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| − | + | 1996) as demonstrated in studies involving curare-induced partial neuromuscular blockade (Ochwadt et al. 1959; Asmussen et al. 1965; Galbo et al. 1987). Thus, partial afferent blockade using local anaesthetics creates a condition of reduced neural feedback in the face of increased feedforward. With this in mind, the resultant net effect on ventilatory and/or circulatory responses during exercise with partly blocked feedback via local anaesthetics depends upon the degree to which the increase in central motor command/feedforward response balances the reduced feedback from the working limb muscles (Amann et al. 2010). As unmyelinalted and [http://en.wikipedia.org/wiki/GPX4 GPX4] lightly myelinated nerve fibres are most sensitive to local anaesthetic agents and represent the afferent arm of the [http://www.selleckchem.com/products/azd9291.html click here] exercise pressor reflex (Kaufman, 2012), light epidural anaesthesia was considered to block cardiovascular responses to exercise. Recently, during a 5 km cycling time trial with light lumbar epidural anaesthesia (0.5% lidocaine; Amann et al. 2008) and during constant-load cycling exercise (1% lidocaine; Friedman et al. 1993), HR and BP were found to remain unaffected. This could falsely be interpreted as a lack of effect of muscle afferents on the pressor response during exercise; however, the findings need to be interpreted with extreme caution. It is critical to note that, in the case of the time-trial exercise (Amann et al. 2008), HR and BP were, during the race with afferent blockade, nearly identical compared with control exercise, despite the substantially lower power output (due to the impact of lidocaine on muscle strength) and therefore metabolic and cardiovascular demand. Consequently, HR and BP were increased out of proportion to the real demand. This indicates that the increased central motor drive, subsequent to the blockage of the inhibitory effects of group III/IV muscle afferents on central motor drive (see [http://www.selleckchem.com/products/ch5424802.html Alectinib datasheet] Amann, 2011 for review), was powerful enough not only to compensate for the missing afferent feedback (i.e. attenuated exercise pressor reflex), but even to increase the circulatory response during exercise further. In the case of the constant-load exercise with lidocaine (Friedman et al. 1993), the lidocaine-evoked increase in central motor drive necessary to maintain the given external workload was strong enough to compensate for the missing feedback, with the net effect of unchanged HR and BP during the exercise. Although these studies, if interpreted with caution, do offer an indirect indication of the role of muscle afferents for the exercise pressor reflex, the associated drug-induced increase in central motor drive masks the cardiovascular consequences associated with blocked afferent feedback. | |
Version du 5 décembre 2016 à 08:58
1996) as demonstrated in studies involving curare-induced partial neuromuscular blockade (Ochwadt et al. 1959; Asmussen et al. 1965; Galbo et al. 1987). Thus, partial afferent blockade using local anaesthetics creates a condition of reduced neural feedback in the face of increased feedforward. With this in mind, the resultant net effect on ventilatory and/or circulatory responses during exercise with partly blocked feedback via local anaesthetics depends upon the degree to which the increase in central motor command/feedforward response balances the reduced feedback from the working limb muscles (Amann et al. 2010). As unmyelinalted and GPX4 lightly myelinated nerve fibres are most sensitive to local anaesthetic agents and represent the afferent arm of the click here exercise pressor reflex (Kaufman, 2012), light epidural anaesthesia was considered to block cardiovascular responses to exercise. Recently, during a 5 km cycling time trial with light lumbar epidural anaesthesia (0.5% lidocaine; Amann et al. 2008) and during constant-load cycling exercise (1% lidocaine; Friedman et al. 1993), HR and BP were found to remain unaffected. This could falsely be interpreted as a lack of effect of muscle afferents on the pressor response during exercise; however, the findings need to be interpreted with extreme caution. It is critical to note that, in the case of the time-trial exercise (Amann et al. 2008), HR and BP were, during the race with afferent blockade, nearly identical compared with control exercise, despite the substantially lower power output (due to the impact of lidocaine on muscle strength) and therefore metabolic and cardiovascular demand. Consequently, HR and BP were increased out of proportion to the real demand. This indicates that the increased central motor drive, subsequent to the blockage of the inhibitory effects of group III/IV muscle afferents on central motor drive (see Alectinib datasheet Amann, 2011 for review), was powerful enough not only to compensate for the missing afferent feedback (i.e. attenuated exercise pressor reflex), but even to increase the circulatory response during exercise further. In the case of the constant-load exercise with lidocaine (Friedman et al. 1993), the lidocaine-evoked increase in central motor drive necessary to maintain the given external workload was strong enough to compensate for the missing feedback, with the net effect of unchanged HR and BP during the exercise. Although these studies, if interpreted with caution, do offer an indirect indication of the role of muscle afferents for the exercise pressor reflex, the associated drug-induced increase in central motor drive masks the cardiovascular consequences associated with blocked afferent feedback.
