Heart failure patients exhibited significantly prolonged exercise on-transition time constants for ventilation compared to matched controls (137 vs 74 seconds, P=0.03).
Case-Control (n=19)
Heart failure patients demonstrate exercise on-transition oxygen store depletion and dyssynchronous ventilatory and gas exchange kinetics, suggesting physiological uncoupling contributes to exercise intolerance.
Absolute Event Rate: 137% vs 74%
p-value: p=0.03
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 (O 2 pulse) couples with effects from abnormal pulmonary gaseous oxygen store (O 2store ) contributions to O 2 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% O 2peak (46 ± 14 vs 125 ± 54‐W, P < .001). Temporal responses across E , O 2 and O 2 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 2stores . Results HF vs controls: τ for E (137 ± 93 vs 74 ± 40‐seconds, P = .03), O 2 (60 ± 40 vs 23 ± 5‐seconds, P = .03) and O 2 pulse (28 ± 18 vs 23 ± 15‐seconds, P = .59). Within HF, τ for E differed from O 2 pulse ( P < .02), but not O 2 . Exercise 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 O 2 ) coupled with dyssynchronous E , O 2 and O 2 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.
Iterson et al. (Sun,) conducted a case-control in Heart failure (n=19). Heart failure vs. Matched controls was evaluated on Phase II on-kinetic time constants (τ) for ventilation (E) (p=0.03). Heart failure patients exhibited significantly prolonged exercise on-transition time constants for ventilation compared to matched controls (137 vs 74 seconds, P=0.03).