Temperature is the most widely trained function. Our understanding of the mechanisms underlying hand-warming and hand-cooling, while still incomplete, has radically changed due to landmark studies by researchers like Robert Freedman. These findings underscore the complexity of the cardiovascular system.
This unit covers Descriptions of most commonly employed biofeedback modalities: Skin temperature, EKG and heart rate (III-A 1-2).
Students completing this unit will be able to discuss:
Two patterns, coupling and fractionation, describe changes observed when monitoring subjects. In coupling, responses change together (heart rate up, blood pressure up). In fractionation, responses change independently (heart rate down, blood pressure up).
Coupling and fractionation reflect the multiple, independent processes that jointly produce these physiological measures. Healthy systems operate chaotically to adapt to rapidly changing demands. Whether responses couple or fractionate during a specific observation period depends on the complicated interplay of subject, task, and environmental variables.
Arteries carry blood away from the heart. Arteries are divided into elastic and muscular arteries, and arterioles.
Elastic arteries are the large arteries like the aorta (shown below) that distribute blood from the heart to muscular arteries. Medium-sized muscular arteries (like the brachial artery) distribute blood throughout the body. Arterioles are almost microscopic (8-50 microns in diameter) that deliver blood to capillaries and anastomoses. Arterioles may control up to 50% of peripheral resistance through their narrow diameter, contractility, and massive surface area that follows a fractal pattern.
Caption: This image illustrates a close and sectioned view of an arteriole. An arteriole is a blood vessel that extends and branches out from an artery and leads to capillaries. Arterioles have thick muscular walls and are the primary site of vascular resistance.
The control of arteriole diameter, which is crucial to regulation of blood pressure and hand temperature, is highly complex. Neural, hormonal, and local controls cooperate to regulate blood flow through arterioles. These control mechanisms play varying roles across our body's organs (Widmaier, Raff, & Strang, 2004).
All arteries have three layers or tunics which surround a hollow lumen or center. The tunica interna or innermost layer responds to chemical messengers released in the bloodstream like epinephrine and norepinephrine. This is a site of chemically-controlled vasodilation (increase in lumen diameter and blood flow) in digits like the fingers.
The tunica media or middle layer is composed of smooth muscle and elastic fibers and is controlled by sympathetic constrictor fibers (C-fibers). This is a site of neurally-controlled vasoconstriction (decrease in lumen diameter and blood flow) in the digits.
Finally, the tunica externa or external layer is composed of a connective tissue sheath.
Veins are blood vessels that route blood from tissues back to the heart. Veins contain the same three layers found in arteries. These layers are thinner in veins due to lower pressure. Smooth muscle allows venules to actively adjust diameter. The venous system is shown below.
Caption: This image illustrates the full male body in anatomical position, with the venous flow of the blood highlighted. Along with the full system of major veins shown, the lungs, heart, and liver are shown with their accompanying circulation via the pulmonary veins, coronary veins, and hepatic vessels.
A venule is a small vein (less than 2 mm in diameter) that collects blood from capillaries and delivers it to a vein. The low return pressure in these vessels requires valves that prevent backward blood flow.
Venules play an important role in controlling return blood flow to the heart due to narrow diameter, contractility, and extensive surface area.
Caption: This image shows a representation of a sectioned vein, and is especially useful alongside our image of an elastic artery. While walls are thick and strong, the vein's walls are not nearly as thick as those of the artery, due to the significantly less pressure that exists in the venous system. A valve can be seen inside the vein, a feature that prevents backflow in veins as their contents are pushed along.
Capillaries are 7-9 microns in diameter and found near almost all cells. Capillaries may directly connect arterioles with venules or they may form extensive networks for rapid exchange of a large volume of substances (nutrients and waste products).
A capillary generally consists of a single layer of endothelium and basement membrane. Change in capillary diameter is passive due to the absence of a smooth muscle layer. In true capillaries that extend from arterioles or metarterioles, a precapillary sphincter controls incoming blood flow. Capillaries exchange nutrients and metabolic end-products between blood vessels and cells. This exchange is aided by 1-micron-thick walls, extensive branching, and massive surface area. Capillary distribution is densest where tissue activity is highest.
