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1 an presented with palpitations and decreased exercise tolerance.
2              Patients with HOCM have reduced exercise tolerance.
3 tion of iron might improve both symptoms and exercise tolerance.
4 or did it decrease cardiomyopathy or restore exercise tolerance.
5 eceptor antagonists abolished differences in exercise tolerance.
6 urthermore, it reduces symptoms and improves exercise tolerance.
7 ansport and utilization of O(2), diminishing exercise tolerance.
8  > or =10 have objective evidence of reduced exercise tolerance.
9 low relaxation and E/Ea > or =10 had reduced exercise tolerance.
10 ostcontraction vasodilatation may compromise exercise tolerance.
11 k of death or MI, but it improved angina and exercise tolerance.
12 y disease (CAD), more severe CAD and a lower exercise tolerance.
13  implications for novel therapies to improve exercise tolerance.
14 ant of exercise hyperventilation and reduced exercise tolerance.
15 f (VE/VCO(2)) in CHF patients with preserved exercise tolerance.
16 atients with known or suspected CAD and high exercise tolerance.
17 le, objective, and physiologic expression of exercise tolerance.
18 fore and after the operation showed improved exercise tolerance.
19 lower V(E); this is associated with improved exercise tolerance.
20 on for Ebstein's anomaly results in improved exercise tolerance.
21  subgroup with symptomatic ischemia and poor exercise tolerance.
22 ronic diabetic neuropathic pain and improves exercise tolerance.
23 ing to short-term improvement in dyspnea and exercise tolerance.
24 acco history developed a cough and decreased exercise tolerance.
25 nt in left ventricular ejection fraction and exercise tolerance.
26 ked sarcolemmal fragility and reduced muscle exercise tolerance.
27  at rest occur in conjunction with excellent exercise tolerance.
28 ible benefits to reduce symptoms and improve exercise tolerance.
29 contribution to ATP synthesis, and increased exercise tolerance.
30 rgement, impaired lung function, and reduced exercise tolerance.
31 ificant improvements in angina frequency and exercise tolerance.
32 duced muscle oxidative function and impaired exercise tolerance.
33 pact on ventricular volume and function, and exercise tolerance.
34 h and nine studies examining their effect on exercise tolerance.
35  a deficit in AMPK activity markedly impairs exercise tolerance.
36  pulmonary neutrophilia and the reduction in exercise tolerance.
37 nd leads to an improvement in LV filling and exercise tolerance.
38 oxidative myofibers, muscle vasculature, and exercise tolerance (33%) are decreased in mdx vs. wild-t
39 ), cough (45%), fatigue (45%), and decreased exercise tolerance (45%).
40 ion group than in the medical-therapy group (exercise tolerance, 5.0 MET [metabolic equivalent] vs. 3
41 1), arterial partial pressure of oxygen, and exercise tolerance 6 months after surgery.
42                                  Increase in exercise tolerance (6 min walk distance) was a potent me
43                              Improvements in exercise tolerance (8 of 10 patients), EF (19 +/- 13%, p
44                             There was better exercise tolerance (9.3+/-2.0 versus 7.3+/-3.1 minutes,
45      Additionally, IG KO mice have a reduced exercise tolerance, a phenotype often associated with di
46   All 5 living patients returned to baseline exercise tolerance after 6 to 16 weeks of follow-up.
47 nexplained exertional dyspnea and diminished exercise tolerance after deployment, an analysis of biop
48                     Both groups had a higher exercise tolerance after training and when breathing oxy
49  substantial relief of symptoms and improved exercise tolerance and also showed reduced or abolished
50 ults highlight a critical role for TBC1D1 in exercise tolerance and contraction-mediated translocatio
51 tors responsible for development of impaired exercise tolerance and disease progression are incomplet
52                    TGA patients have limited exercise tolerance and early mortality due to systemic (
53 ues to show promise as a method of improving exercise tolerance and enhancing oxidative capacity.
54 hypertensive response to exercise, increases exercise tolerance and improves quality of life.
