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date: 21 September 2018

Physical Activity, Physical Fitness, and Anxiety

Summary and Keywords

A historically popular research topic in exercise psychology has been the examination of the exercise-anxiety relationship, with an ever-growing literature exploring the link between exercise and anxiety. In addition to its potential for preventing anxiety and anxiety disorders, an increasing number of studies have examined the utility of physical activity and exercise interventions for the treatment of elevated anxiety and clinical anxiety disorders. A National Institute of Mental Health “state-of-the-art workshop” in 1984 was the first significant call put forth that understanding the anxiety-reducing potential of exercise was important and required further investigation. Since the publication of the evidence that came out of that NIMH workshop in Morgan and Goldston’s 1987 book, “Exercise and Mental Health,” a great deal more has been learned yet key aspects of the relationship between exercise and anxiety remain unknown. There is a great deal of work that remains to make good on the “potential efficacy of exercise.”

Keywords: exercise, anxiolysis, anxiety sensitivity, state anxiety, trait anxiety, panic disorder, tranquilizer effect, biological challenge, dose response

I cannot believe that our muscular vigor will ever be a superfluity. Even if the day ever dawns in which it will not be needed for fighting the old heavy battles against Nature, it will still always be needed to furnish the background of sanity, serenity, and cheerfulness to life, to give moral elasticity to our disposition, to round off the wiry edge of our fretfulness, and make us good-humored and easy of approach . . . And that blessed internal peace and confidence, that acquiescentia in seipso, as Spinoza used to call it, that wells up from every part of the body of a muscularly well-trained human being, and soaks the indwelling soul of him with satisfaction is, quite apart from every consideration of its mechanical utility, an element of spiritual hygiene of supreme significance.

—William James, The Gospel of Relaxation

Perhaps due to the increasingly stressful nature of life in modern society, anxiety and anxiety disorders have become a prevalent mental health concern. The anxiety disorders resulting from such increasing stresses are the most prevalent of the mental illnesses, causing significant distress and impairment of function (Hollander & Simeon, 2003). In the 2015 iteration of the American Psychological Association’s ongoing Stress In America survey, “Paying With Our Health” (American Psychological Association, 2015), many respondents said their stress levels either remained the same (53%) or increased (29%) from 2014 to 2015, with concerns about money and work being the most common sources of stress. Techniques for dealing with stress included watching television or movies, surfing the Internet, listening to music, or exercising (although those reporting high levels of stress about money were more likely to engage in non-exercise techniques to manage their stress). Symptoms associated with stress include irritability, nervousness, lack of interest, fatigue, feeling overwhelmed, and sadness/depression. Women report higher levels of stress than men (5.2 versus 4.5 on a 10-point scale in 2014), and the discrepancy is growing (5.5 versus 5.3 in 2010). Left unresolved, such stress can become chronic and ultimately result in subclinical or clinical levels of mental disorders such as anxiety.

There is mounting evidence that chronic stress, the resultant elevated anxiety, and ultimately anxiety disorders have more than just psychological consequences. For example, Goodwin, Davidson, and Keyes (2009) showed that likelihood of any anxiety disorder was related to incidence of cardiovascular disease (CVD) in a large (N=43,093), non-institutionalized adult sample. Roy-Byrne et al. (2008) noted the importance of understanding how anxiety disorders can influence various medical conditions in terms of the impact on self-care, increased risk and complications of illness, and mortality. There is also mounting evidence that increasing physical activity and exercise not only impacts physical illness but also mental disorders such as anxiety (PAGAC, 2008). This chapter will present what is known about the effectiveness of physical activity/exercise, as well as the impact of physical fitness on anxiety disorders and anxiety more generally.

