The central nervous system (CNS) mediates the distribution of resources to deal with internal and external demands. Perceptions and assumed threats to survival may promote a massive withdrawal of PNS tone and a reciprocal excitation of SNS tone. The trade-off between internal and external needs may be used in developing definitions of stress and homeostasis. In this model stress and homeostasis are interdependent. Homeostasis reflects the regulation of the internal organs and stress reflects the subjugation of internal needs in response to external needs. This is why measuring PNS tone may provide the indexing variable for defining stress and stress vulnerability.
Stress and stress vulnerability can therefore be defined in the absence of major shifts in SNS tone. In research assessing stress in neonates in healthy children, withdrawal of PNS tone to a stressor is paralleled by an increased expression of SNS tone. However, in severely compromised children they may not exhibit SNS reactivity and SNS tone might be low. These children generally have low PNS tone and very little PNS reactivity. Clinically, they would be described as chronically stressed and physiologically unstable. Thus PNS tone withdrawal in relation to SNS tone may define stress and high PNS tone prior to the stressor would represent low stress vulnerability, whilst low PNS tone would represent high stress vulnerability. Individuals therefore exhibiting problems of homeostasis will have the greatest stress vulnerability.
In many physiological systems efficient neural control is manifested as rhythmic physiological variability, and within normal parameters the greater the amplitude of oscillation, the healthier the individual. The greater the amplitude of organized rhythmic physiological variability, the greater the response potential or possible range of behavior. Individuals with attenuated physiological variability would then exhibit a lack of physiological and behavioral flexibility in response to environmental demands. This was the situation observed with severely ill infants.
Stimulation of other PNS afferents seems to give a reflex increase in cardiac vagal tone and therefore the latter seems to reflect the general PNS input to the viscera.
The most readily available measure of PNS activity is derived from heart rate pattern in response to breathing i.e. respiratory sinus arrhythmia. The heart rate increases with inspiration and decreases during expiration under the control of efferent parasympathetic impulses along the vagus nerve. Heart rate patterns, like behavioral processes, are dependent on the status of the nervous system and the quality of neural feedback. Stress results in a disorganization of the rhythmic structure of both behavior and autonomic state. Thus, measures of cardiac vagal tone provide a window into the central processes necessary for organized behavior. If vagal tone is a sensitive index of the functional status of the nervous system, then we would predict that individuals with greater vagal tone would exhibit a greater range of competent behaviors.
The pattern of heart rate reflects the continuous feedback between the CNS and the peripheral autonomic receptors. The primary source of HRV is mediated by phasic increases and decreases in neural efferent output via the vagus nerve to the heart. The greater the range of the phasic increases and decreases, the “healthier” the individual. An attenuation in the range of homeostatic function is paralleled by a reduction in vagal tone.
HRV is a marker of the efficiency of neural feedback mechanisms and may index health status or the individual’s capacity to organize physiological resources to respond appropriately. Thus, the better the “organised” physiological variability, the greater the range of behavior. States characterized by attenuated vagal influences should be paralleled by reduced behavioral flexibility in response to environmental demands. So, not only the basal level of vagal tone (measurable during sleep) is important but also the vagal responsivity during sensory and cognitive challenge. Individuals with greater vagal responsivity as exemplified in larger heart rate acceleration also exhibited fewer signs of distress.
Heart Rate Variability as a Marker of ANS Activities
HRV is based on the time difference between each heartbeat (R-wave) (as above), i.e. the beat-to-beat variability. Each R-wave represents a contraction of the heart and corresponds to the pulse. The beat-to-beat variability is affected by autonomic nervous system activity.
Normally the heartbeat should vary from beat to beat under direct control of both the SNS and PNS (the SNS speeds and the PNS slows the heart rate). HRV is the result of the interaction between these 2 systems. It is accepted by scientists that this interaction at the heart is a reflection of ANS balance or imbalance in the body in general. For example, SNS dominance at the heart is therefore an indication of a general sympathetic dominance in the autonomic nervous system. This would indicate a system under chronic stress and a vulnerability to further stresses. An overactive ANS is an indicator of a system under current stress, with a balanced ANS being important to effective stress coping.
More recent research highlights how our personality and thought processes influence health and also HRV. Sustained positive effective states lead to a clear and definable mode of physiological function that appears to facilitate the body’s natural regenerative processes. Physiological coherence – a sine-wave-like pattern in the heart rhythm, increased heart/brain synchronisation and entrainment between diverse physiological systems occurs after positive thought focus, and positive emotions can produce extended periods of this physiological entrainment.
A healthy physiological system has the following characteristics:
• Efficient neural control
• Rhythmic physiological variability within normal limits
• Greater response-potential to challenge
• Greater range of response behavior
Attenuated physiological variability is associated with a lack of psychological and behavioral flexibility in response to environmental demand. A reduction in HRV is therefore not only an indication of a lack of physiological variability, but also in its broad sense a reflection of reduced psychological and behavioral flexibility.
Although our understanding of the meaning of HRV is far from complete, it seems to be a marker of both dynamic and cumulative load. As a dynamic marker of load, HRV appears to be sensitive and responsive to acute stress. Under laboratory conditions, mental load (including making complex decisions, and public speech tasks) have been shown to lower HRV. As a marker of cumulative wear and tear, HRV has also been shown to decline with the aging process. Although resting heart rate does not change significantly with advancing age, there is a decline in HRV, which has been attributed to a decrease in efferent vagal tone and reduced beta-adrenergic responsiveness. By contrast, regular physical activity (which slows down the aging process) has been shown to raise HRV, presumably by increasing vagal tone.
In short, HRV appears to be a marker of two processes, relevant to the conceptualization of allostatic load: (1) frequent activation (short term dips in HRV in response to acute stress); and (b) inadequate response (long-term vagal withdrawal, resulting in the over-activity of the counter-regulatory system –in this case, the sympathetic control of cardiac rhythm).
Several studies have now suggested a link between negative emotions (such as anxiety and hostility) and reduced HRV. Cross-sectional association between anxiety and reduced HRV (as assessed by two time-domain measures). Lower HRV in individuals who were “highly anxious” according to the Minnesota Multiphasic Personality Inventory.