ライフサイエンスコーパス: oxidative capacity

1 f improving exercise tolerance and enhancing oxidative capacity.

2 ion and a marked increase in skeletal muscle oxidative capacity.

3 sitive satellite cells; (iv) improved muscle oxidative capacity.

4 rcise improves endurance and skeletal muscle oxidative capacity.

5 ling, palmitate oxidation, and mitochondrial oxidative capacity.

6 ermining both resting oxygen consumption and oxidative capacity.

7 reduction in both their resting and maximal oxidative capacity.

8 which fatty acid uptake exceeds the myocyte oxidative capacity.

9 letion during exercise, and impaired maximal oxidative capacity.

10 related to abnormalities of skeletal muscle oxidative capacity.

11 inverse relationship between fibre size and oxidative capacity.

12 RS did not increase oxidative capacity.

13 nuclear protein imbalance, and mitochondrial oxidative capacity.

14 letal muscle due to an upregulation of lipid oxidative capacity.

15 ing, including the increase in mitochondrial oxidative capacity.

16 oavailability of NAD is limiting for maximal oxidative capacity.

17 ogical LVH in part by reducing mitochondrial oxidative capacity.

18 rogram that leads to increased mitochondrial oxidative capacity.

19 ivity in these tissues characterised by high oxidative capacity.

20 sis that the level of lactate is a marker of oxidative capacity.

21 with a net loss of mitochondrial protein and oxidative capacity.

22 of RAS is associated with improved cellular oxidative capacity.

23 ty suggest an important role for low resting oxidative capacity.

24 oscopy (MRS) for estimation of mitochondrial oxidative capacity.

25 in response to sepsis at a cost of decreased oxidative capacity.

26 the interface of fibres of largely different oxidative capacities.

27 ly regulated to avoid large fibres with high oxidative capacities, (2) the anatomical fibre distribut

28 Training increased peak work and oxidative capacities (20-30%), systemic arteriovenous O2

29 ol modifies the lipidomic profile, increases oxidative capacities and decreases glycolysis, in associ

30 ents the resveratrol-induced augmentation in oxidative capacities and the increased PDH activity sugg

31 ncept of a constraint between fibre size and oxidative capacity and 2) indicate the important role of

32 sin heavy chain isoforms with an increase in oxidative capacity and a decrease in glycolytic capacity

33 d, and omohyoid) and results in an increased oxidative capacity and a fast-toward-slow shift in myosi

34 ipose tissue (BAT) mitochondria exhibit high oxidative capacity and abundant expression of both elect

35 d hepatic steatosis, increased mitochondrial oxidative capacity and an increased reliance on fatty ac

36 calcium overload, compromised mitochondrial oxidative capacity and augmented oxidative stress.

37 We evaluated oxidative capacity and circulatory and ventilatory respo

38 has been shown to reduce both muscle-tissue oxidative capacity and endurance in animals.

39 protein 72 (HSP72), which include increased oxidative capacity and enhanced mitochondrial function,

40 ressed in concert with reduced mitochondrial oxidative capacity and fatty acid oxidation (FAO).

41 er adjustment for the same variables, muscle oxidative capacity and free-living total EE were negativ

42 Before and after the intervention, oxidative capacity and gene expression were assessed in

43 nsport, respectively, improves mitochondrial oxidative capacity and glucose metabolism in obese anima

44 training (ET) for increasing skeletal muscle oxidative capacity and improving certain cardiovascular

45 hat iron deficiency without anemia decreased oxidative capacity and increased reliance on carbohydrat

46 ssociated with reduced hepatic mitochondrial oxidative capacity and increased susceptibility to hepat

47 tions in tissues with high energy demand and oxidative capacity and is highly enriched in the heart.

48 This likely indicates increased oxidative capacity and may be a compensatory response to

49 ncreasing age, indicating declines in muscle oxidative capacity and mitochondrial function, respectiv

50 to be responsible for this decline in muscle oxidative capacity and mitochondrial function.

51 altered mitochondrial function with enhanced oxidative capacity and mitochondrial ROS generation, and

52 cal determinants of peak muscle strength and oxidative capacity and muscle biopsy-derived measures of

53 The product of oxidative capacity and muscle volume - the quadriceps ox

54 strate that p66(shc) regulates mitochondrial oxidative capacity and suggest that p66(shc) may extend

55 one number and surface area, suggesting that oxidative capacity and synapse strength are reduced as d

56 be decreased in deprived puffs, because the oxidative capacity and transmitter level in GABAergic ne

57 esis and beta-oxidation that potentiates WAT oxidative capacity and ultimately supports browning.

