ライフサイエンスコーパス: oxygen consumption

1 those describing the body mass dependence of oxygen consumption.

2 a consequence, fails to decrease myocardial oxygen consumption.

3 athways would lead to increased whole-kidney oxygen consumption.

4 o be correlated with wood classification and oxygen consumption.

5 been studied in terms of their influence on oxygen consumption.

6 nisms that underlie the body mass scaling of oxygen consumption.

7 in AG in left BA 44 accompanied by decreased oxygen consumption.

8 is and lactate release, as well as decreased oxygen consumption.

9 rmed a 2 h laboratory ride at 72% of maximal oxygen consumption.

10 siveness, including invasion, migration, and oxygen consumption.

11 f2(-/-)white adipose tissues exhibit greater oxygen consumption.

12 ediates oxaloacetate and NADPH, and impaired oxygen consumption.

13 utively elevated mitochondrial potential and oxygen consumption.

14 ndrial membrane potential, and mitochondrial oxygen consumption.

15 d the increase in cardiac output relative to oxygen consumption.

16 remental improvements in RV size and maximum oxygen consumption.

17 1 expressions, mitochondrial biogenesis, and oxygen consumption.

18 ach unit increase in metabolic equivalent of oxygen consumption.

19 exhibit defective mitochondria and decreased oxygen consumption.

20 simultaneous expired gas analysis to measure oxygen consumption.

21 nt in exercise tolerance as assessed by peak oxygen consumption.

22 ased beta-oxidation of fatty acids (FAO) and oxygen consumption.

23 dehydrogenase activity and slightly elevated oxygen consumption.

24 esses beta-agonist-induced thermogenesis and oxygen consumption.

25 surements of extracellular acidification and oxygen consumption.

26 ly must have exceeded the expected increased oxygen consumption.

27 limitation on exercise testing (reduced peak oxygen consumption, 24+/-1.3 versus 31+/-1.3 mL/kg/min,

28 e, METs (metabolic equivalents of task), and oxygen consumption, (3) methods based on heart rate or (

29 to increased cardiorespiratory fitness (peak oxygen consumption, 44.6+/-5.2 versus 46.3+/-5.4 mL/kg p

30 .5+/-16 versus 80.5+/-14; P<0.0001), maximum oxygen consumption (61+/-17 versus 80+/-12; P<0.0001), a

31 80% (IQR, 70-88%) of predicted, median peak oxygen consumption 62% (IQR, 45-77%) of predicted, and m

32 athletes (mean +/- SEM age: 29 +/- 2 y; peak oxygen consumption: 66.8 +/- 1.3 mL . min(-1)) were stud

33 FpEF displayed worse exercise capacity (peak oxygen consumption, 7.7+/-2.3 versus 10.0+/-3.4 and12.9+

34 submaximal exercise test to estimate maximum oxygen consumption adjusted for body weight in millilite

35 Peak oxygen consumption (adjusted hazard ratio [HR] 0.82, 95%

36 all but significant dose-dependent effect on oxygen consumption after 1 h of exposure, returning to n

37 d mitochondria to immediately increase their oxygen consumption after the addition of the exogenous n

38 % at 500 mug L(-1)), and altered metabolism (oxygen consumption, ammonia excretion, and O/N from 10 m

39 tion becomes uncoupled, leading to increased oxygen consumption and a state of relative adipocyte hyp

40 developed a proliferative defect, increased oxygen consumption and accumulated reactive oxygen speci

41 We recorded oxygen consumption and assessed blood lactate after each

42 c16a have abnormal mitochondria with reduced oxygen consumption and ATP concentration, both of which

43 s associated with pathological mitochondrial oxygen consumption and ATP deficiency.

44 Y5Y neuroblastoma cells demonstrated reduced oxygen consumption and ATP production after doxorubicin,

45 RK-33 antagonized the increase in oxygen consumption and ATP production observed after exp

46 rmal metabolic function compared to impaired oxygen consumption and ATP production observed in mutant

47 tochondrial fitness associated with enhanced oxygen consumption and ATP production than wild-type pod

48 ulated glycogen synthesis; and (d) decreased oxygen consumption and ATP synthesis.

