ライフサイエンスコーパス: exercise capacity

1 and a measure of functional status (such as exercise capacity).

2 levels surge during exercise and IL-6 favors exercise capacity.

3 vidual noninvasive FFR data acutely improves exercise capacity.

4 d protein 1 ablation significantly decreases exercise capacity.

5 mice have increased oxidative metabolism and exercise capacity.

6 training for clinical outcomes or changes in exercise capacity.

7 as were improvements in quality-of-life and exercise capacity.

8 At 14 weeks the mutants displayed reduced exercise capacity.

9 t with lower mitochondrial mass and impaired exercise capacity.

10 s the beneficial effect of spironolactone on exercise capacity.

11 se and that this would lead to impairment in exercise capacity.

12 rminant of right ventricular performance and exercise capacity.

13 ongenital heart disease can improve physical exercise capacity.

14 h rate, persistent hypoglycemia, and limited exercise capacity.

15 osphorylation, muscle ATP depletion and poor exercise capacity.

16 associated with hand weakness and decreased exercise capacity.

17 were independently associated with impaired exercise capacity.

18 e advanced disease and significantly reduced exercise capacity.

19 sed risk of hospitalization and have reduced exercise capacity.

20 nary flow-to-systemic flow ratio or baseline exercise capacity.

21 eatures and increased strength and endurance exercise capacity.

22 atients with Fontan circulation have reduced exercise capacity.

23 ptide or intracardiac pressures, and reduced exercise capacity.

24 scle hypertrophy, and increased strength and exercise capacity.

25 h reduced myocardial deformation and reduced exercise capacity.

26 Peak oxygen consumption reflected exercise capacity.

27 lly improve cardiopulmonary hemodynamics and exercise capacity.

28 ilatory reserve underlying the limitation of exercise capacity.

29 tients maintain normal systolic function and exercise capacity.

30 related to echocardiographic parameters and exercise capacity.

31 y mass index, lung obstruction, dyspnea, and exercise capacity.

32 elivery, thereby impairing VO2 peak and thus exercise capacity.

33 delivery thereby impairing VO2 peak and thus exercise capacity.

34 tiffness, more renal dysfunction, and poorer exercise capacity.

35 s, ischemic etiology, ejection fraction, and exercise capacity.

36 nt difference in favor of ExCR for HRQoL and exercise capacity.

37 hyperinflation, health status, dyspnea, and exercise capacity.

38 RV ejection fraction, functional class, and exercise capacity.

39 The EP group had significantly impaired exercise capacity.

40 hreshold, peak expiratory flow, and muscular exercise capacity.

41 poor lung function, nutritional status, and exercise capacity.

42 hat correlates with reproductive success and exercise capacity.

43 ntervention had a positive effect on maximal exercise capacity.

44 ance of volumetric hematological measures to exercise capacity.

45 n health-related quality-of-life (HRQoL) and exercise capacity.

46 ture interventions might focus on preserving exercise capacity.

47 oglobin (HAH) affects maximal and submaximal exercise capacity.

48 sure at rest and at peak exercise, and lower exercise capacity (101+/-40 versus 122+/-51 W; P=0.02).

49 rance (-11.4 +/- 4.6 Nm/kg, 300 degrees /s), exercise capacity (-2.0 +/- 2.1 ml/kg per minute), low-b

50 sponse effect of potassium nitrate (KNO3) on exercise capacity; (2) the population-specific pharmacok

51 /- 0.1 vs. 36.8 +/- 0.1 degrees C), impaired exercise capacity (269 +/- 11 vs. 336 +/- 14 W), and low

52 t improvement between baseline and follow-up exercise capacity (4.2 +/- 1.8 METs vs. 5.7 +/- 1.9 METs

53 piratory flow (11%), and the extensor muscle exercise capacity (464 J).