58 (mean age 68.8 years) and compared with the oxidative capacity and volume of the quadriceps.

59 on and hormone activation with mitochondrial oxidative capacity and whole-body energy homeostasis.

60 n single skeletal muscle fibres differing in oxidative capacity, and across stimulation intensities u

61 lipid accumulation, increases white adipose oxidative capacity, and enhances whole-body energy expen

62 ed in intramyocellular lipids, mitochondrial oxidative capacity, and insulin resistance.

63 Cultured Fnip1-null muscle fibers had higher oxidative capacity, and isolated Fnip1-null skeletal mus

64 ndgrip exercise, 6-minute walk test, maximal oxidative capacity, and life quality; cardiac function w

65 e of appearance (Ra) and disappearance (Rd), oxidative capacity, and markers for pro-inflammatory pat

66 The complete FAO, the oxidative capacity, and mitochondrial biogenesis were in

67 xcitatory input to maintain their heightened oxidative capacity; and 3) intracortical inhibition medi

68 ction and increased mitochondrial number and oxidative capacity are hallmark features of myocyte diff

69 Skeletal muscle mitochondrial content and oxidative capacity are important determinants of muscle

70 Once induced, this gene program and oxidative capacity are maintained independently of rosig

71 inflammatory state and reduced mitochondrial oxidative capacity are observed in bouts separated by 4

72 y FGF21 in adipocytes enhanced mitochondrial oxidative capacity as demonstrated by increases in oxyge

73 5-coated LDs were positively associated with oxidative capacity but not with insulin sensitivity.

74 chondrial mass in TM cells not only promotes oxidative capacity, but also glycolytic capacity.

75 nesis in skeletal muscle and enhances muscle oxidative capacity, but the signaling mechanisms involve

76 icant increases in mitochondrial content and oxidative capacity (by 40-80%).

77 ted with reduced mitochondrial integrity and oxidative capacity, can be attenuated under conditions o

78 intolerance by further reducing the limited oxidative capacity caused by blocked glycogenolysis.

79 high levels of mitochondrial biogenesis and oxidative capacity characteristic of brown adipose tissu

80 nes in SM high-energy phosphates and reduced oxidative capacity compared with healthy and low-fatigab

81 tivity and cytochrome c protein) and reduced oxidative capacity (complete palmitate oxidation in hepa

82 To determine if abnormal skeletal muscle oxidative capacity contributes to this impaired aerobic

83 We tested the hypothesis that a high oxidative capacity could attenuate lipid-induced IR.

84 expression of enzymes controlling the muscle oxidative capacity (Cpt1, Acox1, Cs, Cycs, Ucp3) and glu

85 Insulin resistance increases and muscle oxidative capacity decreases during aging, but lifestyle

86 findings challenge the notion that increased oxidative capacity defends whole-body energy homeostasis

87 We based our oxidative capacity estimates on the kinetics of changes

88 This study suggests another mechanism, that oxidative capacity exceeds regulated entry of long chain

89 be useful to distinguish black carbon-based oxidative capacity from water-soluble organic-based acti

90 l proliferation, mitochondrial abundance and oxidative capacity, glycogen accumulation, and acquisiti

91 A low fat oxidative capacity has been linked to muscle diacylglyce

92 ce-trained athletes, characterized by a high oxidative capacity, have elevated intramyocellular lipid

93 a in regulating mitochondrial biogenesis and oxidative capacity; however, the precise mechanisms by w

94 tic gluconeogenesis, decreased mitochondrial oxidative capacity, impaired lipid metabolism, and incre

95 th reduced tricarboxylic acid and fatty acid oxidative capacity, impairs mitochondrial energetics.

96 to be the main determinant of mitochondrial oxidative capacity in aging tissues.

97 activator of uncoupling protein 1 (UCP1) and oxidative capacity in BAT.

98 g-induced improvement in skeletal muscle fat oxidative capacity in humans.

99 onstrate that SIRT4 inhibition increases fat oxidative capacity in liver and mitochondrial function i

100 Oxidative capacity in patients was limited by the abilit

101 training has been shown to increase work and oxidative capacity in patients with mitochondrial myopat

102 +RES supplementation significantly increased oxidative capacity in permeabilized muscle fibers (P-tim

103 which mediates mitochondrial biogenesis and oxidative capacity in skeletal muscle (SKM).

