 min. After the animals started running, plasma prolactin levels rose rapidly in both normal and ADM rats, reaching near maximum at 10 min. Close to exhaustion (19.8 +/- 2.9 min for intact rats and 23.5 +/- 4.1 min for ADM) they were still high, remained increased until 30 min, and returned to preexercise levels at 40 min. Icv injections of atropine decreased the time to exhaustion by 67% in intact rats and by 96.2% in ADM and also reduced the exercise-induced PRL release in both intact (50%) and ADM rats (90%). The results showed that prolactin release induced by exercise was dependent on the exercise workload and could be observed as early as after 10 min of running, remaining increased until 30 min. These data indicate that adrenodemedullation does not affect prolactin secretion induced by exercise, although adrenodemedullated rats proved to be more sensitive to the reducing effect of central cholinergic blockade on their maximal capacity for exercise.     

Adipose, muscle and lung tissue lipoprotein lipase activities in young streptozotocin treated rats

Lipoprotein lipase (LPL) activity was studied in adipose, muscle and lung tissues of post-weanling rats 48 and 96 hours after experimentally induced diabetes by streptozotocin administration. Weight gain was reduced, and blood glucose level increased about 3-4 fold above the control level as an indication of the diabetic state. LPL activity in brown and white adipose tissues decreased in diabetic rats to 10-30% of the control level. In soleus muscle the LPL activity was slightly enhanced 96 hours after the streptozotocin injection. In cardiac muscle the LPL activity was markedly increased already 48 hours after the administration of streptozotocin and the increase remained significant until 96 hours. There was in the pulmonary tissue also an increase of LPL activity of diabetic rats, although this was significant only 96 hours after streptozotocin treatment. The results suggest marked tissue specific variation in the LPL activity. Moreover, tissue responses to experimentally induced diabetes vary. In adipose tissue the decrease in the LPL activity suggests that lipid transport to adipocytes is decreased while an increase in skeletal and cardiac muscles and in lung tissue proposes that their lipid utilization is enhanced.     

Pentose phosphate pathway,glutathione-dependent enzymes and antioxidant defense during oxidative stress in diabetic rodent brain and peripheral organs: effects of stobadine and vitamin E

The aim of the present study was to investigate the effects of treatment with antioxidant stobadine (ST) on the activities of enzymes related with pentose phosphate pathway and glutathione-dependent metabolism and the other markers of oxidative stress in brain and peripheral organs of diabetic rats, and to compare the effects of ST treatment alone with the effects of treatments with another antioxidant vitamin E and ST plus vitamin E. Rats were made diabetic by the injection of streptozotocin (STZ; 55 mg/kg IP), and, 2 days later, some control and diabetic rats were left untreated or treated with ST (24.7 mg/kg/day, orally), vitamin E (400–500 U/kg/day, orally), or both substances together. In the brain, although 6-phosphogluconate dehydrogenase activity (6-PGD) did not change, glucose-6-phosphate dehydrogenase activity (G-6PD) was markedly increased in diabetic rats compared with controls; only combined treatment with ST and vitamin E produced a partial prevention on this alteration. The aorta G-6PD and 6-PGD of diabetic rats were 52% and 36% of control values, respectively. Neither single treatments with each antioxidant nor their combination altered the G-6PD and 6-PGD in aorta of diabetic rats. Glutathione peroxidase (GSHPx) activity was increased by STZ-diabetes in brain, heart, and kidney. In diabetic brain, vitamin E alone or combination with ST kept GSHPx at normal levels. Diabetes-induced stimulation in GSHPx did not decrease in response to the treatment with vitamin E in heart and kidney, but was greatly prevented by ST alone. The activity of glutathione reductase (GR) was decreased in brain and heart of diabetic rats. The treatment with each antioxidant or with a combination of both agents completely prevented this deficiency and resulted in further activation of GR in diabetic tissues. Glutathione S-transferase (GST) activity did not significantly change in diabetic brain and aorta. GST was stimulated by all treatment protocols in the brain of diabetic rats and was depressed in aorta of control rats. Catalase (CAT) was activated in diabetic heart but depressed in diabetic kidney. Diabetes-induced abnormalities in CAT activity did not respond to vitamin E alone in heart, was moderately ameliorated by the treatment with this vitamin in kidney, and was completely prevented by ST alone in both tissues. Superoxide dismutase (SOD) activity of brain and heart was unchanged by the diabetes but inhibited in diabetic kidney after the treatment ST alone or ST plus vitamin E. The lipid peroxidation (MDA) was increased in diabetic brain and heart. ST or vitamin E alone partly prevented diabetes-induced increase in MDA in brain and heart; however, antioxidant combination achieved a completely amelioration in MDA of these tissues of diabetic rats. Kidney MDA levels were similar in control and untreated diabetic animals. ST and vitamin E treatments, when applied separately or together, significantly reduced kidney MDA in both control and diabetic rats; and the combined effect of antioxidants was greater than that of each alone. These results are consistent with the degenerative role of hyperglycemia on cellular reducing equivalent homeostasis and antioxidant defense, and provide further evidence that pharmacological intervention of different antioxidants may have significant implications in the prevention of the prooxidant feature of diabetes and protects redox status of the cells.     

