How Motivation Affects Cardiovascular Response: Mechanisms and Applications

Motivation in psychocardiological rehabilitation

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Because of diseases generally display a multifactorial aetiology and symptoms require to be assumed as manifestations of a complex interplay of several factors, the bio-psycho-social approach of illness theorized by Engel remains in the background. Health and illness are not seen as opposite concepts or distinct entities but extremes of a continuum on which individuals constantly flux depending on the quality of their daily-life experiences, influenced by biological e.

Due to this complexity, as well as stated the crucial role of both personal dispositions and intentions in modifying personal attitudes and behaviors, the relevance of setting realistic goal, implementing patient-centered treatments and developing motivational enhancement techniques, is highlighted. Overall, this book represents a well-collated collection of research outcomes, successfully demonstrating the importance of both psychological factors and motivation in the treatment of patients suffering from CV diseases Manzoni et al.

In fact, as extensively discussed through the pages of this volume, the individual's level of initial motivation, reflecting the maximum energy spent by a person for goals attainment, represent one the main predictor of success in preventing and managing CV risk factors Manzoni et al.

However, the text is so densely written than chapters seem to be resources for references rather than flowing text. Despite recent technological changes have made information readily available on the Internet, because of potentially appealing scholars and practitioners from a wide range of areas, together with its acceptable price, this book still constitute a significant source of outcomes and data.

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Journal List Front Psychol v. Published online Nov 6. Author information Article notes Copyright and License information Disclaimer. This article was submitted to Psychology for Clinical Settings, a section of the journal Frontiers in Psychology. Received Aug 20; Accepted Oct The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

No use, distribution or reproduction is permitted which does not comply with these terms. No medicine without psychology: Vulnerable personality and Takotsubo cardiomyopathy consequent to emotional stressful events: Clinical psychology and cardiovascular disease: Health 7 , — Post-traumatic stress disorder, emotional processing and inappropriate implantable cardioverter-defibrillator shocks: Emotion-focused therapy and dietary counseling for obese patients with binge eating disorder: Type D personality is associated with the development of stress cardiomyopathy following emotional triggers.

Depression and blunted reactivity Another possible corollary of reactivity is depression and high levels of depressive symptomatology. However, depression has been related to a variety of physiological adaptations that suggest altered autonomic function. For example, enhancement of cardiac sympathetic activity relative to vagal tone has been reported in those with depression and subclinical depressive symptoms Carney, et al. Thus, the speculation that such autonomic dysregulation in depression may also be manifest as exaggerated cardiovascular reactions to stress is at least superficially appealing.

Unfortunately, none of the aggregate effects were statistically significant. The studies included in the meta-analysis generally tested small samples and few of them adjusted for potential confounding variables such as demographic factors and medication status. Higher depressive symptom scores and possible depression were associated with lower, not higher, cardiovascular reactivity.

The association was still evident following adjustment for socio- demographic, anthropometric, task performance, and medicaton status variables. A contemporary study found a similar direction of relationship. Higher depressive symptomatology was associated with lower, not higher, cardiovascular reactivity to a public speaking stressor York, et al. Again, the relationship survived control for a reasonably comprehensive collection of covariates.

More recently, we have been able to examine the prospective association between cardiovascular reactions to acute stress and symptoms of depression in the West of Scotland Study. Cardiovascular reactions to acute psychological stress were negatively associated with subsequent depressive symptomatology; the lower the reactivity the higher the depression scores five years later. What might be the peripheral mechanisms underlying the link between cardiovascular reactivity and symptoms of depression? One possibility is altered sympathetic nervous system function.

However, the prevailing wisdom is that depression and symptoms of depression are associated with increased, not decreased, sympathetic nervous system activity, as indexed by a shift to enhanced cardiac sympathetic activity relative to vagal tone Carney, et al. However, this tells us only about the tonic state. It does not indicate how the system responds to challenge.

Another possible explanation for the observed association between heart rate reactivity and symptoms of depression is a common genetic pathway. For example, polymorphisms of the serotonin transporter gene 5HTTLPR , which plays a key role in determining the magnitude and duration of both the central and peripheral actions of serotonin, would appear to be implicated in emotional regulation and physiological reactivity.

