Exercise intolerance, slowed pulmonary gas exchange (02 uptake) kinetics, and skeletal muscle dysfunction are characteristic of patients suffering from CHF. To date, it is not known how CHF impacts microvascular function and 02 exchange in skeletal muscle at the start of muscle contractions when the muscle energy (and therefore 02) demands are increased. Dr. Poole's laboratory has assembled a unique combination of established and state-of-the art techniques (intravital microscopy, phosphorescence quenching) to address this problem. My proposed doctoral thesis will test the broad hypothesis that CHF induces microcirculatory dysfunction that impairs 02 transfer from blood to muscle across the onset of contractions. This work will utilize the rat model of CHF that is a widely accepted analog of the human condition and has the major advantages of permitting very invasive studies and also facilitating direct comparison of CHF animals with controls. Development of effective treatments for CHF patients who number over 200,000 Americans per year and millions worldwide is contingent upon resolution of the mechanistic bases for the muscle dysfunction of the CHF patient. In this regard, my doctoral work seeks to address one important potential mechanism for the physical limitations pathognomonic to CHF.