RESUMO
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 (O2 pulse) couples with effects from abnormal pulmonary gaseous oxygen store (O2store ) contributions to VËO2 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% VËO2peak (46 ± 14 vs 125 ± 54-W, P < .001). Temporal responses across VËE , VËO2 and O2 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 O2stores . RESULTS: HF vs controls: τ for VËE (137 ± 93 vs 74 ± 40-seconds, P = .03), VËO2 (60 ± 40 vs 23 ± 5-seconds, P = .03) and O2 pulse (28 ± 18 vs 23 ± 15-seconds, P = .59). Within HF, τ for VËE differed from O2 pulse (P < .02), but not VËO2 . Exercise VËE 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 VËO2 ) coupled with dyssynchronous VËE , VËO2 and O2 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.