Caption: This image shows a close and sectioned view of a capillary, the smallest blood vessel in the human body. Capillaries serve as the junction between arteries and veins, and are characterized by their extremely thin walls, consisting of only a single layer of endothelium cells. Such thin walls function to exchange molecules such as oxygen, water, and carbon dioxide between tissues and blood.
Anastomoses are junctions of two or more vessels that supply the same region. Arteriovenous anastomoses (AV shunts) bypass capillaries and directly connect arterioles to venules. These vessels contain the three layers seen in both arterioles and venules. Smooth muscle allows anastomoses to actively adjust diameter.
Dilation (enlargement of the lumen) of anastomoses shunts blood from the epidermis to the interior (cooling the skin). This mechanism is critical in regulating body heat and is implicated in both Raynaud’s disease and Raynaud’s phenomenon.
Blood pressure is the force exerted by blood as it presses against blood vessels. In clinical practice, blood pressure refers to pressure in arteries. The force that stretches arteries is called cardiac output. Cardiac output is calculated by multiplying stroke volume times heart rate. Stroke volume is the amount of blood ejected by the left ventricle. Heart rate is the number of contractions per minute. Cardiac output is about 5.25 liters/min (70 ml x 75 beats/min) in a normal, resting adult.
Caption: This image illustrates the full male body in the anatomical position with the arterial flow of blood highlighted. The image reveals arterial circulation to the hands, feet, and face, and major branching from the ascending and descending aorta. Also included for anatomical reference are representations of the heart, lungs, and the pulmonary arteries.
Blood leaving the left ventricle meets resistance or friction due to blood viscosity (thickness), blood vessel length, and blood vessel radius. Blood pressure equals cardiac output times resistance. Self-regulation skills that lower blood pressure reduce cardiac output, resistance, or both.
Clinicians measure both systolic and diastolic blood pressures. Systolic blood pressure is the force exerted by blood on arterial walls during contraction of the left ventricle (called systole). This is the upper value when blood pressure is reported and is about 120 mm Hg in young, adult males (under resting conditions). Diastolic blood pressure is the force applied against arteries during ventricular relaxation (called diastole). This is the lower value and is about 80 mm Hg (under resting conditions).
The heart is a hollow, muscular organ, about the size of a closed fist. The heart contains four chambers (two ventricles and two atria) that function as two pumps.
The heart ejects oxygenated blood from the left ventricle to the arterial system. Returning deoxygenated blood enters the right atrium and is pumped by the right ventricle via the pulmonary artery to the lungs. There, wastes are removed and oxygen is replaced. Oxygenated blood returns to the left atrium by the pulmonary vein.
The cardiac cycle consists of systole (heart muscle contraction), and diastole (relaxation). During systole, blood pressure peaks as contraction by the left ventricular ejects blood from the heart. Systolic blood pressure is measured here. During diastole, blood pressure is lowest as the left ventricle relaxes. Diastolic blood pressure is measured at this time.
The sinoatrial (SA) and atrioventricular (AV) nodes are the two internal pacemakers that are primarily responsible for the heart rhythm. The electrocardiogram (ECG) records the action of this electrical conduction system.
In a healthy heart, the SA node initiates each cardiac cycle through spontaneous depolarization of its autorhythmic fibers. The SA node’s firing of about 100 action potentials per minute usually prevents other parts of the conduction system and myocardium (heart muscle) from generating competing potentials. The SA node fires an impulse that travels through the atria (upper heart chambers) to the AV node in about 0.03 s and causes the AV node to fire. The P wave of the ECG is produced as contractile fibers in the atria depolarize and culminates in contraction of the atria (atrial systole).
The AV node can replace an injured or diseased SA node as pacemaker and spontaneously depolarizes 40-60 times per minute. The signal rapidly spreads through the atrioventricular (AV) bundle reaching the top of the septum. These fibers descend down both sides of the septum as the right and left bundle branches and conduct the action potential over the ventricles about 0.2 s after the appearance of the P wave. Conduction myofibers, which extend from the bundle branches into the myocardium, depolarize contractile fibers in the ventricles (lower chambers), resulting in the QRS complex. The ventricles contract (ventricular systole) soon after the emergence of the QRS complex and this continues through the S-T segment. The repolarization of ventricular contractile fibers generates the T wave about 0.4 s following the P wave. The ventricles relax (ventricular diastole) 0.6 s after the P wave begins.
