Endurance exercise training such as marathon can increase the ability of exercise performance. Muscle glycogen is associated with an exercise performance, because glycogen depletion is primary causes of muscle fatigue. This review summarizes the glycogen saving effect according to duration of endurance exercise training. Long-term endurance exercise-induced mitochondrial biogenesis contributes to glycogen saving effect that is reduced glycogen breakdown and lactate accumulation. Glycogen sparing is due to a smaller decrease in adenosine triphosphate and phosphocreatine and a smaller increase in inorganic phosphate in the working muscles. It takes required endurance exercise training for about 4 weeks or more. Single bout or short-term endurance exercise is not sufficient to bring an increase in functional mitochondria. But peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) increases rapidly after single bout of endurance exercise. PGC-1α downregulates glycogenolytic and glycolytic enzymes to reduce muscle glycogen breakdown and lactic acid accumulation after short-term endurance exercise.
Adenosine Triphosphate ; Glycogen* ; Glycogenolysis ; Lactic Acid ; Mitochondria ; Muscle Fatigue ; Muscle, Skeletal* ; Muscles ; Organelle Biogenesis ; Peroxisomes ; Phosphocreatine

OBJECTIVETo study the effect of energy therapy on Ca2+ concentration and Ca2+ -ATP enzyme activity in rat master muscle after unilateral chew, and to discuss the protective action of the exogenous creatine phosphate on rat masseter muscle after unilateral chew.

METHODSThe 20 rats were randomly divided into 4 groups, A: Creatine phosphate normal control group; B: Creatine phosphate experimental group; C: Saline normal control group; D: Saline experimental group. The Ca2+ concentration were determined by atomic absorption spectrophotometry, the activity of the Ca2+ -ATP enzyme were determined by super-micro volume Ca2+ -ATP enzyme kit.

RESULTS(1) The Ca2+ concentration of the extraction side of group D which received the saline injection had significant difference compared with the non-extraction side (P = 0.007), the group C (P = 0.009) and the extraction side of group B (P = 0.01); (2) Ca2+ -ATP enzyme activity of group D were higher than its non-extraction side (P = 0.001), group C (P = 0.003) and the extraction side of group B (P = 0.001); (3) The ultrastructural changes of the rat masseter muscle under transmission electron microscope were as follows: The extraction side of group D have more severe pathological manifestations than non-extraction side. Both the extraction side and the non-extraction side of group B had a similar manifestation to the normal control group.

CONCLUSIONExogenous energy material, creatine phosphate, may have certain degree of protective effect on rat masseter muscles after unilateral chew. And it may become a possible way to improve the injury of the masseter muscle.

Animals ; Calcium ; metabolism ; Calcium-Transporting ATPases ; metabolism ; Masseter Muscle ; physiopathology ; ultrastructure ; Mastication ; Microscopy, Electron, Transmission ; Phosphocreatine ; pharmacology ; Rats

It is clear that creatine plays a reservoir of high energy phosphate bond as creatine phosphate and maintains ATP levels in skeletal muscle and nervous tissues. Creatine and creatine kinase activity are required to utilize creatine phosphate as high energy phosphate. The contents of creatine in testis of rats were determined by the method of Van Pilsum and compared with other organs for the study of the physiological role of creatine in testis. Creatine content of tests was 39.82+/-3.36 ug/g wet tissue compared with skeletal muscle, 52.92+/-10.25 ug/g wet tissue. It was relatively high compared with brain (15.45+/-6.49 ug/g wet tissue), heart (20.0+/-2.91 ug/g wet tissue), kidney (29.55+/-2.52 ug/g wet tissue) and liver (12.68+/-1.94 ug/g wet tissue). Creatinine content of testes (45.84+/-4.08 ug/g wet tissue) was very high, compared with skeletal muscle (24.14+/-7.73 ug/g wet tissue), heart .(23.71+/-4.73 ug/g wet tissue), brain (17.24+/-1.19 ug/g wet tissue), kidney (14.92+/-3.45 ug/g set tissue), and liver (9.59 +/-1.26 ug/g wet tissue). I suppose that creatine in testis of rats may be a part of potent system for generation of ATP from ADP hydrolyzing creatine phosphate.
Adenosine Diphosphate ; Adenosine Triphosphate ; Animals ; Brain ; Creatine Kinase ; Creatine* ; Creatinine ; Heart ; Kidney ; Liver ; Muscle, Skeletal ; Phosphocreatine ; Rats* ; Testis

