scholarly journals Sodium bicarbonate ingestion prior to training improves mitochondrial adaptations in rats

2010 ◽  
Vol 299 (2) ◽  
pp. E225-E233 ◽  
Author(s):  
David J. Bishop ◽  
Claire Thomas ◽  
Tom Moore-Morris ◽  
Michail Tonkonogi ◽  
Kent Sahlin ◽  
...  
Keyword(s):  
Sodium Bicarbonate ◽  
Citrate Synthase ◽  
Training Session ◽  
Oxidative Capacity ◽  
Ion Accumulation ◽  
Hydrogen Ion ◽  
Time To Exhaustion ◽  
Mitochondrial Mass ◽  
Palmitoyl Carnitine ◽  
Male Wistar Rats

We tested the hypothesis that reducing hydrogen ion accumulation during training would result in greater improvements in muscle oxidative capacity and time to exhaustion (TTE). Male Wistar rats were randomly assigned to one of three groups (CON, PLA, and BIC). CON served as a sedentary control, whereas PLA ingested water and BIC ingested sodium bicarbonate 30 min prior to every training session. Training consisted of seven to twelve 2-min intervals performed five times/wk for 5 wk. Following training, TTE was significantly greater in BIC (81.2 ± 24.7 min) compared with PLA (53.5 ± 30.4 min), and TTE for both groups was greater than CON (6.5 ± 2.5 min). Fiber respiration was determined in the soleus (SOL) and extensor digitorum longus (EDL), with either pyruvate (Pyr) or palmitoyl carnitine (PC) as substrates. Compared with CON (14.3 ± 2.6 nmol O2·min−1·mg dry wt−1), there was a significantly greater SOL-Pyr state 3 respiration in both PLA (19.6 ± 3.0 nmol O2·min−1·mg dry wt−1) and BIC (24.4 ± 2.8 nmol O2·min−1·mg dry wt−1), with a significantly greater value in BIC. However, state 3 respiration was significantly lower in the EDL from both trained groups compared with CON. These differences remained significant in the SOL, but not the EDL, when respiration was corrected for citrate synthase activity (an indicator of mitochondrial mass). These novel findings suggest that reducing muscle hydrogen ion accumulation during running training is associated with greater improvements in both mitochondrial mass and mitochondrial respiration in the soleus.

scholarly journals Endurance Is Improved in Female Rats After Living High-Training High Despite Alterations in Skeletal Muscle

2021 ◽  
Vol 3 ◽  
Author(s):  
Alexandra Malgoyre ◽  
Alexandre Prola ◽  
Adelie Meunier ◽  
Rachel Chapot ◽  
Bernard Serrurier ◽  
...  
Keyword(s):  
High Altitude ◽  
Citrate Synthase ◽  
Oxidative Capacity ◽  
Female Rats ◽  
Whole Body ◽  
Aerobic Performance ◽  
Time To Exhaustion ◽  
Altitude Training ◽  
Similar Reduction ◽  
Mitochondrial Mass

Altitude camps are used during the preparation of endurance athletes to improve performance based on the stimulation of erythropoiesis by living at high altitude. In addition to such whole-body adaptations, studies have suggested that high-altitude training increases mitochondrial mass, but this has been challenged by later studies. Here, we hypothesized that living and training at high altitude (LHTH) improves mitochondrial efficiency and/or substrate utilization. Female rats were exposed and trained in hypoxia (simulated 3,200 m) for 5 weeks (LHTH) and compared to sedentary rats living in hypoxia (LH) or normoxia (LL) or those that trained in normoxia (LLTL). Maximal aerobic velocity (MAV) improved with training, independently of hypoxia, whereas the time to exhaustion, performed at 65% of MAV, increased both with training (P = 0.009) and hypoxia (P = 0.015), with an additive effect of the two conditions. The distance run was 7.98 ± 0.57 km in LHTH vs. 6.94 ± 0.51 in LLTL (+15%, ns). The hematocrit increased >20% with hypoxia (P < 0.001). The increases in mitochondrial mass and maximal oxidative capacity with endurance training were blunted by combination with hypoxia (−30% for citrate synthase, P < 0.01, and −23% for Vmax glut−succ, P < 0.001 between LHTH and LLTL). A similar reduction between the LHTH and LLTL groups was found for maximal respiration with pyruvate (−29%, P < 0.001), for acceptor-control ratio (−36%, hypoxia effect, P < 0.001), and for creatine kinase efficiency (−48%, P < 0.01). 3-hydroxyl acyl coenzyme A dehydrogenase was not altered by hypoxia, whereas maximal respiration with Palmitoyl-CoA specifically decreased. Overall, our results show that mitochondrial adaptations are not involved in the improvement of submaximal aerobic performance after LHTH, suggesting that the benefits of altitude camps in females relies essentially on other factors, such as the transitory elevation of hematocrit, and should be planned a few weeks before competition and not several months.