While the SA node generates the fundamental cardiac rhythm, autonomic motor neurons and circulating hormones influence the interbeat interval and force of myocardial contraction. Sympathetic cardiac accelerator nerves (arising from the medulla’s cardiovascular center) increase the rate of spontaneous depolarization in SA and AV nodes, and increase stroke volume by strengthening the contractility of the atria and ventricles. The parasympathetic vagus (X) nerves (also arising from the medulla’s cardiovascular center) decrease the rate of spontaneous depolarization in SA and AV nodes, and slow the heart rate, Heart rate increases often reflect reduced vagal inhibition.
There is a dynamic balance between sympathetic and parasympathetic influences over the heart. Parasympathetic control predominates at rest, resulting in an average heart rate of 75 beats per minute that is significantly slower than the SA node’s intrinsic rate of 100 beats per minute. The parasympathetic branch can slow the heart to 20 or 30 beats per minute, or briefly stop it.
Heart rate is also influenced by circulating hormones and ions. Epinephrine, norepinephrine, and thyroid hormones increase heart rate and contractibility. The cations (positive ions) K+, Ca2+, and Na+ significantly affect cardiac function. While elevated blood levels of K+ and Na+ decrease heart rate and contractibility, elevated Ca2+ levels have the opposite effect (Tortora & Derrickson, 2006).
Heart rate (also called stroke rate) is the number of heartbeats per minute. This value is 75 beats/min for a resting young, adult male. Resting rates slower than 60 beats/minute (bradycardia) and faster than 100 beats/min (tachycardia) may indicate cardiovascular disorder. Athletes show lower heart rates during exercise and rest while maintaining healthy cardiac output due to increased stroke volume. Abnormal or irregular rhythms (like heart block, independent contraction by the atria and ventricles) are called arrhythmias or dysrhythmias.
Analysis of heart rates in healthy individuals reveals a chaotic pattern. Heart rate values are not constant, but instead are unpredictable, due to multiple hormonal and neural control systems. Successive values read from a cardiotachometer, which measures the frequency of ventricular contraction beat-to-beat, might be 65, 78, 72, 86. This illustrates the variability of a healthy heart that can rapidly adapt to changing workloads. Variability is severely reduced in hearts damaged by cardiovascular disease. Below is a BioGraph ® Infiniti heart rate variability (HRV) display.
Heart rate variability (HRV) consists of beat-to-beat changes in heart rate and includes changes in instantaneous heart rates and the R-R intervals between consecutive heartbeats (Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology, 1996).
Low heart rate variability is a marker for cardiovascular disorders, including hypertension, especially with left ventricular hypertrophy; sudden cardiac death, especially due to arrhythmia following myocardial infarction; ventricular arrhythmia; and ischemic heart disease.
Reduced heart rate variability is also seen in disorders with autonomic dysregulation, including: anxiety and depressive disorders, asthma, without acute symptoms, and sudden infant death syndrome.
HRV amplitude decreases with age, increases with adult aerobic capacity, and increases during cardiac rehabilitation programs with a relaxation component. Lehrer (2007) believes that reduced HRV is evidence of vulnerability to physical and psychological stressors, and disease.
HR Max – HR Min is the difference between the highest and lowest heart rates during each respiratory cycle. The range for 20-year-olds is 5-10 beats-per-minute while it is 3-5 beats-per-minute for those over 50. Physically-active individuals show wider ranges than those who are sedentary. HRV biofeedback can increase the range to 50 beats-per-minute during a training session. An important training objective is to increase HR Max – HR Min (Moss, 2004).
Below is a BioGraph ® Infiniti heart rate variability (HRV) display.
The interbeat interval (IBI) is measured as the time interval between the peaks of successive R-waves (initial upward deflection in the QRS complex). The interbeat interval is also called the NN (normal to normal) interval.
