ライフサイエンスコーパス: ventilatory

1 activation of HIF-2alpha strikingly impaired ventilatory acclimatisation to chronic hypoxia (HVRs: 4.

2 latory responses to hypoxia, abrogating both ventilatory acclimatization and carotid body cell prolif

3 nic hypercapnia but alone do not account for ventilatory acclimatization to chronic increased InCO(2)

4 ic ventilatory response (HVR) that is called ventilatory acclimatization to hypoxia (VAH).

5 in CNS respiratory centres is necessary for ventilatory acclimatization to hypoxia (VAH); VAH is a t

6 correlated well with most other measures of ventilatory acclimatization.

7 the initial G(pCO2) is a modest predictor of ventilatory acclimatization.

8 Of note, maintaining ventilatory activity at low carbon dioxide levels is amo

9 Human ventilatory activity persists, during wakefulness, even

10 ng, dynamic kinematic MRI of the thorax, and ventilatory adjustments to single-breath inspiratory loa

11 ycardia, reduction in PCA and an increase in ventilatory amplitude (VAMP) without any changes in vent

12 ted HR 1.10, 95% CI 1.00-1.22, P=0.049), and ventilatory anaerobic threshold (adjusted HR 0.82, 95% C

13 VCO2 was assessed as the slope pre- and post-ventilatory anaerobic threshold (VE/VCO2(pre-VATslope),

14 They reached the ventilatory anaerobic threshold earlier (81.4 +/- 9.5 vs

15 onitoring system revealed the first signs of ventilatory and circulatory deterioration before a chang

16 Ventilatory and electroencephalographic recordings were

17 The magnitude of the ventilatory and haemodynamic responses depended on both

18 Separately, ventilatory and haemodynamic responses to systemic hypox

19 lopmental nicotine exposure (DNE) alters the ventilatory and metabolic response to hyperthermia in ne

20 Coefficients of variation for ventilatory and MSNA burst frequency responses, indicati

21 omparisons across quartiles of corresponding ventilatory and MSNA responses, we found that the magnit

22 Ventilatory and MSNA responsiveness to hyperoxia and hyp

23 The carotid chemoreceptor mediates the ventilatory and muscle sympathetic nerve activity (MSNA)

24 Ventilatory and neurocirculatory (MSNA, blood pressure a

25 Accordingly, we measured ventilatory and neurocirculatory responses to chemorefle

26 alyses to study the association of PPCs with ventilatory and other perioperative variables.

27 Demographic, disease factor, and ventilatory and outcome data were collected, and 328 pat

28 We conclude that the magnitudes of the ventilatory and pulmonary vascular responses to sustaine

29 as found between the magnitudes of pulmonary ventilatory and pulmonary vascular responses.

30 tion, and opens new avenues to study certain ventilatory and speech disorders.

31 Potentiation of the ventilatory and sympathetic drive in response to CC acti

32 arget Vt of 6 ml/kg during neurally adjusted ventilatory assist (NAVA).

33 physiologic efficiency of neurally adjusted ventilatory assist affects patient-important outcomes in

34 iability was higher during neurally adjusted ventilatory assist and ineffective efforts appeared only

35 anical ventilation such as neurally adjusted ventilatory assist are feasible and improve patient phys

36 iratory failure, levels of neurally adjusted ventilatory assist between 0.5 and 2.5 cm H2O/muvolt are

37 Neurally adjusted ventilatory assist improves patient-ventilator synchrony

38 Neurally adjusted ventilatory assist is a ventilatory mode that may lead t

39 nloading were observed for neurally adjusted ventilatory assist levels from 0.5 cm H2O/muvolt (46% [4

40 applied in a random order: neurally adjusted ventilatory assist levels: 0.5, 1, 1.5, 2, 2.5, 3, 4, 5,

41 to determine the impact of neurally adjusted ventilatory assist on patient-ventilator asynchrony, oth

42 Neurally adjusted ventilatory assist provides better patient-ventilator in

43 ical scenarios, the use of neurally adjusted ventilatory assist was associated with significantly red

44 In neurally adjusted ventilatory assist, double triggering occurred sometimes

45 re support ventilation and neurally adjusted ventilatory assist.

46 sisted breathing and with different modes of ventilatory assist.

47 nsistently improved during neurally adjusted ventilatory assist.

48 e time until death or the need for permanent ventilatory assistance.

