ライフサイエンスコーパス: oxidative capacity

1 espiratory exchange rates and higher hepatic oxidative capacity.

2 of RAS is associated with improved cellular oxidative capacity.

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

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

5 f improving exercise tolerance and enhancing oxidative capacity.

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

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

8 rcise improves endurance and skeletal muscle oxidative capacity.

9 ling, palmitate oxidation, and mitochondrial oxidative capacity.

10 ermining both resting oxygen consumption and oxidative capacity.

11 reduction in both their resting and maximal oxidative capacity.

12 which fatty acid uptake exceeds the myocyte oxidative capacity.

13 plained by age-related differences in muscle oxidative capacity.

14 related to abnormalities of skeletal muscle oxidative capacity.

15 ively associated with VO2peak but not muscle oxidative capacity.

16 ch to glycolysis and decreased systemic anti-oxidative capacity.

17 decreased oxygen delivery and reduced muscle oxidative capacity.

18 letal muscle (SkM) dysfunction with impaired oxidative capacity.

19 ce spectroscopy to determine skeletal muscle oxidative capacity.

20 some of the HFD-induced reduction in muscle oxidative capacity.

21 rate constant (k(PCr) ), a measure of muscle oxidative capacity.

22 ous effects on skeletal muscle mitochondrial oxidative capacity.

23 late MEF2 and PGC1a to affect fiber type and oxidative capacity.

24 ed with cardiorespiratory fitness and muscle oxidative capacity.

25 arily because of a decrease in mitochondrial oxidative capacity.

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

27 letion during exercise, and impaired maximal oxidative capacity.

28 inverse relationship between fibre size and oxidative capacity.

29 RS did not increase oxidative capacity.

30 nuclear protein imbalance, and mitochondrial oxidative capacity.

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

32 ing, including the increase in mitochondrial oxidative capacity.

33 oavailability of NAD is limiting for maximal oxidative capacity.

34 ogical LVH in part by reducing mitochondrial oxidative capacity.

35 rogram that leads to increased mitochondrial oxidative capacity.

36 ivity in these tissues characterised by high oxidative capacity.

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

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

39 the interface of fibres of largely different oxidative capacities.

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

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

42 lay an essential role in the skeletal muscle oxidative capacity adaptation and muscle mass control.

43 Mitochondrial oxidative capacity alone or combined with cardiorespirat

44 itrogen species and modifies the atmospheric oxidative capacity along its long-rang transport.

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

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

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

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

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

50 llution components because of their enhanced oxidative capacity and ability to translocate systemical

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

52 Currently, the effects of VML on the oxidative capacity and adaptability of the remaining inj

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

54 ver mitochondria, VWR increased both maximal oxidative capacity and ATP-linked respiration only in HC

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

56 We evaluated oxidative capacity and circulatory and ventilatory respo

57 atmospheric imprint that altered atmospheric oxidative capacity and climate radiative forcing, provid

58 Reduced 1-(13)C-propionate oxidative capacity and decreased levels of plasma and ur

59 uscle of obesity-prone rats, WLM reduced fat oxidative capacity and downregulated genes involved in f

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

61 ccretion but did not improve skeletal muscle oxidative capacity and endurance performance during 10 w

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

63 RB-alpha activation enhances skeletal muscle oxidative capacity and exercise performance, its deletio

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

65 ERR agonists increase mitochondria oxidative capacity and fatty acid use in vitro and in vi

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

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

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

69 se tissue dysfunction, which enhances muscle oxidative capacity and improves beta cell function.TRIAL

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

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

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

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

74 y and lactation would impact skeletal muscle oxidative capacity and lipid metabolism in adolescent of

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

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

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

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

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

80 lpha over-expression rescued the deficits in oxidative capacity and muscle strength.

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

82 altered, suggesting that total mitochondrial oxidative capacity and not trafficking is the main mecha

83 blunted hyperaemia in BAs may reflect lower oxidative capacity and O(2) requirement.

84 occurs in parallel with a decrease in muscle oxidative capacity and respiratory control ratio.

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

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

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

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

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

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

91 ment in pyruvate-driven muscle mitochondrial oxidative capacity and whole-body insulin-stimulated car

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

93 Mitochondrial biogenesis, oxidative capacity, and AMPK-autophagy signaling decreas

94 demonstrated that mitochondrial biogenesis, oxidative capacity, and AMPK-autophagy signaling decreas

95 s in global changes in exercise performance, oxidative capacity, and blood glucose levels.

96 ic emissions of iodine destroy ozone, modify oxidative capacity, and can form new particles in the tr

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

98 , established a kinetic model to predict the oxidative capacity, and examined its removal efficiency

99 after 5 and 10 wk to measure skeletal muscle oxidative capacity, and fasting blood samples were taken

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

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

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

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

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

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

106 by a higher proximal intrinsic mitochondrial oxidative capacity, apparently to support contractile pe

107 Cardiorespiratory fitness and mitochondrial oxidative capacity are associated with reduced walking s

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

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

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

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

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

113 5-coated LDs were positively associated with oxidative capacity but not with insulin sensitivity.

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

115 ed age-related changes in fitness and muscle oxidative capacity, but cannot entirely explain the age-

116 tivity is associated with VO2peak and muscle oxidative capacity, but physical inactivity cannot entir

117 Cold also increased muscle oxidative capacity, but reduced the capacity for mitocho

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

119 tabolism, and they influence redox state and oxidative capacity by altering TCA cycle intermediate co

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

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

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

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

124 Reduced skeletal muscle mass and oxidative capacity coexist in patients with pulmonary em

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

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

127 did increase the mitochondrial turbidity and oxidative capacity, consistent with reduced mitochondria

128 ry fitness and skeletal muscle mitochondrial oxidative capacity contribute to slower walking speeds i

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

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

131 age-related variation in VO2peak and muscle oxidative capacity could be explained on the basis of ph

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

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

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

135 ive muscle, indicating that intrinsic muscle oxidative capacity determines the response to cancer cac

136 B-alpha is a key mediator of skeletal muscle oxidative capacity, enhancing exercise performance when

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

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

139 b (low oxidative capacity) to type IIa (high oxidative capacity) fibres.