Those with long alleles have also been found to exhibit higher blood pressure and heart rate reactions to a laboratory stress task Williams, et al. Further, men who are homozygous for long allele have been found to score lower on measures of anxiety and depression Lesch, et al.

However, a recent meta- analysis reported that the 5HTTLPR genotype did not appear to be associated with major depression, particularly in association with high life events Risch, et al. Nevertheless, this avenue seems worthy of further investigation. Both cross-sectional and prospective analyses were conducted.

Motivation in psychocardiological rehabilitation

Contrary to expectations based on the indicative rather than definitive outcomes of the few previous small scale studies, we found clear evidence that low cardiac reactivity was associated with a greater body mass index, more abdominal adiposity and greater likelihood of being obese. In addition, in prospective analyses low cardiac reactivity was associated with an increased risk of being obese five years later, even taking into account obesity status at the earlier time point. These outcomes withstood adjustment for socio-demographic factors, stress task performance, smoking, and medication status.

For example, after ingestion of a meal, there is a postprandial sympathetic nervous system response as reflected by higher plasma norepinephrine concentrations and an increased low- to high-frequency ratio in the heart rate variability spectrum Tentolouris, et al. However, this effect has been observed to be much smaller in obese as opposed to lean individuals Tentolouris, et al. Further, changes in heart rate and muscle sympathetic nerve stimulation after the infusion of antihypertensive and antihypotensive drugs were found to be significantly smaller in the obese than the non-obese Grassi, et al.

In sum, the finding that it is low cardiac reactivity that characterises obesity would appear to be credible. Indeed, low reactivity, possibly by reflecting generally blunted sympathetic nervous system response to acute challenge, may even be a risk marker for developing obesity. Might blunted reactivity be a marker for motivational dysregulation? Whereas the cardiovascular health consequences of excessive cardiovascular reactivity constitute a coherent whole, it is difficult to see what unites these apparently diverse corollaries of blunted reactivity. Leaving aside self-reported health, as its determinants have yet to be subjected to concerted study, depression and obesity are both characterised, to an extent, by behavioural expressions of disordered motivation.

Here we tentatively explore the possibility that blunted reactivity may be a marker of such motivational dysregulation.

Later in this chapter we review the evidence that common addictions are also associated with blunted reactivity. In such instances, the case that blunted reactivity reflects motivational dysregulation is almost certainly easier to make. For the moment, though, let us focus our attention on obesity and depression. Family and twin studies indicate a genetic predisposition toward obesity. In a study of over Danish adopted children, weight was found to be associated with the weight of their biological but not their adoptive parents Stunkard, et al.

In humans the precise gene candidates have proved elusive, as have the upstream processes that are being influenced by genetics. However, one postulated candidate process is a dysfunctional biological response to food. The authors postulate that this striatal hypo-reponsiveness to food might elicit compensatory overeating. For example, in a recent study depressed patients and controls were exposed to a number of anticipatory conditions, including anticipation of reward money and anticipation of punishment cold pressor.

Again the striatum, which has a central role in processing reward, would appear to be implicated. In an imaging study, there was less activation of the striatum to positive, but not negative, stimuli in depressed patients relative to healthy controls Epstein, et al. In addition, among the depressed group, those with the most blunted striatal response also reported less interest and pleasure in work and hobbies as well as less engagement in such activities.

Although highly speculative, it is possible that blunted cardiovascular reactions to psychological challenge in the obese and those with high levels of depressive symptomatology are a peripheral analogue of this hypo-responsiveness of the central reward system. Stress reactivity and addiction Whiereas it may seem intuitive that excessive physiological reactions to psychological stress might have relevance for the onset or progression of cardiovascular disease and not beyond the bounds of reason that low reactivity might have consequences for other health outcomes, it is perhaps less immediately obvious that stress reactivity might relate to addictive behaviour Lovallo, , However, if our speculations on motivational dysregulation have any merit, then blunted reactivity might conceivably signal risk for addiction.

We have argued elsewhere that our characteristic physiological response tendencies may have origins at three levels in our system Lovallo, Here we will comment only on the highest level of the system because of its special relevance for emotions and behaviours. The brain structures in question, their anatomical interconnections, and their patterns of response to motivating circumstances are currently the subject of much research, and these have been described in some detail Damasio, et al.

