Dynamics of several indices of carbohydrate and lipid metabolism during the period of readaptation after prolonged restriction of movement

Eighty-seven white rats were exposed to prolonged hypokinesia. On 90th hypokinesia day the content of cholesterol, free fatty acids and acetone bodies increased and the content of sugar and triglycerides decreased in blood, the content of glycogen decreased and the content of cholesterol increased in liver and skeletal muscles. On the 15th day after exposure most parameters returned to normal. However, glucose-6-phosphate dehydrogenase in liver and adipose tissue increased and remained elevated till recovery day 60. On the 30th recovery day the changes were similar to those during hypokinesia. On the 90th recovery day the content of triglycerides, cholesterol and acetone bodies in blood grew and the content of triglycerides and glycogen in muscles increased.     

Concentration of collagen, lipids and glycogen in the skeletal muscles of the rat during the recovery period after 15 and 30 days of hypokinesia

On the 15th hypokinetic day carcass mass, glycogen and lipid content in skeletal muscles decreased while collagen content increased. The content of collagen returned to the norm by the 7th day of the recovery period. By that time the glycogen content increased significantly and a week later decreased noticeably. The content of total lipids and triglycerides was higher than the baseline level on the 15th and 30th days of the recovery period. On hypokinesia day 30 carcass mass and glycogen content decreased while collagen content increased. After 30-day hypokinesia glycogen was significantly increased on the 7th day and returned to the norm by the 60th day of the recovery period. Lipid content was elevated only on the 7th day of the recovery period, collagen content returned to the norm on the 15th day of the recovery period. Following 15- and 30-day hypokinesia carcass mass returned to the baseline level by the 30th day of the recovery period.     

Effect of accelerations, hypergravity and hypokinesia on protein metabolism in Japanese quail. I. Effect on muscle composition]

The effect of hypokinesia, hypergravity achieved by centrifugation and additional weight load on the content and composition of proteins and nucleic acids in the chest and pelvic muscles of four groups of quails (Coturnix coturnix japonica) was studied. The first group was used as controls, the second included hypokinetic birds, the third was made of birds with an additional weight load (the load was a double weight of the animal) and the fourth group included birds exposed to acceleration of 3 g. The birds were exposed to the above effects for 1 to 6 hours during 8 days. They were given identical food through forced feeding. The content of total proteins, sarcoplasmatic proteins, DNA and RNA, cholesterol and esterified fatty acids was measured in chest and pelvic muscles. The composition of total lipids was examined in pelvic muscles. The level of corticosterone was determined in the blood plasma. The above experimental variants made it possible to discriminate individual contributions of acceleration, additional weight load and hypo-inesia to the effect. Weight load and acceleration decreased and hypokinesia increased the content of total proteins in the pelvic muscles. During an exposure to acceleration and hypokinesia the content and the portion of sarcoplasmatic proteins decreased and during an exposure to weight load increased significantly. Acceleration did not exert a significant effect on the RNA and DNA content in muscles. The content of esterified fatty acids increased under the influence of acceleration and hypokinesia and decreased significantly under the influence of additional weight.     

Motor activity and the prevention of the sequelae of hypokinesia (according to tissue metabolic indices)

The content of protein, DNA and RNA was measured in rats that had been exposed to 90-day hypokinesia: hypokinesia alternating with unrestrained maintenance and hypokinesia combined with exercises (swimming). Adverse effects of hypokinesia on metabolism seemed to build up. Short-term passive rest was insufficient to make up deficiency in motor activity. The recovery of metabolic disorders after prolonged hypokinesia proceeded in a non-uniform and slow manner: most parameters did not return to the initial level within one month. During the first two weeks exercises produced effects similar to those of hypokinesia. By the 30th and 60th days they shower their normalizing effect on tissue metabolism. When developing work-rest cycles for the people who are exposed to partial hypokinesia during work and do exercises as a countermeasure against hypokinetic effects, biochemical analysis of blood (nonesterified fatty acids, acetone bodies, cholesterol, beta-lipoproteins, urea) and urine (potassium, calcium, creatinine) should be made to measure metabolic processes in tissues.     