54 Respiratory Questionnaire total score), and exercise capacity (47.5 m for the incremental shuttle wa

55 The CAV group patients had lower exercise capacity (5.2 +/- 1.9 versus 6.5 +/- 2.2 metabo

56 00% and residual volume >150%), a restricted exercise capacity (6 min walking distance <450 m), and s

57 Tx, and reason for HTx), corticosteroid use, exercise capacity (6-min walk distance), and quadriceps

58 fibrosis before and after PR with regard to exercise capacity (6-min walking distance [6MWD]) and he

59 us (St. George's Respiratory Questionnaire), exercise capacity (6-min-walk distance [6MWD]), muscle m

60 een emphysema, arterial BV5, and RV(EV) with exercise capacity (6-min-walk distance) and all-cause mo

61 0.7 +/- 123.7 dynes.s.cm(-5), P = 0.013) and exercise capacity (6-min-walk distance, 382.8 +/- 122.3

62 way defect by calculating the improvement in exercise capacity a patient could expect from correcting

63 bute to age-associated reductions in aerobic exercise capacity, a primary predictor of mortality in b

64 We sought to compare clinical features and exercise capacity among patients with HFpEF who were in

65 Both increased exercise capacity and adaptive behavior change are neces

66 in if passive recovery), was correlated with exercise capacity and all-cause mortality over a median

67 Exercise capacity and cardiovascular functional reserve

68 amined the relationship between preoperative exercise capacity and event-free survival in hepatocellu

69 specially benefit from regular monitoring of exercise capacity and exercise counseling.

70 asure, frailty correlated more strongly with exercise capacity and grip strength than with lung funct

71 bstructive pulmonary disease (COPD) improves exercise capacity and health-related quality of life and

72 d lead to clinically meaningful increases in exercise capacity and health-related quality of life.

73 m comprehensive PR can significantly improve exercise capacity and HRQL in LTx candidates to a clinic

74 e 3 key findings were: 1) the association of exercise capacity and HRR is much weaker in severe CHF c

75 emental exercise on a separate day, however, exercise capacity and ICA, MCA Vmean and CCA dynamics we

76 ary MR, however, is associated with impaired exercise capacity and increased mortality.

77 associated with less profound impairment of exercise capacity and is accompanied by derangements of

78 ise is a strong and independent predictor of exercise capacity and is associated with clinical outcom

79 ficient in miR-133a demonstrated low maximal exercise capacity and low resting metabolic rate.

80 The finding of lower exercise capacity and lower blood pressure response shou

81 xercise, participants significantly improved exercise capacity and lower extremity power.

82 failure, which contributes to their impaired exercise capacity and lower quality of life.

83 able electronic devices favorably influences exercise capacity and LV function 6 months later.

84 y with RV volume, and their association with exercise capacity and mortality in ever-smokers with COP

85 utonomic dysfunction and its implications on exercise capacity and mortality in long-term survivors o

86 e, sex, FEV1 percent predicted, and baseline exercise capacity and physical activity levels.

87 failure (HF) and is associated with reduced exercise capacity and poor outcomes.

88 theter VSD closure prevents deterioration in exercise capacity and promotes left ventricular reverse

89 ce this genotype displays enhanced longevity/exercise capacity and protects against cardiovascular/me

90 d abnormal relaxation 5 years later, whereas exercise capacity and pulmonary function abnormalities w

91 e effects of tadalafil--a PDE5 inhibitor--on exercise capacity and quality of life in patients with C

92 hosphodiesterase-5 (PDE5) inhibitors improve exercise capacity and quality of life in patients with i

93 o differences in age, gender, lung function, exercise capacity and quantitative computed tomography b

94 reted by the engineered fibroblasts improved exercise capacity and reduced skeletal-muscle fibrosis.

95 eatine-deficient mice show unaltered maximal exercise capacity and response to chronic myocardial inf

96 at correlate with long-term outcome; namely, exercise capacity and right heart function.

97 Riociguat significantly improved exercise capacity and secondary efficacy end points in p

98 ls, confirm the benefit of ExCR on HRQoL and exercise capacity and support the Class I recommendation

99 ial hypertension and associated with reduced exercise capacity and survival.

100 mten can reduce LVOT obstruction and improve exercise capacity and symptoms in patients with oHCM.

101 Reduced exercise capacity and worsening resting LV-GLS were asso

102 STAA mice have reduced exercise capacity, and cardiac hypertrophy is evident at

103 ted poorer cardiac function, worse treadmill exercise capacity, and greater myocardial scarring.

