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1 his adaptation is mediated by an increase in muscle mitochondria.
2 this increase in endurance is an increase in muscle mitochondria.
3 c muscle fibers and increased the numbers of muscle mitochondria.
4  in L6 and RC13 rodent myocytes and isolated muscle mitochondria.
5 for hydrogen peroxide) compared with control muscle mitochondria.
6 , complex V was less abundant in extraocular muscle mitochondria.
7 ochondria were 40% to 60% lower than in limb muscle mitochondria.
8  of ATP by F1F0-ATPase in heart and skeletal muscle mitochondria.
9  aged 21-87 years on insulin sensitivity and muscle mitochondria.
10 cluding a dramatic proliferation of skeletal muscle mitochondria.
11 he increase in PDK4 protein in gastrocnemius muscle mitochondria.
12  much more abundant in the liver rather than muscle mitochondria.
13 tly on SDS gels, as did CPT I from liver and muscle mitochondria.
14 sport at all points between inspired air and muscle mitochondria.
15 nvestigated in isolated cardiac and skeletal muscle mitochondria.
16 ets occurs despite a concomitant increase in muscle mitochondria; 2) mitochondrial deficiency severe
17 2, also known as MnSod) in muscle tissue and muscle mitochondria, a modest increase in Sod2 in heart
18 g reverse electron transport in rat skeletal muscle mitochondria: a protonmotive force generated by A
19 ic proteins, which enabled identification of muscle mitochondria among mitochondria from other tissue
20 lation reaction network in isolated skeletal muscle mitochondria and attempted to extrapolate these r
21   Thus, fusion dynamically connects skeletal muscle mitochondria and its prolonged loss jeopardizes b
22 ase inhibitor subunit, IF1, in their cardiac muscle mitochondria and show marked IF1-mediated mitocho
23 , subsarcolemmal and interfibrillar skeletal muscle mitochondria) and to determine the pIs of other b
24 lyzed ADP-stimulated respiration of isolated muscle mitochondria, and ADP-stimulated mitochondrial re
25 s of working muscles, fatty acid delivery to muscle mitochondria, and the oxidation of other substrat
26 cellular energetics and metabolism, skeletal muscle mitochondria appear to play a key role in the dev
27  complexes I and IV was lower in extraocular muscle mitochondria (approximately 50% the activity in t
28     These findings demonstrate that skeletal muscle mitochondria are a critical pathological link bet
29 ing, with respiratory uncoupling in skeletal muscle mitochondria, associated with increased uncouplin
30 alcium stimulates NADH synthesis in skeletal muscle mitochondria but not in cardiac mitochondria.
31 entration is low, complex II in rat skeletal muscle mitochondria can generate superoxide or H(2)O(2)
32                 Mammalian liver and striated muscle mitochondria can oxidize exogenous lactate becaus
33 -CoA substrates by liver, heart and skeletal muscle mitochondria differed among the three genotypes.
34 ce mitochondrial dysfunction was assessed in muscle mitochondria from 5 healthy individuals incubated
35 rial oxidative enzyme activity was normal in muscle mitochondria from a CMT2 patient with an MFN2 mut
36                         Cardiac and skeletal muscle mitochondria from ant1(-)/ant1(-) mice had increa
37                     Respirometry of skeletal muscle mitochondria from iPLA(2)gamma(-/-) mice demonstr
38                                     Skeletal muscle mitochondria from penguins that had been either e
39                        In contrast, isolated muscle mitochondria from the type 2 subjects exhibited a
40 a expressing UCP1 and was absent in skeletal muscle mitochondria from UCP3 knockout mice.
41 t expressing UCP1, and is absent in skeletal muscle mitochondria from UCP3 knockout mice.
42 n impaired bioenergetic capacity of skeletal muscle mitochondria in type 2 diabetes, with some impair
43 ing of oxidative phosphorylation in skeletal muscle mitochondria: increased proton transport activity
44 sites produce superoxide/H2O2 using isolated muscle mitochondria incubated in media mimicking the cyt
45 of RYGB with or without exercise on skeletal muscle mitochondria, intramyocellular lipids, and insuli
46              The role of hypoxia on skeletal muscle mitochondria is controversial.
47                                     Skeletal muscle mitochondria isolated from penguins that had neve
48      Here, we provide evidence that skeletal muscle mitochondria lacking UCP3 are more coupled (i.e.
49 of fatty acid hydroperoxides from denervated muscle mitochondria may be an important determinant of m
50 t calcium has a stimulatory role in skeletal muscle mitochondria not apparent in cardiac mitochondria
51                           Skeletal and heart muscle mitochondria of the CAP(R) mice were enlarged and
52  affinity form of IF1 present in the cardiac muscle mitochondria of the pigeon is partially functiona
53 f higher affinity IF1 present in the cardiac muscle mitochondria of the rat is, under these condition
54 we tested the relative capacities of cardiac muscle mitochondria of the three species to avert a pote
55                  To examine whether skeletal muscle mitochondria oxidize lactate, mitochondrial respi
56 d methods to disrupt tissue using kidney and muscle mitochondria preparations as exemplars.
57                           The ANT1-deficient muscle mitochondria produce excess reactive oxygen speci
58 dence of the elevated bioenergetic status of muscle mitochondria relative to their counterparts in th
59     The results demonstrate that extraocular muscle mitochondria respire at slower rates than mitocho
60 thors tested the hypothesis that extraocular muscle mitochondria respire faster than do mitochondria
61        Analysis of bioenergetics in skeletal muscle mitochondria revealed that knock-out of Grx2 (Grx
62 ntact cardiac myocytes and purified skeletal muscle mitochondria, robust mt-cpYFP flashes were accomp
63 tCU "hot spots" can be formed at the cardiac muscle mitochondria-SR associations via localization and
64 uscle insulin resistance despite an increase muscle mitochondria that enhances the capacity for fat o
65 te dehydrogenase kinase activity in skeletal muscle mitochondria that promotes phosphorylation and in
66           We proposed that PGC1alpha enables muscle mitochondria to better cope with a high lipid loa
67                              The capacity of muscle mitochondria to fully oxidize a heavy influx of f
68 ase intramuscular ATP and the ability of mdx muscle mitochondria to meet ATP demand.
69             However, the ability of skeletal muscle mitochondria to sequester Ca2+ released from the
70 AD(P)H reduction levels in isolated skeletal muscle mitochondria under conditions that favored supero
71 uperoxide in respiring isolated rat skeletal muscle mitochondria using hydroethidine.
72 ase activities were measured in rat skeletal muscle mitochondria using, as substrates, the synthesize
73 states were obtained in cardiac and skeletal muscle mitochondria utilizing physiologically relevant c
74                        Complementation among muscle mitochondria was suppressed by both in vivo genet
75 3, 4, and 5 respiration rates in extraocular muscle mitochondria were 40% to 60% lower than in limb m
76                        In addition, skeletal muscle mitochondria were abnormally shaped, and activiti
77 o, isolated rat liver, cardiac, and skeletal muscle mitochondria were incubated with lactate, pyruvat
78 As measured by electron microscopy, skeletal muscle mitochondria were smaller in type 2 diabetic and
79 Qo) has a very high capacity in rat skeletal muscle mitochondria, whereas the flavin site in complex
80 of the exercise-induced adaptive increase in muscle mitochondria, whereas the subsequent increase in
81 tae vesicles isolated from Drosophila flight-muscle mitochondria, which are very rich in ATP synthase
82 Hsp60) is a chaperone localizing in skeletal muscle mitochondria, whose role is poorly understood.

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