scholarly journals Effects of high-intensity training on MCT1, MCT4, and NBC expressions in rat skeletal muscles: influence of chronic metabolic alkalosis

2007 ◽  
Vol 293 (4) ◽  
pp. E916-E922 ◽  
Author(s):  
Claire Thomas ◽  
David Bishop ◽  
Tom Moore-Morris ◽  
Jacques Mercier
Keyword(s):  
Sodium Bicarbonate ◽  
High Intensity ◽  
Skeletal Muscles ◽  
Metabolic Alkalosis ◽  
Citrate Synthase ◽  
Ph Regulation ◽  
Training Session ◽  
High Intensity Training ◽  
Male Wistar Rats ◽  
Intensity Training

This study investigated the effects of high-intensity training, with or without induced metabolic alkalosis, on lactate transporter (MCT1 and MCT4) and sodium bicarbonate cotransporter (NBC) content in rat skeletal muscles. Male Wistar rats performed high-intensity training on a treadmill 5 times/wk for 5 wk, receiving either sodium bicarbonate (ALK-T) or a placebo (PLA-T) prior to each training session, and were compared with a group of control rats (CON). MCT1, MCT4, and NBC content was measured by Western blotting in soleus and extensor digitorum longus (EDL) skeletal muscles. Citrate synthase (CS) and phosphofructokinase (PFK) activities and muscle buffer capacity (βm) were also evaluated. Following training, CS and PFK activities were significantly higher in the soleus only ( P < 0.05), whereas βm was significantly higher in both soleus and EDL ( P < 0.05). MCT1 (PLA-T: 30%; ALK-T: 23%) and NBC contents (PLA-T: 85%; ALK-T: 60%) increased significantly only in the soleus following training ( P < 0.01). MCT4 content in the soleus was significantly greater in ALK-T (115%) but not PLA-T compared with CON. There was no significant change in protein content in the EDL. Finally, NBC content was related only to MCT1 content in soleus ( r = 0.50, P < 0.01). In conclusion, these results suggest that MCT1, MCT4, and NBC undergo fiber-specific adaptive changes in response to high-intensity training and that induced alkalosis has a positive effect on training-induced changes in MCT4 content. The correlation between MCT1 and NBC expression suggests that lactate transport may be facilitated by NBC in oxidative skeletal muscle, which may in turn favor better muscle pH regulation.

Decreased muscle ACE activity enhances functional response to endurance training in rats, without change in muscle oxidative capacity or contractile phenotype

2009 ◽  
Vol 107 (1) ◽  
pp. 346-353 ◽  
Author(s):  
Estelle Habouzit ◽  
Hélène Richard ◽  
Hervé Sanchez ◽  
Nathalie Koulmann ◽  
Bernard Serrurier ◽  
...  
Keyword(s):  
Ace Inhibitor ◽  
Citrate Synthase ◽  
Ace Inhibition ◽  
Oxidative Capacity ◽  
Time To Exhaustion ◽  
Metabolic Efficiency ◽  
Endurance Time ◽  
Female Wistar Rats ◽  
Permeabilized Fibers ◽  
Training Protocol

