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1 to restrict motor unit activation and limit exercise tolerance.
2 vascular rarefaction may be key to restoring exercise tolerance.
3 ificant improvements in angina frequency and exercise tolerance.
4 duced muscle oxidative function and impaired exercise tolerance.
5 pact on ventricular volume and function, and exercise tolerance.
6 h and nine studies examining their effect on exercise tolerance.
7 a deficit in AMPK activity markedly impairs exercise tolerance.
8 pulmonary neutrophilia and the reduction in exercise tolerance.
9 nd leads to an improvement in LV filling and exercise tolerance.
10 Patients with HOCM have reduced exercise tolerance.
11 tion of iron might improve both symptoms and exercise tolerance.
12 or did it decrease cardiomyopathy or restore exercise tolerance.
13 eceptor antagonists abolished differences in exercise tolerance.
14 urthermore, it reduces symptoms and improves exercise tolerance.
15 ansport and utilization of O(2), diminishing exercise tolerance.
16 > or =10 have objective evidence of reduced exercise tolerance.
17 low relaxation and E/Ea > or =10 had reduced exercise tolerance.
18 ostcontraction vasodilatation may compromise exercise tolerance.
19 , Canadian Cardiovascular Society class, and exercise tolerance.
20 k of death or MI, but it improved angina and exercise tolerance.
21 y disease (CAD), more severe CAD and a lower exercise tolerance.
22 implications for novel therapies to improve exercise tolerance.
23 ant of exercise hyperventilation and reduced exercise tolerance.
24 f (VE/VCO(2)) in CHF patients with preserved exercise tolerance.
25 ack restrict motor unit activation and limit exercise tolerance.
26 entral role in the control of metabolism and exercise tolerance.
27 itical speed) was used to evaluate treadmill exercise tolerance.
28 endothelin receptor expression and impaired exercise tolerance.
29 atients with known or suspected CAD and high exercise tolerance.
30 le, objective, and physiologic expression of exercise tolerance.
31 fore and after the operation showed improved exercise tolerance.
32 lower V(E); this is associated with improved exercise tolerance.
33 an presented with palpitations and decreased exercise tolerance.
34 on for Ebstein's anomaly results in improved exercise tolerance.
35 subgroup with symptomatic ischemia and poor exercise tolerance.
36 ronic diabetic neuropathic pain and improves exercise tolerance.
37 ing to short-term improvement in dyspnea and exercise tolerance.
38 mic responsiveness, while increasing maximal exercise tolerance.
39 acco history developed a cough and decreased exercise tolerance.
40 dividuals with desensitized B-ARs or limited exercise tolerance.
41 muscle blood flow during exercise, hindering exercise tolerance.
42 either unable to exercise or have a very low exercise tolerance.
43 ance, shortness of breath, and reductions in exercise tolerance.
44 ad no respiratory symptoms, and enjoyed good exercise tolerance.
45 zed by pain, decline in function and reduced exercise tolerance.
46 task-dependent nature of mechanisms limiting exercise tolerance.
47 iated with reduced systolic augmentation and exercise tolerance.
48 contribution to ATP synthesis, and increased exercise tolerance.
49 altered haemoglobin affinity impacts hypoxic exercise tolerance.
50 nt in left ventricular ejection fraction and exercise tolerance.
51 ked sarcolemmal fragility and reduced muscle exercise tolerance.
52 at rest occur in conjunction with excellent exercise tolerance.
53 ible benefits to reduce symptoms and improve exercise tolerance.
54 rgement, impaired lung function, and reduced exercise tolerance.
55 oxidative myofibers, muscle vasculature, and exercise tolerance (33%) are decreased in mdx vs. wild-t
57 ion group than in the medical-therapy group (exercise tolerance, 5.0 MET [metabolic equivalent] vs. 3
63 etal muscle function, which led to increased exercise tolerance, activation of FAPs, facilitation of
65 fety of exercise provocation tests to assess exercise tolerance after consumption of allergens follow
66 nexplained exertional dyspnea and diminished exercise tolerance after deployment, an analysis of biop
68 substantial relief of symptoms and improved exercise tolerance and also showed reduced or abolished
69 ults highlight a critical role for TBC1D1 in exercise tolerance and contraction-mediated translocatio
70 tors responsible for development of impaired exercise tolerance and disease progression are incomplet
73 ues to show promise as a method of improving exercise tolerance and enhancing oxidative capacity.
