There is uncertainty regarding the physiological mechanisms responsible for activity within the very-low-frequency (VLF) band (Kleiger et al., 2005). The HRV frequency graphic was adapted from Dr. Richard Gevirtz.
The heart's intrinsic nervous system may contribute to the VLF rhythm (Shaffer, McCraty, & Zerr, 2014). The intrinsic ganglia images © 2012 Dr. Andrew Armour and the Institute of HeartMath.
VLF power may also be generated by physical activity (Bernardi et al., 1996), thermoregulatory, renin-angiotensin, and endothelial influences on the heart (Akselrod et al., 1981; Claydon & Krassioukov, 2008). There may be an alpha-adrenergic (norepinephrine-mediated) vascular tone contribution (Lehrer & Gevirtz, 2021; Reid, 1986). PNS activity may contribute to VLF power since parasympathetic blockade almost completely abolishes it (Taylor et al., 1998).
The Case Against A Sympathetic Contribution
SNS nerve bursts occur 1-2 times per second, each lasting 0.5-2 seconds (Macefield & Wallin, 1999). VLF cycles take 25 to 300 seconds per wave. At 0.67 seconds per burst, 37.5 bursts fit in the shortest VLF cycle and 450 in the longest. Therefore, SNS nerve bursts are 37 to 450 times faster than VLF cycles--far too rapid to generate the slow oscillations seen in the VLF band.
In addition, the SNS lacks a mechanism to generate regular, sustained oscillations that comprise VLF oscillations. SNS activity doesn’t rise and fall smoothly like a perfect wave—it reacts spontaneously to stressors, not in a predictable rhythm.
Summary
SNS bursts happen every 0.5–2 seconds.
SNS effects on heart rate last 5–10 seconds.
VLF cycles take 25–300 seconds.
SNS activity is too fast and too irregular to explain VLF power.
Instead, hormonal, thermoregulatory, and vascular mechanisms are the primary sources of VLF oscillations.
Neurotransmitter Kinetics
Sympathetic modulation of heart rate relies on norepinephrine (NE) release at cardiac synapses, which has a slow clearance rate (Esler et al., 1990). NE removal occurs via reuptake and enzymatic degradation, with a half-life of several seconds, limiting SNS-mediated oscillations to cycles shorter than those required to contribute meaningfully to VLF power.
Baroreflex Latency
The sympathetic baroreflex loop operates on a latency of several seconds, with a feedback time that exceeds the typical period of VLF oscillations (Julien, 2006). This suggests that sympathetic fluctuations can only influence the low-frequency (LF, 0.04–0.15 Hz) band, rather than the VLF range.
Cardiac Sympathetic Decay Time
SNS-mediated heart rate adjustments exhibit slow dynamics, with responses occurring on the order of 5–10 seconds or longer (Goldstein et al., 2011). These kinetics are too fast to generate VLF rhythms, which have periods of 25–300 seconds.
Experimental Evidence
SNS blockade studies have shown that beta-blockade (e.g., propranolol) does not significantly reduce VLF power, but it does reduce LF power, suggesting that SNS does not drive VLF oscillations (Taylor et al., 1998).
Denervation studies have revealed that VLF power persists after sympathetic denervation in humans and animals, reinforcing the idea that non-neural mechanisms (e.g., thermoregulation, renin-angiotensin system) are primary contributors (Akselrod et al., 1981; Montano et al., 2001).
Summary
There is uncertainty regarding the precise physiological mechanisms responsible for VLF band activity. Possible contributors include the heart’s intrinsic nervous system, physical activity, and hormonal, thermoregulatory, and endothelial influences. Some evidence suggests an alpha-adrenergic (vascular tone) contribution and a role for the parasympathetic nervous system (PNS), as PNS blockade nearly abolishes VLF power. However, the SNS is unlikely to generate VLF activity because its bursts are 37 to 450 times faster than VLF cycles, and it lacks a mechanism to generate sustained, rhythmic oscillations in this range. Instead, hormonal and vascular processes appear to be the dominant drivers.
Key Takeaways
SNS bursts occur every 0.5–2 seconds, much faster than VLF cycles.
SNS effects on heart rate last 5–10 seconds, too short to generate VLF power.
VLF cycles take 25–300 seconds, far slower than SNS fluctuations.
SNS activity is too fast and irregular to be a primary driver of VLF rhythms.
Hormonal, intrinsic cardiac nervous system, thermoregulatory, and vascular mechanisms are the most likely sources of VLF oscillations.