In the present study, we tested the hypothesis that chronic ANG I-converting enzyme (ACE) inhibition could improve the training-induced improvement in endurance exercise performance and that this could be related to enhanced skeletal muscle metabolic efficiency. Female Wistar rats were assigned to four groups comprising animals either maintained sedentary or endurance trained (Sed and Tr, respectively), and treated or not for 10 wk with an ACE inhibitor, perindopril (2 mg·kg−1·day−1) (Per and Ct, respectively) ( n = 8 each). Trained rats underwent an 8-wk treadmill training protocol that consisted of 2 h/day running at 30 m/min on a 8% decline. Before the start of and 1 wk before the end of experimental conditioning, the running time to exhaustion of rats was measured on a treadmill. The training program led to an increase in endurance time, higher in Tr-Per than in Tr-Ct group (125% in Tr-Ct vs. 183% in Tr-Per groups, P < 0.05). Oxidative capacity, measured in saponin-permeabilized fibers of slow soleus and fast plantaris muscles, increased with training, but less in Tr-Per than in Tr-Ct rats. The training-induced increase in citrate synthase activity also was less in soleus from Tr-Per than Tr-Ct rats. The training-induced increase in the percentage of the type IIa isoform of myosin heavy chain (MHC) (45%, P < 0.05) and type IIx MHC (25%, P < 0.05) associated with decreased type IIb MHC (34%, P < 0.05) was minimized by perindopril administration. These findings demonstrate that the enhancement in physical performance observed in perindopril-treated animals cannot be explained by changes in mitochondrial respiration and/or MHC distribution within muscles involved in running exercise.

Muscle oxidative capacity and work performance after training under local leg ischemia

1990 ◽  
Vol 69 (2) ◽  
pp. 785-787 ◽  
Author(s):  
L. Kaijser ◽  
C. J. Sundberg ◽  
O. Eiken ◽  
A. Nygren ◽  
M. Esbjornsson ◽  
...  
Keyword(s):  
Work Performance ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Training Session ◽  
Oxidative Capacity ◽  
Cycle Ergometer ◽  
Chamber Pressure ◽  
Exercise Tests ◽  
Rubber Membrane ◽  
The Difference

Healthy young men executed supine one-legged cycle training four times per week for 4 wk with legs and the cycle ergometer inside a pressure chamber, the opening of which was sealed by a rubber membrane at the level of the crotch. Each training session started by training one leg under ischemic conditions induced by increased chamber pressure (50 mmHg) at the highest intensity tolerable for 45 min. Then the other leg was trained with the same power profile but normal atmospheric chamber pressure. Before and after the training period, both legs executed one-legged exercise tests under both normal and increased chamber pressure and muscle biopsies were taken from the vastus lateralis. Ischemic training increased performance more than normal training, the difference being greater for exercise executed under ischemic conditions. The difference in performance increase between the legs was paralleled by a greater muscle citrate synthase activity in the ischemically than in the normally trained leg.

Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans

2005 ◽  
Vol 98 (6) ◽  
pp. 1985-1990 ◽  
Author(s):  
Kirsten A. Burgomaster ◽  
Scott C. Hughes ◽  
George J. F. Heigenhauser ◽  
Suzanne N. Bradwell ◽  
Martin J. Gibala
Keyword(s):  
Citrate Synthase ◽  
Training Session ◽  
Interval Training ◽  
Maximal Activity ◽  
Work Capacity ◽  
Control Group ◽  
Endurance Capacity ◽  
Sprint Interval Training ◽  
Oxidative Potential ◽  
Cycle Endurance

Parra et al. ( Acta Physiol. Scand 169: 157–165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change “anaerobic” work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (V̇o2 peak), no study has examined the effect of SIT on “aerobic” exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1–2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at ∼80% V̇o2 peak. Eight recreationally active subjects [age = 22 ± 1 yr; V̇o2 peak = 45 ± 3 ml·kg−1·min−1 (mean ± SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven “all-out” 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 ± 1.0 vs. 4.0 ± 0.7 mmol·kg protein−1·h−1) and resting muscle glycogen content increased by 26% (614 ± 39 vs. 489 ± 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 ± 11 vs. 26 ± 5 min; P < 0.05), despite no change in V̇o2 peak. The coefficient of variation for the cycle test was 12.0%, and a control group ( n = 8) showed no change in performance when tested ∼2 wk apart without SIT. We conclude that short sprint interval training (∼15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.