Defining Anxiety

Encountering stressors can lead to anxiety, which is a normal human emotion. Anxiety is a noticeable, psychophysiological emotional state that is most often characterized by feelings of apprehension, fear or expectations of fear, worry, nervousness, and physical sensations arising from activation of the autonomic nervous system (e.g., increased muscle tension, elevated heart rate, sweating). It has been referred to as an “essential” emotion (Gaudlitz, von Lindenberger, & Strohle, 2012) because responding to dangerous or threatening stressors with anxiety can help ensure survival. This anxiety response can be adaptive if it leads to effective handling of a threat, but it can also be maladaptive. When someone is dealing with chronic stress as a result of multiple stressors (e.g., financial concerns, work pressures and deadlines, relationship issues, lack of sleep, health concerns, juggling a busy schedule, poor dietary habits), he or she can begin to feel a need to be “on guard” all the time. In such instances, the person is experiencing clinical manifestations of anxiety, a feeling that goes beyond “normal” feelings of worry and fear. In the Surgeon General’s Report on Mental Health (U.S. DHHS, 1999), anxiety is defined as the “pathological counterpart of normal fear, manifest by disturbances of mood, as well as of thinking, behavior, and physiological activity” (p. 233). Thus, this normal human emotion becomes pathological (i.e., clinical anxiety or an anxiety disorder) when it results in changes in thoughts and actions, occurs even in the absence of an eliciting event, and when the response is disproportionate and unmanageable (American Psychiatric Association, 2000, p. 299A–C). Because of ever-increasing stressors occurring in life in modern society, anxiety and the various anxiety disorders are increasingly prevalent problems worldwide (Remes, Brayne, van der Linde, & Lafortune, 2016).


Anxiety is a psychophysiological phenomenon (i.e., it manifests with both psychological and physiological symptoms). One (and often several) of the following are used to characterize anxiety: (a) unpleasant feelings (e.g., sense of uncertainty, indecision, sense of dread, feeling burdened or overwhelmed, tenseness); (b) physical symptoms from elevated autonomic nervous system activation (e.g., increased muscle tension, elevated heart rate [HR], or autonomic hyperactivity); (c) altered cognitive processes (e.g., compulsions, persistent obsessions, or unsubstantiated uncertainties related to objects, activities, or situations); (d) altered behavior (e.g., avoidance of situations, restlessness); and (e) vigilance (constantly being on alert for danger or a problem). “Normal” anxiety becomes pathological or clinical anxiety when the number and magnitude of the aforementioned symptoms increases and the degree of suffering and subsequent dysfunction disrupts normal activities. Using established criteria such as those found in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; American Psychiatric Association, 2013) or the International Classification of Diseases (ICD-10; WHO, 1992; or several others), a diagnosis of clinical anxiety is rendered when an anxiety response occurs in the absence of an eliciting event (with the exception of a specific phobia), is disproportionate and is unmanageable (American Psychiatric Association, 2000). A list of the characteristics, along with signs and symptoms, of the major anxiety disorders (i.e., panic disorder, generalized anxiety disorder, posttraumatic stress disorder,1 agoraphobia, social anxiety disorder, and obsessive-compulsive disorder) appears in Table 1.

Table 1. Characteristics, Signs, and Symptoms of Main Anxiety Disorders

PANIC DISORDER/AGORAPHOBIA: Intense fear and discomfort associated with symptoms (mental and physical) including: Sweating, trembling, shortness of breath, chest pain, nausea; fear of dying, or loss of control of emotions

  • Severe, persistent anxiety when in situations where escape may be difficult, or complete avoidance of particular environments (e.g., crowded areas, alone outside of home, travel in bus or plane)

  • Urge to escape or run away, often resulting in seeking urgent help (e.g., emergency room)

  • Often accompanied by major depressive disorder

  • Twice as common in females as males

  • Agoraphobia often evolves after onset of panic disorder

SPECIFIC PHOBIAS: Noticeable and persistent fear, often excessive and disproportionate, invoked by the expected or actual presence of an object or situation (e.g., a certain animal, flying, heights)