PURPOSE: To evaluate the various phosphorus metabolism' of breast tumors with use of in vivo phosphorus-31 (31P) M R spectroscopy (MRS) MATERIALS AND METHODS: Five patients with breast tumor (benign in two, malignant in three) and three normal healthy volunteers participated in this study. All in vivo31P MRS examinations were performed on 1.5 Twhole-body MRI/MRS system by using a Free Induction Decay (FID) pulse sequence. Tl-weighted MR images were used for localization of tumors. Peak areas for each phosphorus metabolite were measured using a Marquart algorithm. RESULTS: Breast carcinoma had a substantially larger phosphomonoester (PME) and a smaller phosphocreatine (PCr) peak intensity than normal breast tissue. This was reflected in the relatively higher PME/PCr ratio of breast carcinomas as well as phosphodiester (PDE)/PCr, inorganic phosphate (Pi)/PCr, and adenosine triphosphate (ATP)/PCr ratios, compared with normal controls. The mean pH value of breast tumor demonstrating the alkaline nature was higher than that of normal controls. Spectral patterns between benign breast disease and normal breast tissue were quite similar, and differentiation was not established. CONCLUSION: Our preliminary study suggests that in vivo 31P MRS is a noninvasive examination which may be useful in the early differentiation of malignant breast tumors from normal and benign conditions. However, normal control and benign conditions could not be characterized on the basis of the phosphorus metabolite ratios.
Adenosine Triphosphate ; Breast Diseases ; Breast Neoplasms* ; Breast* ; Healthy Volunteers ; Humans ; Hydrogen-Ion Concentration ; Magnetic Resonance Spectroscopy* ; Phosphocreatine ; Phosphorus ; Spectrum Analysis

BACKGROUND: It is well known that both thiopental sodium and propofol reduce the cerebral metabolic rate. The author investigated whether these drugs have similar effects on neurobiochemical compounds by using 1H-NMR, which enables noninvasive in vivo measurements of brain biochemistry. METHODS: Six healthy white New Zealand rabbits (2.5-3.0 kg) were studied. A marginal ear vein was punctured for continuous intravenous infusion. Spontaneous breathing was maintained during the anesthesia. Neurobiochemical compounds such as N- acetylaspartate (NAA), choline-containing compounds (Cho), creatine plus phosphocreatine (Cr), myoinositol (MI), and lactate were examined at 30, 45 and 60 min during intravenous anesthesia induced with thiopental sodium (n = 3) and propofol (n = 3). RESULTS: The signals of NAA, Cho, Cr and MI were unchanged during thiopental anesthesia, but the NAA signal was reduced at 45 and 60 min, and that of Cr was reduced from 30 min until the end of the propofol anesthesia. The Cho signal was increased at 45 and 60 min during propofol anesthesia. Thiopental sodium signal were detected through the study, but propofol was detected only at 30 min. On comparing metabolic ratios in the two groups, the ratio of NAA/Cr was reduced and those of Cho/Cr and MI/Cr were higher in propofol group than in the thiopental sodium group. CONCLUSIONS: Our results suggest that thiopental sodium has a cerebral protective function. Howerver, further study is needed upon the cerebral protective function of propofol anesthesia. Propofol is more useful for total intravenous anesthesia than thiopental sodium.
Anesthesia ; Anesthesia, Intravenous* ; Biochemistry ; Brain* ; Creatine ; Ear ; Infusions, Intravenous ; Inositol ; Lactic Acid ; Magnetic Resonance Spectroscopy* ; Phosphocreatine ; Propofol* ; Protons* ; Rabbits ; Respiration ; Thiopental* ; Veins

PURPOSE: The present study examined how changes in cerebral hemodynamics in newborn piglets with bilirubin infusion can be evaluated by near infrared sepctroscopy (NIRS). METHODS: Seventeen newborn piglets were randomly divided into the following three experimental groups: six in the control group (CG) ; seven in the bilirubin infusion group (BG), and four in the bilirubin infusion with 7-nitroindazole group (NG). To achieve the concentration of bilirubin above 20 mg/dL, we injected a bolus of 40 mg/kg of bilirubin intravenously, followed by 30 mg/kg/hr of bilirubin continuous intravenous infusion. All groups were monitored with cerebral hemodynamics using near infrared spectroscopy (NIRS) and their brain cortexes were harvested and the activities of Na+, K+ -ATPase, level of conjugated dienes, ATP and phosphocreatine (PCr) were determined biochemically. RESULTS: No changes took place in CG. In BG and NG, base excess, pH, and MABP decreased, and lactate level in blood increased. Cerebral Na+, K+-ATPase activity and ATP, PCr level in BG significantly decreased and conjugated dienes increased compared to CG. These abnormalities observed in the BG were significantly improved in the NG. In continuous NIRS monitoring, [HbO2], [HbT], and [HbD] in BG were significantlly decreased compared to CG. However these abnormalities between NG and CG were not significantly different. There were no significant differences in ScO2 between the study groups. CONCLUSION: Our study suggests cerebral hemodynamic changes could be monitored by non- invasive NIRS in newborn piglets with bilirubin infusion.
Adenosine Triphosphate ; Bilirubin ; Brain ; Hemodynamics* ; Humans ; Hydrogen-Ion Concentration ; Hyperbilirubinemia ; Infant, Newborn* ; Infusions, Intravenous ; Jaundice ; Kernicterus ; Lactic Acid ; Phosphocreatine ; Polymerase Chain Reaction ; Spectroscopy, Near-Infrared* ; Spectrum Analysis