scholarly journals A Blunted Sympathetic Function and an Enhanced Nitrergic Activity Contribute to Reduce Mesenteric Resistance in Hyperthyroidism

2021 ◽  
Vol 22 (2) ◽  
pp. 570
Author(s):  
Laia Cros-Brunsó ◽  
Laura Camacho-Rodríguez ◽  
Ángel Martínez-González ◽  
Pablo Llévenes ◽  
Mercedes Salaices ◽  
...  
Keyword(s):  
Citrate Synthase ◽  
Purinergic Receptor ◽  
Body Weight Gain ◽  
Electrical Field Stimulation ◽  
Alpha Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Sympathetic Function ◽  
Vasoconstrictor Response ◽  
Relevant Role ◽  
Male Wistar Rats

We aimed to determine whether an experimental model of hyperthyroidism could alter the function of sympathetic and nitrergic components of mesenteric innervation. For this purpose, male Wistar rats were divided into (1) control rats (CT) and (2) rats infused with L-Thyroxine (HT). Body weight gain and adipose tissue accumulation were lower in HT rats, while systolic blood pressure and citrate synthase activity in the soleus muscle were increased by HT. In segments from the superior mesenteric artery, the application of an electrical field stimulation (EFS) induced a vasoconstrictor response, which was lower in arteries from HT animals. The alpha-adrenoceptor antagonist phentolamine diminished EFS-induced vasoconstriction to a lower extent in HT arteries, while the purinergic receptor antagonist suramin reduced contractile response to EFS only in segments from CT. In line with this, noradrenaline release, tyrosine hydroxylase expression and activation and dopamine β hydroxylase expression were diminished in HT. The unspecific nitric oxide synthase (NOS) inhibitor L-NAME increased EFS-induced vasoconstriction more markedly in segments from HT rats. NO release was enhanced in HT, probably due to an enhancement in neuronal NOS activity, in which a hyperactivation of both PKC and PI3K-AKT signaling pathways might play a relevant role. In conclusion, perivascular mesenteric innervation might contribute to reduce the vascular resistance observed in hyperthyroidism.

Fatty acid oxidation and triacylglycerol hydrolysis are enhanced after chronic leptin treatment in rats

2002 ◽  
Vol 282 (3) ◽  
pp. E593-E600 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Arend Bonen ◽  
David J. Dyck
Keyword(s):  
Fatty Acid ◽  
Citrate Synthase ◽  
Uncoupling Protein ◽  
Oxidative Capacity ◽  
Hormone Sensitive Lipase ◽  
Acid Oxidation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Triacylglycerol Hydrolysis ◽  
Hormone Sensitive

Leptin acutely increases fatty acid (FA) oxidation and triacylglycerol (TG) hydrolysis and decreases TG esterification in oxidative rodent muscle. However, the effects of chronic leptin administration on FA metabolism in skeletal muscle have not been examined. We hypothesized that chronic leptin treatment would enhance TG hydrolysis as well as the capacity to oxidize FA in soleus (SOL) muscle. Female Sprague-Dawley rats were infused for 2 wk with leptin (LEPT; 0.5 mg · kg−1 · day−1) by use of subcutaneously implanted miniosmotic pumps. Control (AD-S) and pair-fed (PF-S) animals received saline-filled implants. Subsequently, FA metabolism was monitored for 45 min in isolated, resting, and contracting (20 tetani/min) SOL muscles by means of pulse-chase procedures. Food intake (−33 ± 2%, P < 0.01) and body mass (−12.5 ± 4%, P = 0.01) were reduced in both LEPT and PF-S animals. Leptin levels were elevated (+418 ± 7%, P < 0.001) in treated animals but reduced in PF-S animals (−73 ± 8%, P< 0.05) relative to controls. At rest, TG hydrolysis was increased in leptin-treated rats (1.8 ± 2.2, AD-S vs. 23.5 ± 8.1 nmol/g wet wt, LEPT; P < 0.001). In contracting SOL muscles, TG hydrolysis (1.5 ± 0.6, AD-S vs. 3.6 ± 1.0 μmol/g wet wt, LEPT; P = 0.02) and palmitate oxidation (18.3 ± 6.7, AD-S vs. 45.7 ± 9.9 nmol/g wet wt, LEPT; P < 0.05) were both significantly increased by leptin treatment. Chronic leptin treatment had no effect on TG esterification either at rest or during contraction. Markers of overall (citrate synthase) and FA (hydroxyacyl-CoA dehydrogenase) oxidative capacity were unchanged with leptin treatment. Protein expression of hormone-sensitive lipase (HSL) was also unaltered following leptin treatment. Thus leptin-induced increases in lipolysis are likely due to HSL activation (i.e., phosphorylation). Increased FA oxidation secondary to chronic leptin treatment is not due to an enhanced oxidative capacity and may be a result of enhanced flux into the mitochondrion (i.e., carnitine palmitoyltransferase I regulation) or electron transport uncoupling (i.e., uncoupling protein-3 expression).

