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

E. H. Van Iterson; J. R. Smith; T. P. Olson

doi:10.1111/apha.13063

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

E. H. Van Iterson, J. R. Smith, T. P. Olson

Cardiovascular Medicine

Research output: Contribution to journal › Article › peer-review

5 Scopus citations

Abstract

Aim: In contrast to knowledge that heart failure (HF) patients demonstrate peak exercise uncoupling across ventilation, gas exchange and cardiac haemodynamics, whether this dyssynchrony follows that at the exercise on-transition is unclear. This study tested whether exercise on-transition temporal lag for ventilation relative to gas exchange and oxygen pulse (O₂pulse) couples with effects from abnormal pulmonary gaseous oxygen store (O_2store) contributions to (Formula presented.) O₂ to interdependently precipitate persistently elevated ventilatory demand and low oxidative metabolic capacity in HF. Methods: Beat-to-beat HR and breath-to-breath ventilation and gas exchange were continuously acquired in HF (N = 9, ejection fraction = 30 ± 9%) and matched controls (N = 10) during square-wave ergometry at 60% (Formula presented.) O_2peak (46 ± 14 vs 125 ± 54-W, P <.001). Temporal responses across (Formula presented.) _E, (Formula presented.) O₂ and O₂pulse were assessed for the exercise on-transition using single exponential model Phase II on-kinetic time constants (τ = time to reach 63% steady-state rise). Breath-to-breath gas fractions and respiratory flows were used to determine O_2stores. Results: HF vs controls: τ for (Formula presented.) _E (137 ± 93 vs 74 ± 40-seconds, P =.03), (Formula presented.) O₂ (60 ± 40 vs 23 ± 5-seconds, P =.03) and O₂pulse (28 ± 18 vs 23 ± 15-seconds, P =.59). Within HF, τ for (Formula presented.) _E differed from O₂pulse (P <.02), but not (Formula presented.) O₂. Exercise (Formula presented.) _E rise (workload indexed) differed in HF vs controls (545 ± 139 vs 309 ± 88-mL min⁻¹ W⁻¹, P <.001). Exercise on-transition O_2store depletion in HF exceeded controls, generally persisting to end-exercise. Conclusion: These data suggest HF demonstrated exercise on-transition O_2store depletion (high O_2store contribution to (Formula presented.) O₂) coupled with dyssynchronous (Formula presented.) _E, (Formula presented.) O₂ and O₂pulse kinetics—not attributable to prolonged cardiac haemodynamics. Persistent high ventilatory demand and low oxidative metabolic capacity in HF may be precipitated by physiological uncoupling occurring within the exercise on-transition.

Original language	English (US)
Article number	e13063
Journal	Acta Physiologica
Volume	223
Issue number	4
DOIs	https://doi.org/10.1111/apha.13063
State	Published - Aug 2018

Keywords

HFrEF
O transport
alveolar oxygen
muscle V˙O kinetics
ventilatory efficiency

ASJC Scopus subject areas

Physiology

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10.1111/apha.13063

Cite this

@article{400eb7c3ce164063a145d9ea9a0dfbbe,

title = "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",

abstract = "Aim: In contrast to knowledge that heart failure (HF) patients demonstrate peak exercise uncoupling across ventilation, gas exchange and cardiac haemodynamics, whether this dyssynchrony follows that at the exercise on-transition is unclear. This study tested whether exercise on-transition temporal lag for ventilation relative to gas exchange and oxygen pulse (O2pulse) couples with effects from abnormal pulmonary gaseous oxygen store (O2store) contributions to (Formula presented.) O2 to interdependently precipitate persistently elevated ventilatory demand and low oxidative metabolic capacity in HF. Methods: Beat-to-beat HR and breath-to-breath ventilation and gas exchange were continuously acquired in HF (N = 9, ejection fraction = 30 ± 9%) and matched controls (N = 10) during square-wave ergometry at 60% (Formula presented.) O2peak (46 ± 14 vs 125 ± 54-W, P <.001). Temporal responses across (Formula presented.) E, (Formula presented.) O2 and O2pulse were assessed for the exercise on-transition using single exponential model Phase II on-kinetic time constants (τ = time to reach 63% steady-state rise). Breath-to-breath gas fractions and respiratory flows were used to determine O2stores. Results: HF vs controls: τ for (Formula presented.) E (137 ± 93 vs 74 ± 40-seconds, P =.03), (Formula presented.) O2 (60 ± 40 vs 23 ± 5-seconds, P =.03) and O2pulse (28 ± 18 vs 23 ± 15-seconds, P =.59). Within HF, τ for (Formula presented.) E differed from O2pulse (P <.02), but not (Formula presented.) O2. Exercise (Formula presented.) E rise (workload indexed) differed in HF vs controls (545 ± 139 vs 309 ± 88-mL min−1 W−1, P <.001). Exercise on-transition O2store depletion in HF exceeded controls, generally persisting to end-exercise. Conclusion: These data suggest HF demonstrated exercise on-transition O2store depletion (high O2store contribution to (Formula presented.) O2) coupled with dyssynchronous (Formula presented.) E, (Formula presented.) O2 and O2pulse kinetics—not attributable to prolonged cardiac haemodynamics. Persistent high ventilatory demand and low oxidative metabolic capacity in HF may be precipitated by physiological uncoupling occurring within the exercise on-transition.",

keywords = "HFrEF, O transport, alveolar oxygen, muscle V˙O kinetics, ventilatory efficiency",

author = "{Van Iterson}, {E. H.} and Smith, {J. R.} and Olson, {T. P.}",

note = "Funding Information: The author(s) would like to thank the participants who volunteered for this study. Funding for this work was supported by National Institutes of Health grants HL126638 (TPO) and HL138814 (EHV) and American Heart Association Grant 16POST30260021 (EHV). Publisher Copyright: {\textcopyright} 2018 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd",

year = "2018",

month = aug,

doi = "10.1111/apha.13063",

language = "English (US)",

volume = "223",

journal = "Acta Physiologica",

issn = "1748-1708",

number = "4",

}

TY - JOUR

T1 - 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

AU - Van Iterson, E. H.