有氧运动和谷氨酰胺对二型糖尿病大鼠氧化应激及相关因子表达的影响

目的:探讨有氧运动和谷氨酰胺(Gln)对二型糖尿病(T2MD)大鼠抗氧化应激及炎性因子的影响。方法:用链脲佐菌素(STZ)诱导糖尿病大鼠模型,将成年雄性SD大鼠50只,6周龄,随机分为5组(n=10):包括安静对照组(N)、糖尿病对照组(D)、糖尿病施加有氧运动组(DE)、糖尿病施加谷氨酰胺组(DG)、糖尿病施加有氧运动+谷氨酰胺组(DEG)。6周后,检测干预后糖尿病大鼠糖脂代谢、抗氧化应激及炎性因子等相关指标,并探讨影响炎症反应的可能机制。结果:与N组相比,D组大鼠血清MDA、血糖、TC、TG、胰岛素、瘦素、TNF-α水平均明显升高(P<0.01),血清中SOD、GSH-Px、脂联素、HDL-C的水平均明显降低(P<0.01);与D组相比,三个干预组血清中MDA、血糖、TC、TG、胰岛素、瘦素、TNF-α水平降低,血清中HDL-C、SOD、GSH-Px、脂联素的水平均明显升高(P<0.05,P<0.01),且两者联合对上述指标的改善作用更为明显(P<0.01)。结论:有氧运动和Gln均能缓解糖尿病大鼠糖脂代谢及紊乱、氧化应激损伤及炎症反应,两者联合对其作用优于单一作用。     

Amelioration of hyperlipidemia by low fat diets in chronically streptozotocin-diabetic rats

The effects of reduced dietary fat intake on plasma lipid levels were examined in diabetic rats. One week after induction of diabetes (D) with streptozotocin (65 mg/kg, iv), the animals were fed food pellets consisting of 1.5% (D1.5), 2.5% (D2.5) or 5% (D5) fat for two weeks. Irrespective of the diets, both food and water consumed by untreated diabetic rats were 2- to 5-fold greater respectively compared to normal. Plasma glucose concentrations were also similarly increased. Plasma and skeletal muscle lipid levels were significantly greater than controls in D2.5 and D5, but not in the D1.5 group. Plasma and muscle lipid concentrations correlated directly with fat consumption. In D5 rats receiving insulin treatment, plasma glucose and lipid concentrations were comparable to control values. These findings indicate that the degree of hyperlipidemia in chronically diabetic rats is directly related to dietary fat intake. They also demonstrate that dietary interventions can modulate some of the metabolic abnormalities in diabetes.     

Effects of acute hypobaric hypoxia and exhaustive exercise on AMP-activated protein kinase phosphorylation in rat skeletal muscle

The present study was aimed to explore the changes of phosphorylated AMP-activated protein kinase (pAMPK) level in skeletal muscle after exposure to acute hypobaric hypoxia and exhaustive exercise. Thirty-two male Sprague-Dawley (SD) rats were randomly divided into sea level and high altitude groups. The rats in high altitude group were submitted to simulated 5 000 m of high altitude in a hypobaric chamber for 24 h, and sea level group was maintained at normal conditions. All the rats were subjected to exhaustive swimming exercise. The exhaustion time was recorded. Before and after the exercise, blood lactate and glycogen content in skeletal muscle were determined; AMPK and pAMPK levels in skeletal muscle were detected by Western blot. The results showed that the exhaustion time was significantly decreased after exposure to high altitude. At the moment of exhaustion, high altitude group had lower blood lactate concentration and higher surplus glycogen content in gastrocnemius compared with sea level group. Exhaustive exercise significantly increased the pAMPK/AMPK ratio in rat skeletal muscles from both sea level and high altitude groups. However, high altitude group showed lower pAMPK/AMPK ratio after exhaustion compared to sea level group. These results suggest that, after exposure to acute hypobaric hypoxia, the decrement in exercise capacity may not be due to running out of glycogen, accumulation of lactate or disturbance in energy status in skeletal muscle.     

