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Special Considerations for Psychological Health

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INTRODUCTION

Depression and anxiety are forms of psychological distress, which are often comorbid with each other and with chronic disease. They are commonly encountered by exercise professionals working with healthy and special populations and can affect the capacity for exercise training and testing among healthy and special populations. Exercise professionals should be able to recognize symptoms of depression and anxiety and provide recommendations based on evidence relevant to each patient’s specific needs. This chapter provides a summary of special considerations for exercise testing and training among those with depression and/or anxiety briefly discussed.

Description, Prevalence, and Etiology

The concept of depression is closely related to loss and involves states of grief or bereavement that would naturally occur after, for example, the death of a loved one or after enduring a catastrophic natural disaster. Sustained clinical depression, however, exists in the absence of such loss. Depression presents cognitively (e.g., negative self-appraisals, a pessimistic view of the world, feelings of helplessness, and hopelessness about the future) and somatically (e.g., extreme fatigue, altered sleep, fluctuations in weight) and significantly affects the ability to function. Distinguishing factors between specific depressive disorders include issues of age of onset/timing, duration, and presumed etiology (2).

Anxiety is a negative affective state characterized by worry, apprehension, or tension in the presence of novel or aversive stimuli. Anxiety is closely related to fear and is a normal protective psychological and physiological response in anticipation of the need for fight-or-flight response. Individuals with disproportionate acute anxiety responses for the level of real or perceived threat as well as individuals who frequently experience anxious symptoms in the absence of any real or perceived threat may be suffering from an anxiety disorder (2). The underlying feature common to anxiety disorders is unwarranted sympathetic nervous system (SNS) activation in response to a perceived future threat. Either chronic or episodic SNS activation under circumstances that pose no immediate danger can be highly debilitating and lead to additional health problems (2).

Depressive and anxiety disorders identified in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) are listed in Table 22.1. The DSM-5 marks a reclassification such that (a) depressive disorders are distinct from bipolar disorders, whereas in the fourth edition, these classes of disorders formed one heterogeneous group of mood disorders, and (b) obsessive/compulsive disorder (OCD) and posttraumatic stress disorder (PTSD) are also reclassified as unique from each other and anxiety disorders, unlike in earlier editions (1,2). Interested readers are encouraged to refer to the DSM-5 for detailed descriptions of each disorder. Symptoms of depression and anxiety are listed in Table 22.2, although it should be noted that not everyone experiences the same symptoms, and it is unlikely that any one person would present with all symptoms listed. Depressive and anxiety disorders can only be diagnosed by a mental health care professional according to clinical criteria such as those described in the DSM-5 and are typically treated with pharmacotherapy, psychotherapy, or both.

Anxiety disorders are the most prevalent of mental disorders among adults (2) and are highly comorbid with depression (44). Anxiety disorders and depression are also frequently comorbid with other mental health problems, with about 85% and 76% of cases of generalized anxiety disorder (GAD) and major depressive disorder (MDD), respectively, being comorbid with at least one other mental disorder (44). The United States is ranked highest for 12-month prevalence of anxiety (18.2%) and depression (10%) (67,79), and U.S. citizens have an estimated lifetime risk/lifetime prevalence of 36% and 31.4%, respectively (43). Women are twice as likely to experience anxiety (2) or depression (67) than men. Anxiety and depression are often comorbid with chronic illness, including cardiovascular disease (CVD), hypertension, arthritis, obesity, diabetes, asthma, and chronic obstructive pulmonary disease (COPD). Anxiety and depression increase the risk of morbidity and mortality in clinical samples (15,81), and a recent meta-analysis estimates a 52% increase in the risk of incident CVD in samples reporting clinical or subclinical anxiety at baseline (7). Depression and anxiety represent major public health concerns that are drastically underdiagnosed, as those who do suffer from mental distress often wait many years before seeking treatment (84).

Although the causes of depression and anxiety are not fully understood, the prevalence of comorbidity between depression and anxiety suggests some common underlying etiology. Generally, neurobiological theories of anxiety and depression specify a role for autonomic dysfunction and often overlap. Central and peripheral evidence of autonomic dysfunction in animals and humans has provided a myriad of candidate mechanisms for anxiety and depression. Most early clinical work in depression and anxiety focused on the norepinephrine (NE) and the serotonin (5-hydroxytryptamine [5-HT]) systems, which modulate brain activity in areas involved in regulating mood and the response to stress. Pharmacological interventions continue to target an increase in the activity level of NE and 5-HT for the treatment of depressive and anxiety disorders. More recently, γ-aminobutyric acid (GABA) and glutamate, which both play a major role in neuroplasticity, have been implicated in the etiology of anxiety (8,62) and depression (40). Investigations focused on GABA were prompted by the observed actions of benzodiazepines, which bind to the GABA_A receptor, and have been successful in treating anxiety disorders. Glutamate mediates fear-conditioning and inhibitory-avoidance memory and has been supported in the etiology of anxiety (8). Neurotropic factors in the brain, specifically brain-derived neurotropic factor (BDNF), are important in proliferation, differentiation, and survival of neurons, as well as neurogenesis, synaptic plasticity, and cognitive function, and have been linked to anxiety and depression (56). A downregulation of BDNF expression in the brain could result in neuronal atrophy and cell loss in brain regions associated with depression and anxiety, such as the hippocampus and prefrontal cortex (21). This hypothesis is supported in animal (54) and human studies (14). A growing body of evidence emphasizes a role for inflammatory dysregulation in the etiology depression (57,59). However, the presence of inflammatory biomarkers is neither necessary nor sufficient for a diagnosis of depression (66), especially among those with CVD in whom this relationship is no longer significant (37). An exhaustive review of the evidence for mechanisms underlying depression and anxiety is beyond the scope of this chapter. Overall, several forms of treatment have been successful in relieving symptoms, but our understanding of underlying mechanisms remains incomplete. It is likely that depression and anxiety result from an interaction of genetic, social, environmental, psychological, cognitive, and physiological factors.