  • general categories include animal type (e.g., snakes), natural environment type (e.g., lightning), situational type (e.g., tight spaces), blood/injection/injury type (e.g., needles)

  • accompanied by a variety of physical symptoms (e.g., heart palpitations, sweating, trembling, shortness of breath or a smothering feeling, chest pain/discomfort, nausea/abdominal discomfort) and psychological symptoms (e.g., a feeling of choking, sense of things being unreal, fear of losing control, fear of dying)

  • more than twice as common in females than males

SOCIAL ANXIETY DISORDER (SOCIAL PHOBIA): Marked, persistent anxiety in social situations (e.g., public speaking) where possibility of embarrassment or ridicule is crucial factor

  • preoccupation with concern that others will notice the anxiety symptoms (e.g., trembling, sweating, halting/rapid speech)

  • accompanied by anticipatory anxiety days or weeks prior to feared event

  • more common in females than males

OBSESSIVE-COMPULSIVE DISORDER: Obsessions (e.g., recurrent thoughts or images that are perceived as inappropriate or forbidden), elicit anxiety and distress

  • individual perceives loss of control, thus acts on impulses or thoughts

  • compulsions, including behaviors or thoughts, reduce anxiety associated with obsessions

  • include overt ritual-like behavior (e.g., hand washing) and mental acts (e.g., counting, praying)

  • take long periods of time (up to hours) to complete

  • disorder has fluctuating course, including periods of increased symptoms, usually linked with life stressors

  • equally common in females and males


  • defined by worry lasting more than six months, along with multiple symptoms (e.g., muscle tension, poor concentration, insomnia, irritability)

  • anxiety and worry not attributable to other conditions (e.g., panic disorder, phobias)

  • disorder has fluctuating course, including periods of increased symptoms, usually linked with life stressors

  • twice as common in females than males


  • anxiety and behavioral disturbances following exposure to extreme trauma (e.g., combat, physical assault) that persist for more than one month

  • dissociation—symptom involving perceived detachment from emotional state or body—is critical feature

  • symptoms also include generalized anxiety, hyperarousal, avoidance of situations that trigger memories of trauma, recurrent thoughts

  • occurs in about 9 percent of those exposed to extreme trauma

Note. Adapted from U.S. Department of Health and Human Services (1999, pp. 233–237). Rockville, MD: U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health; American Psychiatric Association (2000, 2013).


In addition to distinctions between “normal” and clinical anxiety, there are both state and trait forms of anxiety that are important for understanding the measurement of anxiety. State anxiety is a noticeable but transient emotional state characterized by feelings of worry, tension, uneasiness, and apprehension along with elevated autonomic nervous system activity (e.g., increased HR, sweaty palms, increased respiration rate, increased muscle tension). Measuring state anxiety thus involves an assessment of how the individual is feeling “right now, at this moment.” As an example, a self-report measure of state anxiety would assess the extent to which an individual feels calm, relaxed, jittery, or frightened.

Trait anxiety, on the other hand, is a more general tendency or predisposition to respond across many situations with apprehension, worry, and nervousness. For example, someone high in trait anxiety would self-report a feeling of increased restlessness, lack of confidence, difficulty in making decisions, and a feeling of inadequacy regardless of the situation. He or she may also have relatively high levels of resting muscle tension. Thus, measuring trait anxiety involves an assessment of how the individual “generally feels.” A self-report measure of trait anxiety would assess the extent to which an individual feels satisfied, feels like a failure, has disturbing thoughts, wishes he or she could be as happy as others, and perseverates on disappointments. Measures of trait anxiety are conceptually analogous to the personality construct of neuroticism/emotionality (Watson & Clark, 1984). Numerous studies have used such measures of neuroticism or emotionality to assess trait anxiety. Because trait anxiety reflects a general predisposition, it conceptually makes sense to assess trait anxiety before and after chronic exercise programs (i.e., exercise programs that last several weeks or months); studies examining acute exercise effects (i.e., single bouts of exercise) would more appropriately use a measure of state anxiety, as the goal is to assess the ongoing experience of anxiety.