49 Accordingly, mTORC1 loss reduces oxygen consumption and causes a severe defect in BAT oxi

50 The iBAT-ablated mice showed higher oxygen consumption and decreased body weight and fat mas

51 an II (MTII), compared to vehicle, increased oxygen consumption and EE and decreased the respiratory

52 epolarized mitochondrial membrane, decreased oxygen consumption and extracellular acidification and i

53 present a technology platform for performing oxygen consumption and extracellular acidification measu

54 The oxygen consumption and extracellular acidification rate,

55 rved in injured nerves, as well as increased oxygen consumption and extracellular acidification rates

56 cidosis is associated with diminished global oxygen consumption and extraction.

57 ite adipose tissue, substantially increasing oxygen consumption and fatty acid beta-oxidation in adip

58 We found that oxygen consumption and fatty acid oxidation were increas

59 ition of BCAT1 activity results in decreased oxygen consumption and glycolysis.

60 The p32 (+/-) mice show increased oxygen consumption and heat production, indicating that

61 tRNAmut cybrids exhibited lower oxygen consumption and higher glucose consumption and la

62 Reduced oxygen consumption and impaired insulin action were reca

63 relevant events that guard against wasteful oxygen consumption and inappropriate cell growth during

64 x I into supercomplexes, leading to impaired oxygen consumption and increased mitochondrial ROS.

65 that MnSOD deletion increased mitochondrial oxygen consumption and induced mitochondrial biogenesis.

66 Based on UV/Vis-spectroscopy, measurement of oxygen consumption and LC-MS detection of intermediates,

67 pEF, and comparable values of predicted peak oxygen consumption and minute-ventilation/carbon dioxide

68 ATPHI islets have an increased basal rate of oxygen consumption and mitochondrial mass.

69 read-out of the system, cellular metabolism, oxygen consumption and morphological integrity detects s

70 anopy tests showed significant reductions in oxygen consumption and of carbon dioxide emission in can

71 uring continuous infusion of linezolid while oxygen consumption and oxygen extraction were diminishin

72 ere found to be substrates for COX, based on oxygen consumption and product formation.

73 late gestation adopts strategies to decrease oxygen consumption and redistribute the cardiac output a

74 KL-treatment increases mitochondrial rate of oxygen consumption and reduces ROS synthesis in wild typ

75 An increase in mitochondrial oxygen consumption and reserve capacity was observed in

76 on and rise in core temperature, yet reduced oxygen consumption and respiratory exchange ratio with a

77 ss of COX activity associated with decreased oxygen consumption and respiratory reserve.

78 hondrial function, attributable to increased oxygen consumption and slightly increased mitochondrial

79 HUVEC oxygen consumption and superoxide and hydrogen peroxide

80 e membrane system was examined by monitoring oxygen consumption and the antiradical and reducing capa

81 er, PDT-induced tumor hypoxia as a result of oxygen consumption and vascular damage can reduce the ef

82 cebo, at 24 weeks, TAPSE decreased, and peak oxygen consumption and VE/CO2 slope were unchanged with

83 ic calcium ([Ca(2+)] i ), insulin secretion, oxygen consumption, and [U-(13)C]glucose metabolism in i

84 Glucose oxidation, oxygen consumption, and ATP production correlated well w

85 -regulated mitochondrial membrane potential, oxygen consumption, and ATP production.

86 In response to CL 316, 243 treatments, oxygen consumption, and BAT thermogenesis were diminishe

87 acterized by increased glycolysis, decreased oxygen consumption, and decreased ATP production in mous

88 with dynamic changes such as thermal power, oxygen consumption, and extracellular acidification rate

89 lower valvuloarterial impedance, myocardial oxygen consumption, and improved myocardial efficiency d

90 gher levels of muscle AMPK, greater rates of oxygen consumption, and increased oxidative phosphorylat

91 onset diabetes, impairs beta-cell mitophagy, oxygen consumption, and insulin secretion.