49 The relative importance of ventilatory, circulatory and peripheral muscle factors i

50 Ventilatory CO(2) and pH chemoreflexes are primarily det

51 lation of arterial pH as determinants of the ventilatory CO(2) chemoreflex.

52 rtantly, TAL also effectively normalized the ventilatory CO2 chemoreflex in BN rats, but TAL did not

53 stems such as breathing and specifically the ventilatory CO2 chemoreflex.

54 without altering P aC O2 or pH and enhanced ventilatory CO2 sensitivity (3.4 +/- 0.4 to 5.1 +/- 0.8

55 ely 22, 41 and 68 mmHg, respectively) on the ventilatory CO2 sensitivity of central chemoreceptors wa

56 by an augmented carotid body and whole body ventilatory CO2 sensitivity.

57 ely disordered breathing pattern and reduced ventilatory CO2 sensitivity.

58 he tidal volume signal (related to medullary ventilatory command), (3) autonomic function, and (4) co

59 ory muscle functional tests reflect distinct ventilatory compensations in LOPD.

60 analysis, we provide the first evidence of a ventilatory component in HRV similar to mammalian respir

61 Ventilatory conditions were grouped based upon the fract

62 reload and decreased cardiac output, whereas ventilatory consequences include increased airway pressu

63 tion may produce significant hemodynamic and ventilatory consequences such as increased intraabdomina

64 er women have a greater degree of mechanical ventilatory constraint (i.e. work of breathing and expir

65 cant differences in the degree of mechanical ventilatory constraint between conditions, the intensity

66 form moderate intensity exercise, mechanical ventilatory constraint does not contribute significantly

67 ally manipulated the magnitude of mechanical ventilatory constraint during moderate-intensity exercis

68 ermine the effect of manipulating mechanical ventilatory constraint during submaximal exercise on dys

69 that changes in the magnitude of mechanical ventilatory constraint within the physiological range ha

70 at patients limited by breathlessness due to ventilatory constraints can be identified as those reach

71 lead to the development of abnormalities in ventilatory control and efficiency, pulmonary congestion

72 d prolonged circulation time, implicates the ventilatory control system and suggests feedback instabi

73 associated pneumonia rates were 9.6 of 1,000 ventilatory days and 19.8 of 1,000 ventilatory days, res

74 of 1,000 ventilatory days and 19.8 of 1,000 ventilatory days, respectively (p = 0.0076).

75 In terms of ventilatory days, ventilator-associated pneumonia rates

76 Survival was compared based on the ventilatory defect and among groups based on the best FE

77 Survival was compared based on the ventilatory defect and among groups based on the best FE

78 Although the type of ventilatory defect on best spirometry does not predict s

79 nary function testing reveals an obstructive ventilatory defect that is typically not reversed by inh

80 Irrespective of the type of ventilatory defect, survival worsened as the best FVC (%

81 ow 60% predicted.Irrespective of the type of ventilatory defect, survival worsened as the best FVC (%

82 nfections 16%), pulmonary (diffusion 79% and ventilatory defects 63%, pulmonary alveolar proteinosis

83 of HIV-infected individuals have obstructive ventilatory defects and reduced diffusing capacity is se

84 abnormal PASP and PAC, whereas a restrictive ventilatory deficit was associated with abnormalities of

85 Opioid-induced ventilatory depression and hypoxemia is common, severe,

86 lished the hypoxic ventilatory response, and ventilatory depression during hypoxia was exacerbated un

87 These data suggest that in ventilatory disorders characterized by reduced inspirato

88 ry neural activity, a characteristic of many ventilatory disorders, leads to inadequate ventilation a

89 usal threshold was estimated as the level of ventilatory drive associated with arousal.

90 This fuels the notion that the human ventilatory drive during wakefulness often results from

91 n which spontaneous biological variations in ventilatory drive repeatedly induce temporary and irregu

92 ion in patients who are dependent on hypoxic ventilatory drive.

93 ic ventilatory response and the mechanism of ventilatory dysfunctions arising from AMPK deficiency.

94 onfidence interval [CI] 0.77-0.88, P<0.001), ventilatory efficiency (adjusted HR 1.10, 95% CI 1.00-1.

95 Ventilatory efficiency (minute ventilation required to e

96 gen consumption (Vo2 [mL/kg per minute]) and ventilatory efficiency (the VE/Vco2 slope).

