LF Power of HRV Could Be the Piezo2 Activity Level in Baroreceptors with Some Piezo1 Residual Activity Contribution

Abstract

Heart rate variability is a useful measure for monitoring the autonomic nervous system. Heart rate variability measurements have gained significant demand not only in science, but also in the public due to the fairly low price and wide accessibility of the Internet of things. The scientific debate about one of the measures of heart rate variability, i.e., what low-frequency power is reflecting, has been ongoing for decades. Some schools reason that it represents the sympathetic loading, while an even more compelling reasoning is that it measures how the baroreflex modulates the cardiac autonomic outflow. However, the current opinion manuscript proposes that the discovery of the more precise molecular characteristics of baroreceptors, i.e., that the Piezo2 ion channel containing vagal afferents could invoke the baroreflex, may possibly resolve this debate. It is long known that medium- to high-intensity exercise diminishes low-frequency power to almost undetectable values. Moreover, it is also demonstrated that the stretch- and force-gated Piezo2 ion channels are inactivated in a prolonged hyperexcited state in order to prevent pathological hyperexcitation. Accordingly, the current author suggests that the almost undetectable value of low-frequency power at medium- to high-intensity exercise reflects the inactivation of Piezo2 from vagal afferents in the baroreceptors with some Piezo1 residual activity contribution. Consequently, this opinion paper highlights how low-frequency power of the heart rate variability could represent the activity level of Piezo2 in baroreceptors.

Does Proprioception Involve Synchronization with Theta Rhythms by a Novel Piezo2 Initiated Ultrafast VGLUT2 Signaling?

“…The low-frequency (LF) power of heart rate variability (HRV) also shows a correlation, albeit a negative one, with voluntary medium to high-intensity exercise at the onset, and this mechanism is theorized to be largely attributed to the activity level of Piezo2 ion channels in the baroreceptors [5]. Furthermore, these Piezo2 ion channels are shown to be the principal mechanotransductory ion channels responsible for proprioception [6].…”

Orthostasis Is Impaired Due to Fatiguing Intensive Acute Concentric Exercise Succeeded by Isometric Weight-Loaded Wall-Sit in Delayed-Onset Muscle Soreness: A Pilot Study

“…The inactivation of Piezo2 channels in response to hyperexcitation during allostatic stress is a homeostatic response [3,33]. Correspondingly, a recent theory postulated that Piezo2 ion channels can be inactivated in baroreceptors during IAE [34]. In that case, the Ca v 1.3 channels in the sinoatrial node (SAN) could be unopposed, with ever-increasing pacemaking during the sustained IAE activity.…”

“…In that case, the Ca v 1.3 channels in the sinoatrial node (SAN) could be unopposed, with ever-increasing pacemaking during the sustained IAE activity. Hence, it means that Piezo2 inactivation in baroreceptors could be the excitatory neural upper limit of entrainment activity between baroreceptors and SAN [34]. However, it is suggested that synchronization deactivation is not complete because Piezo1 can maintain residual entrainment activity from this aspect [34].…”

“…Hence, it means that Piezo2 inactivation in baroreceptors could be the excitatory neural upper limit of entrainment activity between baroreceptors and SAN [34]. However, it is suggested that synchronization deactivation is not complete because Piezo1 can maintain residual entrainment activity from this aspect [34]. The current authors interpret that the athletes produced the observed positive OST after the exercise protocol due to the insufficient abrupt return of Piezo2 reactivation-induced entrainment between baroreceptors and SAN, likely accompanied by hypovolemia and transiently increased hemoconcentration, in which mechanism Piezo1 proteins are also suggested to have a primary role.…”

“…The current authors propose that, when Piezo2 is activated in baroreceptors and synchronized with the cardiac vagal afferents, then cardiac-specific Na v 1.5, in collaboration with Ca v 1.2 and Ca v 1.3, maintains the proper pacing and conduction in the SAN. On the contrary, when Piezo2 is deactivated in baroreceptors, entrainment is suggested to diminish to undetectable levels, and Ca v 1.3 could gain dominance in pacemaking [34,43]. Indeed, animal research shows that Ca v 1.3 is needed for beta-adrenergic-triggered automaticity in SAN pacemaker cells [44].…”