Patients suffering from CHF are limited in their exercise tolerance. One factor leading to the reduced exercise tolerance is believed to involve attenuated oxygen transport to active muscle. In previous reports, peripheral blood flow measures have been used as an index of oxygen transport but there is a disagreement as to whether or not CHF alters the peripheral regulation of blood flow. Among other factors, this uncertainty may be due to differences in oxygen carrying capacity in heterogeneous groups of CHF patients. Lower oxygen carryinmg capacity may result in augmented flow responses in an attempt to optimize oxygen delivery. However, it seems clear that an augmented oxygen extraction from a normal flow response cannot compensate leading to an early activation of muscle glycolosis. A critical factor may be the rate at which oxygen transport increases at the onset of exercise (i.e. oxygen transport kinetics) It is known that a slowed adaption to the onset of exercise can slow the rate at which oxygen uptake occurs (i.e. the rate of delivery may limit the rate of oxygen uptake) thereby increasing the oxygen deficit incurred at the exercise onset, leading to an early and accelerated release of lactate and hydorgen ion. These metabolites are believed to be instrumental in the development of fatigue. The objectives of this study are to investigate the effect of CHF on the rate of increase in blood flow during the transition from rest to steady state handgrip exercise. A second objective is to examine the consequent effect of slowed blood flow kinetics on muscle metabolism. A third objective is to asses the role of forearm edema in the blood flow and oxygen uptake time course. We believe that CHF is associated with a slowed rate of increase in oxygen transport at the onset of exercise. The slower blood flow response may be due to slowed vasodilation and to limb edema.
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