104 IM-AA mice also had impaired motor control, exercise capacity, and grip strength.

105 cluded change in quality of life, submaximal exercise capacity, and left ventricular ejection fractio

106 outcomes: left ventricular EF, peak aerobic exercise capacity, and N-terminal pro-brain natriuretic

107 BAT was safe and significantly improved QOL, exercise capacity, and NT-proBNP.

108 study was to characterize clinical features, exercise capacity, and outcomes in patients with HFpEF w

109 th persistent improvement in lung structure, exercise capacity, and pulmonary hypertension.

110 reduce LV outflow tract obstruction, improve exercise capacity, and relieve symptoms of oHCM in the P

111 nergetic marker), iron status, symptoms, Hb, exercise capacity, and safety.

112 V systolic function during exercise, maximal exercise capacity, and survival.

113 cted patients with CHF does not improve peak exercise capacity; and 3) acutely lowering baseline and

114 time, however, complications such as reduced exercise capacity are seen more frequently.

115 This study identified preoperative exercise capacity as an independent prognostic indicator

116 pressure after MitraClip and improvement in exercise capacity as documented by 6-minute walk test (6

117 ts had improvements in functional status, in exercise capacity as evaluated by 6-min walk test, and i

118 cebo with the primary end point of change in exercise capacity as measured by peak oxygen consumption

119 Exercise capacity as measured by peak oxygen uptake (Vo2

120 opted on the basis of short-term trials with exercise capacity as the primary end point.

121 =0.003) and significantly reduced submaximal exercise capacity, as determined by the oxygen uptake ef

122 continuous training on the change in aerobic exercise capacity, assessed as the peak oxygen consumpti

123 Voluntary exercise capacity, assessed by rats performing rotarod e

124 lts suggest that systematically implementing exercise capacity assessment pre- and post-TAVR may help

125 g TAVR completed both baseline and follow-up exercise capacity assessments at 6 months post-TAVR.

126 ed exacerbated SCD complications and reduced exercise capacity associated with an increase in altitud

127 tistically significant but small increase in exercise capacity at 16 weeks.

128 ic HF was associated with older age, reduced exercise capacity at baseline, and a higher overall rate

129 he increase in LV filling does not influence exercise capacity at this moderate altitude.

130 a clinically significantly greater change in exercise capacity based on the Vo(2)peak values (25% ver

131 We describe the changes in exercise capacity between baseline and 6 months post-TAV

132 ression of the data was performed to compare exercise capacity between survivors exposed or unexposed

133 ass Index, Airflow Obstruction, Dyspnea, and Exercise Capacity (BODE) index (0.31 [0.19 to 0.43]; p<0

134 ass index, airflow obstruction, dyspnea, and exercise capacity (BODE) index.

135 the lung can improve pulmonary function and exercise capacity but its benefit is tempered by signifi

136 Pulmonary rehabilitation (PR) improves exercise capacity, but there is conflicting evidence reg

137 disproportionately smaller hearts and their exercise capacity, cardiac diastolic function, and heart

138 aving reduced cerebral perfusion and maximal exercise capacity, cerebral oxygenation and uptake of la

139 ic response would be associated with greater exercise capacity compared to those with high [Hb] as a

140 effect of inhaled inorganic nitrite on peak exercise capacity, conducted in the National Heart, Lung

141 Exercise capacity correlated with muscle capillarity (r

142 ten in the last 20 years (p=0.039), and mean exercise capacity decreased (p=0.003).

143 an adaptive response resulting in increased exercise capacity despite less oxygen utilization associ

144 mo did not improve LVEF, quality of life, or exercise capacity, despite increases in thiamin concentr

145 d from a high-fat feeding-induced decline in exercise capacity, displaying an approximate doubling of

146 e in skeletal muscle strength and functional exercise capacity due to aging, frailty, and muscle wast

147 Bosentan improves exercise capacity, exercise time, and functional class i

148 est result for obesity via cardiorespiratory exercise capacity (experiment 1, N = 116) or physiologic

149 anied by increased visceral adiposity, lower exercise capacity, failure to maintain core body tempera

150 (DM1) increased their physical activity and exercise capacity following a behavioral intervention.

151 Treadmill exercise capacity, forelimb grip strength, and in vivo m

152 Patients with PAH displayed decreases in exercise capacity ([Formula: see text]o2max) and microci

153 for neladenoson with regard to the change in exercise capacity from baseline to 20 weeks.

