During heavy exercise, the arterial baroreflex and the reflexes evoked by the activation of those afferent nerve endings in the working skeletal muscles that are sensitive to metabolic changes (the so-called muscle metaboreflex) are hypothesized to be activated and, moreover, to interact in ways that lead to the modulation of the primary cardiovascular reflex responses. For the past few years, our group has been investigating the interaction between the arterial baroreflex and the muscle metaboreflex. We have focused our efforts in identifying the effects of muscle metaboreflex activation on the arterial baroreflex regulation of the cardiovascular hemodynamics and muscle sympathetic nerve activity (MSNA) in humans. In a series of studies, we have found that during muscle metaboreflex activation, dynamic carotid baroreflex responses are modulated, as exemplified by the augmentation of the MSNA, leg vascular conductance and blood pressure responses to carotid baroreflex unloading and the shorter suppression period of MSNA, diminished vasodilation, and reduced blood pressure response to carotid baroreflex stimulation. Furthermore, we have found that the modification of the arterial baroreflex-mediated beat-to-beat control of MSNA, which is seen during activation of the muscle metaboreflex (i.e., resetting and an increase in sensitivity), could be a consequence of the alteration in the arterial baroreflex control of both the occurrence and strength of the MSNA burst. In addition, we have demonstrated that the arterial baroreflex beat-to-beat control of MSNA is time-dependently modulated during isometric exercise. We suggest that the modulation of arterial baroreflex function during the activation of muscle metaboreflex is one of the mechanisms for increasing, or maintaining, blood pressure at the required pressure and thereby contributes to the regulation of the cardiovascular system during exercise.