97 with MPRI < 2) was associated with worsened ventilatory efficiency (VE/VCO2) (P < 0.001) but not pea

98 seline in 6-minute walk test distance and in ventilatory efficiency (ventilation/carbon dioxide produ

99 Submaximal exercise parameters, such as ventilatory efficiency and anaerobic threshold, measured

100 These patients had particularly poor ventilatory efficiency compared with patients without hy

101 tilation led to hypocapnia and poor exercise ventilatory efficiency in chronic obstructive pulmonary

102 Impaired ventilatory efficiency is associated with cardiovascular

103 ration, percent predicted peak Vo2 [%ppVo2], ventilatory efficiency) were examined.

104 erent physiologic dimensions of fitness (eg, ventilatory efficiency, exercise blood pressure, peak Vo

105 t improve RV function, exercise capacity, or ventilatory efficiency.

106 ischemia burden was associated with worsened ventilatory efficiency.

107 levels, whereas peak respiratory frequency, ventilatory equivalent for CO2, and IL-6 and IL-1beta le

108 predicted; HR, 0.969; 95% CI, 0.951-0.988), ventilatory equivalent for oxygen (HR, 1.085; 95% CI, 1.

109 on fraction, ventricular dimensions, or peak ventilatory equivalent of oxygen.

110 tion (OR, 11.3; 95% CI, 7.4-17.1; P < .001), ventilatory failure (OR, 12.4; 95% CI, 8.2-18.8; P < .00

111 io [OR], 17.1; 95% CI, 13.8-21.3; P < .001), ventilatory failure (OR, 15.9; 95% CI, 12.8-19.8; P < .0

112 ve pressure modes and their role in managing ventilatory failure in neuromuscular diseases and other

113 outbreaks had a higher proportion of patient ventilatory failure.

114 recordings were analyzed with respect to the ventilatory flow signal to detect preinspiratory potenti

115 tory amplitude (VAMP) without any changes in ventilatory frequency (fV).

116 ntrol respiration, yet mechanisms regulating ventilatory frequency are poorly understood.

117 d standard technique for assessing pulmonary ventilatory function in humans.

118 ch the abdominal muscles took on the primary ventilatory function, whereas the broadened ribs became

119 d with an increased risk of COPD and reduced ventilatory function.

120 ostic group on decline in postbronchodilator ventilatory function.

121 y (CB) chemoreceptor stimulus influenced the ventilatory gain of the central chemoreceptors to CO2 .

122 tance of easily acquired submaximum exercise ventilatory gas exchange measurements in broad populatio

123 that adrenaline release can account for the ventilatory hyperpnoea observed during hypoglycaemia by

124 ssociated condition had significantly longer ventilatory, ICU, and hospital days compared with those

125 al lung fields in a chest CT scan, and mixed ventilatory impairment in a spirometric test were reveal

126 Peak oxygen consumption decreased and ventilatory inefficiency (VE/VCO2 slope) increased with

127 Formula: see text]e/[Formula: see text]co2), ventilatory inefficiency was closely related to PcCO2 (r

128 A responses, we found that the magnitudes of ventilatory inhibition with hyperoxia or excitation with

129 way (BN) rats exhibit an inherent and severe ventilatory insensitivity to hypercapnia but also exhibi

130 Herein, we tested the hypothesis that the ventilatory insensitivity to hypercapnia in BN rats is d

131 atory events may be predisposed to increased ventilatory instability and/or have augmented autonomic

132 to sympathetic nervous system activation and ventilatory instability has been implicated in the patho

133 he rationale for recommendations on selected ventilatory interventions for adult patients with ARDS.

134 pared to matched healthy controls, even when ventilatory limitations (i.e. attainment of maximal vent

135 Ventilatory long-term facilitation can be evoked by brie

136 However, the magnitude of ventilatory long-term facilitation was not enhanced over

137 Secondary outcomes included ventilatory management (including tidal volume [VT] expr

138 The impact of acute kidney injury on the ventilatory management of patients with acute respirator

139 cian recognition of ARDS, the application of ventilatory management, the use of adjunctive interventi

140 syndrome is important for a more customized ventilatory management.

141 the dynamics of the lungs and the effects of ventilatory manoeuvres, including changes in ventilator

142 w affected the stability of upper airway and ventilatory mechanics.

143 Neurally adjusted ventilatory assist is a ventilatory mode that may lead to improved patient-venti

144 on with conventional pneumatically triggered ventilatory modes.

145 We propose that daytime ventilatory oscillations generally result from a chemore

146 elucidates the mechanism underlying daytime ventilatory oscillations in heart failure and provides a

147 LG was defined as the ratio of the ventilatory overshoot to the preceding reduction in vent

148 nder normoxia had resting cardiovascular and ventilatory parameters similar to controls.

