scholarly journals Citrulline/malate promotes aerobic energy production in human exercising muscle

2002 ◽  
Vol 36 (4) ◽  
pp. 282-289 ◽  
Author(s):  
D Bendahan
Keyword(s):  
Energy Production ◽  
Citrulline Malate ◽  
Aerobic Energy Production

Importance of purine nucleotide cycle to energy production in skeletal muscle

1986 ◽  
Vol 251 (5) ◽  
pp. C795-C802 ◽  
Author(s):  
W. F. Flanagan ◽  
E. W. Holmes ◽  
R. L. Sabina ◽  
J. L. Swain
Keyword(s):  
Skeletal Muscle ◽  
Total Energy ◽  
Energy Demand ◽  
Energy Production ◽  
Muscle Tension ◽  
Lactate Production ◽  
Muscle Dysfunction ◽  
Purine Nucleotide ◽  
Purine Nucleotide Cycle ◽  
Aerobic Energy Production

The purpose of this study was to determine the role of the purine nucleotide cycle in aerobic energy production. Rats received either saline or 5-amino-4-imidazolecarboxamide riboside (AICAriboside), a precursor to an inhibitor of adenylosuccinate lyase (AICAR). Muscle tension was quantified during gastrocnemius stimulation, and muscle metabolite content was measured to obtain an estimate of the activity of the enzymes of the cycle. AICAriboside prevented the increase in synthetase and lyase activities observed in control animals during moderate (aerobic) stimulation, and was accompanied by marked muscle dysfunction. Although glycolytic energy production was not impaired in the AICAriboside-treated animals (lactate production occurred), total energy production did not meet energy demand. These results suggest that disruption of the purine nucleotide cycle impairs aerobic energy metabolism. Tetanic (anaerobic) stimulation produced more rapid fatigue in the AICAriboside-treated group. Total energy production was again impaired in the AICAriboside-treated animals, but lactate production was similar in both groups. These findings suggest the loss of the initial aerobic component of energy generation in tetanically stimulated muscle of AICAriboside-treated animals. The results of this study indicate that disruption of the purine nucleotide cycle at the level of the synthetase and lyase reactions is associated with skeletal muscle dysfunction, and suggest that the cycle plays an anapleurotic role in providing citric acid cycle intermediates that enhance aerobic energy production in contracting skeletal muscle.

scholarly journals COVID-19 and hypertension: is the HSP60 culprit for the severe course and worse outcome?

2020 ◽  
Vol 319 (4) ◽  
pp. H793-H796 ◽  
Author(s):  
Hrvoje Jakovac
Keyword(s):  
Energy Production ◽  
Toll Like Receptor ◽  
Hypertensive Patients ◽  
Cytokine Induction ◽  
Third Phase ◽  
Pathological Conditions ◽  
Hsp60 Expression ◽  
Hypertrophic Myocardium ◽  
Circulating Levels ◽  
Aerobic Energy Production

The 60-kDa heat shock protein (HSP60) is a chaperone essential for mitochondrial proteostasis ensuring thus sufficient aerobic energy production. In pathological conditions, HSP60 can be translocated from the mitochondria and excreted from the cell. In turn, the extracellular HSP60 has a strong ability to trigger and enhance inflammatory response with marked proinflammatory cytokine induction, which is mainly mediated by Toll-like receptor binding. Previous studies have found increased circulating levels of HSP60 in hypertensive patients, as well as enhanced HSP60 expression and membrane translocation in the hypertrophic myocardium. These observations are of particular interest, since they could provide a possible pathophysiological explanation of the severe course and worse outcome of severe acute respiratory syndrome coronavirus 2 infection in hypertensive patients, repeatedly reported during the recent coronavirus disease 2019 (COVID-19) pandemic and related to hyperinflammatory response and cytokine storm development during the third phase of the disease. In this regard, pharmacological inhibition of HSP60 could attract attention to potentially ameliorate inappropriate inflammatory reaction in severe COVID-19 patients. Among HSP60 antagonizing drugs, mizoribine is the most intriguing, since it is clinically approved and exerts antiviral activity. However, this topic requires to be further scrutinized.

scholarly journals Mitochondrial responses to prolonged anoxia in brain of red-eared slider turtles

2016 ◽  
Vol 12 (1) ◽  
pp. 20150797 ◽  
Author(s):  
Matthew E. Pamenter ◽  
Crisostomo R. Gomez ◽  
Jeffrey G. Richards ◽  
William K. Milsom
Keyword(s):  
Energy Production ◽  
Citrate Synthase ◽  
Brain Mitochondria ◽  
Freshwater Turtles ◽  
Vertebrate Species ◽  
Low Oxygen ◽  
Oxygen Stress ◽  
Neuronal Signalling ◽  
Mild Uncoupling ◽  
Aerobic Energy Production

Mitochondria are central to aerobic energy production and play a key role in neuronal signalling. During anoxia, however, the mitochondria of most vertebrates initiate deleterious cell death cascades. Nonetheless, a handful of vertebrate species, including some freshwater turtles, are remarkably tolerant of low oxygen environments and survive months of anoxia without apparent damage to brain tissue. This tolerance suggests that mitochondria in the brains of such species are adapted to withstand prolonged anoxia, but little is known about potential neuroprotective responses. In this study, we address such mechanisms by comparing mitochondrial function between brain tissues isolated from cold-acclimated red-eared slider turtles ( Trachemys scripta elegans ) exposed to two weeks of either normoxia or anoxia. We found that brain mitochondria from anoxia-acclimated turtles exhibited a unique phenotype of remodelling relative to normoxic controls, including: (i) decreased citrate synthase and F 1 F O -ATPase activity but maintained protein content, (ii) markedly reduced aerobic capacity, and (iii) mild uncoupling of the mitochondrial proton gradient. These data suggest that turtle brain mitochondria respond to low oxygen stress with a unique suite of changes tailored towards neuroprotection.