154 therapies, all groups showed improvement in exercise capacity, functional class, and natriuretic pep

155 ul in predicting outcomes in those with high exercise capacity (>/=10 metabolic equivalents [METs]) p

156 nts; clinically, those with deterioration of exercise capacity had poorer outcomes.

157 or the means by which this cytokine enhances exercise capacity has been formally established yet.

158 originates from muscle and that to increase exercise capacity, IL-6 must signal in osteoblasts to fa

159 mass and end-diastolic volume increased and exercise capacity improved (by approximately 8%) only in

160 actors independently correlated with reduced exercise capacity improvement included a range of baseli

161 Although exercise capacity improves postheart transplantation (HT

162 Exercise tests revealed an increase in exercise capacity in +/- mice.

163 ction was the predominant limiting factor to exercise capacity in 40% of patients with HFpEF and was

164 We observed decreased forelimb strength and exercise capacity in adult hemizygous male mice starting

165 oderate-intensity exercise training improves exercise capacity in adults with hypertrophic cardiomyop

166 the effect of increasing and lowering HR on exercise capacity in CHF as assessed by symptom-limited

167 tudy sought to clarify the role of the HR on exercise capacity in CHF.

168 e contention that CI contributes to impaired exercise capacity in CHF.

169 assess: 1) the relationship between HRR and exercise capacity in CHF; and 2) the effect of increasin

170 Iron repletion augments exercise capacity in chronic heart failure (HF), but the

171 Exercise capacity in chronic obstructive pulmonary disea

172 moves ventilation as the major constraint to exercise capacity in COPD, allowing maximal muscle funct

173 st positive effect of any current therapy on exercise capacity in COPD; as such, gains in this area s

174 Improved exercise capacity in cyclophilin-D knockout mice associa

175 -5 Inhibition to Improve CLinical Status And EXercise Capacity in Diastolic Heart Failure (RELAX) cli

176 -5 Inhibition to Improve Clinical Status And Exercise Capacity in Diastolic Heart Failure (RELAX) tri

177 -5 Inhibition to Improve Clinical Status and Exercise Capacity in Diastolic Heart Failure with Preser

178 ociated with myocardial fibrosis and reduced exercise capacity in HCM.

179 CK-2066260 treatment improved in-vivo exercise capacity in healthy rats and in a rat model of

180 trial (Inorganic Nitrite Delivery to Improve Exercise Capacity in Heart Failure with Preserved Ejecti

181 ich beetroot juice has been shown to improve exercise capacity in heart failure with preserved ejecti

182 ich beetroot juice has been shown to improve exercise capacity in heart failure with preserved ejecti

183 othesis that NO3(-) supplementation improves exercise capacity in heart failure with preserved ejecti

184 NO3(-) increased exercise capacity in heart failure with preserved ejecti

185 -5 Inhibition to Improve Clinical Status and Exercise Capacity in Heart Failure with Preserved Ejecti

186 ailure, but factors associated with impaired exercise capacity in heart failure with preserved ejecti

187 -5 Inhibition to Improve Clinical Status and Exercise Capacity in HFpEF) was a multicenter randomized

188 ypothesis that heart rate reduction improves exercise capacity in HFpEF.

189 hat peak C(a-v)o2 was a major determinant of exercise capacity in HFpEF.

190 ercise significantly contributes to impaired exercise capacity in HFpEF.

191 iciency did not affect glucose clearance and exercise capacity in lean adult mice.

192 Hemoglobin mass was positively related to exercise capacity in lowlanders at sea level and in Sher

193 Reduced exercise capacity in mice with disrupted musclin signali

194 cise-responsive myokine that acts to enhance exercise capacity in mice.

195 had positive effects but failed to normalize exercise capacity in patients on hemodialysis.

196 er symptoms, and greater quality of life and exercise capacity in patients with heart failure (HF) an

197 Reduced exercise capacity in patients with heart failure (HF) co

198 in improving diastolic function and maximal exercise capacity in patients with heart failure with pr

199 o: 1) assess the impact of ExCR on HRQoL and exercise capacity in patients with HF; and 2) investigat

200 whether therapy with oral iron improves peak exercise capacity in patients with HFrEF and iron defici

201 -type natriuretic peptide levels, and better exercise capacity in patients with ischemic cardiomyopat

202 flammatory response and improve peak aerobic exercise capacity in patients with recently decompensate

203 NMES improves functional exercise capacity in patients with severe COPD by enhanc

204 ignificantly improved pulmonary function and exercise capacity in patients with severe emphysema char

205 Impaired exercise capacity in people with severe TR is related to

206 idative capacity may account for the reduced exercise capacity in Pus1(-/-) mice.