55 horacic radiation therapy (RT) have impaired exercise tolerance and increased cardiovascular mortalit
56 llbeing, but molecular mechanisms underlying exercise tolerance and its plasticity are only partially
57 -dose nitrate therapy significantly improves exercise tolerance and left ventricular size and systoli
58 ble long-term benefit was a trend for better exercise tolerance and less depression of quality of lif
59                      Therefore, increases in exercise tolerance and muscle adaptations are not impair
60                                              Exercise tolerance and New York Heart Association class
61 tion during exercise in hypoxia and restored exercise tolerance and oxidative function to values obse
62                  We determined the effect on exercise tolerance and physiological exercise responses
63 es may help develop strategies for improving exercise tolerance and preventing heat injury.
64 lated lipid metabolism, leading to increased exercise tolerance and protection against diet-induced o
65                                     Improved exercise tolerance and quality of life have been demonst
66 f intravenous iron found improved short-term exercise tolerance and quality of life in patients with
67  perfusion defects, as well as with enhanced exercise tolerance and quality of life.
68 udy of two weeks of losartan (50 mg q.d.) on exercise tolerance and quality of life.
69  persist, but felodipine prevented worsening exercise tolerance and quality of life.
70                                              Exercise tolerance and quality-of-life scores were also
71 tricular resection, including reduced animal exercise tolerance and sudden death in the setting of st
72 hese observations may play a role in reduced exercise tolerance and tachycardia-induced diastolic dys
73 dine produces dose-dependent improvements in exercise tolerance and time to development of ischemia d
74 rease in QRS duration and a deterioration of exercise tolerance and ventricular dysfunction did not p
75 which could be utilized by patients with low exercise tolerance and/or capabilities.
76 populations, particularly those with limited exercise tolerance and/or capabilities.
77 e abnormalities are associated with impaired exercise tolerance, and abnormal HRR predicts increased
78 anadian Cardiovascular Society angina class, exercise tolerance, and antianginal medications), myocar
79 pathy (MM) associated with varying levels of exercise tolerance, and compared responses with those in
80 put, and resulted in weight loss, diminished exercise tolerance, and enhanced susceptibility to induc
81             Data including functional class, exercise tolerance, and hemodynamics were recorded in a
82 uced left ventricular hypertrophy, increased exercise tolerance, and improved quality of life, the op
83 lated with poor functional status, decreased exercise tolerance, and invasive hemodynamics variables.
84 ed with less pulmonary regurgitation, better exercise tolerance, and less QRS prolongation and sympto
85 sociated with improved ventricular function, exercise tolerance, and long-term survival in patients w
86  reduction in anginal symptoms, increases in exercise tolerance, and objective improvements in myocar
87                              Activity level, exercise tolerance, and orthostatic testing could not di
88 al considerations, such as patient symptoms, exercise tolerance, and patient preference.
89  progression, as reflected by lung function, exercise tolerance, and progression-free survival, in pa
90 ostacyclin, PGI2) improves haemodynamics and exercise tolerance, and prolongs survival in severe PPH
91 aningful benefits in lung function, dyspnea, exercise tolerance, and quality of life, with an accepta
92 aningful benefits of improved lung function, exercise tolerance, and quality of life.
93  fraction, New York Heart Association class, exercise tolerance, and quality of life.
94  blood analyses, pulmonary function testing, exercise tolerance, and quality-of-life assessment at 0,
95 in skeletal muscle mitochondrial biogenesis, exercise tolerance, and response to exercise training.
96 rovements in heart failure-related symptoms, exercise tolerance, and reversal of ventricular remodeli
97 m bacterial densities, inflammatory markers, exercise tolerance, and subjective well-being did not ch
98 nduced modest improvements in lung function, exercise tolerance, and symptoms at the cost of more fre
99 s lung tissue and may improve lung function, exercise tolerance, and symptoms in patients with emphys
100 exacerbations, weight gain, quality of life, exercise tolerance, and the total costs of hospital and
101 ysfunction are associated with impairment in exercise tolerance as assessed by peak oxygen consumptio
102 ttle Angina Questionnaire and improvement in exercise tolerance as assessed by treadmill exercise tes
103 s outpatients for assessment of symptoms and exercise tolerance as measured by change in the NYHA cla
104  that lung volume reduction surgery improves exercise tolerance as measured by the 6-min walk distanc
