title: Microvascular oxygen delivery-to-utilization mismatch at the onset of heavy-intensity exercise in optimally treated patients with CHF.
abstract: Impaired muscle blood flow at the onset of heavy-intensity exercise may transiently reduce microvascular O(2) pressure and decrease the rate of O(2) 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 beta-blockers) may have improved microvascular O(2) delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O(2) uptake (Vo(2)) kinetics. We assessed the rate of change of pulmonary Vo(2) (Vo(2)(p)), (estimated) fractional O(2) extraction in the vastus lateralis (approximately Delta[deoxy-Hb+Mb] by near-infrared spectroscopy), and cardiac output (Qt) during high-intensity exercise performed to the limit of tolerance (Tlim) in 10 optimally treated sedentary patients (ejection fraction = 29 + or - 8%) and 11 controls. Sluggish Vo(2)(p) and Qt kinetics in patients were significantly related to lower Tlim values (P < 0.05). The dynamics of Delta[deoxy-Hb+Mb], however, were faster in patients than controls [mean response time (MRT) = 15.9 + or - 2.0 s vs. 19.0 + or - 2.9 s; P < 0.05] with a subsequent response "overshoot" being found only in patients (7/10). Moreover, tauVo(2)/MRT-[deoxy-Hb+Mb] ratio was greater in patients (4.69 + or - 1.42 s vs. 2.25 + or - 0.77 s; P < 0.05) and related to Qt 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 Vo(2)(p) kinetics and tolerance to heavy-intensity exercise in nontrained patients.
authors.affiliation: Pulmonary Function and Clinical Exercise Physiology Unit (SEFICE), Division of Respiratory Diseases, Department of Medicine, Federal University of Sao Paulo (UNIFESP), São Paulo.
authors.forename: Priscila Abreu
authors.initials: PA
authors.lastname: Sperandio
authors.forename: Audrey
authors.initials: A
authors.lastname: Borghi-Silva
authors.forename: Adriano
authors.initials: A
authors.lastname: Barroco
authors.forename: Luiz Eduardo
authors.initials: LE
authors.lastname: Nery
authors.forename: Dirceu R
authors.initials: DR
authors.lastname: Almeida
authors.forename: J Alberto
authors.initials: JA
authors.lastname: Neder
mesh_terms: D000222:Adaptation, Physiological; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002302:Cardiac Output; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D016022:Case-Control Studies; D004359:Drug Therapy, Combination; D017079:Exercise Tolerance; D006333:Heart Failure / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D008297:Male; D008706:Methemoglobin / Q000378:metabolism; D008833:Microcirculation; D008875:Middle Aged; D008929:Mitochondria, Heart / Q000378:metabolism; D008931:Mitochondria, Muscle / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism*; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption; D011446:Prospective Studies; D011659:Pulmonary Gas Exchange; D052097:Quadriceps Muscle / Q000098:blood supply* / Q000378:metabolism*; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D002317:Cardiovascular Agents; D006454:Hemoglobins; C100003:deoxyhemoglobin; D008706:Methemoglobin; D010100:Oxygen