It has been postulated that central nervous system disorders characterized by convulsive seizures are caused by alterations in one or more cerebral metabolism especially in cellular energy metabolism, electrolyte metabolism and glutamate metabolism. In the present study, alterations in cerebral energy metabolism, cellular electrolyte metabolism and glutamate metabolism were studied to investigate biochemical nature of cerebral disturbances in rats injected intraperitoneally with massive doses of penicillin. Also carried out were in vitro experiments by which direct effects of penicillin on concentrations of high energy compounds and Na+, K+-ATPase activity in the brains were determined. Intraperitoneal injections of pencillin G sodium(1,000,000 I.U. per kg body weight) to rats twice daily for 3 to 5 days resulted in significant decreases in cerebral concentrations of ATP, phosphocreatine and lactate, suggesting that penicillin induces cerebral dysfunctions by inhibiting energy production. While cerebral Na+, K+-ATPase activity and brain K+ content were significantly decreased in rats with penicllin-induced cerebral dysfunctions, brain Na+ and water contents were significantly increased. Observations that, in rats with penicillin-induced cerebral dysfunctions, the fall in high-energy phosphate contents in the brain took place as rapidly as the cation shifts indicate that alterations in both energy metabolism and electrolyte metabolism in the brain may be responsible for cerebral dysfunctions induced by penicillin. These assumptions were further supported by the findings that Na+, K+-ATPase activity and high-energy phosphate contents in the isolated cerebral hemispheres were profoundly affected by the addition of penicillin to the medium in which in vitro experiment was carried out. While the activity of glutamine synthetase in the brain was increased in rats exhibiting cerebral dysfunctions induced by penicillin, the activity of glutamine dehydrogenase was significantly decreased. Significance of changes in activities of these two brain enzymes in penicillin-induced cerebral dysfunctions was not immediately understood. It may be possible, however, that penicillin may influence glutamate contents in the brain directly orindirectly through the alteration of these two brain enzyme activities so as to modify the cerebral functions.
Adenosine Triphosphate ; Animals ; Brain ; Central Nervous System Diseases ; Cerebrum ; Energy Metabolism ; Glutamate-Ammonia Ligase ; Glutamic Acid ; Glutamine ; Injections, Intraperitoneal ; Lactic Acid ; Metabolism ; Oxidoreductases ; Penicillins* ; Phosphocreatine ; Rats ; Seizures

This study was performed to assess the accuracy of 31P magnetic resonance spectroscopy(MRS) in the evaluation of myocardial ischemia in cats. Twelve cats underwent myocardial ischemia and reperfusion induced by 90 minutes ligation followed by 90 minutes recirculation of the left anterior descending coronary artery (LAD). MRS was performed using a 4.7T Biospec MRS/MRI system (Bruker, Switzerland). An inner diameter 1.5cm-sized doubly tuned surface coli was used for the collection of the MR signal. The coli was implanted to the epicardial surface at the expected area of infarction. 31P MRS was acquired before and during the periods of ischemia and reperfusion with 5-minute to 30-minute of intervals. After completion of the 31P MRS study, animals were sacrificed and the hearts were excised for 2,3,5-triphenyl tetrazolium chloride (TTG0 histochemical staining. The area of infarct was measured on the photographs of TTG stained heart slices using a computer programmed planimetry and the results were compared with those of the 31P MRS study. The level of phosphocreatine (PCr) was decreased to 28.2±6.9% of the baseline level 90 minutes after occlusion and recovered to 43.8±4.8% of the baseline level at the end of the reperfusion. A 50% depletion of PCr was reached 5 minutes after the LAD occlusion. The ATP was decreased to a 26.6±3.6% of the baseline level 90 minutes after occlusion and recovered to a 35.9±6.0 of the baseline level 90 minutes after reperfusion. The decreasing rate of ATP was slower than that of PCr showing a 50% of depletion 15 minutes after occlusion. The PCr/ATP ratio was 1.16±0.09 at the baseline, decreased to 0.88±0.07 at 30 minutes of occlusion, and then progressively increased during the late ischemic and reperfused periods. The ratio of the infarcted area to the effective signal area of the surface coli was inversely correlated to the ATP (r=0.68) and PCr (r=0.40) levels obtained at the end of reperfusion. In conclusion, 31P MRS reflects the changes in myocardial high energy phosphorous metabolism during the actue ischemia and reperfusion. If on adequate localization technique is feasible, 31P MRS can be used clinically in the diagnosis and monitoring of the patients with acute myocardial infarction.
Adenosine Triphosphate ; Animals ; Cats* ; Coronary Vessels ; Diagnosis ; Heart ; Humans ; Infarction ; Ischemia ; Ligation ; Metabolism ; Myocardial Infarction* ; Myocardial Ischemia ; Phosphocreatine ; Polymerase Chain Reaction ; Reperfusion ; Spectrum Analysis*