Psychological Measures

Because anxiety can be manifested both psychologically and physiologically, it can be assessed in several ways. Exercise research has most commonly assessed anxiety using self-report inventories or questionnaires. Although there are many different questionnaires to choose from, those most commonly used include the Spielberger State–Trait Anxiety Inventory (STAI; Spielberger, 1983), the Tension subscale of the Profile of Mood States (POMS; McNair, Droppleman, & Lorr, 1981), the Tension subscale of the Activation Deactivation Adjective Check List (AD ACL; Thayer, 1986), and the Anxiety Sensitivity Index (ASI; Peterson & Reiss, 1993). These instruments have been fine for use in non-clinical samples, but other measures that have been used for either diagnosis of anxiety disorders or for assessing symptoms of clinical anxiety include the Beck Anxiety Inventory (BAI; Beck, Epstein, Brown, & Steer, 1988), Generalized Anxiety Disorder 7 (GAD-7; Spitzer, Kroenke, Williams, & Löwe, 2006), Hamilton Anxiety Rating Scale (HARS; Hamilton, 1959), Hospital Anxiety & Depression Scale (HADS; Zigmond & Snaith, 1983), and the Patient Health Questionnaire 4 (PHQ-4; Kroenke, Spitzer, Williams, & Löwe, 2009). These measures are often used in conjunction with clinician diagnosis from diagnostic criteria (DSM, ICD-10) or through structured clinical interviews. Even if a measure may not be valid for diagnostic purposes, it could be used to track changes as a function of some intervention.

Physiological Measures

Because anxiety occurs with physical symptoms, measures of physiological activation or arousal (e.g., increased HR, muscle tension, or sweaty palms) have been used as indices of anxiety. Using a single physiological measure implicitly assumes that such physiological indices are a direct reflection of anxiety, which although a questionable assumption, has been the approach taken in numerous investigations. It would be more appropriate to use a battery of physiological measures to account for individual differences in responding (Stern, Ray, & Quigley, 2001), but this is rarely done.

Increased activity in skeletal muscle, indicative of somatic tension, is often a salient feature of elevated anxiety (e.g., wobbliness or being unsteady, shaky or jittery, trembling hands) and can be measured via electromyography (EMG). Anxiety can also be manifested in the cardiovascular system (e.g., heart pounding), measured through changes in blood pressure or HR (or numerous other measures of cardiovascular activation) and in the electrodermal system (e.g., hot/cold sweats, face flushed), measured via skin responses (e.g., galvanic skin response, palmar sweating, skin temperature). Due to the close connection to the stress response, anxiety responses are likely to have neurochemical components (e.g., increases in catecholamines, cortisol); such measures could also be useful. Although not often studied in the human exercise–anxiety literature, an ever-expanding literature continues to advance our understanding of the neurochemistry of anxiety and how exercise influences such pathways (e.g., Gaudlitz et al., 2012; Gaudlitz et al., 2013; Greenwood & Fleshner, 2013).


It was noted in the Surgeon General’s Report (USDHHS, 1999) that anxiety disorders are the most prevalent of the mental disorders (Regier et al., 1990); this remains the case (Bandelow & Michaelis, 2015; Steel et al., 2014). Anxiety disorders, in order of decreasing lifetime population prevalence, include social phobia (13%–16%), specific phobias (10%), posttraumatic stress disorder (PTSD; 7%–9%), generalized anxiety disorder (GAD; 5%–7%), agoraphobia (6%), panic disorder (PD; 2%–4%), and obsessive-compulsive disorder (OCD; 2%–3%) (Hollander & Simeon, 2003). The anxiety disorders contribute significantly to the disease and disability burden of nations worldwide (Tully & Cosh, 2013; Watkins et al., 2013).

