Exercise on‐transition uncoupling of ventilatory, gas exchange and cardiac hemodynamic kinetics accompany pulmonary oxygen stores depletion to impact exercise intolerance in human heart failure

Iterson, Erik H. Van; Smith, Joshua R.; Olson, Thomas P.

doi:10.1111/apha.13063

Cited by 6 publications

(7 citation statements)

References 55 publications

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“…While it is plausible that widening of the arteriovenous O 2 content gradient may have driven the training benefit previously observed for exercise O 2 pulse in CF, 9 we suggest that this is unlikely because in the steady-state condition (ie, submaximal exercise), the arteriovenous O 2 content gradient is expected to be invariable, and most of the rise in O 2 pulse from the rest to submaximal exercise transition is commensurate with changes that occur in SV. 51 Again, the effect of training on normalV . O 2 , O 2 pulse, and HR responses reported in Gruber et al 9 was generally mirrored across submaximal and maximal exercise performance. There is also no evidence to date suggesting widening of the arteriovenous O 2 content gradient in response to increased O 2 metabolic demand is enhanced and/or an adaptive mechanism able to compensate for impaired cardiac hemodynamics in CF.…”

Section: Discussionmentioning

confidence: 74%

Exercise Stroke Volume in Adult Cystic Fibrosis: A Comparison of Acetylene Pulmonary Uptake and Oxygen Pulse

Iterson

Baker

Wheatley

et al. 2018

Clin Med Insights Circ Respir Pulm Med

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Cardiac hemodynamic assessment during cardiopulmonary exercise testing (CPET) is proposed to play an important role in the clinical evaluation of individuals with cystic fibrosis (CF). Cardiac catheterization is not practical for routine clinical CPET. Use of oxygen pulse (O2pulse) as a noninvasive estimate of stroke volume (SV) has not been validated in CF. This study tested the hypothesis that peak exercise O2pulse is a valid estimate of SV in CF. Measurements of SV via the acetylene rebreathe technique were acquired at baseline and peak exercise in 17 mild-to-moderate severity adult CF and 25 age-matched healthy adults. We calculated O2pulse=V.O2HR. Baseline relationships between SV and O2pulse were significant in CF (r = .80) and controls (r = .40), persisting to peak exercise in CF (r = .63) and controls (r = .73). The standard error of estimate for O2pulse-predicted SV with respect to measured SV was similar at baseline (14.1 vs 20.1 mL) and peak exercise (18.2 vs 13.9 mL) for CF and controls, respectively. These data suggest that peak exercise O2pulse is a valid estimate of SV in CF. The ability to noninvasively estimate SV via O2pulse during routine clinical CPET can be used to improve test interpretation and advance our understanding of the impact cardiac dysfunction has on exercise intolerance in CF.

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Section: Discussionmentioning

confidence: 74%

Exercise Stroke Volume in Adult Cystic Fibrosis: A Comparison of Acetylene Pulmonary Uptake and Oxygen Pulse

Iterson

Baker

Wheatley

et al. 2018

Clin Med Insights Circ Respir Pulm Med

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“…4,26,27 The absolute and temporal responsiveness of oxidative metabolism reflected in _ VO 2 constitutes whole-body physiological reactivity to imposed work-rates expected to lead to _ VO 2 and work-rate linearization within the power-time domain oxygen flow-independent zone of CPET. [28][29][30] This sub-gas exchange VO 2 measurements at rest, respectively. Panels (c) and (d): absolute or body weight corrected _ VO 2 measurements at peak exercise, respectively.…”

Section: Discussionmentioning

confidence: 97%

“…The absolute and temporal responsiveness of oxidative metabolism reflected in V·O2 constitutes whole-body physiological reactivity to imposed work-rates expected to lead to V·O2 and work-rate linearization within the power–time domain oxygen flow-independent zone of CPET. 28–30 This sub-gas exchange threshold proportionality for the V·O2–work-rate relationship can be expected to persist to peak exercise provided the absence of overreliance on substrate-level metabolism. 28–30 Accordingly, our contrasting observations for physiological responses (including V·O2/W and ΔV·O2/ΔW) across patient stratifications suggests for the first time that the balanced ability of oxidative and substrate level metabolic pathways to accommodate a surge in oxygen flow-dependent metabolic demand is interrupted by confounding effects of obesity and/or low Hgb content.…”

Section: Discussionmentioning

confidence: 97%

Obesity and hemoglobin content impact peak oxygen uptake in human heart failure

Iterson

Kim

Uithoven

et al. 2018

Eur J Prev Cardiolog

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Background: Exercise intolerance, obesity, and low hemoglobin (hemoglobin<13 and <12 g/dl, men/women, respectively) are common features of heart failure. Despite serving as potent contributors to metabolic dysfunction, the impact of obesity and low hemoglobin on exercise intolerance is unknown. This study tested the hypotheses, compared with non-obese (NO) heart failure with normal hemoglobin, (a) counterparts with low hemoglobin and obesity or nonobesity will demonstrate reduced peak exercise oxygen uptake; (b) obese with normal hemoglobin will demonstrate decreased peak exercise oxygen uptake; (c) compared across stratifications, obese with low hemoglobin will demonstrate the sharpest decrement in peak exercise oxygen uptake. Methods: Adults with heart failure (n ¼ 315; left ventricular ejection fraction 40%; 77% men) (Group 1: normal hemoglobin and non-obese, n ¼ 137; Group 2: low hemoglobin and non-obese, n ¼ 51; Group 3: normal hemoglobinþobesity, n ¼ 89; Group 4, n ¼ 38: low hemoglobinþobesity; body mass index ¼ 26 AE 3, 26 AE 2, 34 AE 4, 34 AE 4 kg/m 2 , respectively) completed treadmill cardiopulmonary exercise testing as part of routine clinical management. Peak exercise oxygen uptake was measured via standard metabolic system. Results: There were no group-wise differences for heart failure class, gender, left ventricular ejection fraction, and resting cardiopulmonary function. Group 1 demonstrated increased peak exercise oxygen uptake versus Groups 2-4 (20 AE 6 versus 17 AE 6, 17 AE 5, 13 AE 4 ml/kg/min, respectively; all p < 0.001); whereas Group 4 peak exercise oxygen uptake was reduced versus all groups (p < 0.001). Additionally, both body mass index (R 2 ¼ 0.10) and hemoglobin (R 2 ¼ 0.12) were significant predictors of peak exercise oxygen uptake in Group 1; which were relationships not mirrored for Groups 2-4. Conclusion: These data suggest obesity together with low hemoglobin are potent contributors to impaired peak exercise oxygen uptake and, hence, oxidative metabolic capacity. In diverse populations of heart failure where obesity and/or low hemoglobin are present, it is important to consider these features together when interpreting peak exercise oxygen uptake and underlying exercise limitations.

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“…Peak V.O2 is also assumed to represent coupling between oxidative metabolic capacity and energetic demand. Still, HF patients have also been observed to demonstrate integrative pathophysiology involving alveoli and O 2 transport [5–9], which are features recognized to impact oxidative metabolic capacity. As such, in contrast to what has been observed in healthy adults [10–14], it has not been tested whether O 2 transport involving the alveolar airspace and, hence, V.O2 measurement at the mouth is confounded during sea-level room air exercise.…”

Section: Introductionmentioning

confidence: 99%