Intensity of lipid peroxidation in the tissues of rats during hypokinesia

The intensity of lipid peroxidation in the homogenates and mitochondria of the liver, heart and skeletal muscle of hypokinetic rats was measured. The primary products of lipid peroxidation, i. e., diene conjugates, were accumulated in all tissues on hypokinesia days 3, 15, and 30. The content of the final product--malonic dialdehyde--in the mitochondria increased on hypokinesia days 15 and 30. The low level of NADPH--and ascorbate-dependent lipid peroxidation in the mitochondria at early stages of hypokinesia (up to 15 days) and diene conjugates in homogenates on hypokinesia day 7 can be attributed to an activation of the protective systems of the organism against the immobilization stress. It is suggested that at early stages of hypokinesia the process of lipid peroxidation, or to be more precise lipid hydroperoxidation can be blocked.     

Lipid peroxidation in tissues of rats exposed to head-down tilt, exercise or immobilization stress

Lipid peroxidation in tissues of rats exposed to antiorthostatic hypokinesia (-15 degrees) for 60 days, heavy-load exercise (swimming) and 2-hour immobilization was investigated polarographically. Antiorthostatic hypokinesia produced activation of free-radical lipid peroxidation in skeletal muscles, myocardium and plasma which reached a peak on hypokinesia day 3 and remained elevated by day 60. Exercise and immobilization applied during hypokinesia led to an accumulation of endogenous lipid peroxidation products in skeletal muscles and in the heart, although in a lesser degree. It is postulated that during hypokinesia lipid peroxidation is most probably activated due to the following factors: increased activity of the hormonal component of the sympathicoadrenal system, accumulation of excessive quantities of free fatty acids, and reduced activity of anti-oxidant enzymes.     

Activation of lipid peroxides in the liver during hypokinesia and its prevention by antioxidants

Experiments on white rats showed that exposure to hypokinesia increased peroxidation of unsaturated fatty acids of lipids of cell membranes, decreased the content of sulfhydryl groups, and increased the content of disulphide groups. This was very marked during the first 4-7 days, i.e., during the time of a distinct stress-reaction. At later stages the rate of free radical processes decreased slightly. In the recovery period that followed 7-day hypokinesia lipid peroxidation in the rats gradually returned to normal. The initiation of free radical reactions during hypokinesia can be prevented by means of antioxidants (acetate tocopherol, sodium selenite) and syrepar.     

Succinate dehydrogenase and cytochrome oxidase activity in rat tissues during prolonged hypokinesia

The activity of cytochrome oxidase in the liver, skeletal muscles, kidneys, brain and lungs of 56 white rats decreased on days 15 and 60 of the hypokinetic study. The activity of succinate dehydrogenase significantly lowered in the brain and slightly diminished in the lungs and skeletal muscles on the same days. The activity of succinate dehydrogenase in the liver increased on the 90th hypokinetic day.     

Influence of glycogen on liver density: computed tomography from a metabolic perspective

The liver is a metabolically active organ with a radiographic density that can be modified by its glycogen and fat content. In rhesus monkeys an increase in liver glycogen induced by glucose loading was accompanied by an increase in attenuation values on computed tomography and a decrease in total liver fat. Conversely, fasting depleted glycogen, increased fat, and decreased liver attenuation. Acute glycogen depletion without significant change in fat was induced by administration of glucagon and accompanied by a decrease in attenuation. These results along with in vitro measurements of glycogen solutions suggest that an increase of approximately 3 Hounsfield units can be expected for each percent increase in liver glycogen content.     

Biochemical aspects of overtraining in endurance sports : the metabolism alteration process syndrome

Recent studies have shown that endurance overtraining could result from successive and cumulative alterations in metabolism, which become chronic during training. The onset of this process is a biochemical alteration in carbohydrate (saccharide) metabolism. During endurance exercises, the amount of saccharide chains from two blood glycoproteins (alpha(2)-macroglobulin and alpha(1)-acid glycoprotein) was found to have decreased, i.e. concentrations of these proteins remained unchanged but their quality changed. These saccharide chains were probably used for burning liver glycogen stores during exercise. This step was followed by alterations in lipid metabolism. The most relevant aspect of this step was that the mean chain length of blood fatty acids decreased, i.e. the same amount of fatty acids were found within the blood, but overtrained individuals presented shorter fatty acids than well-trained individuals. This suggests that alterations appeared in the liver synthesis of long-chain fatty acids or that higher peroxidation of blood lipoparticles occurred. For the final step of this overtraining process, it was found that these dysfunctions in carbohydrate/lipid metabolism led to the higher use of amino acids, which probably resulted from protein catabolism. The evolution of three protein concentrations (alpha(1)-acid glycoprotein, alpha(2)-macroglobulin and IgG(3)) correlated with this amino acid concentration increase, suggesting a specific catabolism of these proteins. At this time only, overtraining was clinically diagnosed through conventional symptoms. Therefore, this process described successive alterations in exercise metabolism that shifted from the main energetic stores of exercise (carbohydrates and lipids) towards molecular pools (proteins) normally not substantially used for the energetic supply of skeletal muscles. Now, a general biochemical model of the overtraining process may be proposed which includes most of the previously identified metabolic hypotheses.     

