Decrease In Phosphocreatine Levels Research Articles

Metabolic recovery in Atlantic salmon fry and parr following forced activity

Atlantic salmon Salmo salar fry and parr were subjected to 5 min of forced activity and the subsequent changes in oxygen consumption and ammonia excretion rates were evaluated over a 24 h period. In a second experiment, individual Atlantic salmon fry and parr were freeze‐clamped in liquid nitrogen, before, immediately following a 5 min activity period, or after periods of recovery up to 2 h. Samples were analysed for whole body phosphocreatine (PCr), ATP and lactate. Five minutes of forced activity resulted in significant increases in both oxygen consumption and ammonia excretion rates. Changes in the oxygen consumption rates were greater in the parr compared with the fry. In contrast, the post‐exercise ammonia excretion rates were nearly twice as high for the fry compared with the parr. Exercise also caused a marked decrease in PCr levels (c. 47 and 65% in fry and parr, respectively), no change in ATP levels and a significant increase in lactate levels in Atlantic salmon fry and parr. Recovery of PCr occurred quickly (between 15 and 30 min) in fry and parr. Although the post‐activity levels of lactate were lower in fry (c. 3 μmol g−1) compared with parr (c. 14 μmol g−1), lactate levels returned to control levels within 60 min in fry, but it took >2 h for this metabolite to recover in parr. Compared with parr, these findings show that Atlantic salmon fry possess a reduced anaerobic capacity, and these results are consistent with the theoretical and experimental evidence that smaller fish support burst swimming through aerobic processes.

Decrease in phosphocreatine level in skeletal muscle of SIV-infected rhesus macaques correlates with decrease in intracellular glutathione.

Loss of skeletal muscle tissue (cachexia) is one of the hallmarks of HIV infection. It has been found (1) that creatine kinase, i.e., an enzyme of pivotal importance in muscular mitochondrial energy metabolism, is inhibited by oxidative glutathiolation, and (2) that reduced glutathione (GSH) is decreased in skeletal muscle of SIV-infected rhesus monkeys. We, therefore, have studied the phosphocreatine (P-Cr) levels. Muscle tissue from SIV-infected macaques showed significantly decreased P-Cr but normal creatine (Cr), ATP, and ADP when compared with uninfected macaques. Individual P-Cr levels were significantly correlated with GSH. Our findings may explain the dysregulation of energy metabolism in cachexia.

Neither Moderate Hypoxia nor Mild Hypoglycaemia Alone Causes Any Significant Increase in Cerebral [Ca2±i: Only a Combination of the Two Insults Has This Effect.: A 31P and 19F NMR Study

(1) The energy state and free intracellular calcium concentration ([Ca2+]i) of superfused cortical slices were measured in moderate hypoxia (approximately 65 microM O2), in mild hypoglycaemia (0.5 mM glucose), and in combinations of the two insults using 19F and 31P NMR spectroscopy. (2) Neither hypoxia nor hypoglycaemia alone caused any significant change in [Ca2+]i. Hypoxia caused a 40% fall in phosphocreatine (PCr) content but not in ATP level, and hypoglycaemia produced a slight fall in both (as expected from previous studies). These changes in the energy state recovered on return to control conditions. (3) A combined sequential insult (hypoxia, followed by hypoxia plus hypoglycaemia) produced a 100% increase in [Ca2+]i and a decrease in PCr level to approximately 25% of control. The reverse combined sequential insult (hypoglycaemia, followed by hypoglycaemia plus hypoxia) had the same effect. On return to control conditions there was some decrease in [Ca2+]i and a small increase in PCr content, but neither recovered to control levels. (4) Exposure of the tissue to the combined simultaneous insult (hypoxia plus hypoglycaemia) immediately after the control spectra had been recorded resulted in a fivefold increase in [Ca2+]i and a similar decrease in PCr level to 20-25% of control. There was little if any change of [Ca2+]i or PCr level on return to control conditions. (5) These results are discussed in terms of metabolic adaptation of some but not all of the cortical cells to the single type of insult, which renders the tissues less vulnerable to the combined insult.

Muscle bioenergetics in skiers: studies using NMR spectroscopy.

