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1 Science Applied to Biological Systems , university of cagliari, cagliari, Italy; Biomedical Sciences, university of sassari, sassari, Italy; Biological Science, university of torino, torino, Italy
2 Science Applied to Biological Systems , university of cagliari, cagliari, Italy
3 Science Applied to Biological Systems, university of cagliari, Italy
4 Biomedical Sciences, university of sassari, sassari, Italy
5 Cardiovascular and Neurological Sciences, university of cagliari, cagliari, Italy
6 Biological Science, university of torino, torino, Italy
7 Science Applied to Biological Systems, university of cagliari, cagliari, Italy
* To whom correspondence should be addressed. E-mail: crisafulli{at}tiscali.it.
The muscle metaboreflex is enhanced in chronic heart failure (CHF) patients, and this fact has been associated with the early fatigue shown by these patients in response to exercise. In animal studies of CHF it was found that the limited capacity to enhance ventricular performance is responsible for a functional shift from a cardiac output (CO) to a systemic vascular resistance (SVR) increase in the mechanism by which the cardiovascular system raises blood pressure in response to the metaboreflex. However, the existence of this functional shift is still unknown in humans. The present study was undertaken to test the hypothesis that a similar hemodynamic response was present also in humans with CHF. The hemodynamic response to metaboreflex activation obtained through post-exercise ischemia was assessed in nine patients with CHF and nine healthy controls (CTL) by means of impedance cardiography. The main results were that: 1) the blood pressure rise due to the metaboreflex was similar in the two groups; 2) the CTL group achieved the blood pressure response via CO-increase; the CHF group via SVR increase; 3) stroke volume (SV) was enhanced in the CTL group and decreased in the CHF group. This study demonstrates that in CHF patients metaboreflex recruitment causes a functional shift from flow-increase to peripheral vasoconstriction in the mechanism through which blood pressure is increased. The incapacity to enhance cardiac performance and SV is probably the primary cause of this cardiovascular alteration.
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