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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/H1720    most recent 00596.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Sperandio, P. A. Articles by Neder, J. A. PubMed PubMed Citation Articles by Sperandio, P. A. Articles by Neder, J. A.

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

¹Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo (UNIFESP), São Paulo; ²Division of Cardiology, Department of Medicine, Federal University of Sao Paulo (UNIFESP), São Paulo; and ³Cardiopulmonary Laboratory, Nucleus of Research in Physical Exercise, Federal University of São Carlos (UFSCar), São Carlos, SP, Brazil

Submitted July 6, 2009 ; accepted in final form September 4, 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 β-blockers) may have improved microvascular O₂ delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O₂ uptake (O₂) kinetics. We assessed the rate of change of pulmonary O₂ (O_2p), (estimated) fractional O₂ extraction in the vastus lateralis ([deoxy-Hb+Mb] by near-infrared spectroscopy), and cardiac output (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 O_2p and 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, 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 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 adjustments still play a prominent role in limiting O_2p kinetics and tolerance to heavy-intensity exercise in nontrained patients.

blood flow; chronic heart failure; hemodynamics; near-infrared spectroscopy; oxygen consumption