scholarly journals Creatine supplementation and muscles: From metabolism to medical practice

2021 ◽  
Vol 16 (3) ◽  
pp. 317-321
Author(s):  
Romana VULTURAR ◽  
◽  
Bianca JURJIU ◽  
Marc DAMIAN ◽  
Anca BOJAN ◽  
...  
Keyword(s):  
Functional Performance ◽  
Energy Content ◽  
Exercise Physiology ◽  
Creatine Supplementation ◽  
High Energy ◽  
Muscle Physiology ◽  
High Energy Phosphates ◽  
Long Term Effects ◽  
Muscle Disorders ◽  
Atp Production

Creatine has become the most popular dietary supplement in sport and exercise physiology. In humans creatine is synthesized by the kidneys, pancreas and liver and transported mainly into brain, skeletal and cardiac muscle. Phosphocreatine is a high-energy content molecule, essential for the ADP to ATP conversion during intensive physical activity. Creatine and phosphocreatine are crucial in the energy shuttle system of high-energy phosphates between the mitochondrial ATP production and the cytosolic ATP consumption. Creatine supplementation increases lean body mass acting on myogenic regulatory factors. During muscular recovery, creatine supplementation regulates the regeneration process by reduction of muscle damage-induced inflammation and oxidative stress, activation and proliferation of satellite cells and regulation of calcium transport in muscle. The effects of creatine supplementation on muscle physiology are beneficial in anaerobic/aerobic exercises. In several muscle disorders (muscular dystrophies, in idiopathic inflammatory myopathies) creatine improved functional performance, but apparently not in metabolic myopathies; in McArdle diseases it may even have paradoxical effects. More research is warranted to better understand the short and long-term effects and safety of creatine supplementation among adolescents or elderly, as well as in different types of muscle diseases; for the two enzymatic genetic defects of creatine biosynthesis – arginine: glycine amidinotransferase (AGAT) and guanidinoacetate methyltransferase (GAMT), respectively – normal neurodevelopment has been achieved in early initiation of creatine therapy.

Responses of beta-adrenoceptor in rat soleus to phosphorus compound levels and/or unloading

1994 ◽  
Vol 266 (5) ◽  
pp. C1257-C1262 ◽  
Author(s):  
Y. Ohira ◽  
K. Saito ◽  
T. Wakatsuki ◽  
W. Yasui ◽  
T. Suetsugu ◽  
...  
Keyword(s):  
Contractile Activity ◽  
Creatine Supplementation ◽  
High Energy ◽  
Hindlimb Suspension ◽  
Phosphorus Compounds ◽  
High Energy Phosphates ◽  
High Energy Phosphate ◽  
Gravitational Unloading ◽  
Beta Adrenoceptor ◽  
Muscle Contractile

Responses of beta-adrenoceptor (beta-AR) in rat soleus to gravitational unloading and/or changes in the levels of phosphorus compounds by feeding either creatine or its analogue beta-guanidinopropionic acid (beta-GPA) were studied. A decrease in the density of beta-AR (about -35%) was induced by 10 days of hindlimb suspension, but the affinity of the receptor was unaffected. Suspension unloading tended to increase the levels of adenosine triphosphate and phosphocreatine and decrease inorganic phosphate. Even without unloading, the beta-AR density decreased after an oral creatine supplementation (about -20%), which also tended to elevate the high-energy phosphate levels in muscle. However, an elevation of beta-AR density was induced (about +36%) after chronic depletion of high-energy phosphates by feeding beta-GPA (about +125%). Data suggest that the density of beta-AR in muscle is elevated if the high-energy phosphate contents are chronically decreased and vice versa. However, it may not be directly related to the degree of muscle contractile activity.