75 horacic radiation therapy (RT) have impaired exercise tolerance and increased cardiovascular mortalit
76 te that targeted inhibition of Fn14 improves exercise tolerance and inhibits denervation-induced musc
77 llbeing, but molecular mechanisms underlying exercise tolerance and its plasticity are only partially
78 -dose nitrate therapy significantly improves exercise tolerance and left ventricular size and systoli
79 ble long-term benefit was a trend for better exercise tolerance and less depression of quality of lif
81 tion showed functional impairment (decreased exercise tolerance and muscle strength) in APP(SWE)/PS1
83 tion during exercise in hypoxia and restored exercise tolerance and oxidative function to values obse
87 lated lipid metabolism, leading to increased exercise tolerance and protection against diet-induced o
89 f intravenous iron found improved short-term exercise tolerance and quality of life in patients with
94 tricular resection, including reduced animal exercise tolerance and sudden death in the setting of st
95 hese observations may play a role in reduced exercise tolerance and tachycardia-induced diastolic dys
96 dine produces dose-dependent improvements in exercise tolerance and time to development of ischemia d
97 rease in QRS duration and a deterioration of exercise tolerance and ventricular dysfunction did not p
100 e abnormalities are associated with impaired exercise tolerance, and abnormal HRR predicts increased
101 anadian Cardiovascular Society angina class, exercise tolerance, and antianginal medications), myocar
103 pathy (MM) associated with varying levels of exercise tolerance, and compared responses with those in
105 put, and resulted in weight loss, diminished exercise tolerance, and enhanced susceptibility to induc
107 uced left ventricular hypertrophy, increased exercise tolerance, and improved quality of life, the op
108 ted with reduced diastolic function, reduced exercise tolerance, and increased pulmonary congestion a
109 lated with poor functional status, decreased exercise tolerance, and invasive hemodynamics variables.
110 ed with less pulmonary regurgitation, better exercise tolerance, and less QRS prolongation and sympto
111 sociated with improved ventricular function, exercise tolerance, and long-term survival in patients w
112 o have abnormal lung function tests, reduced exercise tolerance, and may be at increased risk for dev
113 in preclinical models and improves symptoms, exercise tolerance, and mortality in refractory angina p
114 reduction in anginal symptoms, increases in exercise tolerance, and objective improvements in myocar
117 progression, as reflected by lung function, exercise tolerance, and progression-free survival, in pa
118 ostacyclin, PGI2) improves haemodynamics and exercise tolerance, and prolongs survival in severe PPH
119 F levels, impaired cardiac function, reduced exercise tolerance, and pulmonary oedema; PAD4-/- mice w
120 s left ventricular ejection fraction (LVEF), exercise tolerance, and quality of life among patients w
121 aningful benefits in lung function, dyspnea, exercise tolerance, and quality of life, with an accepta
124 blood analyses, pulmonary function testing, exercise tolerance, and quality-of-life assessment at 0,
125 in skeletal muscle mitochondrial biogenesis, exercise tolerance, and response to exercise training.
126 rovements in heart failure-related symptoms, exercise tolerance, and reversal of ventricular remodeli
127 m bacterial densities, inflammatory markers, exercise tolerance, and subjective well-being did not ch
128 nduced modest improvements in lung function, exercise tolerance, and symptoms at the cost of more fre
129 s lung tissue and may improve lung function, exercise tolerance, and symptoms in patients with emphys
130 lysis, impaired cardiac function and reduced exercise tolerance, and that the level of altitude would
131 exacerbations, weight gain, quality of life, exercise tolerance, and the total costs of hospital and
132 ysfunction are associated with impairment in exercise tolerance as assessed by peak oxygen consumptio
133 ttle Angina Questionnaire and improvement in exercise tolerance as assessed by treadmill exercise tes
134 s outpatients for assessment of symptoms and exercise tolerance as measured by change in the NYHA cla
135 that lung volume reduction surgery improves exercise tolerance as measured by the 6-min walk distanc
140 hanges in lung function, quality of life, or exercise tolerance between roflumilast- and placebo-trea
141 umber of clinical parameters, lung function, exercise tolerance, biomarkers, and amount of emphysema
144 d QRS duration were univariate predictors of exercise tolerance, but only t-IVT and CAD were independ
145 s is thought to contribute to a reduction in exercise tolerance, but the relative contribution of a c
147 ure, and blood flow (by 33-66%) and improved exercise tolerance (by 75%) in the dystrophic mice.