207 nd abnormal HRR were associated with reduced exercise capacity in RT patients.

208 models of PAH and improves hemodynamics and exercise capacity in selected patients with PAH.

209 Impact of Late Sodium Current Inhibition on Exercise Capacity in Subjects with Symptomatic Hypertrop

210 cular physiology in vivo, leading to reduced exercise capacity in the fight-or-flight response and de

211 of factors, beyond the lungs, that influence exercise capacity in this patient population and may, ul

212 These results (1) show higher exercise capacity in Tibetans without the erythropoietic

213 dose of ivabradine does not adversely affect exercise capacity in unselected CHF patients.

214 e spironolactone group showed improvement in exercise capacity (increment in peak VO2 [2.9 ml/min/kg

215 ass index, airflow obstruction, dyspnea, and exercise capacity index (adjusted beta = 0.169; 95% CI,

216 ass index, airflow obstruction, dyspnea, and exercise capacity) index, -1.8 points (all P < 0.05).

217 Low aerobic exercise capacity is a risk factor for diabetes and a st

218 alth benefits of exercise, understanding how exercise capacity is regulated is a question of paramoun

219 tem cell treatment in performance status and exercise capacity, left ventricular ejection fraction, a

220 -naive patients, particularly with regard to exercise capacity, left ventricular ejection fraction, l

221 demonstrated that exercise training improved exercise capacity, lower extremity muscle strength, and

222 eart Association functional class II to III, exercise capacity <80% of normal, left ventricular eject

223 Treatment with mavacamten improved exercise capacity, LVOT obstruction, NYHA functional cla

224 eak exercise was an independent predictor of exercise capacity (maximal oxygen uptake, p = 0.004) and

225 In those with serial testing, a decline in exercise capacity may be a marker of clinical deteriorat

226 Dynamic assessment of preoperative exercise capacity may be a useful predictor of postopera

227 5 years of age without PVR and with a normal exercise capacity may have had a definitive primary repa

228 Exercise capacity measured as peak oxygen consumption (V

229 unrecognized myocardial infarction, reduced exercise capacity, nondiagnostic electrocardiographic ch

230 n left ventricular (LV) function and maximal exercise capacity observed under hypobaric hypoxia.

231 rial hypertension; improved hemodynamics and exercise capacity occurred in medium- and high-dose grou

232 tor only in osteoblasts exhibit a deficit in exercise capacity of similar severity to the one seen in

233 compared with a placebo had no effect on the exercise capacity or clinical status of patients with he

234 did not result in significant improvement in exercise capacity or clinical status.

235 Tadalafil does not improve exercise capacity or quality of life despite exerting pu

236 ntricular mass nor did it improve submaximal exercise capacity or quality of life.

237 Each trial provided IPD on HRQoL or exercise capacity (or both), with follow-up of 6 months

238 rtan on right ventricular ejection fraction, exercise capacity, or quality of life.

239 ing, sildenafil did not improve RV function, exercise capacity, or ventilatory efficiency.

240 iciency, high-dose oral iron did not improve exercise capacity over 16 weeks.

241 To determine direct effects of dietary Pi on exercise capacity, oxygen uptake, serum nonesterified fa

242 uptake) and submaximal (6-min walk distance) exercise capacity (p < 0.01 for both).

243 iastolic function but did not affect maximal exercise capacity, patient symptoms, or quality of life

244 s, obese patients with HFpEF displayed worse exercise capacity (peak oxygen consumption, 7.7+/-2.3 ve

245 ction (E/e') on echocardiography and maximal exercise capacity (peak VO2) on cardiopulmonary exercise

246 g the defective steps that impair each one's exercise capacity (peak Vo2).

247 chronic kidney disease (CKD) exhibit reduced exercise capacity, poor physical function and symptoms o

248 cal implications of a lack of improvement in exercise capacity post-TAVR.

249 amining the clinical impact of variations in exercise capacity post-transcatheter aortic valve replac

250 tients undergoing TAVR did not improve their exercise capacity postprocedure.