Local cerebral glucose utilization during status epilepticus in newborn primates

1989 ◽  
Vol 256 (6) ◽  
pp. C1160-C1167 ◽  
Author(s):  
D. G. Fujikawa ◽  
B. E. Dwyer ◽  
R. R. Lake ◽  
C. G. Wasterlain
Keyword(s):  
Status Epilepticus ◽  
Temporal Cortex ◽  
High Energy ◽  
High Energy Phosphates ◽  
Long Term Effects ◽  
Energy Demands ◽  
Fold Level ◽  
Frontoparietal Cortex ◽  
Glucose Supply

The effect of bicuculline-induced status epilepticus (SE) on local cerebral metabolic rates for glucose (LCMRglc) was studied in 2-wk-old ketamine-anesthetized marmoset monkeys, using the 2-[14C]-deoxy-D-glucose autoradiographical technique. To estimate LCMRglc in cerebral cortex and thalamus during SE, the lumped constant (LC) for 2-deoxy-D-glucose (2-DG) and the rate constants for 2-DG and glucose were calculated for these regions. The control LC was 0.43 in frontoparietal cortex, 0.51 in temporal cortex, and 0.50 in thalamus; it increased to 1.07 in frontoparietal cortex, 1.13 in temporal cortex, and 1.25 in thalamus after 30 min of seizures. With control LC values, LCMRglc in frontoparietal cortex, temporal cortex, and dorsomedial thalamus appeared to increase four to sixfold. With seizure LC values, LCMRglc increased 1.5- to 2-fold and only in cortex. During 45-min seizures, LCMRglc in cortex and thalamus probably increases 4- to 6-fold initially and later falls to the 1.5- to 2-fold level as tissue glucose concentrations decrease. Together with our previous results demonstrating depletion of high-energy phosphates and glucose in these regions, the data suggest that energy demands exceed glucose supply. The long-term effects of these metabolic changes on the developing brain remain to be determined.

Contraction Failure of Skeletal Muscle of Rats Recovering from Critical Illness

1997 ◽  
Vol 92 (2) ◽  
pp. 189-195 ◽  
Author(s):  
Olav E. Rooyackers ◽  
Matthijs K. C. Hesselink ◽  
Anton J. M. Wagenmakers
Keyword(s):  
Skeletal Muscle ◽  
Critical Illness ◽  
Muscle Tension ◽  
High Energy ◽  
High Energy Phosphates ◽  
Maximal Aerobic Capacity ◽  
Tension Development ◽  
Atp Production ◽  
Stimulation Period ◽  
Subsequent Loss

1. Most patients recovering from critical illness experience enhanced fatiguability. Previously we have shown that zymosan-induced critical illness in rats is attended by a decreased mitochondrial content (maximal aerobic capacity) in skeletal muscle. We investigated whether this decrease results in an increased reduction in high-energy phosphates and a subsequent loss of contractility during in situ electrical stimulation in rats recovering from zymosan treatment. 2. Plantar-flexor muscles of the hindlimb were electrically stimulated via the innervating nerve to develop maximal isometric tetanic contraction. 3. Decreased concentrations of ATP were measured in gastrocnemius muscle of zymosan-treated rats, both at rest and after stimulation, in comparison with ad libitum-fed and pair-fed control rats. However, no differences in the stimulation-induced decreases in high-energy phosphate levels and changes in other metabolites, except ADP, were observed between the groups. Tension development in the zymosan-treated rats was, however, about 85% less compared with the pair-fed controls during the whole stimulation period. 4. We conclude that the primary cause of the loss of muscle tension in zymosan-treated rats is an insensitivity of skeletal muscle to stimulation via the nerve. An additional derangement in ATP production is, however, indicated by the comparable decreases in energy substrates during development of a dramatically lower tension.

scholarly journals Observation of intramyocellular lipids by means of 1H magnetic resonance spectroscopy

1999 ◽  
Vol 58 (4) ◽  
pp. 841-850 ◽  
Author(s):  
Chris Boesch ◽  
Jacques Décombaz ◽  
Johannes Slotboom ◽  
Roland Kreis
Keyword(s):  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
High Energy ◽  
Muscle Physiology ◽  
High Temporal Resolution ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Intramyocellular Lipids ◽  
Before And After ◽  
Recovery Protocols

Magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) are being increasingly used for investigations of human muscle physiology. While MRI reveals the morphology of muscles in great detail (e.g. for the determination of muscle volumes), MRS provides information on the chemical composition of the tissue. Depending on the observed nucleus, MRS allows the monitoring of high-energy phosphates (31P MRS), glycogen (13C MRS), or intramyocellular lipids (1H MRS), to give only a few examples. The observation of intramyocellular lipids (IMCL) by means of 1H MRS is non-invasive and, therefore, can be repeated many times and with a high temporal resolution. MRS has the potential to replace the biopsy for the monitoring of IMCL levels; however, the biopsy still has the advantage that other methods such as those used in molecular biology can be applied to the sample. The present study describes variations in the IMCL levels (expressed in mmol/kg wet weight and ml/100 ml) in three different muscles before and after (0, 1, 2, and 5 d) marathon runs for a well-trained individual who followed two different recovery protocols varying mainly in the diet. It was shown that the repletion of IMCL levels is strongly dependent on the diet post exercise. The monitoring of IMCL levels by means of 1H MRS is extremely promising, but several methodological limitations and pitfalls need to be considered, and these are addressed in the present review.

scholarly journals Efficiency of human skeletal muscle in vivo: comparison of isometric, concentric, and eccentric muscle action

1997 ◽  
Vol 83 (3) ◽  
pp. 867-874 ◽  
Author(s):  
T. W. Ryschon ◽  
M. D. Fowler ◽  
R. E. Wysong ◽  
A.-R. Anthony ◽  
R. S. Balaban
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Production Rate ◽  
Human Skeletal Muscle ◽  
Atp Synthesis ◽  
High Energy ◽  
High Energy Phosphates ◽  
Muscle Action ◽  
Atp Production

Ryschon, T. W., Fowler, R. E. Wysong, A.-R. Anthony, and R. S. Balaban. Efficiency of human skeletal muscle in vivo: comparison of isometric, concentric, and eccentric muscle action. J. Appl. Physiol. 83(3): 867–874, 1997.—The purpose of this study was to estimate the efficiency of ATP utilization for concentric, eccentric, and isometric muscle action in the human tibialis anterior and extensor digitorum longus in vivo. A dynamometer was used to quantitate muscle work, or tension, while simultaneous 31P-nuclear magnetic resonance data were collected to monitor ATP, phosphocreatine, inorganic phosphate, and pH. The relative efficiency of the actions was estimated in two ways: steady-state effects on high-energy phosphates and a direct comparison of ATP synthesis rates with work. In the steady state, the cytosolic free energy dropped to the lowest value with concentric activity, followed by eccentric and isometric action for comparative muscle tensions. Estimates of ATP synthesis rates revealed a mechanochemical efficiency [i.e., ATP production rate/work (both in J/s)] of 15.0 ± 1.3% in concentric and 34.7 ± 6.1% in eccentric activity. The estimated maximum ATP production rate was highest in concentric action, suggesting an activation of energy metabolism under these conditions. By using direct measures of metabolic strain and ATP turnover, these data demonstrate a decreasing metabolic efficiency in human muscle action from isometric, to eccentric, to concentric action.

Na-H exchange in myocardium: effects of hypoxia and acidification on Na and Ca

1990 ◽  
Vol 259 (6) ◽  
pp. C940-C948 ◽  
Author(s):  
S. E. Anderson ◽  
E. Murphy ◽  
C. Steenbergen ◽  
R. E. London ◽  
P. M. Cala
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Magnetic Resonance ◽  
Atpase Activity ◽  
Time Course ◽  
High Energy ◽  
High Energy Phosphates ◽  
Atp Production ◽  
31P Nuclear Magnetic Resonance ◽  
Regulatory Capacity ◽  
Na Uptake

Historically, increase in cell Na content during ischemic and hypoxic episodes were thought to result from impaired ATP production causing decreased Na(+)-K(+)-ATPase activity. Here we report the results of testing the alternate hypothesis that hypoxia-induced Na uptake is 1) the result of increased entry, as opposed to decreased extrusion 2) via Na-H exchange operating in a pH regulatory capacity and that cell Ca accumulation occurs via Na-Ca exchange secondary to collapse of the Na gradient. We used 23Na-, 19F-, and 31P-nuclear magnetic resonance (NMR) to measure intracellular Na content (Nai), Ca concentration [( Ca]i), pH (pHi), and high-energy phosphates in Langendorff-perfused rabbit hearts. When the Na(+)-K(+)-ATPase was inhibited by ouabain and/or K-free perfusion, hearts subjected to hypoxia gained Na at a rate greater than 10 times that of normoxic controls [during the first 12.5 min Nai increased from 7.9 +/- 5.8 to 34.9 +/- 11.0 (SD) meq/kg dry wt compared with 11.1 +/- 16.3 to 13.6 +/- 9.0 meq/kg dry wt, respectively]. When normoxic hearts were acidified using a 20 mM NH4Cl prepulse technique, pHi rapidly fell from 7.27 +/- 0.24 to 6.63 +/- 0.12 but returned to 7.07 +/- 0.10 within 20 min, while Na uptake was similar in rate and magnitude to that observed during hypoxia (24.5 +/- 13.4 to 132.1 +/- 17.7 meq/kg dry wt). During hypoxia and after NH4Cl washout, increases in [Ca]i were similar in time course to those observed for Na.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Mitochondrial Substrate-Level Phosphorylation as Energy Source for Glioblastoma: Review and Hypothesis