105                         These changes affect exercise tolerance, as indicated by the positive correla
106                   Exercise training improved exercise tolerance, as measured by increases in peak VO2
107                                              Exercise tolerance at 12 months had increased by a media
108                 The primary endpoint was the exercise tolerance at 12 months.
109 hanges in lung function, quality of life, or exercise tolerance between roflumilast- and placebo-trea
110 umber of clinical parameters, lung function, exercise tolerance, biomarkers, and amount of emphysema
111 d QRS duration were univariate predictors of exercise tolerance, but only t-IVT and CAD were independ
112                                Limitation of exercise tolerance by dyspnea is common in the elderly a
113 ure, and blood flow (by 33-66%) and improved exercise tolerance (by 75%) in the dystrophic mice.
114           The impact of these constraints on exercise tolerance cannot be determined from this invest
115 included functional class and improvement in exercise tolerance, cardiac index, and mean pulmonary ar
116       Finally, Tyk2(-/-) mice show decreased exercise tolerance compared to wild-type littermates.
117 ores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P <
118 nts with ERVSP > or = 40 mm Hg had decreased exercise tolerance compared with those with ERVSP <40 mm
119 rachial index, forced expiratory volume, and exercise tolerance, did not change the results.
120 roved collateral vessel function and enhance exercise tolerance during routine physical activity.
121 d desaturation, we evaluated improvements in exercise tolerance facilitated by a wearable, 1-lb, noni
122 m to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induce
123 r patients have had sustained improvement in exercise tolerance, from 3.5 mo to 4.5 yr after stent pl
124     Baseline predictors of survival included exercise tolerance, functional class, right atrial press
125 most instances, an associated improvement in exercise tolerance has been reported.
126 erfusion imaging (MPI) in patients with high exercise tolerance has not been established.
127                      The role of miR-133a in exercise tolerance has not been fully elucidated.
128                         Cardiac symptoms and exercise tolerance improved from baseline to a similar d
129 he hypothesis that intravenous iron improves exercise tolerance in anemic and nonanemic patients with
130  both TKO and TXNIP(SKM-/-) mice had reduced exercise tolerance in association with muscle-specific i
131 ACE DD genotype is associated with decreased exercise tolerance in CHF, possibly mediated by altered
132  prominently, CAD, are major determinants of exercise tolerance in DCM.
133 n vivo, which has important implications for exercise tolerance in health and certain disease states
134 hether chronotropic incompetence and reduced exercise tolerance in HF are attributable to beta-blocka
135           Oxygen therapy improves submaximal exercise tolerance in hypoxemic patients with chronic ob
136  training intensity and evidence of gains in exercise tolerance in laboratory testing.
137 ing in "leaky" channels that cause decreased exercise tolerance in mice.
138   (The Influence of Heart Rate Limitation on Exercise Tolerance in Pacemaker Patients [TREPPE]; NCT02
139           Spinal anesthesia enhanced cycling exercise tolerance in patients with COPD, mostly by redu
140      We assessed the effect of losmapimod on exercise tolerance in patients with COPD.
141 giotensin II (Ang II) blockade would improve exercise tolerance in patients with diastolic dysfunctio
142 is study was to identify the determinants of exercise tolerance in patients with Ebstein's anomaly.
143 fferent rate or rhythm control strategies on exercise tolerance in patients with HFpEF and AF is warr
144 e mechanisms linking dynamic obstruction and exercise tolerance in patients with hypertrophic obstruc
145 e that may thereby improve lung function and exercise tolerance in patients with pulmonary hyperinfla
146 ernal counterpulsation improves symptoms and exercise tolerance in patients with symptomatic coronary
147 eintroduced to alleviate dyspnea and improve exercise tolerance in selected patients with emphysema.
148 oplasty may improve flow rates, comfort, and exercise tolerance in severe emphysema.
149  supplementation on endothelial function and exercise tolerance in stable coronary artery disease (CA
150                    We hypothesized that good exercise tolerance in such patients treated medically is
151 ting demonstrated significant improvement in exercise tolerance in TAC/DOCA mice that expressed N2BAs
152 itins, which improves diastolic function and exercise tolerance in the TAC/DOCA model.