149 We conclude that changes in the ventilatory pattern after ALI result not only from senso

150 l inflammation has a role in determining the ventilatory pattern after ALI.

151 ecture that autonomously generates a desired ventilatory pattern in response to dynamic changes in ar

152 ion has an essential role in determining the ventilatory pattern of ALI rats.

153 One week later, we recorded the ventilatory pattern of the rat pups using flow-through p

154 Compared with the ventilatory pattern of the sham rat pups, injured rat pu

155 i increases fR and the predictability of the ventilatory pattern similar to rats with ALI.

156 ts, which increased fR and predictability of ventilatory pattern variability (VPV) after 2 h.

157 ry (ALI) increases respiratory rate (fR) and ventilatory pattern variability (VPV), but also evokes p

158 drug, mitigates the effect of ALI on fR and ventilatory pattern variability.

159 and respiratory cycle duration to evoke this ventilatory pattern.

160 o be a useful spirometric tool for assessing ventilatory patterns and impairment severity.

161 Furthermore, the finding of a hypomorphic ventilatory phenotype in untreated HIF-2alpha S305M muta

162 dent RTN neuronal activation and rescued the ventilatory phenotype.

163 The ventilatory phenotypes associated with both inducible an

164 /-) rats, HKD failed to restore the observed ventilatory phenotypes.

165 Both injurious ventilatory protocols developed comparable levels of phy

166 erfused lungs were allocated to one of three ventilatory protocols for 3 hours: control group receive

167 omly allocated to one of the three following ventilatory protocols for 4 hours: spontaneous breathing

168 nical levels, which was due to an increasing ventilatory rate rather than an increase in tidal volume

169 These results are promising for the use of ventilatory ratio as a simple bedside index of impaired

170 the secondary outcome, we tested the role of ventilatory ratio as an outcome predictor.

171 Ventilatory ratio correlates well with Vd/Vt in ARDS, an

172 Ordinal groups of ventilatory ratio had significantly higher Vd/Vt.

173 The ventilatory ratio is a simple bedside index that can be

174 Ventilatory ratio is defined as [minute ventilation (ml/

175 Ventilatory ratio positively correlated with Vd/Vt.

176 Ventilatory ratio was independently associated with incr

177 RDS, we tested the association of Vd/Vt with ventilatory ratio.

178 urray lung injury score, 3.14 +/- 0.53; mean ventilatory ratios, 2.6 +/- 0.8) with evidence of hyperc

179 Baseline ventilation, ventilatory recruitment threshold and the slope of the v

180 ores the state dependence of the hypercapnic ventilatory reflex (HCVR).

181 One week after CB excision, the hypoxic ventilatory reflex was greatly reduced as expected, wher

182 n in 21% O2 were normal, whereas the hypoxic ventilatory reflex was still depressed (95.3%) and hypox

183 mediates a large portion of the hypercapnic ventilatory reflex, regulates breathing differently duri

184 (CCs) are considered a dominant mechanism in ventilatory regulation.

185 control subjects in association with higher ventilatory requirements.

186 ation, rate of oxygen consumption (VO2), and ventilatory reserve (ventilation/maximum ventilatory vol

187 in vivo significantly decreased the hypoxic ventilatory response (Delta VE control 74 +/- 6%, Delta

188 phy, SH attenuated the acute (5 min) hypoxic ventilatory response (HVR) and caused a high incidence o

189 n minute ventilation (V(E) ) and the hypoxic ventilatory response (HVR) has not been sufficiently stu

190 ABSTRACT: The hypoxic ventilatory response (HVR) is biphasic, consisting of a

191 ease in baseline ventilation and the hypoxic ventilatory response (HVR) occurring over days to weeks

192 rease of resting ventilation and the hypoxic ventilatory response (HVR) that is called ventilatory ac

193 increase in ventilation, termed the hypoxic ventilatory response (HVR).

194 ing of the mechanisms underlying the hypoxic ventilatory response and highlight the significance of p

195 /or AMPK-alpha2 are required for the hypoxic ventilatory response and the mechanism of ventilatory dy

196 Heightened neural drive promoting a ventilatory response beyond that required to overcome an

197 s exhibited a significantly enhanced hypoxic ventilatory response compared to AV-CHF rats.