ASN NEURO ◽  
2018 ◽  
Vol 10 ◽  
pp. 175909141881826 ◽  
Author(s):  
Christos Chinopoulos ◽  
Thomas N. Seyfried
Keyword(s):  
Atp Synthase ◽  
Adenine Nucleotide ◽  
Tricarboxylic Acid Cycle ◽  
Atp Synthesis ◽  
High Energy ◽  
Adult Brain ◽  
High Energy Phosphates ◽  
Atp Production ◽  
Substrate Level Phosphorylation ◽  
Substrate Level

Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers. Ultrastructural and biochemical evidence shows that GBM cells exhibit mitochondrial abnormalities incompatible with energy production through oxidative phosphorylation (OxPhos). Under such conditions, the mitochondrial F0-F1 ATP synthase operates in reverse at the expense of ATP hydrolysis to maintain a moderate membrane potential. Moreover, expression of the dimeric M2 isoform of pyruvate kinase in GBM results in diminished ATP output, precluding a significant ATP production from glycolysis. If ATP synthesis through both glycolysis and OxPhos was impeded, then where would GBM cells obtain high-energy phosphates for growth and invasion? Literature is reviewed suggesting that the succinate-CoA ligase reaction in the tricarboxylic acid cycle can substantiate sufficient ATP through mitochondrial substrate-level phosphorylation (mSLP) to maintain GBM growth when OxPhos is impaired. Production of high-energy phosphates would be supported by glutaminolysis—a hallmark of GBM metabolism—through the sequential conversion of glutamine → glutamate → alpha-ketoglutarate → succinyl CoA → succinate. Equally important, provision of ATP through mSLP would maintain the adenine nucleotide translocase in forward mode, thus preventing the reverse-operating F0-F1 ATP synthase from depleting cytosolic ATP reserves. Because glucose and glutamine are the primary fuels driving the rapid growth of GBM and most tumors for that matter, simultaneous restriction of these two substrates or inhibition of mSLP should diminish cancer viability, growth, and invasion.

scholarly journals Cerebral energetic effects of creatine supplementation in humans

2007 ◽  
Vol 292 (4) ◽  
pp. R1745-R1750 ◽  
Author(s):  
J. W. Pan ◽  
K. Takahashi
Keyword(s):  
Human Brain ◽  
Creatine Supplementation ◽  
Significant Negative Correlation ◽  
High Energy ◽  
Muscle Physiology ◽  
High Energy Phosphate ◽  
Healthy Human ◽  
Fractional Increase ◽  
And Shifts ◽  
Induced Changes

There has been considerable interest in the use of creatine (Cr) supplementation to treat neurological disorders. However, in contrast to muscle physiology, there are relatively few studies of creatine supplementation in the brain. In this report, we use high-field MR 31P and 1H spectroscopic imaging of human brain with a 7-day protocol of oral Cr supplementation to examine its effects on cerebral energetics (phosphocreatine, PCr; ATP) and mitochondrial metabolism ( N-acetyl aspartate, NAA; and Cr). We find an increased ratio of PCr/ATP ( day 0, 0.80 ± 0.10; day 7, 0.85 ± 09), with this change largely due to decreased ATP, from 2.7 ± 0.3 mM to 2.5 ± 0.3 mM. The ratio of NAA/Cr also decreased ( day 0, 1.32 ± 0.17; day 7 1.18 ± 0.13), primarily from increased Cr (9.6 ± 1.9 to 10.1 ± 2.0 mM). The Cr-induced changes significantly correlated with the basal state, with the fractional increase in PCr/ATP negatively correlating with the basal PCr/ATP value ( R = −0.74, P < 0.001). As NAA is a measure of mitochondrial function, there was also a significant negative correlation between basal NAA concentrations with the fractional change in PCr and ATP. Thus healthy human brain energetics is malleable and shifts with 7 days of Cr supplementation, with the regions of initially low PCr showing the largest increments in PCr. Overall, Cr supplementation appears to improve high-energy phosphate turnover in healthy brain and can result in either a decrease or an increase in high-energy phosphate concentrations.