92 2-mutant RV showed impaired palmitate-linked oxygen consumption, and metabolomics analysis showed red

93 reduced mitochondrial mass, ATP production, oxygen consumption, and mitochondrial protein synthesis

94 Atpenin A5 partially inhibits oxygen consumption, and neither hypoxia nor atpenin A5 i

95 ics of tissue lactate, of tissue glucose and oxygen consumption, and of the BOLD signal as reported i

96 clusively to mitochondria largely normalizes oxygen consumption, and the growth advantage of these ce

97 dissociation constant of 13 mum Steady-state oxygen consumption assays show that NADPH efficiently re

98 rometric detection was carried out following oxygen consumption at -0.7V vs. the Ag reference electro

99 nge in exercise capacity as measured by peak oxygen consumption at baseline and at 16 weeks.

100 ective evidence of exercise limitation (peak oxygen consumption at maximal exercise [o2 peak] <80% pr

101 dence, to further clarify the application of oxygen consumption at ventilatory threshold, to describe

102 oblasts derived from the patient reveal that oxygen consumption, ATP output and reactive oxygen speci

103 ased mitochondrial DNA (mtDNA) copy numbers, oxygen consumption, ATP synthesis, and expression of gen

104 y a few attempts to describe the kinetics of oxygen consumption based on the chemical composition of

105 declined from 8.0 to 7.5, calcification and oxygen consumption both decreased, suggesting a reduced

106 ffected by prednisolone while heart rate and oxygen consumption both increased significantly througho

107 se from ATTM reduces metabolism (measured as oxygen consumption) both in vivo in awake rats and ex vi

108 on of reactive oxygen species; (3) increased oxygen consumption but decreased ATP production (an ener

109 creased glucose and palmitate metabolism and oxygen consumption, but maintained power and function.

110 e micelles, have been determined in terms of oxygen consumption by a Clark electrode in an oxygen-tig

111 The kinetics of oxygen consumption by different oenological tannins were

112 cardiac output, arterial oxygen content, and oxygen consumption by the upper body.

113 cavenging activity (measured by DPPH assay), oxygen consumption capacity and ability to reduce wine c

114 nd finally, to assay metabolism, we measured oxygen consumption, carbon dioxide production, and body

115 Finally, the Rosa-Lkb1 mice had much reduced oxygen consumption, carbon dioxide production, and energ

116 on R6/2 mice to directly determine rates of oxygen consumption (CMRO2) and assess mitochondrial func

117 accompanied by significantly higher food and oxygen consumption, compared to wild type mice.

118 Mitochondrial oxygen consumption constitutes a mechanism for stimulati

119 Peak oxygen consumption decreased and ventilatory inefficienc

120 With increasing energy state, oxygen consumption decreases rapidly until a threshold i

121 Silencing MICU1 in vitro increases oxygen consumption, decreases lactate production, inhibi

122 As the temperature dependence of oxygen consumption depends on activity levels, these fin

123 ident with a large decrement in peak rate of oxygen consumption during aerobic exercise, respectively

124 rmation of the tumour based on the increased oxygen consumption during cancer cell proliferation.

125 rease and subsequent reduction in myocardial oxygen consumption during disease progression indicates

126 y and lipid profiles combined with increased oxygen consumption during high-fat-diet-induced obesity.

127 d using the DPPH test and the measurement of oxygen consumption during the autoxidation of oils rich

128 n skeletal muscle, we examined mitochondrial oxygen consumption, dynamics, and biogenesis and changes

129 s that of pyruvate kinase (PKM2) and reduces oxygen consumption, eliciting a metabolic state that con

130 EX significantly increased peak oxygen consumption (EX, 26.7+/-7.0 mL/kg per minute; UC,

131 Levels of oxygen consumption, extraction, creatinine fall and frac

132 e were no group differences in average daily oxygen consumption, fasted blood glucose or plasma free

133 in Ad-FLD mice was associated with increased oxygen consumption, fat utilization, and the expression

134 S to measure the recovery kinetics of muscle oxygen consumption following a approximately 15 s isomet

135 balanced increase in lactate production and oxygen consumption following activation, with proportion

136 e primary outcome measure was change in peak oxygen consumption from baseline to 16 weeks.