198 rebrovascular reactivity and the hypercapnic ventilatory response in 11 healthy subjects (five female

199 tivation of the muscle metaboreflex causes a ventilatory response in COPD patients but not in healthy

200 Excessive ventilatory response in this group was associated with h

201 ignificant differences in any of the central ventilatory response indices were found between CB normo

202 poxia, contrary to the view that the hypoxic ventilatory response is determined solely by increased c

203 ene (c-fos) expression to assess the hypoxic ventilatory response of mice with conditional deletion o

204 ion of Tac1-Pet1 neuron activity blunted the ventilatory response of the respiratory CO2 chemoreflex,

205 n minute ventilation (V(E) ) and the hypoxic ventilatory response to 10% O(2) (HVR) in C57BL/6J mice

206 nalysis, our results showed that LG, AT, the ventilatory response to arousal and nadir end-tidal carb

207 ttent hypoxia also led to an increase in the ventilatory response to arousal.

208 region influences baseline breathing or the ventilatory response to CO(2) in conscious male Wistar r

209 P2Y(2) from smooth muscle cells blunted the ventilatory response to CO(2), and re-expression of P2Y(

210 ing hypoventilation, apnea, and a diminished ventilatory response to CO(2).

211 ed in RTN neurons, essentially abolished the ventilatory response to CO2.

212 The ventilatory response to exercise requires substantial ch

213 cle afferents in reflex control of the human ventilatory response to exercise.

214 RATIONALE: An increased ventilatory response to exertional metabolic demand (hig

215 6-/-) rats showed up to 45% reduction in the ventilatory response to graded hypercapnic acidosis vs.

216 monstrate that the EP3R is important for the ventilatory response to hypercapnia.

217 pH, but there was a further reduction in the ventilatory response to hypercapnic acidosis.

218 th subtle but significant alterations in the ventilatory response to hyperthermia in neonatal rats.

219 ed an interference in the cardiovascular and ventilatory response to hypoxia.

220 vel of chemosensitivity as determined by the ventilatory response to hypoxia.

221 The ventilatory response to inhaled CO(2) of mice was marked

222 and, when silenced, observed blunting of the ventilatory response to inhaled CO2Tac1-Pet1 neurons thu

223 In wakefulness, the ventilatory response to normoxic hypercapnia is higher i

224 KEY POINTS: The ventilatory response to reduced oxygen (hypoxia) is biph

225 The ventilatory response was abolished and the haemodynamic

226 y recruitment threshold and the slope of the ventilatory response were similar between pre-HDTBR and

227 gene, erythrocytosis, and augmented hypoxic ventilatory response, all hallmarks of Egln1 loss of fun

228 ha2 deletion virtually abolished the hypoxic ventilatory response, and ventilatory depression during

229 bition of CD73 in vivo decreased the hypoxic ventilatory response, reduced the hypoxia-induced heart

230 16-/-) rats also had a nearly absent hypoxic ventilatory response, suggesting major contributions of

231 en sensing and the initiation of the hypoxic ventilatory response, yet the gene expression profile of

232 nt the hyperventilation nor abnormal hypoxic ventilatory response.

233 ponsiveness to acute hypoxia and the hypoxic ventilatory response.

234 CSE using morpholinos attenuated the hypoxic ventilatory response.

235 play a pivotal role in promoting the hypoxic ventilatory response.

236 cular reactivity to CO(2) or the hypercapnic ventilatory response.

237 terozygous PHD2 deficiency, enhances hypoxic ventilatory responses (HVRs: 7.2 +/- 0.6 vs. 4.4 +/- 0.4

238 oxygen detection and the cardiovascular and ventilatory responses of fish to hypoxia, we hypothesize

239 m neurochemistry is associated with impaired ventilatory responses to acute hypoxia and mortality.

240 Experimental evidence, including exaggerated ventilatory responses to CO2 and prolonged circulation t

241 rons, increased apnea frequency, and blunted ventilatory responses to CO2.

242 nary vascular resistance and more pronounced ventilatory responses to exercise, lower pulmonary arter

243 It was concluded that ventilatory responses to hypoxia and hyperoxia do not pr

244 g, intracellular signalling and promotion of ventilatory responses to hypoxia in adult and larval zeb

245 ed to inhibit tumor growth, rapidly impaired ventilatory responses to hypoxia, abrogating both ventil

246 the exposure, measurements were made of the ventilatory sensitivities to acute isocapnic hypoxia (G(

247 onclude that, in conscious, behaving humans, ventilatory sensitivities to progressive, steady-state,

248 gether with the evidence of severely blunted ventilatory sensitivity to CO2 in mice with conditional

249 HIF prolyl hydroxylase, PHD2, show enhanced ventilatory sensitivity to hypoxia and carotid body hype

250 Ventilatory sensitivity to hypoxia increases in response

251 2alpha enzyme-substrate couple in modulating ventilatory sensitivity to hypoxia.

