Abstract

Aging and chronic heart failure (CHF) both manifest alterations in the regional blood flow (BF) response and contribute to a reduced exercise (EX) capacity. Since the majority of the CHF patient population is elderly, it is imperative to understand the extent to which aging itself alters BF in this disease. PURPOSE To determine the effects of aging on the hemodynamic and regional BF response to submaximal EX in rats with CHF induced by myocardial infarction. METHODS Heart rate (HR), mean arterial pressure (MAP), and BF to different organs (kidneys, splanchnic organs, and 28 hindlimb muscles) were determined at rest (R) and during treadmill EX (20 m/min, 5% grade) with radiolabeled microspheres in young (Y; 6–8 month old, 412 ± 11 g, n = 11) and old (O; 27–29 month old, 494 ± 10 g, n = 8) Fischer 344 × Brown Norway rats with similar degrees of left ventricular (LV) dysfunction and CHF (LV end-diastolic pressure: Y: 24 ± 2 vs. O: 22 ± 2 mmHg, P > 0.05). RESULTS HR and MAP at R were similar between Y and O rats. BF at R was higher in spleen (274 ± 64 vs. 161 ± 17 ml/min/100g, P < 0.05) but lower in liver (96 ± 14 vs. 185 ± 39 ml/min/100g, P < 0.05) of Y vs. O rats. Skeletal muscle BF (SMBF) at R was similar for the 28 hindlimb (HLD) muscles in Y and O rats. HR and MAP increased during EX, but the HR response was blunted in O when compared to Y rats (Y: 546 ± 8 vs. O: 395 ± 9 bpm, P < 0.05). O rats demonstrated a greater reduction in abdominal organ BF in response to EX (Y: 35 ± 9 vs. O: 77 ± 6 %, P < 0.05). Moreover, BF during EX was elevated in 14 and reduced in 5 of the 28 HDL muscles of O vs. Y rats and this contributed to the greater SMBF response found in O CHF rats (Y: 78 ± 5 vs. O: 100 ± 11 ml/min/100g, P < 0.05). CONCLUSION O CHF rats respond to submaximal EX with a greater reduction in BF to the abdominal organs, and a greater increase in BF to the HDL musculature as a whole. The greater increase in HDL BF found in the O vs. Y CHF rat is primarily due to augmented BF responses found in muscles containing a majority of fast-twitch glycolytic fibers. Supported by NIH AG19228 & HL50306

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