AU - Smith, J. R.

AU - Olson, T. P.

N1 - Funding Information: The author(s) would like to thank the participants who volunteered for this study. Funding for this work was supported by National Institutes of Health grants HL126638 (TPO) and HL138814 (EHV) and American Heart Association Grant 16POST30260021 (EHV). Publisher Copyright: © 2018 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd

PY - 2018/8

Y1 - 2018/8

N2 - Aim: In contrast to knowledge that heart failure (HF) patients demonstrate peak exercise uncoupling across ventilation, gas exchange and cardiac haemodynamics, whether this dyssynchrony follows that at the exercise on-transition is unclear. This study tested whether exercise on-transition temporal lag for ventilation relative to gas exchange and oxygen pulse (O2pulse) couples with effects from abnormal pulmonary gaseous oxygen store (O2store) contributions to (Formula presented.) O2 to interdependently precipitate persistently elevated ventilatory demand and low oxidative metabolic capacity in HF. Methods: Beat-to-beat HR and breath-to-breath ventilation and gas exchange were continuously acquired in HF (N = 9, ejection fraction = 30 ± 9%) and matched controls (N = 10) during square-wave ergometry at 60% (Formula presented.) O2peak (46 ± 14 vs 125 ± 54-W, P <.001). Temporal responses across (Formula presented.) E, (Formula presented.) O2 and O2pulse were assessed for the exercise on-transition using single exponential model Phase II on-kinetic time constants (τ = time to reach 63% steady-state rise). Breath-to-breath gas fractions and respiratory flows were used to determine O2stores. Results: HF vs controls: τ for (Formula presented.) E (137 ± 93 vs 74 ± 40-seconds, P =.03), (Formula presented.) O2 (60 ± 40 vs 23 ± 5-seconds, P =.03) and O2pulse (28 ± 18 vs 23 ± 15-seconds, P =.59). Within HF, τ for (Formula presented.) E differed from O2pulse (P <.02), but not (Formula presented.) O2. Exercise (Formula presented.) E rise (workload indexed) differed in HF vs controls (545 ± 139 vs 309 ± 88-mL min−1 W−1, P <.001). Exercise on-transition O2store depletion in HF exceeded controls, generally persisting to end-exercise. Conclusion: These data suggest HF demonstrated exercise on-transition O2store depletion (high O2store contribution to (Formula presented.) O2) coupled with dyssynchronous (Formula presented.) E, (Formula presented.) O2 and O2pulse kinetics—not attributable to prolonged cardiac haemodynamics. Persistent high ventilatory demand and low oxidative metabolic capacity in HF may be precipitated by physiological uncoupling occurring within the exercise on-transition.

AB - Aim: In contrast to knowledge that heart failure (HF) patients demonstrate peak exercise uncoupling across ventilation, gas exchange and cardiac haemodynamics, whether this dyssynchrony follows that at the exercise on-transition is unclear. This study tested whether exercise on-transition temporal lag for ventilation relative to gas exchange and oxygen pulse (O2pulse) couples with effects from abnormal pulmonary gaseous oxygen store (O2store) contributions to (Formula presented.) O2 to interdependently precipitate persistently elevated ventilatory demand and low oxidative metabolic capacity in HF. Methods: Beat-to-beat HR and breath-to-breath ventilation and gas exchange were continuously acquired in HF (N = 9, ejection fraction = 30 ± 9%) and matched controls (N = 10) during square-wave ergometry at 60% (Formula presented.) O2peak (46 ± 14 vs 125 ± 54-W, P <.001). Temporal responses across (Formula presented.) E, (Formula presented.) O2 and O2pulse were assessed for the exercise on-transition using single exponential model Phase II on-kinetic time constants (τ = time to reach 63% steady-state rise). Breath-to-breath gas fractions and respiratory flows were used to determine O2stores. Results: HF vs controls: τ for (Formula presented.) E (137 ± 93 vs 74 ± 40-seconds, P =.03), (Formula presented.) O2 (60 ± 40 vs 23 ± 5-seconds, P =.03) and O2pulse (28 ± 18 vs 23 ± 15-seconds, P =.59). Within HF, τ for (Formula presented.) E differed from O2pulse (P <.02), but not (Formula presented.) O2. Exercise (Formula presented.) E rise (workload indexed) differed in HF vs controls (545 ± 139 vs 309 ± 88-mL min−1 W−1, P <.001). Exercise on-transition O2store depletion in HF exceeded controls, generally persisting to end-exercise. Conclusion: These data suggest HF demonstrated exercise on-transition O2store depletion (high O2store contribution to (Formula presented.) O2) coupled with dyssynchronous (Formula presented.) E, (Formula presented.) O2 and O2pulse kinetics—not attributable to prolonged cardiac haemodynamics. Persistent high ventilatory demand and low oxidative metabolic capacity in HF may be precipitated by physiological uncoupling occurring within the exercise on-transition.

KW - HFrEF

KW - O transport

KW - alveolar oxygen

KW - muscle V˙O kinetics

KW - ventilatory efficiency

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U2 - 10.1111/apha.13063

DO - 10.1111/apha.13063

M3 - Article

C2 - 29575588

AN - SCOPUS:85044740555

SN - 1748-1708

VL - 223

JO - Acta Physiologica

JF - Acta Physiologica

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M1 - e13063

ER -

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

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