Sedentary human subjects (n = 6) and two homogeneous groups of athletes, trained for down-hill skiing (n = 5) and cross-country skiing (n = 7), were subjected to cardiorespiratory testing and to evaluation of the bioenergetics of calf muscles by means of Phosphorus Nuclear Magnetic Resonance Spectroscopy. The exercise consisted of successive plantar flexions performed at graded fractions of the maximal voluntary contraction force. It appears from this study that the decrease in phosphocreatine level induced by exercise at 80% of maximal voluntary contraction, was smaller in the muscles of athletes who trained for cross-country skiing, than in the muscles of down-hill skiers and control subjects. Intracellular acidosis was virtually absent in cross-country athletes. The rate of restitution of phosphocreatine, after the exercise, was higher in both groups of skiers, compared to sedentary subjects. The maximal oxygen consumption and the maximal alactic power were higher in athletes than in sedentary subjects. NMR data and mechanical measurements are used in consideration with functional systemic indexes to characterize the capabilities of skiers.

Energetic metabolism in hypothyroid skeletal muscle, as studied by phosphorus magnetic resonance spectroscopy.

Phosphorus nuclear magnetic resonance spectroscopy was used to investigate the muscle bioenergetics in different hypothyroid states. Using the thenar muscle group as reference, 2 patients with chronic and severe hormonal deficiency, 3 patients with subacute hypothyroidism, and 8 patients with moderate thyroid insufficiency with isolated high blood TSH levels were studied at rest, during exercise, and during subsequent recovery. The patients were compared with 15 control subjects. Only 1 patient presented a clinical myopathy. The intracellular pH and the relative measurements of inorganic phosphate, phosphocreatine, phosphodiesters, and ATP were directly calculated from phosphorus spectra. Resting muscle showed a significant rise in the inorganic phosphate to ATP ratio. In working hypothyroid muscle, a more important decrease in phosphocreatine levels was noted in patients with chronic and subacute thyroid deficiency, while the intracellular pH fall was greater in all hypothyroid patients than in control subjects. The phosphocreatine recovery rate was lower in all deficient patients, reflecting a probable mitochondrial metabolism impairment. These results are consistent with a defect of the high energy phosphate metabolism in hypothyroidism, even in moderate or recent hormonal deficiency.

Effect of decreased pH on force and phosphocreatine in mammalian skeletal muscle

Phosphocreatine (PCr) and intracellular pH changes were monitored by 31P-NMR spectroscopy in isolated, arterially perfused cat biceps and soleus muscles, while the pH of the CO2-bicarbonate buffered perfusate was decreased from 7.1-7.4 to 6.4-6.7 by increasing the CO2 in the equilibrating gas from 5 to up to 70%. In biceps (fast twitch) muscles, intracellular pH decreased from 7.0 to 6.6 (30% CO2, 30 degrees C), peak tetanic force decreased by 8%, but the rise and relaxation times of tetanic were not significantly changed. In soleus muscles, intracellular pH decreased from 7.0 to 6.6 (30% CO2, 30 degrees C), peak tetanic force was unchanged, but the rise and relaxation times of tetani were increased by 27 and 112%, respectively. In both muscles greater decreases in tetanic force were observed during repetitive or ischemic stimulation, which resulted in intracellular pH similar to that produced by hypercapnia. Contrary to previous reports, there was no significant decrease in PCr level in either muscle type with decreased intracellular pH. In the soleus at 30 degrees C there was a significant increase in PCr level with decreased pH.

冠動脈結紮によるイヌ心筋の代謝変動におよぼすCarteolol前投与の効果

Effects of coronary artery ligation on myocardial glycogenolysis were studied in the endo- and epicardial layers of the left ventricular wall in dogs pretreated with 10 or 100 microgram/kg (i.v.) of carteolol, a potent beta-adrenergic blocking agent. Coronary artery ligation was performed by ligating one of the small branches of the left anterior descending coronary artery. In control (saline-pretreated) dogs, an increase in phosphorylase alpha activity and an increase in breakdown of glycogen were observed in both endo- and epicardial layers after coronary artery ligation. In the presence of 10 or 100 microgram/kg of carteolol, however, increases in phosphorylase alpha activity and increase in breakdown of glycogen were not observed in either the endo or epicardial layers. These results indicate that pretreatment of the dog with carteolol inhibits the increase in glycogenolysis caused by coronary artery ligation. Nevertheless, carteolol did not completely inhibit the coronary artery ligation-induced increase in glucose-6-phosphate and lactate levels, and the coronary artery ligation-induced decrease in phosphocreatine level, particularly in the endocardial layers.