Preparticipation Health Screening, Medical History, and Physical Examination

Exercise professionals should assess risk for depression and anxiety among patients reporting symptoms. Brief screening tools for depression and anxiety used in primary care (e.g., the Brief Patient Health Questionnaire or the Patient Health Questionnaire Depression Scale, the Hospital Anxiety and Depression Scale) can be useful to the exercise professional in assessing patient symptoms (52). Those who indicate more than minimal symptoms of depression and/or anxiety as indicated by scores calculated using the validated scoring criteria for the chosen measure/screening tool or those whose symptoms persist for more than few weeks should be referred for a clinical evaluation by a mental health care professional (52) to rule out other causes for symptoms, check for comorbidities, and develop an appropriate treatment plan. Individuals with any level of symptoms can also be referred to several community resources that are able to provide diagnostic, treatment, or support services, such as family practice or internal medicine physicians, community mental health centers, outpatient clinics, social agencies, family service, self-help groups, or religious organizations. Exercise professionals should make themselves familiar with the resources in their area. As with all personal or sensitive issues, exercise professionals should be tactful, empathetic, and knowledgeable when discussing symptoms of depression and/or anxiety and referring patients to diagnostic screening, counseling, or other forms of assistance.

In the case that someone expresses such hopelessness or depression that suicide risk is suspected, immediate action is necessary. You may call their mental health professional, refer them to a local suicide or crisis center, call the National Hopeline Network (1-800-SUICIDE, available 24 h a day), or have them taken directly to a hospital emergency room. It is important that the person be accompanied to the treatment center and not left alone until professional help is available. Exercise professionals are encouraged to visit https://hopeline.com to learn more about the National Hopeline Network.

Exercise Testing Considerations

Individuals with depression and/or anxiety are less active than others (13), contributing to a lower level of physical conditioning. A recent meta-analysis reported a modest relationship between MDD and cardiorespiratory fitness (CRF) (effect size [ES] = −0.16, 95% confidence interval [CI] = [−0.21, −0.10]), such that greater symptom severity was associated with reduced CRF (64). Anxiety is also inversely related to CRF, and there is some evidence that this relationship is mediated by individual perceptions of anxiety symptoms in response to stress (82). Exercise professionals might expect an individual with symptoms of depression and/or anxiety to perform below average for their age, gender, and health status during aerobic exercise testing. Fortunately, the cumulative evidence supports the efficacy of exercise programs for improving CRF in clinically depressed samples (78), and there appear to be no contraindications to participation in regular exercise programs to improve CRF for those suffering from depression and/or anxiety in the absence of other contraindicated conditions.

Of particular relevance to CRF testing among samples with depression and anxiety is the autonomic modulation of the cardiovascular response to exercise. Autonomic balance modulates the cardiovascular response to stress. Measures of heart rate variability (HRV) are accepted as indexes for autonomic balance and regulated emotional responding (4) and provide indices of autonomic tone that have prognostic value (23). Higher levels of variability are related to cardiovascular fitness and reflect a higher level of physical conditioning and autonomic balance. Reduced HRV indicates an autonomic imbalance resulting from reduced parasympathetic drive, increased sympathetic drive to the heart, or both. HRV is related to a number of modifiable and nonmodifiable risk factors for CVD (80) and is thought to be an important factor in assessing cardiovascular risk (23). It could be expected that cardiovascular responses to exercise might be altered among individuals with depressive and/or anxiety disorders, as autonomic dysregulation is implicated in their etiology. Reduced HRVs are reported repeatedly in these clinical populations (25,42,50,51).

An imbalance in autonomic signaling to the heart, indicated by reduced HRV, may result in an elevated resting heart rate (HR), abnormal sinus tachycardia with postural changes (i.e., standing from a recumbent position), and abnormal or inadequate HR responses to exercise (e.g., chronotropic incompetence) (23). Reduced HRV is strongly supported as a robust predictor for the development of abnormal arrhythmias and cardiac mortality in patients with postmyocardial infarction (45). The relationship between reduced HRV among depressed and anxious samples and autonomic regulation of cardiovascular responses during exercise testing is understudied or underreported. Most investigations report on the effect of cardiovascular fitness on the autonomic response to psychological stress (39). Work is needed to test for significant differences in autonomic modulation of cardiovascular responses to graded maximal and submaximal exercise tests in samples with clinical depression and/or anxiety.

Exercise professionals should use caution when testing and training individuals taking psychoactive medication. Although limited, evidence suggests that there may be interactive effects of exercise and drugs commonly used to treat anxiety and depression. Exercise may have an additive or antagonistic effect on psychological symptoms when combined with pharmacotherapy (9). For example, one report suggests that selective serotonin reuptake inhibitors (SSRIs) may increase the risk of rhabdomyolysis after eccentric exercise (47). Of specific relevance to cardiorespiratory exercise testing is the occasional use of β-blockers, which inhibit the HR response to exercise, to minimize physical symptoms when an anxiety-provoking event is anticipated. Exercise professionals should ask their patients if they are currently taking any prescription medications that fall under the classifications listed in Box 22.1, as additional precautions may be necessary to ensure safety during training. Psychoactive medication does not act uniformly between individuals, and the dosage must often be adjusted for optimal therapeutic effect (11). Interactive effects between exercise and antidepressants and anxiolytics are not well understood. More work is necessary to provide clear guidelines for exercise prescription among populations taking psychoactive medications (9).

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