We are grateful to C. F. Notarius and J. S. Floras for their interest in our recent article (Fisher et al. 2010) and for highlighting the previous work they performed in patients with heart failure indicating a potential role for muscle metaboreflex-mediated cardiac sympatho-excitation (Notarius et al. 2001). The alterations in neural cardiovascular regulation that occur during exercise in heart failure have been an intense area of investigation for quite some time, with often inconsistent findings leading to lively debate (Piepoli & Coats, 2007). However, this debate has centred largely on the regulation of sympathetic vasoconstrictor tone, blood pressure or ventilation, rather than on heart rate per se. As such, the significantly elevated heart rate observed during isolated muscle metaboreflex activation with post-exercise muscle ischaemia (PEI) in heart failure patients compared with healthy controls reported by Notarius et al. (2001) is particularly intriguing. These findings concur with our speculations derived from autonomic blockade studies in healthy young subjects. Indeed, the muscle metaboreflex can increase cardiac sympathetic drive and heart rate during PEI in humans, an effect that appears enhanced when reductions in cardiac parasympathetic control are manifest. However, it should be noted that a muscle metaboreflex-mediated increase in heart rate in the setting of heart failure does not seem to be a universal observation (Piepoli et al. 1996; Carrington et al. 2004). The reason for these discrepant findings is unclear but may be explained by heterogeneity in the patient populations and muscle groups studied as well as the intensity of muscle metaboreflex activation achieved. In regards to the latter, an advantage of both our work (Fisher et al. 2010) and the study of Notarius et al. (2001) is that multiple graded intensities of handgrip and PEI were utilized, thus maximizing muscle metaboreflex activation. Indeed, it appears that robust muscle metaboreflex activation may be needed to discern clear reflex-mediated heart rate effects. Interestingly, in the study of Notarius et al. (2001) a sustained heart rate elevation was observed during PEI despite 71% of the heart failure patients taking a β-1 blocker. As such, it may be of interest to specifically examine the heart rate responses of those patients that were not on a β-1 blocker. One might speculate that the greatest heart rate elevation would be seen in this group, perhaps indicating another benefit of β-blockade in heart failure patients. Due to its prognostic significance, the kinetics of heart rate recovery from exercise has received much attention. Indeed, a rapid heart rate recovery following exercise has been attributed to vagal reactivation and a sign of healthy heart rate control (Imai et al. 1994), whilst a delayed heart rate recovery is a powerful independent predictor of mortality even in low risk patients (Cole et al. 1999). However, the precise mechanisms underlying the rate of heart rate recovery from exercise have remained obscure in humans (i.e. central command, metaboreflex, mechanoreflex, arterial baroreflex); although we believe our recent data may be somewhat helpful in this regard. We suggest that in humans, as has been previously shown in dogs (O’Leary, 1993), the activation of metabolically sensitive muscle afferents can elicit a sympathetically mediated tachycardia that is ordinarily masked during PEI by the over-riding reactivation of cardiac parasympathetic activity due to arterial baroreflex activation and/or loss of inhibitory central command and muscle mechanoreflex inputs to parasympathetic neurons (Fisher et al. 2010). Although there are obvious differences between exercise recovery under occluded versus free flow conditions, it is plausible that in clinical situations where exaggerated skeletal muscle afferent activity is coupled with impairments in cardiac parasympathetic reactivation, sustained elevations in heart rate and a more sluggish heart rate recovery would be evident in the period immediately following exercise. The data of Notarius et al. (2001) add weight to this contention. Overall, these collective studies in animals (O’Leary, 1993), healthy humans (Fisher et al. 2010) and heart failure patients (Notarius et al. 2001) tend to corroborate one another, which is encouraging in light of the present emphasis on clinical translational science.