Background: Ischemic preconditioning (IP) is the exposure to brief periods of circulatory occlusion and reperfusion in order to protect local or systemic organs against subsequent bouts of ischemia. IP has been shown to improve exercise performance and to delay fatigue. It has been hypothesized that IP lowers the sensation of fatigue by reducing the discharge of group III and IV nerve endings, which also regulate hemodynamics during the metaboreflex. We hypothesized that if the preconditioning reduces the discharge of group III and IV nerve endings then can reduce also the blood pressure response during the metaboreflex. Objective: The purpose of this study is to verify if IP reduces the blood pressure response during the metaboreflex and if improves exercise performance. Methods: Fourteen healthy males (age between 25-48 years) participated in this study. They underwent the following randomly assigned protocol: control exercise recovery session (CER) test, post-exercise muscle ischemia (PEMI) test, PEMI after IP (IP-PEMI) test. The exercises was performed with dynamic handgrip. Hemodynamics were evaluated by echocardiography and impedance cardiography. Results: We found that after IP the mean arterial pressure response was reduced in comparison with the PEMI test (+3.37±6.41 vs. +9.16±7.09 mmHg; P < 0.05). It was reduced because of a lower stroke volume during the IP-PEMI in comparison with the PEMI test (-1.43±15.35 vs. +10.28±10.479 ml; P < 0.05). Conclusions: The main result of the present investigation was that IP was able to reduce the blood pressure response during the metaboreflex activation. The IP seems to change hemodynamics mainly because it impairs the capacity to augment venous return and to recruit the cardiac pre-load reserve. It was hypothesized that this is the consequence of an increased nitric oxide production which reduces the possibility to constrict venous capacity vessels.

Il precondizionamento ischemico e la regolazione dell'apparato cardiovascolare: ruolo delle terminazioni nervose libere III e IV

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2016-03-18

Abstract

Background: Ischemic preconditioning (IP) is the exposure to brief periods of circulatory occlusion and reperfusion in order to protect local or systemic organs against subsequent bouts of ischemia. IP has been shown to improve exercise performance and to delay fatigue. It has been hypothesized that IP lowers the sensation of fatigue by reducing the discharge of group III and IV nerve endings, which also regulate hemodynamics during the metaboreflex. We hypothesized that if the preconditioning reduces the discharge of group III and IV nerve endings then can reduce also the blood pressure response during the metaboreflex. Objective: The purpose of this study is to verify if IP reduces the blood pressure response during the metaboreflex and if improves exercise performance. Methods: Fourteen healthy males (age between 25-48 years) participated in this study. They underwent the following randomly assigned protocol: control exercise recovery session (CER) test, post-exercise muscle ischemia (PEMI) test, PEMI after IP (IP-PEMI) test. The exercises was performed with dynamic handgrip. Hemodynamics were evaluated by echocardiography and impedance cardiography. Results: We found that after IP the mean arterial pressure response was reduced in comparison with the PEMI test (+3.37±6.41 vs. +9.16±7.09 mmHg; P < 0.05). It was reduced because of a lower stroke volume during the IP-PEMI in comparison with the PEMI test (-1.43±15.35 vs. +10.28±10.479 ml; P < 0.05). Conclusions: The main result of the present investigation was that IP was able to reduce the blood pressure response during the metaboreflex activation. The IP seems to change hemodynamics mainly because it impairs the capacity to augment venous return and to recruit the cardiac pre-load reserve. It was hypothesized that this is the consequence of an increased nitric oxide production which reduces the possibility to constrict venous capacity vessels.
18-mar-2016
ischemic preconditioning
metaboreflex
metaboriflessi
precondizionamento ischemico
Corona, Francesco
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11584/266650
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