SDNN is the standard deviation of the interbeat interval measured in milliseconds. SDNN values predict both morbidity and mortality. Patients with SDNN values below 50 ms are classified as unhealthy, 50-100 ms have compromised health, and above 100 ms are healthy. Movement to a higher category increases a patient’s probability of survival. For example, a shift from low to moderate SDNN can decrease mortality 400% (Kleiger et al., 1987). Increasing SDNN is an important training goal of HRV biofeedback (Moss, 2004).
Below is a BioGraph ® Infiniti heart rate variability (HRV) display.
The pNN50 is the percentage of adjacent N-to-N intervals that differ from each other by more than 50 milliseconds. This may be a more reliable index than the SDNN for the brief samples used in biofeedback. At least a 2-min sample is required to calculate an accurate pNN50.
The respiratory cycle functions as an oscillator and generates heart rate variability via the nucleus ambiguous system. Inhalation inhibits vagal nerve slowing of the heart (increasing heart rate), while exhalation restores vagal slowing (decreasing heart rate). This respiration-driven heart rhythm is termed respiratory sinus arrhythmia (RSA) and contributes to the high frequency (HF) component of heart rate variability described in the next section (Gevirtz & Lehrer, 2003).
Heart rate variability is produced by the interaction of multiple regulatory mechanisms that operate on different time scales (Moss, 2004).Spectral analysis separates heart rate variability into its component rhythms that operate within different frequency bands. The Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (1996) has divided heart rate oscillations into the following bands:
The ultra low frequency (ULF) band (below 0.0033 Hz) represents very slow-acting biological processes and is too gradual to train using conventional biofeedback.
The very low frequency (VLF) band (0.005-0.05 Hz) may represent sympathetic activation. Worry and rumination increase the power of this waveform.
The low frequency (LF) band (0.05-0.15 Hz) may represent the influence of both the parasympathetic and sympathetic branches and blood pressure regulation via baroreceptors or blood pressure receptors (Lehrer, 2007). Meditation and slow breathing, like the “tanden breathing” practiced by Rinzai Zen monks, increase the power of this waveform.
The high frequency (HF) or respiratory band (0.15-.40 Hz) represents the inhibition and activation of the vagus nerves by breathing at normal rates (Moss, 2004).
Below is a BioGraph ® Infiniti heart rate variability (HRV) display.
Evgeny Vaschillo (Lehrer, Vaschillo, & Vaschillo, 2004) proposes that each client has a unique resonant frequency around 0.1 Hz within the low frequency (LF) band that optimizes health. Clients can maximize heart rate variability at this resonant frequency by creating a “relaxed mental state, with a positive emotional tone, breathing diaphragmatically at a rate of about 5-7 breaths per minute” (Moss, 2004).
Each of these components is critical. Respiration rate is important because breathing is an oscillator that drives the heart rhythm. A respiration rate of 6 breaths per minute drives the heart rate at 0.1 Hz (6/60 = .1). Positive emotional tone is important because the sympathetic nervous system activation caused by negative emotions can increase power in the very low frequency (VLF) band at the expense of low frequency (LF) power.
When individuals breathe at their personal resonant frequency between 4.5 to 7 breaths per minute, heart rate and blood pressure oscillations are 180 degrees out of phase. Inhaling increases heart rate and decreases blood pressure, which causes the baroreceptor system to further increase heart rate. Exhaling decreases heart rate and increases blood pressure, which causes the baroreceptor system to further decrease heart rate (Lehrer, 2007).
Slow diaphragmatic breathing coupled with a positive emotional tone maximizes heart rate variability in the low frequency (LF) range because it superimposes the effects of three oscillators: slow breathing, parasympathetic and sympathetic activity, and blood pressure regulation. This, in turn, increases total heart rate variability measured by indices like SDNN, pNN50, and HR Max - Min.
Moss has conceptualized HRV biofeedback “as a process of training an active balancing between the sympathetic and parasympathetic branches’ effects on the heart rhythm” (Shaffer & Moss, 2006).