Protection of ischemic myocardium by inhibition of contracture in isolated rat heart

1996 ◽  
Vol 271 (6) ◽  
pp. H2515-H2519 ◽  
Author(s):  
M. Tani ◽  
H. Hasegawa ◽  
Y. Suganuma ◽  
K. Shinmura ◽  
Y. Kayashi ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Recovery Of Function ◽  
Ischemia Reperfusion ◽  
High Energy ◽  
Isolated Rat Heart ◽  
Ischemic Myocardium ◽  
Low Flow ◽  
High Dose ◽  
High Energy Phosphates ◽  
Atp Production

Protection of the ischemic myocardium by pretreatment with a high dose of 2,3-butanedione monoxime (BDM) is attributed to the enhancement of glycolytic ATP production rather than to the inhibition of contracture during mild ischemia. Our objective was to investigate whether the inhibition of contracture would protect the arrested heart during prolonged ischemia. Isolated perfused rat hearts were subjected to 30 min of low-flow ischemia followed by reperfusion. Ischemic hearts were treated with BDM (5 mmol/l) after beating stopped. BDM ameliorated the increase in intraventricular pressure after ischemia without significant changes in ATP levels and with a decreased accumulation of lactate. BDM treatment accelerated the recovery of function and high-energy phosphates with reduced myocardial Ca2+ overload. The results of this study suggested that inhibition of contracture can protect the heart from ischemia-reperfusion injury.

Glycolysis is necessary to preserve myocardial Ca2+ homeostasis during beta-adrenergic stimulation

1993 ◽  
Vol 264 (3) ◽  
pp. H670-H678 ◽  
Author(s):  
K. Nakamura ◽  
H. Kusuoka ◽  
G. Ambrosio ◽  
L. C. Becker
Keyword(s):  
Diastolic Pressure ◽  
Superconducting Magnet ◽  
High Energy ◽  
Left Ventricular ◽  
19F Nmr ◽  
High Energy Phosphates ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Atp Production ◽  
Developed Pressure

Although ATP derived from glycolysis represents only a small fraction of total myocardial ATP production, metabolic compartmentation may result in preferential use of glycolytic ATP for certain membrane activities, including pumping of Ca2+ from the cytoplasm. We tested this hypothesis by looking for evidence of Ca2+ overload in normoxic perfused rabbit hearts given iodoacetate (IAA, 50 microM) to block glycolysis and isoproterenol (Iso, 0.05 microM) to stimulate Ca2+ entry. The hearts beat isovolumically and were perfused with 16 mM glucose and 5 or 10 mM pyruvate (to preserve oxidative metabolism) in a superconducting magnet for 31P-nuclear magnetic resonance (NMR) measurements of high energy phosphates or 19F-NMR measurements of intracellular free Ca2+ concentration ([Ca2+]i). IAA by itself had no effect on left ventricular (LV) developed pressure, end-diastolic pressure, pressure-rate product, or tissue high-energy phosphates. During exposure to Iso, mean LV end-diastolic pressure increased from 10.7 to 49.3 mmHg in hearts pretreated with IAA (n = 7) but did not change in control hearts (n = 7). During Iso, there were substantial reductions in developed pressure, ATP, and phosphocreatine in IAA-treated hearts but not in control hearts. After exposure to IAA and Iso, a doubling of diastolic [Ca2+]i was observed with 19F-NMR. In IAA-treated hearts, reduction of perfusate Ca2+ concentration from 2.5 to 0.6 mM during Iso exposure (n = 6) prevented the mechanical dysfunction and decrease in high-energy phosphates. These findings suggest that glycolysis is necessary to preserve myocardial Ca2+ homeostasis during beta-adrenergic stimulation.

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