153 pact on operating lung volumes, dyspnea, and exercise tolerance in these patients.
154 ated and comparable to enalapril in terms of exercise tolerance in this short-term (12-week) study of
155  in immunofluorescence assays (P < 0.05) and exercise tolerance in treadmill tests (P < 0.05), wherea
156 g allograft dysfunction can be subdivided by exercise tolerance in two groups, and quality of life (Q
157                          At 12 months, total exercise tolerance increased by a median of 65 s in the
158 s been independently associated with reduced exercise tolerance, increased heart failure hospitalizat
159                       RV dysfunction impairs exercise tolerance independent of LV dysfunction.
160 in GLUT4(-/-)HK(Tg) show that HK II improves exercise tolerance, independent of its effects on MGU.
161                                Although high exercise tolerance is associated with an excellent progn
162                                              Exercise tolerance is decreased in patients with pulmona
163 ay, therefore, dictate intensities for which exercise tolerance is determined by the magnitude of fat
164            In addition, dyspnea is lessened, exercise tolerance is increased, and measured pulmonary
165                                      Maximal exercise tolerance is reduced in PPH, but gas exchange r
166 he age of 3-4 mo, and maximal stress-induced exercise tolerance is reduced, indicating impaired physi
167 or heart responds abnormally to exercise and exercise tolerance is reduced.
168 therapy, improves symptoms, quality of life, exercise tolerance, left ventricular function, and the s
169 gly, we hypothesized that pacing may improve exercise tolerance long-term in this syndrome.
170            During the 12-month intervention, exercise tolerance (maximum treadmill workload and 6-min
171 dvanced lung allograft dysfunction regarding exercise tolerance might result from altered IC and impa
172                                     Impaired exercise tolerance, mitochondrial biogenesis, and muscle
173                               After 6 weeks, exercise tolerance, myocardial function, and end-organ f
174                  Improvement in symptoms and exercise tolerance occurred in all patients, and a signi
175                 Supplemental oxygen improves exercise tolerance of normoxemic and hypoxemic chronic o
176   Losmapimod did not cause an improvement in exercise tolerance or lung function, despite being well-
177 acoronary infusion of rFGF2 does not improve exercise tolerance or myocardial perfusion but does show
178 ng: an improvement of at least 25 percent in exercise tolerance or pulmonary-function tests or resolu
179 res of patient benefit, including changes in exercise tolerance or quality-of-life scores.
180 ed with a greater improvement in symptoms or exercise tolerance or with a reduction in the rate of de
181 erance, such as advanced age, diabetes, poor exercise tolerance, or history of myocardial infarctions
182  oxygen saturation is the major predictor of exercise tolerance, oxygen saturation at peak exercise a
183 ith reduced muscle mass, abnormal indexes of exercise tolerance (peak V(O2), V(E)/V(CO2) slope), ejec
184 ymptomatic state (NYHA class, P<0.05), lower exercise tolerance (peak VO(2), P<0.05), and pronounced
185                          Substudies included exercise tolerance, plasma hormone and cytokines, echoca
186  costs of chronic inflammation and to foster exercise tolerance provide a rationale for therapeutic u
187 rtant clinical implications, such as reduced exercise tolerance, quality of life, and even survival.
188 domized, single-blinded study, EECP improved exercise tolerance, quality of life, and NYHA functional
189 he placebo group, P=.01) but did not improve exercise tolerance, quality of life, or the need for hos
190 ideline included mortality; hospitalization; exercise tolerance; quality of life; and cardiovascular
191 patients with otherwise unexplained impaired exercise tolerance; recurrent lower airways infection; a
192                                              Exercise tolerance reflects the integrative capacity of
193      Baseline assessments were angina class, exercise tolerance, Seattle angina questionnaire for qua
194                                              Exercise tolerance significantly improved at 3 months (n
195 y class (MD, -0.58; 95% CI, -1.00 to -0.16), exercise tolerance (standardized MD, 0.331; 95% CI, 0.08
196  in brachial artery endothelial function and exercise tolerance, suggesting a potential mechanism by
197 py use from baseline for pulmonary function, exercise tolerance, survival, hospital admission, and ad
198                    Demographics, spirometry, exercise tolerance, symptom questionnaires, CFTR genetic
199 Case series have shown that EECP can improve exercise tolerance, symptoms and myocardial perfusion in
200 a and enhances functional capacity during an exercise tolerance test (ETT) in patients with coronary
201 on or myocardial infarction (MI), with a pre-exercise tolerance test (ETT) likelihood of CAD > or =0.