Actively phosphorylating mitochondria are more resistant to lactic acidosis than inactive mitochondria

1999 ◽  
Vol 277 (2) ◽  
pp. C288-C293 ◽  
Author(s):  
M. Tonkonogi ◽  
K. Sahlin
Keyword(s):  
Lactic Acid ◽  
Lactic Acidosis ◽  
Energy Production ◽  
Reaction Medium ◽  
Mitochondrial Oxygen Consumption ◽  
Physiological Conditions ◽  
Skeletal Muscle Mitochondria ◽  
Potassium Lactate ◽  
Menten Constant ◽  
Aerobic Energy Production

Oxidative phosphorylation of isolated rat skeletal muscle mitochondria after exposure to lactic acidosis in either phosphorylating or nonphosphorylating states has been evaluated. Mitochondrial respiration and transmembrane potential (ΔΨm) were measured with pyruvate and malate as the substrates. The addition of lactic acid decreased the pH of the reaction medium from 7.5 to 6.4. When lactic acid was added to nonphosphorylating mitochondria, the subsequent maximal ADP-stimulated respiration decreased by 27% compared with that under control conditions ( P < 0.05), and the apparent Michaelis-Menten constant ( K m) for ADP decreased to 10 μM vs. 20 μM ( P< 0.05) in controls. In contrast, maximal respiration and ADP sensitivity were not affected when mitochondria were exposed to acidosis during active phosphorylation in state 3. Acidosis significantly increased mitochondrial oxygen consumption in state 4 (post-state 3), irrespective of when acidosis was induced. This effect of acidosis was attenuated in the presence of oligomycin. The addition of lactic acid during state 4 respiration decreased ΔΨm by 19%. The ratio between added ADP and consumed oxygen (P/O) was close to the theoretical value of 3 in all conditions. The addition of potassium lactate during state 3 (i.e., medium pH unchanged) had no effect on the parameters measured. It is concluded that lactic acidosis has different effects when induced on nonphosphorylating vs. actively phosphorylating mitochondria. On the basis of these results, we suggest that the influence of lactic acidosis on muscle aerobic energy production depends on the physiological conditions at the onset of acidity.

Oxidative damage and decreased aerobic energy production due to ingestion of polyethylene microplastics by Chironomus riparius (Diptera) larvae

2021 ◽  
Vol 402 ◽  
pp. 123775 ◽  
Author(s):  
Carlos J.M. Silva ◽  
Ana L. Patrício Silva ◽  
Diana Campos ◽  
Ana L. Machado ◽  
João L.T. Pestana ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Energy Production ◽  
Chironomus Riparius ◽  
Diptera Larvae ◽  
Aerobic Energy Production

Cardiac enzyme activities in fetal and adult pregnant and nonpregnant sheep exposed to high-altitude hypoxemia

1995 ◽  
Vol 79 (4) ◽  
pp. 1286-1289 ◽  
Author(s):  
T. Ohtsuka ◽  
R. D. Gilbert
Keyword(s):  
High Altitude ◽  
Energy Production ◽  
Citrate Synthase ◽  
Reaction Products ◽  
Wet Weight ◽  
Nonpregnant Adult ◽  
The Right ◽  
Enzyme Changes ◽  
Aerobic Energy Production

We measured pyruvate kinase (PK), citrate synthase (CS), and lactate dehydrogenase (LDH) activities in the right and left ventricles of fetal, maternal, and nonpregnant adult sheep exposed to high altitude (3,820 m) for 112 days and compared them with control groups of animals kept at sea level. Enzymes were assayed by the spectrophotometric appearance of reaction products specific to each enzyme, and activity was expressed as micromoles per minute per gram of wet weight of tissue. In control sheep, CS activity was significantly higher in both ventricles of the pregnant and nonpregnant adult compared with the fetus. However, LDH and PK activities were only higher in the left ventricle of the nonpregnant adult compared with the fetus. Long-term hypoxemia significantly increased LDH activities in fetal (57 and 53%), pregnant adult (29 and 27%), and non-pregnant adult (25 and 24%) right and left ventricles, respectively. CS activities also increased in fetal (90 and 97%), pregnant adult (43 and 39%), and nonpregnant adult (46 and 48%) right and left ventricles, respectively. However, PK activity was not affected by altitude in any group of animals. In the fetal heart, which uses lactate as its primary metabolic fuel, these enzyme changes may help enhance aerobic energy production during hypoxemia. In the adult heart, which relies on free fatty acids as well as glucose for energy production, the significance of these enzyme changes is less clear.

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