149 included functional class and improvement in exercise tolerance, cardiac index, and mean pulmonary ar
151 ores for a given work rate leading to poorer exercise tolerance compared with their counterparts (P <
152 nts with ERVSP > or = 40 mm Hg had decreased exercise tolerance compared with those with ERVSP <40 mm
154 roved collateral vessel function and enhance exercise tolerance during routine physical activity.
155 dily implementable approaches for evaluating exercise tolerance enabling exercise prescriptions at ap
156 d desaturation, we evaluated improvements in exercise tolerance facilitated by a wearable, 1-lb, noni
157 m to be required for body weight regulation, exercise tolerance, fatty acid oxidation, or cold-induce
158 r patients have had sustained improvement in exercise tolerance, from 3.5 mo to 4.5 yr after stent pl
159 Baseline predictors of survival included exercise tolerance, functional class, right atrial press
163 erobic capacity ( V O(2) max) and submaximal exercise tolerance (i.e. speed-duration relationship) du
165 ease co-morbidities, will assist recovery of exercise tolerance in a variety of conditions that limit
166 he hypothesis that intravenous iron improves exercise tolerance in anemic and nonanemic patients with
167 both TKO and TXNIP(SKM-/-) mice had reduced exercise tolerance in association with muscle-specific i
168 on is hypothesized to contribute to impaired exercise tolerance in cardiovascular disease, but it rem
169 ACE DD genotype is associated with decreased exercise tolerance in CHF, possibly mediated by altered
172 n vivo, which has important implications for exercise tolerance in health and certain disease states
174 imulator, vericiguat, on quality of life and exercise tolerance in heart failure patients with preser
175 hether chronotropic incompetence and reduced exercise tolerance in HF are attributable to beta-blocka
180 (The Influence of Heart Rate Limitation on Exercise Tolerance in Pacemaker Patients [TREPPE]; NCT02
181 indings may have widespread implications for exercise tolerance in patient populations who experience
184 giotensin II (Ang II) blockade would improve exercise tolerance in patients with diastolic dysfunctio
185 is study was to identify the determinants of exercise tolerance in patients with Ebstein's anomaly.
186 fferent rate or rhythm control strategies on exercise tolerance in patients with HFpEF and AF is warr
187 e mechanisms linking dynamic obstruction and exercise tolerance in patients with hypertrophic obstruc
188 e that may thereby improve lung function and exercise tolerance in patients with pulmonary hyperinfla
189 ernal counterpulsation improves symptoms and exercise tolerance in patients with symptomatic coronary
190 eintroduced to alleviate dyspnea and improve exercise tolerance in selected patients with emphysema.
192 supplementation on endothelial function and exercise tolerance in stable coronary artery disease (CA
194 ting demonstrated significant improvement in exercise tolerance in TAC/DOCA mice that expressed N2BAs
197 ated and comparable to enalapril in terms of exercise tolerance in this short-term (12-week) study of
198 in immunofluorescence assays (P < 0.05) and exercise tolerance in treadmill tests (P < 0.05), wherea
199 g allograft dysfunction can be subdivided by exercise tolerance in two groups, and quality of life (Q
201 s been independently associated with reduced exercise tolerance, increased heart failure hospitalizat
203 in GLUT4(-/-)HK(Tg) show that HK II improves exercise tolerance, independent of its effects on MGU.
206 ay, therefore, dictate intensities for which exercise tolerance is determined by the magnitude of fat
209 he age of 3-4 mo, and maximal stress-induced exercise tolerance is reduced, indicating impaired physi
211 therapy, improves symptoms, quality of life, exercise tolerance, left ventricular function, and the s
214 dvanced lung allograft dysfunction regarding exercise tolerance might result from altered IC and impa
219 Losmapimod did not cause an improvement in exercise tolerance or lung function, despite being well-
220 acoronary infusion of rFGF2 does not improve exercise tolerance or myocardial perfusion but does show
221 ng: an improvement of at least 25 percent in exercise tolerance or pulmonary-function tests or resolu
223 ed with a greater improvement in symptoms or exercise tolerance or with a reduction in the rate of de
224 erance, such as advanced age, diabetes, poor exercise tolerance, or history of myocardial infarctions
225 oxygen saturation is the major predictor of exercise tolerance, oxygen saturation at peak exercise a
226 ith reduced muscle mass, abnormal indexes of exercise tolerance (peak V(O2), V(E)/V(CO2) slope), ejec
227 ymptomatic state (NYHA class, P<0.05), lower exercise tolerance (peak VO(2), P<0.05), and pronounced
229 costs of chronic inflammation and to foster exercise tolerance provide a rationale for therapeutic u
230 rtant clinical implications, such as reduced exercise tolerance, quality of life, and even survival.