137 tion of respiration of animals and inorganic oxygen consumption from microbe respiration in sediment.

138 itochondrial membrane potential and cellular oxygen consumption (from 59 +/- 5 to 34 +/- 1 micromol o

139 ATP synthesis, oxygen consumption, generation of reactive oxygen specie

140 cell metabolic response to SFB, we measured oxygen consumption, generation of reactive oxygen specie

141 Tests for ATP hydrolysis / synthesis, oxygen consumption, glycolytic metabolism and viability

142 ailability, microvascular function, and host oxygen consumption have not been assessed in pediatric m

143 During EVKP lower levels of oxygen consumption, higher oxygen extraction, a lower de

144 at the CDC and YMC interact to separate high oxygen consumption (HOC) from DNA replication to prevent

145 Peak oxygen consumption (HR 0.81, 95% CI 0.77-0.86, P<0.01) a

146 and exhibit increased energy expenditure and oxygen consumption in beige and white fat depots.

147 atment demonstrated an immediate decrease in oxygen consumption in both parasitic (Haemonchus contort

148 d elevated both intracellular ATP levels and oxygen consumption in cardiomyocytes in vitro and in viv

149 ss dependence of oxygen diffusion to that of oxygen consumption in endotherms and ectotherms.

150 It was accompanied by larger increases in oxygen consumption in FHM1 mice, leading to tissue anoxi

151 Oxygen consumption in freshly isolated mitochondria from

152 31% and 23% increase in unloaded myocardial oxygen consumption in healthy and postischemic pigs, res

153 Oxygen consumption in its deep waters leads to the build

154 oped pressure (LVDP), coronary flow rate and oxygen consumption in LANG and LWHs.

155 ndent and -independent energy biogenesis and oxygen consumption in mice without a concomitant increas

156 f reactive oxygen species and lower rates of oxygen consumption in mitochondria.

157 lycolysis and fatty acid oxidation-dependent oxygen consumption in NK cells, but only glycolysis is r

158 Paradoxically, HFD further increases oxygen consumption in part by inducing thermogenesis and

159 ill exercise testing and measurement of peak oxygen consumption in patients with CHF due to left vent

160 ease in the ratio of l-lactate production to oxygen consumption in primary hippocampal cultures.

161 uffer from a severe deficit in mitochondrial oxygen consumption in response to the respiratory comple

162 Indeed, compared with control animals, oxygen consumption in the kidneys of claudin-2-null mice

163 ne monoxide abolished all surplus myocardial oxygen consumption in the OM-treated hearts.

164 a failure of palmitoylcarnitine to stimulate oxygen consumption in the PAH RV.

165 Diabetes did not affect oxygen consumption in the photoreceptors in either dark

166 SIRT5-/- mice revealed that SIRT5 regulates oxygen consumption in the presence of complex I, complex

167 studying the kinetics of dissolved oxygen consumption in the presence of suspended NP's and

168 Total copper correlated more closely with oxygen consumption in the wine compared to total iron, a

169 eart, endothelial nitric oxide (NO) controls oxygen consumption in the working heart through paracrin

170 energy expenditure and reduced mitochondrial oxygen consumption in white adipose tissue, brown adipos

171 Renal oxygen consumption increased only in nonseptic animals (

172 liver mitochondria, SR4 similarly increased oxygen consumption independent of adenine nucleotide tra

173 uppressor ofUcp1expression) decreasedUcp1and oxygen consumption inNrf2-deficient fibroblasts.