Two nationwide probability surveys published in the mid-1990s further highlight the prevalence of such disabling mental conditions. In the National Comorbidity Survey (Kessler et al., 1994), the one-year prevalence rate (i.e., percentage of individuals diagnosed with a disorder within the previous 12 months) for any mental disorder was 23.4%. This included a one-year prevalence rate of 18.7% for any anxiety disorder. The National Comorbidity Survey Replication study put the one-year prevalence rate for any anxiety disorder at 18.1% (Kessler et al., 2005). The Epidemiological Catchment Area Study (Regier et al., 1993) estimated a 19.5% one-year prevalence rate for any mental disorder, which included 13.1% for any anxiety disorder. A best estimate of the one-year prevalence rates from these studies has been calculated at 16.4% for any anxiety disorder (USDHHS, 1999), but various epidemiological surveys show a range of 8.4%–21.3% (Bandelow & Michaelis, 2015). Of all cases of anxiety disorder, roughly 22.8% were deemed severe, 33.7% were moderate, and 43.5% were mild (Kessler et al., 2005). Although Kessler et al. (2005) caution against interpreting temporal trends, anxiety disorders continue to be the most prevalent of the mental disorders (Bandelow & Michaelis, 2015; Steel et al., 2014).

The cost of such prevalent anxiety disorders is quite significant, beyond the human suffering that cannot be measured. This includes both direct medical costs (e.g., counseling, hospitalization, emergency room treatment) and indirect workplace costs (DuPont et al., 1996; Greenberg et al., 1999; Marciniak et al., 2005), the greatest of which derive from lost productivity (i.e., presenteeism) rather than absenteeism. Anxiety is also a predisposing factor in drug and substance abuse (Smith & Book, 2008), which further adds to the cost of the disorder.


Clinical anxiety is often treated with medication (i.e., pharmacotherapy) and “talk therapy” (i.e., psychotherapy). Both of these options are often expensive and time consuming, albeit readily available and generally effective. But those who really need the help rarely get it (Herring et al., 2014). Pharmacotherapies used to treat anxiety include benzodiazepines (e.g., diazepam), which inhibit neurotransmitter systems and have sedative effects, and antidepressants (e.g., clomipramine, a tricyclic antidepressant, or specific serotonin reuptake inhibitors such as sertraline and fluoxetine). Although primarily used in the treatment of depressive disorders, antidepressants are also used to help treat anxiety because they have anti-anxiety properties. While they can provide an effective treatment, medication usually requires extended periods of use and are not effective for everyone; in addition, they often come with side effects (e.g., withdrawal symptoms when medication is stopped, sexual dysfunction, weight gain, disturbed sleep; see Lader, 2015).

Psychotherapy has long been considered a standard treatment for anxiety as well as depression. There are numerous types of psychotherapy (e.g., cognitive behavioral therapy [CBT], psychodynamic therapy, exposure therapy), but CBT is apparently best suited for dealing with anxiety disorders. The idea is to treat the individual by helping them to better understand their own mental illness (USDHHS, 2016). Such therapies attempt to help in determining cause-effect relationships among the person’s thoughts, feelings, and behaviors and then in developing strategies and techniques for reducing anxiety symptoms and dysfunctional behaviors (USDHHS, 1999). CBT involves some combination of relaxation training, thought restructuring, psychological education, and changing behavioral responses to anxiety-provoking situations (Gaudlitz et al., 2012). Therapy that is conducted within a finite time period (i.e., time-limited therapy) is often a hallmark in such treatments. While these psychotherapies are designed to help the affected person cope with the anxiety and its symptoms, they also have their shortcomings. Treatment can take a long time (e.g., weeks, months, years), and there is greater financial cost associated with it. The effectiveness and safety of such talk therapies have even been questioned. Ekkekakis (2013) summarizes the growing skepticism surrounding psychotherapy as an effective form of treatment, particularly in comparison to placebo treatments. Such dissatisfaction may explain, in part, the steady (~3% from 1987 to 2007; Ekkekakis, 2013) and even declining rate of treatment (Mojtabai & Olfson, 2008).