104 oth NeuroAR and MyoAR mice exhibited reduced oxidative capacity in skeletal muscles, as well as a shi

105 n primates the high ratio of transaminase to oxidative capacity in the entire gastrointestinal tract

106 le flux is a central mechanism of restricted oxidative capacity in this disorder.

107 he effect of exercise training on muscle fat oxidative capacity in vivo.

108 is abundantly expressed in tissues with high oxidative capacity, including the heart and type I skele

109 While oxidative capacity increased 25% in WL + EX (compared wi

110 s, including decreased hepatic mitochondrial oxidative capacity, increased hepatic expression of de n

111 le by W191G represents an example of how the oxidative capacity inherent in the heme prosthetic group

112 in mtDNA copy number proportional to tissue oxidative capacities is demonstrated in skeletal muscle

113 Whether decreased oxidative capacity is a cause or consequence of diabetes

114 cardiac metabolic profile and mitochondrial oxidative capacity is a viable therapeutic strategy.

115 letal muscle combined with low mitochondrial oxidative capacity is associated with insulin resistance

116 Oxidative capacity is decreased in type 2 diabetes.

117 mechanisms by which mitochondrial fatty acid oxidative capacity is diminished in response to hypoxia,

118 ells balance lipid storage and mitochondrial oxidative capacity is poorly understood.

119 In contrast, mitochondrial oxidative capacity is transiently upregulated in the liv

120 Muscle mitochondrial oxidative capacity is unchanged at the onset but decreas

121 a for diabetes exhibit reduced mitochondrial oxidative capacity is unclear; addressing this question

122 is to evaluate whether lactate, a marker of oxidative capacity, is associated with incident diabetes

123 inally, the apelin-stimulated improvement of oxidative capacity led to decreased levels of acylcarnit

124 abolism related to mitochondrial content and oxidative capacity may account for the reduced exercise

125 ese data indicate that reduced mitochondrial oxidative capacity may contribute to cardiac dysfunction

126 d in heart failure and that impaired aerobic-oxidative capacity may play a role in the limitation of

127 Disruptions in FSHD myogenesis and oxidative capacity may therefore not arise from a positi

128 pression resulted in increased mitochondrial oxidative capacity measured by cellular respiration and

129 II substrates, followed by uncoupled maximal oxidative capacity measured in the presence of these com

130 Despite greatly decreased oxidative capacity, muscle tissue from patients deficien

131 le of adult Myo-Cre/Flox-MCIP1 mice, whereas oxidative capacity, myoglobin content, and mitochondrial

132 suggests that resveratrol might improve the oxidative capacities of cancer cells through the CamKKB/

133 e JCI, Mori et al. link WNT signaling to the oxidative capacity of adipocytes during obesity.

134 vity and Cox7a1 protein levels affecting the oxidative capacity of brown adipose tissue and thus non-

135 systemic energy homeostasis and the overall oxidative capacity of insulin target tissues.

136 chondrial fatty acid metabolism and elevated oxidative capacity of insulin-target tissues.

137 We provide data suggesting normal oxidative capacity of mitochondria in insulin-resistant

138 Here, we explored the oxidative capacity of nano-magnetite (Fe3O4) having appr

139 t mineral-only results may underestimate the oxidative capacity of natural systems with biotic and ab

140 The improvement in the oxidative capacity of skeletal muscle may be a key compo

141 and thus links endothelial FA uptake to the oxidative capacity of skeletal muscle, potentially preve

142 Ozone depletion events can change the oxidative capacity of the air by affecting atmospheric h

143 part of the radical cycles that control the oxidative capacity of the atmosphere and lead to the for

144 roxyl radicals (OH) are known to control the oxidative capacity of the atmosphere but their influence

145 quence, of a more accurate prediction of the oxidative capacity of the atmosphere.

146 f galactose to culture medium improves total oxidative capacity of the cells and ameliorates fatty ac

147 in mitochondrial content, as well as a lower oxidative capacity of the mitochondria with age.