174 Oxygen consumption is also increased nearly 2.5-fold inN

175 Here we show that chromoplast oxygen consumption is stimulated by the electron donors

176 found that the sperm of species with higher oxygen consumption/lactate excretion rate ratios were ab

177 or patients in the lowest quartile with peak oxygen consumption </=15.3 mL/kg/min were 14% at 5 years

178 The primary outcome was peak oxygen consumption, measured with cardiopulmonary exerci

179 ptides derived from glycinin was analyzed by oxygen consumption measurements, absorbance and mass spe

180 as determined by simultaneous measurement of oxygen consumption, membrane potential and hydrogen pero

181 Peak oxygen consumption (milliliters per kilogram of body wei

182 nction, which was observed by a reduction in oxygen consumption, mitochondrial potential, and glycoly

183 Tissue level oxygen consumption (MRO2) was determined and used to cal

184 se metabolism, and metformin, which inhibits oxygen consumption, normalized lupus T cell functions in

185 Diabetes increased mitochondrial oxygen consumption (OCR) at complex II-IV.

186 ce-trained males, with a mean +/- SD maximal oxygen consumption of 58.2 +/- 5.3 mL . min(-1), followe

187 stance of greater than 440 m, peak volume of oxygen consumption of greater than 15 mL/min/kg, right a

188 rmined the role of neural stimulation in the oxygen consumption of several organs, established many o

189 he little difference of the time of complete oxygen consumption on concentration of different antioxi

190 , and sildenafil did not improve TAPSE, peak oxygen consumption, or VE/VCO2 in patients with pulmonar

191 , whereas loss of NLRX1 results in increased oxygen consumption, oxidative stress, and subsequently a

192 lar resistance (P<0.0001) and decreased peak oxygen consumption (P=0.0001).

193 and exercise performance as assessed by peak oxygen consumption (peak VO2) (CRC group 21.8 ml/kg/min;

194 us) ferric carboxymaltose (FCM) affects peak oxygen consumption [peak VO2], an objective measure of e

195 en consumption (r = -0.598, P < 0.001), peak oxygen consumption per kilogram (r = -0.474, P < 0.001),

196 Fitness was measured by peak oxygen consumption, percentage of body fat (adiposity) b

197 , measured alone or in combination with peak oxygen consumption, predict death from heart failure.

198 d, lower blood pressure response, lower peak oxygen consumption predicted, and higher minute ventilat

199 ation from scans such as blood flow rate and oxygen consumption provides new perspectives on the dise

200 action fraction (OEF), whereas outer retinal oxygen consumption (QO2) relies on oxygen availability b

201 exercise also correlated inversely with peak oxygen consumption (r = -0.598, P < 0.001), peak oxygen

202 efficiency defined as stroke work/myocardial oxygen consumption (r=0.63-0.65; all P<0.01).

203 ho developed BPD or died had a lower maximal oxygen consumption rate (mean +/- SEM, 107 +/- 8 vs. 235

204 Results indicate that MPP(+)-induced loss in oxygen consumption rate (OCR) and ATP production by mito

205 The mitochondrial oxygen consumption rate (OCR) increased in 1alpha,25(OH)

206 urs, we conduct a high-throughput screen for oxygen consumption rate (OCR) reduction and identify a n

207 nover and proton leak to basal mitochondrial oxygen consumption rate (OCR).

208 etabolites (glucose, lactate, pyruvate), and oxygen consumption rate (OCR).

209 The circadian rhythmicity of oxygen consumption rate (Vo2) was disrupted in aged obes

210 Compared to M-MO, GM-MO displayed higher oxygen consumption rate and aerobic glycolysis (extracel

211 cells (E10) induced a drop in mitochondrial oxygen consumption rate and impairment of cellular bioen

212 e presence of oxygen, profoundly reduced the oxygen consumption rate and increased the extracellular

213 observed that TSPO deficiency decreased the oxygen consumption rate and mitochondrial membrane poten

214 The oxygen consumption rate and NAD(P)H oxidation levels inc

215 lts showed no significant differences in the oxygen consumption rate between white and red wines, and

216 reases of brown-specific signature genes and oxygen consumption rate by EPA were concurrent with up-r

217 The results indicate that the oxygen consumption rate follows second-order kinetics de

218 -coated microRNA-211 partially augmented the oxygen consumption rate in PIG3V cells.