模拟高原低氧应激环境下大鼠内分泌代谢的变化研究

目的：探索高原低氧应激环境对大鼠糖脂代谢的影响。方法：将大鼠随机分为对照组和低压缺氧应激组,缺氧组大鼠置模拟海拔6 000m低压舱内48h×3次,实验结束后,缺氧组从低压氧舱中取出后立即断头处死,测定血糖,胰岛素,采用稳态模型HOMAβ评估胰岛β细胞功能,测定血脂（TC、TG、LDL-C、HDL-C）,称量脏器重量,测定肝、肌糖原含量。结果：相比较正常组,Hypoxia组大鼠血糖值稍有降低,但胰岛素水平显著升高（P〈0.05）。Hypoxia组大鼠的HOMAβ高于正常对照组。脏器重量结果显示,Hypoxia组大鼠的肾脏重量显著降低（P〈0.05）,脾脏、肝脏重量显著升高（P〈0.01,P〈0.05）,肾上腺重量有下降趋势。与正常对照组相比,Hypoxia组大鼠TC含量显著增高（P〈0.01）;Hypoxia组大鼠肝糖原显著升高（P〈0.05）,而肌糖原显著降低（P〈0.01）;Hypoxia组大鼠TRH、TSH、T3具有下降趋势,仅TSH具有统计学意义（P〈0.01）,而T4显著升高（P〈0.05）。结论：高原低氧应激条件下,大鼠机体呈现血糖降低,胰岛功能增强,肝糖原储备增加,肌糖原储备减少,糖脂代谢紊乱。     

低肌糖原含量促进运动诱导大鼠骨骼肌IL-6基因转录的可能信号通路

目的:探讨低肌糖原含量促进运动诱导的骨骼肌白细胞介素6(interleukin-6,IL-6)基因转录的增加与核转录因子κB(Nuclear factor kappa B,NF-κB)及p38丝裂原激活的蛋白激酶(Mitogen-activated protein kinase,p38MAPK)信号通路激活的关系。方法:空白对照组(n=8)大鼠不运动,其余80只大鼠分为正常肌糖原组和低肌糖原组两大组,每组40只,先进行2 h跑台运动(消耗肌糖原),运动后24 h内采取不同膳食干预,低肌糖原组大鼠运动后6 h喂食低糖饲料,正常肌糖原组运动后即刻喂食标准饲料,这样运动24 h后低肌糖原组大鼠肌糖原含量与空白对照组相比显著降低(P<0.05),而正常肌糖原组大鼠肌糖原含量与空白对照组相比无显著性差异(P>0.05)。然后两个大组进行定量负荷运动,分别于运动前、运动30 min即刻、运动2 h即刻、运动2 h后恢复3 h和恢复6 h宰杀大鼠取材,测定血清IL-6蛋白含量、肌糖原含量、骨骼肌NF-κB及p38MAPK蛋白含量和骨骼肌IL-6 mRNA水平。结果:与运动前相比,低肌糖原组和正常肌糖原组大鼠运动2h即刻骨骼肌IL-6 mRNA水平、骨骼肌核磷酸化NF-κB蛋白含量、骨骼肌核磷酸化p38MAPK蛋白含量均显著上升(P<0.05)。与运动2 h即刻相比,低肌糖原组与正常肌糖原组运动后3 h及运动后6 h骨骼肌IL-6 mRNA水平增加,骨骼肌核磷酸化p38MAPK蛋白含量下降,而骨骼肌核磷酸化NF-κB蛋白含量运动后3 h上升,运动6 h后下降。运动2 h即刻、运动2 h后3 h及运动2 h后6 h,低肌糖原组与正常肌糖原组上述三指标均有显著性差异(P<0.05)。结论:低肌糖原含量促进运动引起的骨骼肌IL-6基因转录增加可能是通过激活NF-κB和p38MAPK信号通路实现的。     