For quite some time, physical activity (e.g., exercise) has been examined as a potential tool in both the prevention and the treatment of anxiety (Martinsen & Raglin, 2007; PAGAC, 2008). The National Institute of Mental Health felt strongly enough about the need for examination of the anxiolytic (anxiety-reducing) effects of exercise that a “state-of-the-art workshop” was convened by the Office of Prevention at the NIMH in 1984 with a published summary of that evidence (Morgan & Goldston, 1987). In a follow-up volume, Morgan (1997) stated “it is important to quantify the psychotherapeutic effect of physical activity” (p. xiii). Although there exists a school of thought that some of the anxiety disorders (e.g., phobias) would not be affected by exercise (because they are linked to specific situations or objects; Dunn, Trivedi, & O’Neal, 2001), this is not a uniformly accepted viewpoint (Johnsgard, 1989, 2004). Prior to presenting the major findings of research examining the influence of physical activity on both “normal” anxiety and clinical anxiety, it is useful to define what constitutes physical activity and physical fitness.

Defining Physical Activity and Physical Fitness

Although often viewed as similar, physical activity and physical fitness are related but very different (see Caspersen, Powell, & Christenson, 1985). Physical activity is often defined as “bodily movements that cause increases in physical exertion beyond that which occurs during normal activities of daily living” (Lox, Martin, Ginis, & Petruzzello, 2014, p. 4). Exercise, which will be referred to often here, is physical activity done in leisure time, most often in an attempt to maintain or increase some aspect of physical fitness.

Physical fitness is the capacity to perform muscular work, referring “primarily to components related to health, the most important being cardiorespiratory endurance, body composition, flexibility, and strength and endurance of certain skeletal muscles” (Blair, Kohl, & Powell, 1987, p. 53). Unfortunately, when the term “physical fitness” is used, it is often in reference to only the cardiorespiratory (aerobic) portion of overall fitness. As noted, physical activity and exercise are related to physical fitness, but they are not strongly related. Someone could have a high degree of some aspect of fitness (e.g., cardiorespiratory endurance or VO2max) and not necessarily be very physically active; likewise, a highly active individual may not have the expected high level of fitness. Because fitness is a physical characteristic (like height or body mass), it is believed to have a fairly strong genetic basis. With all of this in mind, this article will specifically refer to physical activity, exercise, or fitness as appropriate and will avoid using them interchangeably. It is also worth noting that much of what is known about the effects of physical activity and exercise on anxiety is based on activities that are primarily aerobic in nature (i.e., not much is known about how other aspects of fitness influence the relationship).

Physical Fitness and Anxiety

Although there have been numerous investigations of the exercise-anxiety relationship, there has not been much in the way of examination of the fitness-anxiety relationship. Landers and Petruzzello (1994) summarized what was known at the time about links between physical fitness (i.e., primarily cardiovascular capacity) and anxiety. The collaboration between T. K. Cureton (exercise physiologist) and Raymond Cattell (personality psychologist) created the basis for much of the early work (Cureton, 1963). In general, this early work supported the inverse relationship between fitness and trait levels of anxiety or emotionality (Cattell, 1960). One example was Ismail and Young (1976), who had participants undertake a four-month physical fitness program that met 3 d∙wk−1 for 90 min∙session−1. Resting blood pressure, submaximal HR and minute ventilation, maximal oxygen uptake, and percent of lean body mass were all assessed before and after the fitness program as was personality (via Cattell’s 16 Personality Factor questionnaire). Ismail and Young showed relationships between fitness and emotional stability (conceptually analogous to trait anxiety) at both pre- and post-program. They speculated that the pre-program relationships indicate emotional instability is tied to a lack of fitness and, as a result of physical training designed to increased fitness, emotional stability is developed. Young (1979) showed that a 10-week exercise program not only improved various indices of fitness but also resulted in a reduction of trait anxiety (M effect size (ES) = −0.23). Landers and Petruzzello noted an average ES of nearly –0.40, with higher levels of fitness being associated with lower levels of trait anxiety.