202 postinfarction angina or a strongly positive exercise tolerance test (ETT) typically had cost-effecti
203 , exercise, and nuclear models by use of pre-exercise tolerance test (ETT), post-ETT, and nuclear inf
204 , CA, and Washington DC, USA, who had had an exercise tolerance test between 1986, and 2011.
205                         Deterioration in all exercise tolerance test parameters occurred in patients
206 s were similar in the 2 approaches, with the exercise tolerance test result exerting the greatest lev
207 cumented coronary artery disease, a positive exercise tolerance test, and stable chronic angina pecto
208 Efficacy was evaluated at 90 and 180 days by exercise tolerance test, myocardial nuclear perfusion im
209  depression > or =1 mm from baseline) during exercise tolerance testing (ETT) was examined in patient
210 dical treatment and, if stable, predischarge exercise tolerance testing (n = 1106).
211 principally in middle-aged men, suggest that exercise tolerance testing can provide independent progn
212                           Although screening exercise tolerance testing detects severe coronary arter
213                                              Exercise tolerance testing has been proposed as a means
214 le cohort studies demonstrate that screening exercise tolerance testing identifies a small proportion
215 ta-blocker therapy underwent cardiopulmonary exercise tolerance testing under 2 conditions in random
216  disease events (relative risk with abnormal exercise tolerance testing, 2.0 to 5.0).
217 nsional echocardiography, Holter monitoring, exercise tolerance testing, and ajmaline provocation.
218  to limiting angina during bicycle exercise (exercise tolerance tests), performed at trough of drug a
219 musclin secretion in mice results in reduced exercise tolerance that can be rescued by treatment with
220 al care resulted in an improvement in median exercise tolerance that was modest and of uncertain clin
221 th chronic heart failure (CHF) and preserved exercise tolerance, the value of cardiopulmonary exercis
222 - 0.8 mo) showed significant improvements in exercise tolerance: The distance covered over a 6 min wa
223 to guide management of patients with limited exercise tolerance, those at highest risk for perioperat
224         TMR lowered angina scores, increased exercise tolerance time, and improved patients' percepti
225           PTMR was associated with increased exercise tolerance time, low morbidity, lower angina sco
226 stress allows an assessment of the patient's exercise tolerance, to be performed while adequately str
227 ly associated with decreased muscle mass and exercise tolerance; untreated LH/FSHD was associated wit
228                                              Exercise tolerance using a bicycle ergometer showed incr
229                                              Exercise tolerance was assessed on a treadmill.
230                                This improved exercise tolerance was caused in part by an increase in
231 f patients were relieved of angina symptoms, exercise tolerance was improved, complications were mini
232                                              Exercise tolerance was increased at 90 days in all group
233                                              Exercise tolerance was not significantly different betwe
234                                              Exercise tolerance was observed.
235                                              Exercise tolerance was reduced in GLUT4(-/-) compared to
236                    Similarly, improvement in exercise tolerance was significantly greater in low-dose
237                             In vivo, maximal exercise tolerance was significantly impaired only in I7
238 nflammation, lung mechanical properties, and exercise tolerance were determined at different time poi
239 ion, and subjective and objective changes in exercise tolerance were end points.
240                    Chronic cough and reduced exercise tolerance were reported by 66% and 21% of parti
241            The F110I mutation impaired acute exercise tolerance, whereas R278C did not.
242 ng patients in the assessment of symptoms or exercise tolerance while expanding the range of patients
243 often performed in stable patients with good exercise tolerance who have not been treated with proven
244 ion) and 60 patients with stage B HF (normal exercise tolerance with left ventricular hypertrophy, an
245 s with elevated HDGF had significantly lower exercise tolerance, worse New York Heart Association fun

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