Key result
Heart failure lowers cardiac output and impairs skeletal muscle blood flow during exercise.
Why the study?
The effects of chronic left ventricular volume overload on cardiocirculatory hemodynamics and cardiac output distribution during acute exhaustive exercise were not well characterized.
Does acute exhaustive treadmill exercise alter cardiocirculatory hemodynamics and cardiac output distribution in a rat model of chronic left ventricular volume overload?
Does acute exhaustive treadmill exercise alter cardiocirculatory hemodynamics and cardiac output distribution in a rat model of chronic left ventricular volume overload?
In a rat model of volume overload-induced heart failure, exercise leads to attenuated cardiac output distribution to skeletal muscles and increased distribution to the coronary bed.
Exercise-induced skeletal muscle hypoperfusion in volume-overload HF rats warrants caution extrapolating to patients; leaves open mechanisms of CO redistribution in human HF.
A rat model for chronic left ventricular volume overload (a-v fistula, 2 mo) was used to test the effects of acute exhaustive treadmill exercise (EX) (5 min, 70 ft/min, 0 degrees grade) on cardiocirculatory hemodynamics and cardiac output (CO) distribution during heart failure (HF). Control (C) and HF rats were studied at rest (R) and during the last minute of EX. Heart rate (HR), mean arterial pressure (MAP), and left ventricular end-diastolic (LVEDP) pressure were recorded and CO, blood flow (BF) to various regions, and total CO distribution were determined by the radioactive microsphere technique. In HF, biventricular hypertrophy and elevated LVEDP at R were correlated with an average shunt size equaling 37% of total CO. In both groups, CO and HR rose during EX with no change in MAP. Systemic CO in HF was reduced compared to C during both R and EX. BF to splanchnic, renal, cutaneous, and testicular circulations was compromised at R in HF, whereas only skeletal muscle BF was compromised in HF during EX. Data for CO distribution suggest that the major effect of HF during R was increased delivery to the coronary and the skeletal muscle beds at the expense of the cutaneous and renal beds, whereas %CO to the cerebral, hepatic, and gastrointestinal beds was spared. During EX, %CO to skeletal muscle beds in HF was attenuated compared to C, whereas that to the coronary bed was increased with no change in other regions.
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Flaim et al. (1980) studied Chronic left ventricular volume overload (heart failure). Chronic left ventricular volume overload (a-v fistula) vs. Control rats was evaluated on Cardiocirculatory hemodynamics and cardiac output distribution. In a rat model of heart failure, systemic cardiac output was reduced compared to controls at rest and during exercise, with attenuated blood flow to skeletal muscle beds during exercise.
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