BACKGROUND: Ischemia-reperfusion myocardial injury is an important factor to determine the early and the late mortality of transplanted patients. Recently, modulation of the cytosolic NADH/NAD+ ratio by pyruvate and aspartate was tested to protect the heart from ischemia-reperfusion injury. MATERIAL AND METHOD: We added pyruvate and aspartate to the University of Wisconsin solution, and evaluated their effect on myocardial protection. We used 16 piglet(age 1 to 3 days) hearts. Eight hearts were arrested with and stored in the University of Wisconsin solution(UW solution) for 24 hours(control group), and the other eight hearts were arrested with and stored in the modified UW solution added pyruvate(3 mmol/L) and aspartate(2 mmol/L)(test group). All hearts underwent modified reperfusion with blood cardioplegic solution followed by conversion to a left-sided working model with perfusion from a support pig. And then, we measured stroke work index(SWI), high-energy phosphate stores, and myocardial water content of the hearts. SWI was calculated at left ventricular end-diastolic pressures of 3, 6, 9, and 12 mmHg after 60 and 120 minutes reperfusion, respectively. RESULT: At 60 minutes and 120 minutes after reperfusion, SWI was higher in the test group than in the control group significantly. The levels of AMP, ADP, ATP of the test group were also higher. But, the creatine phosphate level and myocardial water content were similar in the two groups. CONCLUSION: From these results, we could prove that pyruvate and aspartate enhance cardiac contractility and high-energy phosphate stores after ischemia.
Adenosine Diphosphate ; Adenosine Triphosphate ; Aspartic Acid* ; Cardioplegic Solutions ; Cytosol ; Heart ; Humans ; Ischemia ; Mortality ; Perfusion ; Phosphocreatine ; Pyruvic Acid* ; Reperfusion ; Reperfusion Injury ; Stroke ; Wisconsin*

Patients with chronic renal failure(CRF) suffer from muscular dysfunction of varying degrees. 31P-nuclear magnetic resonance(NMR) spectroscopic studies of skeletal muscle have shown that these patients have less energy reservoir. Chronic metabolic acidosis has been known to decrease intracellular pH in rat muscle. We investigated the effect of correction of metabolic acidosis with sodium bicarbonate on muscle energy metabolism. Eight patients(6M, 2F) with CRF(creatinine clearance <20ml/min/1.73m2) who were clinically stable and had serum bicarbonate level less than 18mEq/L were included. The median age was 48 years (range; 29-56 years). The patients were treated with daily doses of 3 gram sodium bicarbonate for 3 months. Phosphocreatine to inorganic phosphate ratio(PCr/Pi) and intracellular pH were measured with 31P-NMR spectroscopy, at resting, nadir and maximum recovery state after all-out exercise, before and after correction of acidosis. Plasma bicarbonate level increased from 16.2+/-0.9 to 21.9+/-1.1mmol/L(p<0.05). Creatinine clearance, hematocrit and serum albumin did not change during the study period. The exercise capacity, as measured by the time holding the weight, did not improve with sodium bicarbonate treatment. PCr/Pi ratio at resting state was 7.0+/-1.9 before treatment, which did not change after treatment, 6.2+/-0.8, although plasma bicarbonate level increased significantly. The ratio reached bottom immediately after the all-out exercise(the nadir state) and then recovered toward preexercise value. The PCr/Pi ratio at nadir and maximum recovery state were not different between before and after treatment. The intracellular pH became more acidotic immediately after exercise, but no difference was found between before and after sodium bicarbonate treatment in resting state, nadir or maximum recovery state. With our results, we conclude that the partial correction of acidosis does not improve energy reserve and serum albumin in CRF patients.
Acidosis* ; Animals ; Creatinine ; Energy Metabolism* ; Hematocrit ; Humans ; Hydrogen-Ion Concentration ; Kidney Failure, Chronic* ; Muscle, Skeletal ; Phosphocreatine ; Plasma ; Rats ; Serum Albumin ; Sodium Bicarbonate ; Spectrum Analysis