Microvascular oxygen delivery-to-utilization mismatch at the onset of heavy-intensity exercise in optimally treated patients with CHF

Abstract

Microvascular oxygen delivery-to-utilization mismatch at the onset of heavy-intensity exercise in optimally treated patients with CHF. Am J Physiol Heart Circ Physiol 297: H1720 –H1728, 2009. First published September 4, 2009; doi:10.1152/ajpheart.00596.2009.— Impaired muscle blood flow at the onset of heavy-intensity exercise may transiently reduce microvascular O2 pressure and decrease the rate of O2 transfer from capillary to mitochondria in chronic heart failure (CHF). However, advances in the pharmacological treatment of CHF (e.g., angiotensin-converting enzyme inhibitors and third generation -blockers) may have improved microvascular O2 delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O2 uptake (V˙ O2) kinetics. We assessed the rate of change of pulmonary V˙ O2 (V˙ O2p), (estimated) fractional O2 extraction in the vastus lateralis ([deoxy-Hb Mb] by near-infrared spectroscopy), and cardiac output (Q˙ T) during high-intensity exercise performed to the limit of tolerance (Tlim) in 10 optimally treated sedentary patients (ejection fraction 29 8%) and 11 controls. Sluggish V˙ O2p and Q˙ T kinetics in patients were significantly related to lower Tlim values (P 0.05). The dynamics of [deoxy Hb Mb], however, were faster in patients than controls [mean response time (MRT) 15.9 2.0 s vs. 19.0 2.9 s; P 0.05] with a subsequent response “overshoot” being found only in patients (7/10). Moreover, V˙ O2/MRT-[deoxy-Hb Mb] ratio was greater in patients (4.69 1.42 s vs. 2.25 0.77 s; P 0.05) and related to Q˙ T kinetics and Tlim (R 0.89 and 0.78, respectively; P 0.01). We conclude that despite the advances in the pharmacological treatment of CHF, disturbances in “central” and “peripheral” circulatory adjust ments still play a prominent role in limiting V˙ O2p kinetics and tolerance to heavy-intensity exercise in nontrained patients