219 Mitochondrial oxygen consumption rate increases early and decreases du

220 They also confirm that the oxygen consumption rate is influenced by temperature in

221 depletion from serum blunts the induction of oxygen consumption rate observed in tubule cells treated

222 oxic conditions, decreased the mitochondrial oxygen consumption rate of cultured cells and mice.

223 analyze the onset of the pathology, maximal oxygen consumption rate of left ventricular permeabilize

224 Oxygen consumption rate was clearly related to the level

225 Net flux (oxygen consumption rate) is determined by demand for ATP

226 O-induced basal leak respiration and overall oxygen consumption rate, along with increased triglyceri

227 thermogenic activation of EPA by increasing oxygen consumption rate, brown-specific marker genes, an

228 The lower oxygen consumption rate, changes in lipid and metabolite

229 Mechanistically, SCH772984 increased the oxygen consumption rate, indicating that these cells rel

230 scavenging DPPH, and, even without modifying oxygen consumption rate, it protected quite well wine co

231 the mutant did not exhibit major changes in oxygen consumption rate, mitochondrial membrane potentia

232 cose metabolism, without impacting the basal oxygen consumption rate.

233 P/ADP ratio, CO2 and lactate production, and oxygen consumption rate.

234 ex I of the respiratory chain, decreased the oxygen consumption rate.

235 sufficient to decrease the maximal cellular oxygen consumption rate.

236 ting of the wines studied according to their oxygen consumption rate.

237 wever, M-MO exhibited a significantly higher oxygen consumption rate/ECAR ratio.

238 Significant oxygen-consumption-rate/reactive oxygen species cause dr

239 Oxygen Consumption Rates (OCRs) are faster with higher c

240 d mitochondrial dysfunction evidenced by low oxygen consumption rates (OCRs), complex activities, ATP

241 inoma cells overexpressing TIGAR have higher oxygen consumption rates and ATP levels when exposed to

242 As a consequence, oxygen consumption rates and intracellular ATP concentra

243 hondrial levels of RMRP, in turn suppressing oxygen consumption rates and modestly reducing mitochond

244 The Mcl-1 transgene increased oxygen consumption rates and mROS expression in mock-inf

245 iffusion, have been linked to differences in oxygen consumption rates and/or aerobic activity levels

246 sensitive, and using a population of cells, oxygen consumption rates could be calculated down to a s

247 ombine to match oxygen diffusion capacity to oxygen consumption rates in both air- and water-breathin

248 tiproliferative activities and inhibition of oxygen consumption rates in cells were distinctly differ

249 at match the reduced hindlimb blood flow and oxygen consumption rates in IUGR fetal sheep.

250 rates match reduced hindlimb blood flow and oxygen consumption rates in the IUGR fetus.

251 errucosus continuously showed 15-36% reduced oxygen consumption rates indicating metabolic depression

252 In particular, the substantially lower oxygen consumption rates of ectotherms of a given body m

253 ted in significantly increased mitochondrial oxygen consumption rates, ATP production rates, and enha

254 ired glucose uptake, mitochondrial function, oxygen consumption rates, glycolysis, lactic acid, and A

255 roduces cells with gene expression profiles, oxygen consumption rates, nitric oxide production levels

256 arly in relation to the body mass scaling of oxygen consumption rates.

257 ased basal, spare, and maximal mitochondrial oxygen consumption rates.

258 eases glucose uptake, lactate secretion, and oxygen consumption rates; inhibition of glucose consumpt

259 Extracellular acidification and oxygen consumptions rates, respective measures of glycol

260 riate data techniques identify six different Oxygen-Consumption-Rates (OCRs) as required to completel

261 d redox state, increased maximum and reserve oxygen consumption ratio (OCR) and higher VDAC protein l

262 educed anaerobic glycolysis and an increased oxygen consumption ratio.

