Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA.
Acta Physiol (Oxf). 2018 Aug;223(4):e13063. doi: 10.1111/apha.13063. Epub 2018 Apr 1.
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 (O pulse) couples with effects from abnormal pulmonary gaseous oxygen store (O ) contributions to V˙O to interdependently precipitate persistently elevated ventilatory demand and low oxidative metabolic capacity in HF.
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˙O (46 ± 14 vs 125 ± 54-W, P < .001). Temporal responses across V˙ , V˙O and O pulse 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 .
HF vs controls: τ for V˙ (137 ± 93 vs 74 ± 40-seconds, P = .03), V˙O (60 ± 40 vs 23 ± 5-seconds, P = .03) and O pulse (28 ± 18 vs 23 ± 15-seconds, P = .59). Within HF, τ for V˙ differed from O pulse (P < .02), but not V˙O . Exercise V˙ rise (workload indexed) differed in HF vs controls (545 ± 139 vs 309 ± 88-mL min W , P < .001). Exercise on-transition O depletion in HF exceeded controls, generally persisting to end-exercise.
These data suggest HF demonstrated exercise on-transition O depletion (high O contribution to V˙O ) coupled with dyssynchronous V˙ , V˙O and O pulse 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.
与心力衰竭（HF）患者在通气、气体交换和心脏血液动力学方面表现出的峰值运动解耦知识相反，这种解耦是否发生在运动过渡时尚不清楚。本研究旨在测试通气相对于气体交换和氧脉冲（O 脉冲）的运动过渡时滞是否与异常肺气体氧储存（O ）对 V˙O 的贡献作用相耦合，以独立预测 HF 中持续升高的通气需求和低氧化代谢能力。
在 HF（N = 9，射血分数 = 30 ± 9%）和匹配对照组（N = 10）中，在 60% V˙O（46 ± 14 与 125 ± 54-W，P <.001）的方波运动时，连续采集逐搏 HR 和逐呼吸通气和气体交换。使用单指数模型 II 相动力学时间常数（τ = 达到 63%稳态上升的时间）评估运动过渡时 V˙、V˙O 和 O 脉冲的时间响应。使用呼吸气体分数和呼吸流量来确定 O 。
HF 与对照组相比：V˙（137 ± 93 与 74 ± 40 秒，P =.03）、V˙O（60 ± 40 与 23 ± 5 秒，P =.03）和 O 脉冲（28 ± 18 与 23 ± 15 秒，P =.59）的 τ。在 HF 中，V˙的 τ与 O 脉冲不同（P <.02），但与 V˙O 不同。HF 与对照组相比，运动时 V˙上升（工作量指数）不同（545 ± 139 与 309 ± 88-mL min W ，P <.001）。HF 中的运动过渡 O 耗竭超过对照组，通常持续到运动结束。
这些数据表明，HF 表现出运动过渡时的 O 耗竭（高 O 对 V˙O 的贡献），同时伴有 V˙、V˙O 和 O 脉冲动力学的解耦-这不能归因于延长的心脏血液动力学。HF 中持续升高的通气需求和低氧化代谢能力可能是由运动过渡时发生的生理解耦引起的。