252 collected retrospectively and demographics, ventilatory settings and ABG results were recorded.

253 ation of tension pneumothorax depends on the ventilatory status of the patient.

254 We demonstrated that ventilatory status, nusinersen treatment, demographic, a

255 ns of tension pneumothorax differ by subject ventilatory status.

256 Biotrauma due to injurious ventilatory strategies can lead to the release of mediat

257 has been the development of lung-protective ventilatory strategies, based on our understanding of th

258 potential for lung recruitment may guide the ventilatory strategy in acute respiratory distress syndr

259 bjective was to review the impact of initial ventilatory strategy on mortality and the risks related

260 ICU and were expected to continue to receive ventilatory support for longer than the next calendar da

261 Adult patients with ventilatory support for more than 60 days.

262 ht (OR, 3.41; 95% CI, 1.61-7.26), and use of ventilatory support for the newborn (OR, 2.85; 95% CI, 1

263 s less than 3 months old who did not require ventilatory support for whom brain MRI was indicated.

264 ions of domiciliary medical technology, home ventilatory support has either led or run in parallel wi

265 maternal benzodiazepine treatment, rates of ventilatory support increased by 61 of 1000 neonates and

266 zes the trends and growing evidence base for ventilatory support outside the hospital.

267 One of the great advances in ventilatory support over the past few decades has been t

268 ciated with a shorter duration of mechanical ventilatory support than was early parenteral nutrition

269 Titrating ventilatory support to maintain normal levels of inspira

270 nd with an increased frequency of oxygen and ventilatory support use.

271 The mean duration of ventilatory support was 10 days (range, 9-11); the mean

272 h confirmed H1N1 pneumonia and on mechanical ventilatory support were randomized to receive adjuvant

273 Organ Failure Assessment score, duration of ventilatory support, and mortality.

274 organ failure, required prolonged mechanical ventilatory support, and resulted in a high workload for

275 ith high rates of pneumonia, requirement for ventilatory support, and short- and long-term mortality.

276 mes included in-hospital mortality, need for ventilatory support, intensive care unit (ICU) admission

277 associated with an increase in intensity of ventilatory support, NIV failure, and intensive care uni

278 e care unit admission, the need for invasive ventilatory support, the length of hospital stay, or the

279 if they met eligibility criteria for partial ventilatory support, tolerated pressure support ventilat

280 evious myocardial infarction, renal disease, ventilatory support, use of circulatory support, glycopr

281 s lung-protective ventilation during partial ventilatory support, while maintaining diaphragm activit

282 ut might be advantageous because it provides ventilatory support.

283 gan dysfunction, and need for vasopressor or ventilatory support.

284 mortality and often necessitating mechanical ventilatory support.

285 , broad-spectrum antibiotics, and mechanical ventilatory support.

286 maintaining diaphragm activity under partial ventilatory support.

287 minor respiratory interventions, and use of ventilatory support.

288 creasing the risk for failed liberation from ventilatory support.

289 of spasm control that can avoid the need for ventilatory support.

290 7 ml/kg/min, P = 0.81) and heart rate at the ventilatory threshold (H = 78 +/- 6 vs. C = 78 +/- 4% pe

291 ardiopulmonary exercise testing to determine ventilatory threshold (VT).

292 stably low at exercise intensities below the ventilatory threshold but rise rapidly at higher intensi

293 traint during moderate-intensity exercise at ventilatory threshold in healthy older men and women.

294 of knee extensor muscles (P=0.008), and the ventilatory threshold power (P=0.02) were also significa

295 stably low at exercise intensities below the ventilatory threshold, a parameter that can be defined d

296 ts performed three 6-min bouts of cycling at ventilatory threshold, in a single-blind randomized mann

297 ify the application of oxygen consumption at ventilatory threshold, to describe CPX variables with an

298 est, two submaximal levels of exercise below ventilatory threshold, to simulate real-world scenarios/

299 sitivity was measured as the RSNA and minute ventilatory (VE) responses to hypoxia and hypercapnia.

300 and ventilatory reserve (ventilation/maximum ventilatory volume ratio [VE/MVV]) were measured continu