Gevirtz (2005) proposes that each individual has separate heart rate (0.75-11 Hz or 4.5-6.6 times per minute) and blood pressure (0.02-.05 Hz or 1-3 times per minute) resonant frequencies that depend on the baroreflex (blood pressure regulation reflex). 0.1 Hz biofeedback stimulates the baroreflex and maximizes both the baroreflex and heart rate variability.
Ejection of blood from the left ventricle during systole produces a pulse wave. Pulse wave velocity is the rate of pulse wave movement through the arteries. This is measured by placing pressure transducers (motion sensors) at two points along the arterial system (like the brachial and radial arteries of the same arm). The interval required for the pulse wave to move between these points is called transit time (TT). Pulse wave velocity is used as an indirect measure of blood pressure change. Researchers have reported correlations with average and systolic (but not diastolic) blood pressure changes during stress tests.
Skin temperature recorded from the fingers or toes is mainly determined by blood flow through the small arterioles of the skin. Temperature increases are produced by arteriole vasodilation (increased lumen size), while decreases result from arteriole vasoconstriction (decreased lumen size). The classic and incorrect view is that a single mechanism, the sympathetic vasoconstrictor fiber, produces both hand-warming and hand-cooling. According to this model, slow firing rates dilate arterioles producing hand-warming, while faster rates constrict producing cooling. Recent studies have shown that this model is incomplete.
There are two main classes of adrenergic receptors, alpha and beta. There are two alpha-adrenergic receptors (α1 and α2) and three beta-adrenergic receptors (β1, β2, and β3). All adrenergic receptors bind to a G-protein. Activation of α1 alpha-adrenergic receptors by epinephrine or norepinephrine mediates the vasoconstriction produced by sympathetic C-fibers, while activation of β2 beta-adrenergic receptors is responsible for vasodilation (Fox, 2006).
The current view is that hand-cooling and hand-warming are produced by different mechanisms. These blood flow changes seem to involve neural, hormonal, and local processes.
Hand-cooling is mainly controlled by vasoconstricting sympathetic nerves that act on alpha-adrenergic receptors. Circulating hormones and local factors also reduce arteriolar diameter (Widmaier, Raff, & Strang, 2004).
Hand-warming is primarily due to circulating hormones and local vasodilators. There are no vasodilating nerves in the fingers (although they exist in the forearm). Freedman (1991) has shown that hand-warming is produced by a non-neural beta-adrenergic agent.
After sympathetic vasoconstrictor nerves are severed during a sympathectomy, Raynaud’s patients still may experience painful vasospasms due to a continuing local fault in arteriovenous anastomoses. Dilation of anastomoses in response to cold (or associated stimuli) shunts blood from the skin to the body’s core. Also, sympathectomies do not prevent hormone release into the general circulation or volume transmission of agents like norepinephrine.
Temperature response to stimuli is slower than changes in blood volume pulse (.5-2 s compared to 20-30 s) and shows greater inertia.
volume pulse (BVP) is the phasic change in blood volume with each heartbeat. It
is the vertical distance between the minimum value (trough) of one pulse
wave and the maximum value (peak) of the next measured using a photoplethysmograph (PPG) (sensor shown below).
The large-scale changes seen in blood volume pulse in hands that are not cold make this modality very helpful when patients reach a plateau in hand-warming. Shifting to blood volume pulse will allow the patient to receive greater resolution feedback.
The shape of the blood volume pulse waveform can indicate loss of arterial elasticity and decreased pulse transit time that is associated with aging and hypertension (Izzo & Shykoff, 2001). Peper, Harvey, Lin, Tylova, and Moss (2007) compared BVP waveforms and blood pressure values for two parents and their teenage daughter in the recordings below.
Caption: Comparison of finger BVP recording of parents (62-year-old father and 52- year-old mother) and child (17-year-old daughter). The mother has borderline hypertension. The absence of the dicrotic notch in the borderline-hypertensive (top) tracing suggests a stiffening of the arteries indicating increased blood pressure.
BVP amplitude can provide valuable information about a client's cognitive and emotional responses as shown in the recording below from Peper, Harvey, Lin, Tylova, and Moss (2007).