缺氧习服大鼠骨骼肌葡萄糖代谢特点研究

目的 :探讨缺氧习服后组织物质代谢特点。方法 :将大鼠置模拟海拔 5 0 0 0m低压舱内 ,30d后取动脉血 ,测定血气、血糖等 ;取双后肢骨骼肌用3 H 脱氧葡萄糖测定葡萄糖摄取率 ,用葡萄糖氧化酶法测定葡萄糖、糖原含量 ;用酶法测定ATP、磷酸肌酸、乳酸水平 ,并以平原动物作为对照组进行对比分析。结果 :与对照组相比 ,缺氧组血糖、骨骼肌葡萄糖摄取率、葡萄糖含量显著增加 ,而糖原显著降低 ,骨骼肌ATP、磷酸肌酸、乳酸在缺氧组与对照组之间没有显著性差异。结论 :经过缺氧习服之后 ,组织能量代谢能达到平衡状态 ,葡萄糖利用能力加强     

Contractile properties of skeletal muscles of rats after flight on "Kosmos-1887"

Contractile properties of skeletal muscles of rats were investigated using glycerinated muscle preparations that were obtained from Cosmos-1887 animals flown for 13 days (plus 2 days on the ground) and from rats that remained hypokinetic for 13 days on the ground. In the flow rats, the absolute mass of postural muscles remained unchanged while their relative mass increased; this may be attributed to their enhanced hydration which developed during the first 2 days after landing. Strength losses of the postural muscles were less significant than after previous flights. Comparison of the Cosmos-1887 and hypokinesia control data has shown that even 2-day exposure to 1 G after 13-day flight can modify drastically flight-induced changes.     

急性递增负荷跑台运动对小鼠腓肠肌自噬和葡萄糖转运功能的影响

目的:观察急性递增负荷跑台运动对腓肠肌自噬和葡萄糖转运功能的影响,探讨运动激活自噬对骨骼肌葡萄糖转运功能的作用.方法:健康雄性4周龄ICR小鼠适应性喂养3天,然后随机分为安静对照组(Con组,n=6只)和急性递增负荷跑台运动组(n=24只).急性递增负荷跑台运动组小鼠运动力竭后根据恢复时间再分为运动后即刻组(0h组,n...     

Status of the lipid phase of plasma membranes of the rat heart after repeated exposure to an alternate magnetic field of 50 Hz frequency

The concentration of lipids and spectrum of phospholipids in plasma membranes of hearts of rats exposed for 15 times to intermittent (1:2) alternative magnetic field of 50 Hz and 9.4 mT were measured. This exposure lead to accumulation of lipids and increase of free fatty acids, triacylglycerides, cholesterol esters and phospholipids (although to a smaller extent). The cholesterol/phospholipids ratio decreased significantly. The spectrum of phospholipids was similar to that in the controls, except for phosphatidyl inositol whose content grew.     

La récupération après l'exercice. Analyse de la réplétion des réserves énergétiques

According to the intensity and the duration of exercise, depletion of substrates may be important. After exhaustive exercise the muscular store of creatine phosphate (CP) could be almost entirely depleted while the ATP store is half depleted. The resynthesis of both substrates occurs rapidly (5 min) during recovery. However, the repletion of CP is totally inhibited if the local circulation to the muscle is occluded. It is suggested that the initial fast phase of CP resynthesis is limited by the availability of oxygen whereas the subsequent slow phase is limited by the hydrogen ion transport out of the muscle.After liver glycogen is depleted by prolonged exercise, gluconeogenesis becomes necessary through lactate, pyruvate, glycerol and amino acids. As estimated from splanchnic uptake of gluconeogenic precursors, 60–65% of newborn glucose leave the liver and are taken up by the muscles which have been active. Total repletion of liver glycogen is completed 48 h after cessation of exercise with adequate glucose supply.Rapid muscle glycogen occurs in response to carbohydrate feeding following prolonged exercise, leading sometimes to supercompensation. Usually the repletion of glycogen is completed after 24 h if a normal diet (55% carbohydrate) is taken up by the subject. The synthesis of glycogen depends on several factors namely, (1) a persistent increase in glucose uptake by the muscle following exercise, up to 4–6 h, (2) an increase in insulin sensitivity which persists for 4 h following the exercise, (3) an inverse relation between the active form of glycogen synthase and glycogen content, (4) lactate which is rapidly incorporated into glycogen in fast-twitch fibres. It seems probable that glucose is the major substrate for glycogen synthesis in muscle following prolonged exercise of moderate intensity. In contrast, short bouts of heavy exercise result in glycogen repletion from lactate which could play an extended role in this context. Eventually, the regulation of glycogen resynthesis in muscles and liver following exercise depends on several ligands which operate on different key-enzymes.After prolonged physical exercise, lipoprotein lipase activity in skeletal muscle remains increased for several hours or days according to the type of exercise. Post-exercise ketosis occurs in untrained subjects and may be due to a lower carbohydrate intake than that of athletes. Hepatic malonyl-CoA, in subjects who have sufficient liver glycogen, is likely to be the responsible factor for the degree of post-exercise ketosis between trained and untrained subjects.Increased sensitivity to insulin after exercise also stimulates amino acid transport in red fibre muscles. After short bouts of exercise, protein synthesis rates in muscles appear to decrease in the first hour after exercise, but in the second hour after work increase to levels greater than normal.‘Substrate cycles’ appear to be involved in the ‘ultra slow’ component of post-exercise oxygen consumption. It has been calculated that substrate cycles and the repletion of glycogen and protein could account for an extra oxygen uptake of 50 l for a period of 12 h following prolonged and intensive exercise.     