Abstract 294: Alterations in Cerebral Mitochondrial Dynamics and Mitochondrial Mass After Successful Cardiopulmonary Resuscitation in a Porcine Model of Pediatric Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Kumaran Senthil ◽  
Marco M Hefti ◽  
Michael Karlsson ◽  
Ryan W Morgan ◽  
Johannes Ehinger ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Protein Expression ◽  
Citrate Synthase ◽  
Mitochondrial Dynamics ◽  
Coronary Perfusion Pressure ◽  
Short Chain ◽  
Coronary Perfusion ◽  
Mitochondrial Mass ◽  
Convergence Point ◽  
Neurologic Function

Introduction: A critical convergence point for neurologic injury following cardiac arrest is cerebral mitochondrial (Mt) dysfunction, regulated by Mt dynamics (balance of fusion and fission). Both fusion and fission are important to Mt homeostasis under normal conditions; however, under stress fission can decrease Mt mass and signal apoptosis, while fusion promotes oxidative phosphorylation efficiency. Our group has previously shown hemodynamic directed CPR (HD-CPR) improves Mt bioenergetics compared to AHA depth-guided CPR (DG-CPR), which correlated with better neurologic function. Hypothesis: Compared to DG-CPR, HD-CPR will result in cerebral cortical protein expression consistent with Mt fusion and preservation of mitochondrial mass 24 hours post-ROSC. Methods: One-month-old piglets were designated into three groups: 1) DG-CPR (n=5); 2) HD-CPR (n=5; goal SBP 90 mmHg, goal coronary perfusion pressure 20mmHg); 3) Shams (n=7). Groups 1 and 2 underwent 7 minutes of asphyxia, VF, 10-20 min of CPR, and post-ROSC therapies to maintain hemodynamic, oxygenation and ventilation goals. The primary outcomes were immunoblot quantification of cortical proteins for fusion (Opa-1, Opa-1 long to short chain ratio, MFN-2), fission (DRP-1), and citrate synthase activity for Mt mass. Groups shown as median and IQR and analyzed by Kruskal-Wallis, then Dunn’s multiple comparisons. Results: HD-CPR subjects had increased total Opa-1 expression compared to sham (1.52 [1.02,1.69] vs. 0.47 [0.34,0.51], p=0.001). Opa-1 long to short chain ratio was higher in HD-CPR than both sham (0.64 [0.46,0.92] vs. 0.28 [0.25,0.36], p=0.025) and DG-CPR (0.26 [0.26,0.31], p=0.018). There were no differences in MFN-2 or DRP-1 expression between groups. Mt mass was lower in DG-CPR than sham (11.02 [10.15,12.29] vs. 13.9 [12.35,15.63], p=0.029), but preserved in HD-CPR. Discussion: Piglets treated with HD-CPR exhibited protein expression consistent with Mt fusion, as evidenced by upregulation of total Opa-1, elevated Opa-1 long to short chain ratio, and preservation of Mt mass compared to standard AHA depth guided CPR strategy. We speculate that neurotherapeutics that target Mt dynamics could further improve brain Mt bioenergetics and neurologic function after pediatric CA.