231 domized, single-blinded study, EECP improved exercise tolerance, quality of life, and NYHA functional
232 he placebo group, P=.01) but did not improve exercise tolerance, quality of life, or the need for hos
233 ideline included mortality; hospitalization; exercise tolerance; quality of life; and cardiovascular
234 patients with otherwise unexplained impaired exercise tolerance; recurrent lower airways infection; a
236 Baseline assessments were angina class, exercise tolerance, Seattle angina questionnaire for qua
238 y class (MD, -0.58; 95% CI, -1.00 to -0.16), exercise tolerance (standardized MD, 0.331; 95% CI, 0.08
239 in brachial artery endothelial function and exercise tolerance, suggesting a potential mechanism by
240 py use from baseline for pulmonary function, exercise tolerance, survival, hospital admission, and ad
242 Case series have shown that EECP can improve exercise tolerance, symptoms and myocardial perfusion in
244 a and enhances functional capacity during an exercise tolerance test (ETT) in patients with coronary
245 on or myocardial infarction (MI), with a pre-exercise tolerance test (ETT) likelihood of CAD > or =0.
246 postinfarction angina or a strongly positive exercise tolerance test (ETT) typically had cost-effecti
247 , exercise, and nuclear models by use of pre-exercise tolerance test (ETT), post-ETT, and nuclear inf
251 s were similar in the 2 approaches, with the exercise tolerance test result exerting the greatest lev
252 cumented coronary artery disease, a positive exercise tolerance test, and stable chronic angina pecto
253 Efficacy was evaluated at 90 and 180 days by exercise tolerance test, myocardial nuclear perfusion im
255 depression > or =1 mm from baseline) during exercise tolerance testing (ETT) was examined in patient
257 principally in middle-aged men, suggest that exercise tolerance testing can provide independent progn
260 le cohort studies demonstrate that screening exercise tolerance testing identifies a small proportion
261 ta-blocker therapy underwent cardiopulmonary exercise tolerance testing under 2 conditions in random
263 nsional echocardiography, Holter monitoring, exercise tolerance testing, and ajmaline provocation.
264 ography, cardiac magnetic resonance imaging, exercise tolerance testing, and biomarker assessment.
267 dulthood caused male mice to underperform at exercise tolerance tests compared to their control and f
268 to limiting angina during bicycle exercise (exercise tolerance tests), performed at trough of drug a
269 musclin secretion in mice results in reduced exercise tolerance that can be rescued by treatment with
270 al care resulted in an improvement in median exercise tolerance that was modest and of uncertain clin
271 th chronic heart failure (CHF) and preserved exercise tolerance, the value of cardiopulmonary exercis
272 - 0.8 mo) showed significant improvements in exercise tolerance: The distance covered over a 6 min wa
273 to guide management of patients with limited exercise tolerance, those at highest risk for perioperat
276 stress allows an assessment of the patient's exercise tolerance, to be performed while adequately str
277 ly associated with decreased muscle mass and exercise tolerance; untreated LH/FSHD was associated wit
281 f patients were relieved of angina symptoms, exercise tolerance was improved, complications were mini
288 and hypoxic (HVR) ventilatory responses, and exercise tolerance were assessed at the end of a 6 week
289 nflammation, lung mechanical properties, and exercise tolerance were determined at different time poi
294 tory muscle oxygen delivery and compromising exercise tolerance, which may be improved by therapeutic
295 ng patients in the assessment of symptoms or exercise tolerance while expanding the range of patients
296 often performed in stable patients with good exercise tolerance who have not been treated with proven
298 ion) and 60 patients with stage B HF (normal exercise tolerance with left ventricular hypertrophy, an
299 ior pilot studies have shown improvements in exercise tolerance with single-dose and short-term inorg
300 s with elevated HDGF had significantly lower exercise tolerance, worse New York Heart Association fun