Caption: This figure shows psychophysiological responses during a standardized stress protocol. The participant’s responsiveness to internal and external physical and emotional stressors is vividly depicted in the variations of BVP amplitude. The pattern portrays decreases in amplitude in BVP signal in response to prompts such as sighs and claps that triggered sympathetic activation. In this participant, eye closure during the protocol evoked an unanticipated and large decrease in the BVP amplitude compared to any of the physical or imagined stress conditions. This unanticipated decrease in BVP may be interpreted as a kind of anticipatory anxiety.
Below is a BioGraph ® Infiniti blood volume pulse (BVP) display.
The advantage of temperature, when a patient is successful, is that it measures blood flow in absolute units (blood volume pulse is in relative units) and is a better index of relaxation since it changes more gradually as shown in the BioGraph ® Infiniti temperature display below.
Gender differences have been consistently found in hand temperature. Men show finger temperatures of 87.8-91.4 degrees F, while women range from 84.2-87.8 degrees F (in a 74 degree room).
Clinicians usually consider finger temperatures above 90 degrees F (in a 74 degree F room) to be relatively relaxed. Temperatures exceeding 90 degrees do not mean that all major systems are relaxed. For example, a patient could present with warm hands and strongly contracted upper trapezius muscles.
A current hypothesis is that there is a linear relationship between blood vessel diameter and finger temperature up to 95 degrees F and that above this threshold, arteriole dilation increases nonlinearly. If this hypothesis were confirmed, it would justify training patients to warm their hands above 95 degrees to produce maximum clinical effects.
Hand temperature is affected by social interactions. Taub’s research demonstrated a person effect. An impersonal experimenter was less successful in teaching temperature self-regulation (2/22 successes) than a warm, friendly experimenter (20/21 successes).
Environmental temperature (temperatures below 68 degrees F may produce downward drift) and metabolic activity affect blood flow to the digits. Finally, respiration rates below 6 breaths per minute increase percentage CO2 (pCO2), which dilates blood vessels.
Now that you have completed this module, describe how this module has changed your understanding of hand-warming. Also, explain when blood volume pulse feedback could be more useful than temperature biofeedback.
Akselrod, S., Gordon, D., Ubel, F. A., et al. (1981). Power spectrum analysis of heart rate fluctuation: A quantitative probe of beat-to-beat cardiovascular control. Science, 213, 220-222.
Andreassi, J. L. (2000). Psychophysiology: Human behavior and physiological response. Hillsdale, NJ: Lawrence Erlbaum and Associates, Inc.
Cacioppo, J. T., & Tassinary, L. G. (Eds.). (1990). Principles of psychophysiology. New York: Cambridge University Press.
Carney, R. M., Blumenthal, J. A., Stein, P. K., Watkins, L., Catellier, D., Berkman, L. F., Czajkowski, S. M., O’Connor, C., Stone, P. H., & Freedland, K. E. (2001). Depression, heart rate variability, and acute myocardial infarction. Circulation, 104(17), 2024-2028.
Del Pozo, J. M., & Gevirtz, R. N. (2003). Complementary and alternative care for heart disease. Biofeedback, 31(3), 16-17.
Del Pozo, J. M., Gevirtz, R. N., Scher, B., & Guarneria, E. (2004). Biofeedback treatment increases heart rate variability in patients with known coronary artery disease. American Heart Journal, 147(3), G1-G6.
Fox, S. I. (2006). Human physiology (9th ed.). New York: McGraw-Hill.
Gevirtz, R. N. (2000). Resonant frequency training to restore homeostasis for treatment of psychophysiological disorders. Biofeedback, 27, 7-9.
Gevirtz, R. N. (2003). The promise of HRV biofeedback: Some preliminary results and speculations. Biofeedback, 31(3), 18-19.
Gevirtz, R. N. (2005). Heart rate variability biofeedback in clinical practice. AAPB Fall workshop.
Gevirtz, R. N., & Lehrer, P. (2003). Resonant frequency heart rate biofeedback. In M. S. Schwartz, & F. Andrasik (Eds.). (2003). Biofeedback: A practitioner's guide (3rd ed.). New York: The Guilford Press.
Giardino, N. D., Chan, L., & Borson, S. (2004). Combined heart rate variability and pulse oximetry biofeedback for chronic obstructive pulmonary disease. Applied Psychophysiology and Biofeedback, 29(2), 121-133.
