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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| 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. |
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| Authors: | Van Iterson, E. H., Smith, J. R., Olson, T. P. |
| Source: | Acta Physiologica. Aug2018, Vol. 223 Issue 4, p1-1. 14p. 2 Charts, 3 Graphs. |
| Subjects: | Heart failure, Ergometry, Exercise, Pulmonary gas exchange, Respiration |
| Abstract: | 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 V ˙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% V ˙O2peak (46 ± 14 vs 125 ± 54‐W, P < .001). Temporal responses across V ˙E, V ˙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 V ˙E (137 ± 93 vs 74 ± 40‐seconds, P = .03), V ˙O2 (60 ± 40 vs 23 ± 5‐seconds, P = .03) and O2pulse (28 ± 18 vs 23 ± 15‐seconds, P = .59). Within HF, τ for V ˙E differed from O2pulse (P < .02), but not V ˙O2. Exercise V ˙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 V ˙O2) coupled with dyssynchronous V ˙E, V ˙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. [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | 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 V ˙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% V ˙O2peak (46 ± 14 vs 125 ± 54‐W, P < .001). Temporal responses across V ˙E, V ˙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 V ˙E (137 ± 93 vs 74 ± 40‐seconds, P = .03), V ˙O2 (60 ± 40 vs 23 ± 5‐seconds, P = .03) and O2pulse (28 ± 18 vs 23 ± 15‐seconds, P = .59). Within HF, τ for V ˙E differed from O2pulse (P < .02), but not V ˙O2. Exercise V ˙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 V ˙O2) coupled with dyssynchronous V ˙E, V ˙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. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 17481708 |
| DOI: | 10.1111/apha.13063 |