148 e activity (mU/g wet wt) correlates with the oxidative capacity of the muscles, being lowest in type

149 Given the oxidative capacity of the neutrophil NADPH oxidase, we s

150 Reactive halogens influence the oxidative capacity of the troposphere directly as oxidan

151 fects of Sul-121, a novel compound with anti-oxidative capacity, on hyperresponsiveness (AHR) and inf

152 by changes in skeletal muscle mitochondrial oxidative capacity or oxidant emissions, nor were there

153 ning did not alter (p > 0.05) MHC phenotype, oxidative capacity, or antioxidant enzyme activity in th

154 decrease tension per unit muscle mass, fiber oxidative capacity, or motor endplate size.

155 he recruitment of muscle fibres differing in oxidative capacity, or slowed blood flow (Q) kinetics is

156 In addition, the oxidative capacity per mitochondrial volume (0.22 +/- 0.

157 Oxidative capacity per quadriceps volume was reduced to

158 ed from reductions in both muscle volume and oxidative capacity per volume in the elderly and appears

159 This study determined the decline in oxidative capacity per volume of human vastus lateralis

160 that elderly subjects had nearly 50 % lower oxidative capacity per volume of muscle than adult subje

161 High free-living total EE and low muscle oxidative capacity predict high rates of fat gain.

162 Lactate, an indicator of oxidative capacity, predicts incident diabetes independe

163 s well as activated the higher mitochondrial oxidative capacity programme and fatty acid oxidation th

164 Despite this increase in mitochondrial oxidative capacity, run time to exhaustion at various in

165 The observed defect in oxidative capacity seen in p66(shc-/-) cells is partiall

166 d COX transcript levels in tissues with high oxidative capacities such as red soleus muscle or liver,

167 increase of its contribution to total brain oxidative capacity, suggesting that it was not the major

168 rom mitoNEET-null mice demonstrate a reduced oxidative capacity, suggesting that mito- NEET is an imp

169 apacity causes reduced hepatic mitochondrial oxidative capacity that increases susceptibility to both

170 troy ozone (O3), oxidize mercury, and modify oxidative capacity that is relevant for the lifetime of

171 egulates mitochondrial activity and enhances oxidative capacity through an AMPK-SIRT1-PGC1alpha-depen

172 oupled duroquinol oxidation measures maximal oxidative capacity through complex III.

173 In adipocytes, lack of SFRP5 stimulated oxidative capacity through increased mitochondrial activ

174 ric ozone and it influences the atmosphere's oxidative capacity through its reaction with the hydroxy

175 ) results in hypertrophic muscle with a high oxidative capacity thus violating the inverse relationsh

176 a in brown adipocytes, thereby expanding the oxidative capacity to match enhanced fatty acid supply.

177 lleagues, showing that reduced mitochondrial oxidative capacity underlies the accumulation of intramu

178 rdiac output (delivery), and skeletal muscle oxidative capacity (utilization).

179 Moreover, enhancing fatty acid oxidative capacity via exercise training is not sufficie

180 o, phosphorylation potential (PP), and total oxidative capacity (Vmax).

181 Oxidative capacity was 50 % lower in the elderly vs. the

182 Age-related decline in mitochondrial oxidative capacity was absent in endurance-trained indiv

183 Total oxidative capacity was concentrated in skeletal muscle a

184 he maximal oxidative phosphorylation rate or oxidative capacity was estimated from the PCr recovery r

185 Furthermore, peak oxidative capacity was higher in the transgenics as comp

186 Quadriceps oxidative capacity was linearly correlated with delta VO

187 In vivo muscle oxidative capacity was not different in fa/fa animals co

188 Fatty acid oxidative capacity was similar between muscles of WT and

189 capacity and muscle volume - the quadriceps oxidative capacity - was 36 % of the adult value in the

190 IMCL levels and skeletal muscle oxidative capacity were determined in vivo, using locali

191 resistance and indices of the rate of muscle oxidative capacity were unchanged in both groups.

192 olite pools have no major negative impact on oxidative capacity, whereas reductions beyond a critical

193 proves insulin sensitivity and mitochondrial oxidative capacity while decreasing resting energy expen

194 The decline in quadriceps oxidative capacity with age resulted from reductions in

195 s of mitochondrial content to the decline in oxidative capacity with age.

196 well as how mitochondria can increase their oxidative capacity with increased demand.

197 volunteers, we measured the skeletal muscle oxidative capacity with the use of high-resolution respi

198 ation of plasma lactate at rest, a marker of oxidative capacity, with incident cardiovascular outcome

199 This was accompanied by a decline in muscle oxidative capacity, without alterations in skeletal musc