Glossary
alpha-adrenergic (norepinephrine-mediated) vascular tone contribution: the regulation of blood vessel constriction by norepinephrine acting on alpha-adrenergic receptors, potentially contributing to very-low-frequency oscillations.
denervation studies: research experiments that examine physiological changes after the removal or disruption of nerve supply, often used to assess autonomic contributions to heart rate variability.
endothelial influences: factors related to the endothelium, the inner lining of blood vessels, that regulate vascular tone and contribute to long-term cardiovascular oscillations.
intrinsic cardiac nervous system: a network of neurons within the heart that regulates local cardiac function independently of central autonomic control.
low-frequency band: a heart rate variability frequency range (0.04–0.15 Hz) associated with both sympathetic and parasympathetic nervous system influences on cardiac function.
norepinephrine (NE): a neurotransmitter released by sympathetic nerve endings that increases heart rate and vascular tone, playing a key role in autonomic regulation.
parasympathetic blockade: the pharmacological inhibition of parasympathetic nervous system activity, which significantly reduces very-low-frequency power in heart rate variability.
parasympathetic nervous system: the branch of the autonomic nervous system responsible for slowing heart rate and promoting rest-and-digest functions.
renin-angiotensin: a hormonal system that regulates blood pressure and fluid balance, contributing to long-term cardiovascular variability, including very-low-frequency oscillations.
SNS blockade studies: research that examines the effects of inhibiting sympathetic nervous system activity, often using beta-blockers, to assess its contribution to heart rate variability.
SNS burst: a short-lived increase in sympathetic nerve activity, occurring 1–2 times per second, which influences heart rate and vascular function.
sympathetic nervous system: the branch of the autonomic nervous system responsible for increasing heart rate, blood pressure, and metabolic activity in response to stress.
thermoregulation: the body's process of maintaining a stable internal temperature through physiological adjustments such as sweating, shivering, and blood vessel dilation or constriction.
very-low-frequency (VLF) band: a heart rate variability frequency range (0.0033–0.04 Hz) influenced by non-neural mechanisms such as hormonal, thermoregulatory, and vascular factors.
References
Akselrod et al. (1981): Akselrod, S., Gordon, D., Ubel, F. A., Shannon, D. C., Berger, A. C., & Cohen, R. J. (1981). Power spectrum analysis of heart rate fluctuation: A quantitative probe of beat-to-beat cardiovascular control. Science, 213(4504), 220–222. https://doi.org/10.1126/science.6166045​
Bernardi, L., Valle, F., Coco, M., Calciati, A., & Sleight, P. (1996). Physical activity influences heart rate variability and very-low-frequency components in Holter electrocardiograms. Cardiovascular Research, 32, 234-237. https://doi.org/10.1016/0008-6363(96)00081-8
Claydon, V. E., & Krassioukov, A. V. (2008). Clinical correlates of frequency analyses of cardiovascular control after spinal cord injury. American Journal of Physiology—Heart and Circulatory Physiology, 294(2), H668-H678. https://doi.org/10.1152/ajpheart.00869.2007
Esler, M., Jennings, G., Lambert, G., Meredith, I., Horne, M., & Eisenhofer, G. (1990). Overflow of catecholamine neurotransmitters to the circulation: Source, fate, and functions. Physiological Reviews, 70(4), 963–985. https://doi.org/10.1152/physrev.1990.70.4.963
Goldstein, D. S. (2011). Sympathetic neurocirculatory physiology in human subjects. Clinical Autonomic Research, 21(2), 69–79. https://doi.org/10.1007/s10286-010-0094-1
Julien, C. (2006). The enigma of Mayer waves: Facts and models. Cardiovascular Research, 70(1), 12–21. https://doi.org/10.1016/j.cardiores.2005.11.008​
Kleiger, R. E., Stein, P. K., & Bigger, J. T. (2005). Heart rate variability: Measurement and clinical utility. Annals of Noninvasive Electrocardiology, 10(1), 88–101. https://doi.org/10.1111/j.1542-474X.2005.10101.x
Lehrer, P. M., & Gevirtz, R. (2021). BCIA HRV Biofeedback didactic workshop. Association for Applied Psychophysiology and Biofeedback.
Macefield, V. G., & Wallin, B. G. (1999). Firing properties of single postganglionic sympathetic neurones in awake human subjects. Autonomic Neuroscience: Basic and Clinical, 81(1–2), 59–64. https://doi.org/10.1016/S1566-0702(00)00129-8
Montano, N., Gnecchi-Ruscone, T., Porta, A., Lombardi, F., Pagani, M., & Malliani, A. (1996). Power spectrum analysis of heart rate variability to assess the changes in sympathovagal balance during graded orthostatic tilt. Circulation, 94(10), 2646–2652. https://doi.org/10.1161/01.CIR.94.10.2646
Reid, J. (1986). Alpha-adrenergic receptors and blood pressure control. The American Journal of Cardiology, 57(9), 6E-12E . https://doi.org/10.1016/0002-9149(86)90716-2 Shaffer, F., McCraty, R., & Zerr, C. L. (2014). A healthy heart is not a metronome: An integrative review of the heart’s anatomy and heart rate variability. Frontiers in Psychology. doi:10.3389/fpsyg.2014.01040
Taylor, J. A., Carr, D. L., Myers, C. W., & Eckberg, D. L. (1998). Mechanisms underlying very-low-frequency RR-interval oscillations in humans. Circulation, 98(6), 547–555. https://doi.org/10.1161/01.CIR.98.6.547