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 osphorylation, muscle ATP depletion and poor exercise capacity.

3 associated with hand weakness and decreased exercise capacity.

4 were independently associated with impaired exercise capacity.

5 e advanced disease and significantly reduced exercise capacity.

6 sed risk of hospitalization and have reduced exercise capacity.

7 eatures and increased strength and endurance exercise capacity.

8 atients with Fontan circulation have reduced exercise capacity.

9 ptide or intracardiac pressures, and reduced exercise capacity.

10 scle hypertrophy, and increased strength and exercise capacity.

11 h reduced myocardial deformation and reduced exercise capacity.

12 Peak oxygen consumption reflected exercise capacity.

13 lly improve cardiopulmonary hemodynamics and exercise capacity.

14 ilatory reserve underlying the limitation of exercise capacity.

15 tients maintain normal systolic function and exercise capacity.

16 related to echocardiographic parameters and exercise capacity.

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

18 s relationship with ventricular function and exercise capacity.

19 d protein 1 ablation significantly decreases exercise capacity.

20 ipating in the study and 22 demonstrated low exercise capacity.

21 as tested by cardiac magnetic resonance and exercise capacity.

22 were independently associated with decrease exercise capacity.

23 ac abnormalities that translate into reduced exercise capacity.

24 rated muscle fatigue, and impaired endurance exercise capacity.

25 in basal low-cardiac performance and limited exercise capacity.

26 in SCD patients with increased TRV and a low exercise capacity.

27 stantially increasing fatigue resistance and exercise capacity.

28 allow improved cardiac filling and improved exercise capacity.

29 mice have increased oxidative metabolism and exercise capacity.

30 stained benefits in hemodynamic function and exercise capacity.

31 orrects diastolic dysfunction, and increases exercise capacity.

32 y and thereby improve diastolic function and exercise capacity.

33 ture interventions might focus on preserving exercise capacity.

34 training for clinical outcomes or changes in exercise capacity.

35 At 14 weeks the mutants displayed reduced exercise capacity.

36 t with lower mitochondrial mass and impaired exercise capacity.

37 s the beneficial effect of spironolactone on exercise capacity.

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

39 rminant of right ventricular performance and exercise capacity.

40 ongenital heart disease can improve physical exercise capacity.

41 ected as low and high responders had similar exercise capacities.

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

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

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

45 /- 0.1 vs. 36.8 +/- 0.1 degrees C), impaired exercise capacity (269 +/- 11 vs. 336 +/- 14 W), and low

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

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

48 00% and residual volume >150%), a restricted exercise capacity (6 min walking distance <450 m), and s

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

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

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

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

53 was to evaluate the mechanisms for improved exercise capacity after endurance exercise training (ET)

54 muscle function) contribute to the improved exercise capacity after ET in HFPEF.

55 th single-ventricle physiology have abnormal exercise capacity after the Fontan operation.

56 r peak oxygen consumption (2 RCTs) to assess exercise capacity after up to 52 weeks of treatment.

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

58 rment of right ventricular function, reduced exercise capacity and a poor prognosis.

59 Both increased exercise capacity and adaptive behavior change are neces

60 nd 2008, we assessed the association between exercise capacity and all-cause mortality in 5314 male v

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

62 ac function in vivo, as indicated by reduced exercise capacity and cardiac hypertrophy.

63 Exercise capacity and cardiovascular functional reserve

64 o Tadalafil) study, tadalafil 40 mg improved exercise capacity and delayed clinical worsening.

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

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

67 reverse ventricular remodeling and improved exercise capacity and health status compared with placeb

68 Imatinib improved exercise capacity and hemodynamics in patients with adva

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

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

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

72 mproves ventilator efficiency, improves peak exercise capacity and improves quality of life in select

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

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

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

76 rtant role in determining both basal aerobic exercise capacity and its improvement by training.

77 the effects of treatment with ivabradine on exercise capacity and left ventricular filling in patien

78 and/or LV diastolic dysfunction will improve exercise capacity and long-term outcomes in sickle cell

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

84 inverse and independent association between exercise capacity and mortality risk.

85 Peak exercise capacity and oxygen consumption did not differ

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

87 erone is an independent predictor of reduced exercise capacity and poor clinical outcomes in patients

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

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

90 Riociguat significantly improved exercise capacity and pulmonary vascular resistance in p

91 or sildenafil, inhaled treprostinil improves exercise capacity and quality of life and is safe and we

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

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

94 to the needs of these patients could improve exercise capacity and quality of life or reduce costs to

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 ctively test the association between aerobic exercise capacity and survivability (aerobic hypothesis)

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

100 Exercise capacity and symptoms of exertional intolerance

101 Exercise capacity and tolerance were reduced in HFpEF co

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

103 amined at rest and during exercise (40% peak exercise capacity) and separated post hoc into a moderat

104 rmined if deletion of Cox7a1 would (1) limit exercise capacity, and (2) alter genes responsible for s

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

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

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

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

109 essed symptoms and measured creatine kinase, exercise capacity, and muscle strength before and after

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

111 diseases (LHD), negatively impacts symptoms, exercise capacity, and outcome.

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

113 her B-type natriuretic peptide levels, lower exercise capacity, and poorer quality of life.

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

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

116 ific mutant mice affects thermal adaptation, exercise capacity, and systemic arterial pressure.