To review quite briefly, these structures involve the extended amygdala system including the striatum , the prefrontal cortex, and feedback from the body to these areas. The extended amygdala is now understood to be the core structure in forming emotional responses to danger as well as things we may wish to obtain Rolls, Persons in whom the amygdala has been damaged or lost through disease are emotionally unresponsive and have a tendency to fail to avoid danger Adolphs, et al. Still other evidence implicates two prefrontal areas as being critically involved in this process of appraising events and the forming of responses to coping with these events; these are the dorsolateral prefrontal cortex, an area shown to be critical for the operation of working memory Ungerleider, , and the anterior cingulate gyrus and related sections of the cortex that bring together information concerning the approach-avoidance value of events with formulations of response strategies Barch, et al.

George Koob has described extensive alteration of neurochemical communication among these structures and among these areas as experimental animals are exposed to increasing amounts of self-administered drugs of abuse Koob, , and recent work shows actual reconfiguration of neural connectivity in these areas following alcohol exposure Xie, et al.

How Motivation Affects Cardiovascular Response : Mechanisms and Applications

In short, these structures and their patterns of interaction will affect not only our physiology, but also our feelings and behaviours. If we are willing to accept this perspective, then it becomes highly plausible that physiological reactivity might not only signal risk for ill health but also may serve as a window into less obvious conditions, such as the addictions.

Although we strongly suspect that brain areas associated with differences between individuals in physiological reactivity to stress are the same ones involved in a range of other disorders, addictions among them, this contention needs strong confirmation through the use of neuroimaging. Research is beginning to emerge of physiological response tendencies in light of resting patterns and reactivity-related activity of the limbic system and prefrontal cortex Gianaros, et al. Smoking, alcoholism, and blunted reactivity At a peripheral level, there is emerging evidence that low or blunted cardiovascular and cortisol reactivity is characteristic of those with substance dependencies and may indeed be a general marker for risk of addiction Lovallo, It is unlikely that these effects reflect temporary abstinence during stress testing and its effects on stress task engagement Roy, et al.

Blunted cardiovascular reactivity has been observed in female smokers regardless of whether they were wearing a nicotine replacement patch or not Girdler, et al. Thus, low reactivity not only characterises those addicted to smoking; it may also be a risk marker of some prognostic significance Lovallo, , In addition, relatively low reactivity would appear to be a characteristic of non-alcoholics with a family history of alcoholism. The data suggest that low reactivity may not only be a characteristic of those with a dependency, it may actually pre-date the addiction and signal risk of future addiction.

Accordingly, in blunted reactivity we may have a marker of motivational dysregulation linked to inherited risk of a wide range of addictions Lovallo, Conclusions The prevailing evidence testifies that large magnitude cardiovascular reactions to acute psychological stress place individuals at risk for the upward drift of resting blood pressure and hypertension, as well as atherosclerosis and increased left ventricular mass.

However, it is low, not high, reactivity that appears to be associated with depression, predicts the development of obesity, and is implicated in poor self-reported health. Finally, research also indicates that blunted cardiovascular and cortisol reactivity is characteristic of individuals with an alcohol or tobacco dependence and, indeed, may predict risk of addiction and the likelihood of relapse following abstinence.

It would appear that, depending on the outcomes in question, departures from the norm in either direction may pose problems, suggesting that in both instances the system is operating in a biased state, whether at the level of the higher central nervous system, at the level of the hypothalamus and brainstem, or at the level of the periphery. One of the challenges is to understand the neural substrates of both hypo- and hyper-reactivity to acute stress. The data conform to an inverted-U model where high and low reactivity can be considered maladaptive depending on the outcome in question.

The inverted-U has a substantial pedigree in psychophysiology.

References

Accordingly, we may simply be putting a few new clothes on a much loved but rather old doll. It is important to appreciate at this stage, however, that a model which conceives of continuous positive associations between reactivity and some outcomes and continuous negative associations between reactivity and other outcomes can also fit the results.

We depict these two models in Figures 2 and 3. Time will tell which best serves any revision of the reactivity hypothesis. Although we strongly suspect that brain areas associated with physiological reactivity differences between individuals are the same ones involved in a range of other disorders including addictions, this contention needs strong confirmation through the use of neuroimaging and prospective studies. Nevertheless, at this stage, it would appear that blunted, as well as excessive, reactivity may be a maladaptive response.

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