Our primary research objective centered on the examination of high and low-frequency sound stimuli's influence on heart-brain coupling. By quantifying the wavelet coherence between heart rate variability and electroencephalogram envelopes from thirty-one subjects exposed to periods of silence or high (880Hz) or low pitch (110 Hz) sounds, we discerned three crucial insights: both sound stimuli types were associated with reduced heart rates; low-pitch sounds showed a notably lower HF normalized power compared to silence; and HRV-EEG coherence significantly varied between the high-pitch sound and both the silence and low-pitch sound for the heart rate variability's low-frequency band and EEG's Beta band.
Our findings suggest that sustained high and low-pitch sounds might decrease heart rate relative to silence, potentially pointing to a calming or focusing influence of these sounds on the autonomic nervous system. The broader implications of these insights for real-world scenarios are considerable. While sound-induced heart rate reduction might be therapeutic, potentially aiding relaxation or anxiety management, it might also pose challenges. For instance, consistent exposure to specific frequencies during tasks demanding precision and concentration might adversely affect performance due to physiological changes. While few studies directly assess simple sound stimuli's effect on heart rate, relevant research corroborates our observations. Specifically, findings from Nakajima et al. (29) and Veternik et al. (2008) (30) mirrored our observations, but a cause-effect relationship between sound and heart rate modifications necessitates more extensive research.
Regarding HRV frequency bands' power, our data did not manifest significant variations between silence, high, and low-pitch conditions. This contrasts with Hori et al. (2005) (32) that reported elevated HF power values for subjects exposed to a 110 Hz sine wave versus 880 Hz. While our data hinted at a slightly heightened normalized power in the HF for the high-pitch condition compared to silence and low-pitch sounds, the difference was subtle. In essence, our observations align more with Nakajima et al. (2016b) (29), where music at a higher frequency exhibited the highest normalized HF power among all tested scenarios.
As for the heart brain coupling, we observed a notably diminished coherence for the high-pitch sound stimulus relative to both the silent and low-pitch stimuli, within the low-frequency band of heart rate variability and the EEG's Beta band. In our methodology, electrodes were chiefly positioned over the frontal and temporal scalp regions. The frontal lobes, corresponding to these placements, are instrumental in executive functions, decision-making, and emotional regulation (16, 33, 34), while temporal electrodes are crucial for auditory processing (18, 35). Our data highlight a region-specific involvement contingent on auditory stimuli, consistent with prior findings that sound processing can modulate heart rate, respiratory rate, and blood pressure (35), and influence brainwave patterns (36).
The reduced coherence between the Beta band and LF HRV in studied brain areas warrants further contemplation. Beta brainwaves, typically oscillating between 12–30 Hz, correlate with active, analytical cognition, predominant during alertness, concentrated attention, and problem-solving. Conversely, HRV's low-frequency band (0.04–0.15 Hz) signifies both sympathetic and parasympathetic nervous system activities, reflecting baroreflex dynamics (37). Hence, the observed coherence reduction during the high-pitch stimulus could indicate a discord between cognitive alertness (as evidenced by Beta EEG patterns) and autonomic regulation (as represented by HRV-LF) under this auditory scenario, leading to asynchronous fluctuations in both attentional and autonomic states when juxtaposed against the high-pitch and silent conditions.
Our observations might hint at a distinct neurocardiac response to auditory stimuli (38), possibly implicating the frontal and temporal brain sectors in deciphering varied sound frequencies. This concurs with studies elucidating the continuous bidirectional communication between the heart and brain (4). The salient coherence deviations, particularly in the beta range, emphasize the need to comprehend the nuanced relationship between sound frequencies and their bearing on heart-brain interplay, in harmony with research indicating variable modulation of this interaction by different auditory stimuli (36).
Although literature regarding synchronization between EEG and HRV in relation to sound stimuli is limited, a few studies have broached the profound heart-brain interplay during music exposure. Stuldreher et al. (2020) discerned that physiological synchrony across EEG, electrodermal activity, and heart rate can flag attention-critical temporal events (39). Bernardi et al., (2005) (5) observed that even brief musical or specific sound exposure could instigate cardiovascular alterations in the T4 temporal region, likely linked to neurological and behavioral transitions. In a similar vein, Blood and Zatorre (2001) (40) cataloged discernible cerebral blood flow changes when participants listened to personally chosen music. Building upon these findings, Bigliassi et al., (41) postulated interconnected frameworks governing modulation of specific heart rate components and distinct EEG patterns. They hypothesized that music might affect fatigue sensations via neural resynchronization, subsequently impacting exercise intensity sustainability. Importantly, the selection of sound frequency, and its subsequent effects on heart-brain coherence, has ramifications for auditory therapy, neurofeedback, and even binaural beats meditation. Such observations suggest that the coherence alterations are not simply serendipitous but might be leveraged for precise therapeutic or relaxation protocols.
Interestingly, EEG-HRV coupling has been indicated in epilepsy (3) and throughout sleep cycles (24). Piper et al. documented significant coherence between an HRV low-frequency sub-band (0.08–0.12 Hz) and the EEG δ envelope (1.5-4 Hz), apparent in both preictal and immediate postictal seizure phases (3). Jurysta et al., meanwhile, found coherence between normalized high-frequency HRV and all-band EEG power spectra (24). These findings intimate that specific sound stimuli might play roles in either mitigating or inducing epileptic seizures and in either enhancing or degrading sleep quality.
However, establishing a linear cause-effect triad amongst sound, cerebral activity, and heart rate is intricate (42). Asserting, for example, that heart rate invariably 'ascends' during silence or 'descends' upon sound exposure compared to a baseline remains premature. Various factors—including sound stimuli attributes (like frequency, volume), individual physiological sound reactions, and the auditory presentation context—might influence these mechanisms. A sound frequency might activate cerebral regions or neural circuits that subsequently sway the autonomic nervous system, thereby adjusting heart rate. Conversely, heart rate alterations post-sound might adjust brain activity, rendering the EEG alterations we detect as reactive. Another conceivable postulate posits that sounds might independently and directly act on both the brain and heart rate, without a unidirectional cause-effect dynamic. Alternatively, anticipatory factors, mindfulness, or even latent cognitive activities during silence might modulate heart rate.
Our research augments the burgeoning literature probing the intricate relationship between auditory stimuli and neurocardiac dynamics. By assiduously investigating HRV and EEG coherence under varied sound stimuli through wavelet coherence frequency analysis, we present a comprehensive view of auditory influences on neuro-cardiac intersections. Nonetheless, additional studies are imperative to clarify these dynamics and to validate or refute the postulates of our discussion and their potential real-world applications.
In our experiments, we deployed Bose QuietComfort 15 Acoustic Noise Cancelling Headphones for sound relay. Recognized for their superior noise-cancellation, it's paramount to note that such a feature might subtly alter the frequency response characteristics, potentially influencing the integrity of the sound stimuli. Future investigations should consider utilizing headphones with meticulously documented response profiles and contemplate the potential ramifications of active noise-canceling attributes on their results.
In summation, our use of wavelet coherence frequency analysis between HRV and EEG envelopes showcases the capability of different sound frequencies to markedly alter heart-brain synchronization. Fundamentally, our results emphasize that varied auditory stimuli can induce diverse modifications in this interplay. These revelations beckon additional research, especially given the possible therapeutic or adverse implications for a range of patients or scenarios. As the field of biomedical engineering continues to evolve and integrate more deeply with neuroscience and cardiology, studies like ours highlight the promise and complexities inherent in understanding and potentially leveraging the nuanced interactions of the human body's systems.