251 associated with a significant improvement in exercise capacity, pulmonary arterial pressure, and qual

252 lopurinol failed to improve clinical status, exercise capacity, quality of life, or left ventricular

253 wer lobes correlated with the improvement in exercise capacity, reflecting surgical success.

254 pEF), but its clinical profile and impact on exercise capacity remain unclear.

255 and left ventricular function declined, peak exercise capacity remained stable.

256 g, self-rated general health, and functional exercise capacity, respectively).

257 We assessed exercise capacity (spiroergometry), cardiac function (ec

258 The increased exercise capacity suggests that decelerated fat infiltra

259 ot have better quality of life or submaximal exercise capacity than did patients who received placebo

260 on skeletal muscle fatty acid metabolism and exercise capacity that is independent of obesity and car

261 impaired diastolic ventricular function and exercise capacity that may be related to myocardial fibr

262 In patients >35 years of age with normal exercise capacity, there was mild residual right ventric

263 We defined age-specific exercise capacity thresholds to guide assessment of mort

264 e "exercise-resistant" and unable to improve exercise capacity through exercise training.

265 sin inhibition to improve symptom burden and exercise capacity through reducing LV outflow tract obst

266 , it may aid in the translation of increased exercise capacity to greater participation in activities

267 limiting left ventricular (LV) function and exercise capacity under chronic hypoxaemia at high altit

268 Clinical profiles and exercise capacity varied across definitions, with peak o

269 other clinical events, safety, and change in exercise capacity (VO(2peak)) and health-related quality

270 tion via lumbar intrathecal fentanyl on peak exercise capacity ( VO2 peak) and the contributory mecha

271 action (HFrEF) exhibit severe limitations in exercise capacity ( VO2 peak).

272 After 4 weeks, exercise capacity, Vo2 peak and ischemic threshold incre

273 exercise results in substantial benefits in exercise capacity ( VO2max ), cardiovascular function at

274 energic stimulation were limited and maximal exercise capacity was compromised.

275 Low functional exercise capacity was defined as </= 300 m walked during

276 Moreover, maximal exercise capacity was enhanced after induction of Crtc2

277 Exercise capacity was evaluated by the 6-minute walk tes

278 Despite these effects in isolated muscle, exercise capacity was not altered in MLC-Cre:GRK2(fl/fl)

279 Also, exercise capacity was reduced and lung weight increased.

280 f any given O2 pathway defect on a patient's exercise capacity was strongly influenced by comorbid de

281 lysis of the O2 pathway in HFpEF showed that exercise capacity was undermined by multiple defects, in

282 uding ST-segment depression, chest pain, and exercise capacity, was used as the outcome of the exerci

283 Patients with low exercise capacity were defined as 6-min walk test <50% p

284 differences in systo-diastolic function and exercise capacity were observed comparing normal and low

285 heart failure symptoms, quality of life, and exercise capacity were observed.

286 gen uptake, voluntary physical activity, and exercise capacity were significantly reduced in TWEAK-Tg

287 ociety grading of angina pectoris class, and exercise capacity were used as covariates in the multiva

288 th such myocardial hypoxia exhibited reduced exercise capacity when compared with wild-type mice.

289 c incompetence) are strongly associated with exercise capacity, whereas resting measures of ventricul

290 Heart failure is associated with diminished exercise capacity, which is driven, in part, by alterati

291 sal vagal motor nucleus dramatically impairs exercise capacity, while optogenetic recruitment of the

292 logical basis for the progressive decline of exercise capacity with aging and in diverse disease stat

293 al activity preserves cardiac metabolism and exercise capacity with aging but has limited effect on a

294 ompared with usual care resulted in improved exercise capacity with high short-term costs.

295 is study sought to define the association of exercise capacity with left ventricular hypertrophy (LVH

296 t the RELAX trial observed no improvement in exercise capacity with sildenafil treatment in subjects

297 he authors sought to identify improvement in exercise capacity with spironolactone in the subset of p

298 ort-term treatment with ivabradine increased exercise capacity, with a contribution from improved lef

299 Most had exercise capacity within normal range (z peak o2=-0.91+/

300 vagal activity are strongly associated with exercise capacity, yet a causal relationship has not bee