Herbs, D., Gevirtz, R. N., & Jacobs, D. (1994). The effect of heart rate pattern biofeedback for the treatment of essential hypertension. Biofeedback and Self-regulation, 19(3), 281 Abstract.
Ironson, G., Taylor, C. B., Boltwood, M., Bartzokis, T., Dennis, C., Chesney, M., Spitzer, S., & Segall, G. M. (1992). Effects of anger on left ventricular ejection fraction in coronary artery disease. American Journal of Cardiology, 70(3), 281-285.
Izzo, J. L., & Shykoff, B. E. (2001). Arterial stiffness: Clinical relevance, measurement, and treatment. Review Cardiovascular Medicine, 2(1), 29-34, 37-40.
Kleiger, R. E., Miller, J. P., Bigger, J. T., et al., and the Multicenter Post-Infarction Research Group. (1987). Decreased heart rate variability and its association with increased mortality after acute myocardial infarction. American Journal of Cardiology, 59, 256-262.
Lacey, J. I. (1967). Somatic response patterning and stress: Some revisions of activation theory. In M. H. Appley & R. Trumbell (Eds.), Psychological stress: Issues in research (pp 14-42). New York: Appleton-Century-Crofts.
Lacey, J. I., & Lacey, B. C. (1964). Cardiac deceleration and simple visual reaction in a fixed foreperiod experiment. Paper presented at the meeting of the Society for Psychophysiological Research, Washington, D.C.
Lehrer, P. M. (2007). Biofeedback training to increase heart rate variability. In P. M. Lehrer, R. M. Woolfolk, & W. E. Sime (Eds.). Principles and practice of stress management (3rd ed.). New York: The Guilford Press.
Lehrer, P. M., Smetankin, A., & Potapova, T. (2000a). Respiratory sinus
arrhythmia biofeedback therapy for asthma: A report of 20 unmedicated
pediatric cases using the Smetankin method. Applied Psychophysiology
and Biofeedback, 25, 193-200.
Lehrer, P. M., Vaschillo, E. V., & Vaschillo, B. (2004). Heartbeat synchronizes with respiratory rhythm only under specific circumstances. Chest, 126(4), 1385-1386.
Lehrer, P., Vaschillo, E., Vaschillo, B., Lu, S-E, Scardella, A., Siddique, M, & Habib, R. (2004). Biofeedback treatment for asthma. Chest, 126, 352-361.
MacLean, B. (2004). The heart and the breath of love. Biofeedback, 32(4), 21-25.
McCraty, R., Atkinson, M., Tiller, W. A. (1995). The effects of emotion on short term heart rate variability using power spectrum analysis. American Journal of Cardiology, 76.
Moss, D. (2004). Heart rate variability (HRV) biofeedback. Psychophysiology Today, 1, 4-11.
Papillo, J. F., & Shapiro, D. (1990). The cardiovascular system. In J. T. Cacioppo & L. G. Tassinary (Eds.) Principles of psychophysiology: Physical, social, and inferential elements (pp. 456 - 512). Cambridge: Cambridge University Press.
Peper, E., Harvey, R., Lin, I., Tylova, H., & Moss, D. (2007). Is there more to blood volume pulse than heart rate variability, respiratory sinus arrhythmia, and cardio-respiratory synchrony? Biofeedback, 35(2), 54-61.
Shaffer, F., & Moss, D. (2006). Biofeedback. In Y. Chun-Su, E. J. Bieber, & B. Bauer (Eds.). Textbook of complementary and alternative medicine (2nd ed.). Abingdon, Oxfordshire, UK: Informa Healthcare.
Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology (1996). Heart rate variability: Standards of measurement, physiological interpretation, and clinical use. Circulation, 93, 1043-1065.
Tortora, G. J., & Derrickson, B. H. (2006). Principles of anatomy and physiology (11th ed.). New York: John Wiley & Sons, Inc.
Widmaier, E. P., Raff, H., & Strang, K. T. (2004). Human physiology: The mechanisms of body function (9th ed.). Boston: McGraw-Hill.