Joshua F Lee1, Zachary Barrett-O'Keefe2, Ashley D Nelson3, Ryan S Garten1, John J Ryan4, Jose N Nativi-Nicolau4, Russell S Richardson5, D Walter Wray6. 1. Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City, UT, United States; Geriatric Research, Education, and Clinical Center, VA Medical Center, Salt Lake City, UT, United States. 2. Geriatric Research, Education, and Clinical Center, VA Medical Center, Salt Lake City, UT, United States; Department of Exercise & Sport Science, University of Utah, Salt Lake City, UT, United States. 3. Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City, UT, United States. 4. Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah, Salt Lake City, UT, United States. 5. Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City, UT, United States; Geriatric Research, Education, and Clinical Center, VA Medical Center, Salt Lake City, UT, United States; Department of Exercise & Sport Science, University of Utah, Salt Lake City, UT, United States. 6. Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City, UT, United States; Geriatric Research, Education, and Clinical Center, VA Medical Center, Salt Lake City, UT, United States; Department of Exercise & Sport Science, University of Utah, Salt Lake City, UT, United States. Electronic address: walter.wray@hsc.utah.edu.
Abstract
BACKGROUND: Exercise intolerance is a hallmark symptom of heart failure patients with preserved ejection fraction (HFpEF), which may be related to an impaired ability to appropriately increase blood flow to the exercising muscle. METHODS: We evaluated leg blood flow (LBF, ultrasound Doppler), heart rate (HR), stroke volume (SV), cardiac output (CO), and mean arterial blood pressure (MAP, photoplethysmography) during dynamic, single leg knee-extensor (KE) exercise in HFpEF patients (n=21; 68 ± 2 yrs) and healthy controls (n=20; 71 ± 2 yrs). RESULTS: HFpEF patients exhibited a marked attrition during KE exercise, with only 60% able to complete the exercise protocol. In participants who completed all exercise intensities (0-5-10-15 W; HFpEF, n=13; Controls, n=16), LBF was not different at 0 W and 5 W, but was 15-25% lower in HFpEF compared to controls at 10 W and 15 W (P<0.001). Likewise, leg vascular conductance (LVC), an index of vasodilation, was not different at 0 W and 5 W, but was 15-20% lower in HFpEF compared to controls at 10 W and 15 W (P<0.05). In contrast to these peripheral deficits, exercise-induced changes in central variables (HR, SV, CO), as well as MAP, were similar between groups. CONCLUSIONS: These data reveal a marked reduction in LBF and LVC in HFpEF patients during exercise that cannot be attributed to a disease-related alteration in central hemodynamics, suggesting that impaired vasodilation in the exercising skeletal muscle vasculature may play a key role in the exercise intolerance associated with this patient population.
BACKGROUND: Exercise intolerance is a hallmark symptom of heart failurepatients with preserved ejection fraction (HFpEF), which may be related to an impaired ability to appropriately increase blood flow to the exercising muscle. METHODS: We evaluated leg blood flow (LBF, ultrasound Doppler), heart rate (HR), stroke volume (SV), cardiac output (CO), and mean arterial blood pressure (MAP, photoplethysmography) during dynamic, single leg knee-extensor (KE) exercise in HFpEF patients (n=21; 68 ± 2 yrs) and healthy controls (n=20; 71 ± 2 yrs). RESULTS: HFpEF patients exhibited a marked attrition during KE exercise, with only 60% able to complete the exercise protocol. In participants who completed all exercise intensities (0-5-10-15 W; HFpEF, n=13; Controls, n=16), LBF was not different at 0 W and 5 W, but was 15-25% lower in HFpEF compared to controls at 10 W and 15 W (P<0.001). Likewise, leg vascular conductance (LVC), an index of vasodilation, was not different at 0 W and 5 W, but was 15-20% lower in HFpEF compared to controls at 10 W and 15 W (P<0.05). In contrast to these peripheral deficits, exercise-induced changes in central variables (HR, SV, CO), as well as MAP, were similar between groups. CONCLUSIONS: These data reveal a marked reduction in LBF and LVC in HFpEF patients during exercise that cannot be attributed to a disease-related alteration in central hemodynamics, suggesting that impaired vasodilation in the exercising skeletal muscle vasculature may play a key role in the exercise intolerance associated with this patient population.
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