117 ) were independent correlates of increase in exercise capacity, and therapy with ivabradine (beta = 0

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

119 f survivors free from late PVR and with good exercise capacity are not well described in a literature

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

121 or who would be expected to have a very high exercise capacity are unlikely to have coronary stenosis

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

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

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

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

126 Exercise capacity as measured by peak oxygen uptake (Vo2

127 as associated with a significant increase in exercise capacity as measured by units of pooled SDs (ne

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

129 =0.003) and significantly reduced submaximal exercise capacity, as determined by the oxygen uptake ef

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

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

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

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

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

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

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

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

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

139 vidence that genetic segregation for aerobic exercise capacity can be linked with longevity and are u

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

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

142 -terminal pro-brain natriuretic peptide, and exercise capacity compared with intracoronary route.

143 associated with a significant improvement in exercise capacity compared with placebo.

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

145 Exercise capacity correlated with muscle capillarity (r

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

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

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

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

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

151 Relationships between sTfR and exercise capacity, functional class, and all-cause morta

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

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

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

155 , fewer comorbidities, better functional and exercise capacity, higher percent diffusing capacity of

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

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

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

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

160 atio were independently associated with poor exercise capacity in a large cohort of patients with sic

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

162 y exercise testing is often used to evaluate exercise capacity in adults with congenital heart diseas

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

164 l muscle atrophy was associated with reduced exercise capacity in affected males but not in heterozyg

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

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

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

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

169 Exercise capacity in chronic obstructive pulmonary disea

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

171 -5 Inhibition to Improve CLinical Status And EXercise Capacity in Diastolic Heart Failure (RELAX) cli

172 -5 Inhibition to Improve Clinical Status And Exercise Capacity in Diastolic Heart Failure (RELAX) tri

173 -5 Inhibition to Improve Clinical Status and Exercise Capacity in Diastolic Heart Failure with Preser

174 d no effect on hemodynamics, LV geometry, or exercise capacity in healthy, previously sedentary senio

175 ng therapy is under investigation to improve exercise capacity in heart failure (HF).

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

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

178 -5 Inhibition to Improve Clinical Status and Exercise Capacity in Heart Failure with Preserved Ejecti

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

180 may enhance cardiovascular function and thus exercise capacity in heart failure with preserved ejecti

181 trial (Inorganic Nitrite Delivery 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 ich beetroot juice has been shown to improve exercise capacity in heart failure with preserved ejecti

184 -5 Inhibition to Improve Clinical Status and Exercise Capacity in HFpEF) was a multicenter randomized

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

186 ercise significantly contributes to impaired exercise capacity in HFpEF.

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

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

189 Reduced exercise capacity in mice with disrupted musclin signali

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

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

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

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

194 Ts) reporting the effects of testosterone on exercise capacity in patients with HF.

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

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

197 lthough sildenafil has been shown to improve exercise capacity in patients with pulmonary arterial hy

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

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

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

201 Exercise hemodynamics and exercise capacity in patients with SSc spectrum-associat

202 ermine whether testosterone therapy improves exercise capacity in patients with stable chronic HF.

203 to describe the changes in hemodynamics and exercise capacity in patients with systemic sclerosis (S

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

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

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

207 o determine whether sildenafil could improve exercise capacity in SCD patients with increased TRV and

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

209 A1 transgene, which also rescued the loss of exercise capacity in Sgcd(-/-) mice.

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

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

212 are associated with marked abnormalities in exercise capacity in these patients.

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

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

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

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

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

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

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

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

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

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

225 5 years of age without PVR and with a normal exercise capacity may have had a definitive primary repa

226 Exercise capacity measured as peak oxygen consumption (V

227 NT-proBNP levels were associated with exercise capacity (n = 198) (maximum workload: beta = -0

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

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

230 t recipients, no significant improvements in exercise capacity or cardiovascular risk factors such as

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

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

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

234 This exercise intervention did not improve exercise capacity or quality of life in older patients w

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

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

237 ce interval, -1.3% to 3.9%; P=0.34), maximum exercise capacity, or quality of life.

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

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

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

241 class (p < 0.05), correlated negatively with exercise capacity (p = 0.027), and values >28.1 nmol/l i

242 area was an independent predictor of maximum exercise capacity (P=0.003).

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

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

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

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

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

252 Median lifespan for low exercise capacity rats was 28% to 45% shorter than high

253 , which demonstrated a modest improvement in exercise capacity, reduction of symptoms, and improved s

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

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

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

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

258 rted physical functioning and low functional exercise capacity, respectively.

259 ssociated with improvement in lung function, exercise capacity, respiratory muscle strength, and vent

260 Mdivi-1 improves exercise capacity, right ventricular function, and hemod

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

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

263 CHF, and it contributes to the limitation in exercise capacity that accompanies this condition.

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

265 For each 1-MET increase in exercise capacity, the adjusted hazard for death was 12%

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

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

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

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

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

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

272 Neither LV mass nor exercise capacity was affected by alagebrium.

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

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

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

276 Exercise capacity was increased in oxfenicine-treated mi

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

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

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

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

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

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

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

284 , abnormal heart rate recovery, or decreased exercise capacity) were associated with increased risk (

285 al conditions but show significantly reduced exercise capacity when challenged to run.

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

287 ning, low responders failed to improve their exercise capacity, whereas high responders improved by 5

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

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

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

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

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

293 es in several measures of muscle strength or exercise capacity with atorvastatin, but more atorvastat

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