263 nd relaxation, and also decreases whole-body oxygen consumption, reduces spontaneous activity, increa

264 Indirect calorimetry demonstrated increased oxygen consumption, respiratory exchange ratio, and ener

265 The new method is yielding lower oxygen consumption than previously reported, as it is on

266 on- and time-dependent, relying on increased oxygen consumption that triggered enhanced production of

267 ficiency was assessed by relating myocardial oxygen consumption to the cardiac work indices, stroke w

268 an dopaminergic SH-SY5Y cells as examined by oxygen consumption, trypan blue, 3-(4,5-dimethylthiazol-

269 onse that was characterized by a decrease in oxygen consumption, Ucp1 expression, and lipolysis.

270 ronic high-fat diet fed mice had lower basal oxygen consumption under FCCP-induced maximal respiratio

271 creased mitochondrial content, and increased oxygen consumption upon activation with cAMP analogs.

272 ches, we demonstrate that tamoxifen inhibits oxygen consumption via inhibition of mitochondrial compl

273 Patients underwent measurement of peak oxygen consumption (Vo2 [mL/kg per minute]) and ventilat

274 high throughput measurements of the rates of oxygen consumption (VO2) and hydrogen peroxide (H2O2) em

275 e primary outcome measures of peak power and oxygen consumption (VO2) and secondary measures related

276 eart rate (HR), BT, motor activity (MA), and oxygen consumption (Vo2) were measured 24 h/d at normal

277 EMGdi, ventilation, rate of oxygen consumption (VO2), and ventilatory reserve (venti

278 Exercise capacity measured as peak oxygen consumption (VO2, mL/kg/min; co-primary outcome)

279 The maximal rate of oxygen consumption (VO2max) showed the closest associati

280 e and after weight loss and included maximal oxygen consumption (VO2max), resting blood pressure, fas

281 r transplantation patients had lower maximal oxygen consumption (VO2max/kg) (37.5 +/- 9.3 mL/kg per m

282 men and men, respectively, at 50% of maximum oxygen consumption [Vo2peak]) (n = 73); high-amount, low

283 At 16 weeks, the change in mean peak oxygen consumption was +1.35 (95% CI, 0.50 to 2.21) mL/k

284 Average oxygen consumption was 1.1 +/- 0.2 mL/kg per minute.

285 On exercise stress test, maximum oxygen consumption was 76+/-16% predicted.

286 The increased unloaded myocardial oxygen consumption was confirmed in OM-treated mouse hea

287 Microvascular oxygen consumption was greater in sickle cell patients t

288 M compared with controls, whereas myocardial oxygen consumption was lower in HOCM.

289 In anaesthetised rats, renal oxygen consumption was not affected, and filtration frac

290 ause of a higher cardiac mass, total cardiac oxygen consumption was significantly higher in HOCM than

291 sgenic mouse islets, whereas glucose-induced oxygen consumption was unchanged.

292 Renal oxygen delivery increased while renal oxygen consumption was unchanged.

293 Maximal whole-body and mitochondrial oxygen consumption were not different between obese and

294 edance (ie, global afterload) and myocardial oxygen consumption were reduced by -11% and -12% (P=0.03

295 d that glutamine exposure potently increased oxygen consumption, whereas glutamine deprivation select

296 ) hearts, but did not improve ADP-stimulated oxygen consumption, which was likely caused by the 33-51

297 ty, stimulating mitochondrial biogenesis and oxygen consumption while inducing antioxidant enzymes.

298 mice by quantifying myocardial perfusion and oxygen consumption with (11)C-acetate (PET) and by measu

299 n chemostat and measured DNA replication and oxygen consumption with high temporal resolution at diff

300 l blood flow by laser Doppler flowmetry, and oxygen consumption with measurement of the oxygen tissue