Lipid metabolic indices in man during head-down tilt hypokinesia and their correction

Twenty one test subjects exposed to head-down tilt for 120 days were subdivided to four groups: Group 1--nine subjects used as controls, Group 2--three bed rested subjects who performed regular exercises, Group 3--four bed rested subjects who were given selected drugs, including Vitamin F-99 that influenced lipid metabolism, and Group 4--four bed rested subjects who performed regular exercises and received Vitamin F-99. At different stages of bed rest and recovery the content of lipoprotein fractions and lipids of different classes in serum was measured by thin-layer chromatography. The concentration of cholesterol in biliary lipids was determined. In Group 1 and 2 subjects bed rest led to a drastic and significant increase of cholesterol esters in blood, a decrease of phospholipids, variations of triglycerides and non-esterified fatty acids, and a lower percentage content of alpha-lipoproteins. The use of Vitamin F-99 produced positive changes in the above parameters of lipid metabolism (it normalized the level of cholesterol and phospholipids). In Group 4 subjects the effect of exercise combined with drugs was most distinct.     

Examination of skeletal muscles of rats after a short-term flight on Cosmos-1667

Using morphological and histochemical methods, skeletal muscles (soleus, gastrocnemius), quadriceps and biceps muscles) of Wistar-SPF rats flown for 7 days on Cosmos-1667 were investigated. The short-term exposure to microgravity led to muscle atrophy which primarily involved myofibers with a high level of oxidative metabolism and a low level of ATPase activity. The percentage composition of myofibers of different types remained unchanged. The soleus muscle showed the greatest changes which included both atrophic and dystrophic shifts. Muscle atrophy developed together with metabolic changes that resulted in glycogen accumulation and decreased SDH activity. After return to Earth's gravity microcirculation disorders were seen only in the soleus muscle.     

Role of fat metabolism in exercise

Fat and carbohydrate are the two major energy sources used during exercise. Either source can predominate, depending upon the duration and intensity of exercise, degree of prior physical conditioning, and the composition of the diet consumed in the days prior to a bout of exercise. Fatty acid oxidation can contribute 50 to 60 per cent of the energy expenditure during a bout of low intensity exercise of long duration. Strenuous submaximal exercise requiring 65 to 80 per cent of VO2 max will utilize less fat (10 to 45 per cent of the energy expended). Exercise training is accompanied by metabolic adaptations that occur in skeletal muscle and adipose tissue and that facilitate a greater delivery and oxidation of fatty acids during exercise. The trained state is characterized by an increased flux of fatty acids through smaller pools of adipose tissue energy. This is reflected by smaller, more metabolically active adipose cells in smaller adipose tissue depots. Peak blood concentrations of free fatty acids and ketone bodies are lower during and following exercise in trained individuals, probably due to increased capacity of the skeletal musculature to oxidize these energy sources. Trained individuals oxidize more fat and less carbohydrate than untrained subjects when performing submaximal work of the same absolute intensity. This increased capacity to utilize energy from fat conserves crucial muscle and liver glycogen stores and can contribute to increased endurance. Further benefits of the enhanced lipid metabolism accompanying chronic aerobic exercise training are decreased cardiac risk factors. Exercise training results in lower blood cholesterol and triglycerides and increased high density lipoprotein cholesterol. High-fat diets are not recommended because of their association with atherosclerotic heart disease. Recent evidence suggests that low-fat high-carbohydrate diets may increase blood triglycerides and reduce high density lipoproteins. This suggests that the chronic ingestion of diets that are extreme in their composition of either fat or carbohydrate should be approached with caution in health-conscious athletes, as well as in sedentary individuals.