Capillary tortuosity in rat soleus muscle is not affected by endurance training

1989 ◽  
Vol 256 (4) ◽  
pp. H1110-H1116 ◽  
Author(s):  
D. C. Poole ◽  
O. Mathieu-Costello ◽  
J. B. West
Keyword(s):  
Exercise Training ◽  
Citrate Synthase ◽  
Metabolic Response ◽  
Oxidative Capacity ◽  
Treadmill Running ◽  
Female Rats ◽  
Capillary Length ◽  
Direct Function ◽  
Musculus Soleus ◽  
Muscle Changes

The total capillary length available for blood-tissue transfer is determined by the number and orientation of the capillaries. Therefore, whether capillary tortuosity changes with exercise training has important implications for peripheral gas exchange. To determine the effects of exercise training on capillary orientation and capillary length per volume of muscle fiber [Jv(c,f)] female rats were trained by treadmill running (30 m/min, up to 60 min/day, 5 days/wk) for 4 wk. Muscles from control and trained rats were perfusion fixed at sarcomere lengths (l) ranging from 1.59 to 2.15 microns, and morphometric techniques were used to estimate capillary orientation and Jv(c,f). Training increased (P less than 0.05) musculus soleus oxidative capacity 35% [as estimated from citrate synthase activity: 24.7 +/- 1.4 to 34.7 +/- 1.0 (SE) mumol.g-1.min-1], capillary-to-fiber ratio 30% (2.17 +/- 0.06 to 2.83 +/- 0.05), and Jv(c,f) 32% (1,886 +/- 73 to 2,496 +/- 180 mm-2). Capillary tortuosity (as determined from comparisons of transverse and longitudinal sections) was a direct function of l in control and trained rats and contributed 17-73% of capillary length above that estimated from capillary counts on transverse sections. We conclude that capillary tortuosity in m. soleus is unchanged by training. Therefore, Jv(c,f) increases as a consequence of increased capillary number. M. soleus citrate synthase activity is best correlated with Jv(c,f) and not with capillary counts on transverse sections. We hypothesize that training-induced muscle changes of capillary geometry improve O2 delivery to skeletal muscle and may therefore alter the metabolic response (e.g., lactate accumulation) to exercise after training.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Perinatal maturation of rat kidney mitochondria

1995 ◽  
Vol 305 (2) ◽  
pp. 675-680 ◽  
Author(s):  
B Prieur ◽  
L Cordeau-Lossouarn ◽  
A Rotig ◽  
J Bismuth ◽  
J P Geloso ◽  
...  
Keyword(s):  
Respiratory Chain ◽  
Atp Synthase ◽  
Nuclear Dna ◽  
Citrate Synthase ◽  
De Novo ◽  
Adenine Nucleotide ◽  
Rat Kidney ◽  
Oxidative Capacity ◽  
Respiratory Chain Complexes ◽  
Kidney Mitochondria

In the rat kidney, NaK-ATPase activity increased between days 19 and 20 of gestation (+50%) and between 1 and 24 h after birth (+20%), requiring an increased energy supply. In order to determine whether mitochondrial changes were involved, renal mitochondrial development was investigated from day 19 of gestation to 1 day after birth. Slot-blot analyses of mitochondrial-DNA/nuclear-DNA ratio and determination of citrate synthase activity showed a doubling in the mitochondrial pool between days 19 and 20 of gestation. In isolated mitochondria, oxygen consumption remained unchanged between days 19 and 20 of gestation, and then it was enhanced between days 20 and 21 of gestation (+70%) and between 1 and 24 h after birth (+50%). We also focused on one of the respiratory-chain complexes, ATP synthase, and measured its activity and content during the perinatal period. We demonstrated increases in both activity and content of ATP synthase between days 20 and 21 of gestation and between 1 and 24 h after birth, thus suggesting that changes in ATP synthase activity are ascribed to an increase in the mitochondrial density of ATP synthase complexes. Moreover, the mitochondrial ATP/ADP ratio only increased between 1 and 24 h (+90%), indicating a critical step in the renal respiratory-chain maturation at that time. We therefore conclude that the postnatal enhancement of renal mitochondrial oxidative capacity might depend on protein synthesis de novo and on changes in the adenine nucleotide concentrations.

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