The main limitation of this work is that it is largely, if not exclusively, cross-sectional. While there are longitudinal studies showing reductions in trait anxiety following some period of exercise training (Petruzzello et al., 1991), these studies often lack measures of fitness. One exception is the work of Sexton, Maere, and Dahl (1989), which examined the effects of an eight-week exercise program (30 min, 3–4 d∙wk−1, walking or jogging) with a six-month follow-up in a sample of symptomatic neurotics. Anxiety (and depressive) symptoms, derived from several measures, were both significantly reduced regardless of whether patients walked (ES= −0.94) or jogged (ES= −1.58), with changes maintained at follow-up (ESs= −1.12, 1.46, respectively). Aerobic capacity was significantly increased both immediately post-program as well as six-months post-program in both walkers (ESs=0.19, 0.43, respectively) and joggers (ESs=1.01, 1.01, respectively), with no difference between the two groups. Sexton et al. (1989) noted a significant relationship between aerobic capacity and anxiety levels, with greater fitness levels associated with lower anxiety, even after accounting for initial aerobic capacity and age. Although not all studies have found such a relationship, this result provides evidence that anxiety reduction is associated with an increase in actual fitness and not just in physical activity. This study also highlights the fact that exercise intensity is not necessarily important for psychological improvements; the effects were comparable for both walking and running. Sexton et al. (1989) noted as well that the patients rated exercise as more important than medication and psychotherapy in their improvement.

An exception is a study by Córdoba-Torrecilla et al. (2016), which examines relationships between measured components of fitness (e.g., cardiorespiratory, muscular strength, flexibility) and anxiety in a sample of women with fibromyalgia. Notably, 61% of the sample of 439 women had moderate (≥30) or severe (≥45) anxiety on the trait anxiety version of Spielberger’s STAI (Spielberger, 1983). Using regression analyses, Córdoba-Torrecilla et al. (2016) demonstrated negative, albeit modest, associations between anxiety and fitness. Another approach to understanding this relationship is to examine what happens to parameters of fitness in individuals who are diagnosed with an anxiety disorder. Lever-van Milligen et al. (2016) examined hand-grip strength and lung function (via peak flow during expiration) in nearly 2,500 adults (66% female; ~1,900 of whom had remitted or current depressive and/or anxiety disorder) over a six-year period. Over the course of the six years, individuals with current disorders (no differences were seen between depressive and anxiety disorders) had weaker grip strength and lung function than healthy controls. They also showed that greater severity of symptoms was associated with weaker physical function. Lever-van Milligen et al. (2016) concluded that their findings imply an influence of depressive or anxiety disorders on physical function not only at a single point in time but also over the course of time.

Several studies have assessed various fitness parameters before and after an exercise training intervention, some in clinical samples (Broocks et al.,1998; Herring et al., 2011, 2012), others in non-clinical samples using anxiety induction techniques (Broocks et al., 2001), and others in samples of patients with various illnesses (e.g., fibromyalgia, cancer) also having anxiety symptoms (Herring, O’Connor, & Dishman, 2010). Most of these studies assess changes in fitness but do not examine the magnitude of these changes on anxiety. The meta-analysis by Herring et al. (2010) did show that the occurrence of a fitness change did not have a differential effect on the magnitude of the anxiolytic effect. A separate review by Stonerock et al. (2015) also showed a lack of consistent improvement in aerobic fitness in exercise intervention studies.