140 le phenotype, microvascular composition, and oxidative capacity following injury and recovery.

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

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

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

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

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

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

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

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

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

150 The reduced oxidative capacity in brown adipocytes and the developme

151 mitochondrial DNA copy number, and augments oxidative capacity in cultured neonatal mouse cardiomyoc

152 Assessment of the oxidative capacity in fresh adipose tissue explants coul

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

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

155 Oxidative capacity in patients was limited by the abilit

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

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

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

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

160 proved exercise capacity likely by improving oxidative capacity in SkM.

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

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

163 esponse to 2HB exposure leads to an improved oxidative capacity in vitro.

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

165 terial occlusions, is associated with muscle oxidative capacity in vivo.

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

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

168 ion was unchanged, estimated skeletal muscle oxidative capacity increased in VWR groups.

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

170 This leads to enhanced mitochondrial oxidative capacity, increased muscle NADH content, and h

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

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

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

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

175 Impaired muscle mitochondrial oxidative capacity is associated with future cognitive i

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

177 Higher in vivo muscle oxidative capacity is associated with preserved brain st

178 Oxidative capacity is decreased in type 2 diabetes.

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

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

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

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

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

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

185 ilability was hypothesized to reflect muscle oxidative capacity (k(HIGH) ) and the difference in k be

186 enhance skeletal muscle mass content and/or oxidative capacity, leading to autophagy activation in s

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

188 ed mitochondrial content and function (i.e., oxidative capacity), loss of mitochondrial network organ

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

190 rine air pollutants interact and atmospheric oxidative capacity may be enhanced.

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

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

193 n and neonatal upregulation of mitochondrial oxidative capacity may protect against oxidative stress

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

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

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

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

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

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

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

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

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

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

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

205 ecovery of phosphocreatine, a measure of the oxidative capacity of muscles, as assessed by (31) P MR

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

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

208 Reducing the mitochondrial B-oxidative capacity of PDGFRB+ cells via inducible expres

209 ondrial function, most notably a decrease in oxidative capacity of platelets and muscle, and greater

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

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

212 n other large Criegee intermediates and that oxidative capacity of some Criegee intermediates is smal

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

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

215 inland and urban regions, which increase the oxidative capacity of the atmosphere and serve as source

216 The hydroxyl radical (OH) sets the oxidative capacity of the atmosphere and, thus, profound

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

218 sence of high Cl(2) significantly alters the oxidative capacity of the atmosphere, with a factor of 2

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

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

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

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

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

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

225 ed mitochondrial function, thereby enhancing oxidative capacity of thermogenic tissues.

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

227 ere not due to age-related changes in muscle oxidative capacity or ATP flux.

228 hamber did not strongly change the toxicity (oxidative capacity or mutagenicity) of biogas combustion

229 xture of several ferrocenes suggest a finite oxidative capacity or oxidant concentration.

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

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

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

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

234 0.037, respectively), despite similar muscle oxidative capacity, oxidative and total ATP flux in both

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

236 Oxidative capacity per quadriceps volume was reduced to

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

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

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

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

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

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

243 vestigate why this muscle exhibits a greater oxidative capacity proximally, we tested whether the spa

244 e driven by a higher intrinsic mitochondrial oxidative capacity proximally.

245 VO2peak (R(2) = 0.323, P < 0.001) and muscle oxidative capacity (R(2) = 0.086, P = 0.011).

246 The oxidative capacity rapidly degraded 1,4-dioxane, carbama

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

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

249 y outcomes were ex vivo muscle mitochondrial oxidative capacity, substrate oxidation and ectopic fat

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

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

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

253 rance and insulin sensitivity, and increased oxidative capacity, supported by upregulation of key met

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

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

256 t MS/CIS patients suffer from abnormally low oxidative capacity that results in disrupted neural deve

257 To maintain oxidative capacity, the SkM secretes myokines such as mu

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

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

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

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

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

263 o assess the contribution of skeletal muscle oxidative capacity to age-related reductions in VO2peak

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

265 th an increase in the ratio of type IIb (low oxidative capacity) to type IIa (high oxidative capacity

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

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

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

269 Higher in vivo skeletal muscle oxidative capacity via MR spectroscopy (post-exercise re

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

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

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

273 Total oxidative capacity was concentrated in skeletal muscle a

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

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

276 Quadriceps oxidative capacity was linearly correlated with delta VO

277 Oxidative capacity was lower at metamorphosis than in la

278 Muscle oxidative capacity was measured from the phosphocreatine

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

280 concomitant with further reduction of muscle oxidative capacity was observed.

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

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

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

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

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

286 oteome suggests an increase in mitochondrial oxidative capacity, which could compensate for the energ

287 ed by myostatin inhibition, leads to loss of oxidative capacity, which further compromises metabolica

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

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

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

291 rial function, and decreased skeletal muscle oxidative capacity with greater ROS production when comp

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

293 lationships of skeletal muscle mitochondrial oxidative capacity with physical performance and perceiv

294 ter cell lipid metabolism, and higher muscle oxidative capacity with reduced ROS production than OB.

295 ng, but improved lipid metabolism and muscle oxidative capacity with reduced ROS.

296 study to link skeletal muscle mitochondrial oxidative capacity with subjective reports of cancer-rel

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

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

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

300 ed whether age-related impairments in muscle oxidative capacity would result in a greater accumulatio