Metabolic and endocrine responses to prolonged exercise in rats under beta 2-adrenergic blockade

The respective roles of allosteric regulators and catecholamines in the control of muscle glycogen breakdown during exercise remain a matter of controversy. This study was designed to reassess the role of the sympathoadrenal system during prolonged exercise in rats. Animals were studied at rest or after treadmill exercise (28 m.min-1; 8% slope) to exhaustion in a control situation or following administration of a specific beta 2-adrenergic receptor antagonist (ICI 118,551, 1 mg.kg-1, i.v.). Running times to exhaustion were 54 and 36 min in control and treated rats, respectively. For the purpose of comparison, another group of control rats was studied after a 36-min exercise bout. The reduction in endurance in treated rats was associated with an impairment in glycogen utilization, as measured by muscle glycogen stores, in soleus muscle but not in superficial vastus lateralis or gastrocnemius lateralis muscles. Utilization of liver glycogen stores was similar in the two groups of animals, but plasma glucose (7 vs. 13 mM) and lactate (4 vs. 7 mM) levels were significantly lower in rats under beta-blockade than in control rats run for 36 min. Plasma free fatty acid and glycerol concentrations were not significantly different between groups. On the other hand, plasma epinephrine concentration was significantly higher in treated rats (13 vs. 5 mM), which might reflect a compensatory increase in adrenal activity. These results suggest that glycogen breakdown during prolonged exercise is under the control of the sympathoadrenal system in predominantly slow-twitch but not in predominantly fast-twitch muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

A Preliminary and Qualitative Metallomics Study of Mercury in the Muscle of Fish from Amazonas, Brazil

In this study, we report the effect of zinc supplementation on the distribution of elements in kidney tissue of diabetic rats subjected to acute swimming exercise. Diabetes was induced by two subcutaneous injections of 40 mg/kg of streptozotocin within a 24-h period. Zinc was given intraperitoneally at a dose of 6 mg/kg per day for a period of 4 weeks. The rats (n = 80) were equally divided into eight study groups: controls, zinc-supplemented, swimming, diabetic, zinc-supplemented diabetic, zinc-supplemented swimming, diabetic swimming, and zinc-supplemented diabetic swimming. The levels of lead, cobalt, molybdenum, chromium, boron, magnesium, iron, copper, calcium, zinc, and selenium were determined in the kidney tissue samples by ICP-AES. Higher molybdenum, calcium, zinc, and selenium values were found in both swimming and nonswimming diabetic rats. Significantly higher iron values were found in swimming, diabetic, diabetic swimming, and zinc-supplemented diabetic swimming rats (p < 0.001). Diabetic, zinc-supplemented diabetic, diabetic swimming, and zinc-supplemented diabetic swimming rats had the highest copper values. These results show that zinc supplementation normalized the higher levels of molybdenum, calcium, selenium, and iron levels seen in diabetic rats, indicating that zinc may have a regulatory effect on element metabolism in kidney tissue.     

Regulation of glycogen metabolism in rat respiratory muscles during exercise

The effect of prolonged exercise on the glycogen level in the respiratory muscles (diaphragm--D, external intercostal--IE and internal--II) has been studied in four groups of rats: 1-control, 2-fasted for 24 h, 3-treated with nicotinic acid and 4-treated with propranolol. There was a sharp reduction in glycogen level in each muscle after 30 min exercise in the control and fasted groups. Exercise till exhaustion further lowered the glycogen level in D in the control group and in IE and II in the fasted group. In the fasted group, the level of glycogen in each muscle, at rest, and after 30 min exercise, and in IE and II muscles after exercise till exhaustion was lower than in the control group. Nicotinic acid did not affect the glycogen level either at rest or during exercise as compared with the control group. Propranolol increased the glycogen level in the muscles at rest and during 30 min exercise. It partially prevented glycogen mobilization in D and IE and fully in II during exercise till exhaustion. In the control group, 24 and 48 h after exercise till exhaustion, the level of glycogen in each muscle exceeded the resting control value. It is concluded that exercise-induced glycogen metabolism in the respiratory muscles differs in some respects from that in the limb or heart muscles.