It has been consistently shown that physically fit individuals typically have less anxiety than their unfit counterparts (Landers & Petruzzello, 1994). More fit individuals may “simply” be living healthier lifestyles (e.g., more activity, better nutrition, better sleep). After examining the effects of exercise training programs (which often have the aim of improving cardiovascular fitness), Landers and Petruzzello (1994) concluded that trait (i.e., more general) levels of anxiety appear to decrease after participation in these chronic activity protocols, often in addition to increasing parameters of fitness. Further, these reductions seem to be greater with longer training programs (Petruzzello et al., 1991).

Research on Exercise and Anxiety

Popular or folk wisdom posits that physical activity or exercise is a useful tool in alleviating anxiety symptoms and anxiety disorders (De Moor et al., 2008), but what is known regarding the anxiolytic effects of exercise? This question can be answered in several different ways with different sources of data. What follows examines evidence for the anxiolytic effects of exercise, including the evidence for preventing anxiety symptoms or disorders from developing, the alleviation of symptoms in non-clinical samples, and for treatment of such symptoms in individuals with clinically diagnosed disorders. Most of the studies have examined the efficacy of exercise as a treatment for alleviating anxiety symptoms in non-clinically anxious samples, even though those with clinically diagnosed anxiety disorders may derive the greatest benefit from exercise interventions (Salmon, 2001). Fortunately, this is slowly changing, and more studies are being published that use clinically diagnosed samples.

Based on coverage of studies, the quantitative review by Petruzzello et al. (1991) remains the most comprehensive review of the exercise-anxiety literature, comprising three separate meta-analyses (one each for state anxiety, trait anxiety, psychophysiological indices of anxiety) and more than 120 studies examining the exercise-anxiety relationship. Numerous narrative reviews (Gaudlitz et al., 2012; Ströhle, 2009; Wolff et al., 2011) and quantitative reviews of the literature have since appeared (Ensari, Greenlee, Motl, & Petruzzello, 2015; Landers & Petruzzello, 1994; Long & van Stavel, 1995; Martinsen & Raglin, 2007; McDonald & Hodgdon, 1991; Physical Activity Guidelines Advisory Committee, 2008; Raglin, 1997; Rosenbaum et al., 2015; Schlicht, 1994; Stonerock et al., 2015; Wipfli, Rethorst, & Landers, 2008), including a meta-analysis of meta-analyses (Rebar et al., 2015), but none has shown any striking differences from the Petruzzello and colleagues review.

Evidence for Preventive Effects

Physical activity and exercise have been implicated as important lifestyle behaviors in the prevention of anxiety symptoms and disorders. Classic examples include the work of Stephens (1988), who showed in four large Canadian samples (ranging in size from 3,025 to 23,791 adults) that greater self-reported physical activity was associated with better mental health. This included fewer symptoms of anxiety (along with fewer symptoms of depression). De Moor et al. (2006), in a population-based study of over 19,000 adolescent and adult twins and their families in the Netherlands, showed that those individuals who exercised had lower trait anxiety than those who were sedentary. A cross-sectional study by Kavussanu and McAuley (1995) showed that individuals who self-reported being either sedentary or low active (<0.5 d∙wk−1, <25 min∙session−1) had significantly greater trait anxiety than either moderately (~3 d∙wk−1, 40 min∙session−1) or high active (~5 d∙wk−1, 45 min∙session−1) participants (ESs= 0.58, 0.71, respectively). Together this suggests that regular physical activity may lead to less trait anxiety even in non-anxious populations.

Goodwin (2003) examined the relationship between regular physical activity (i.e., “How often do you get physical exercise—either on your job or in a recreational activity?”) and mental disorders, including a variety of anxiety disorders (e.g., GAD, panic attack, and agoraphobia), using National Comorbidity Survey data. In this large representative sample (N = 5,877 adults, 15–54 years old), 63% reported regular physical exercise, while the remainder reported either occasional, rare, or no exercise. Goodwin’s analysis revealed that those who engaged in regular physical exercise had a reduced likelihood of several anxiety disorders including GAD, agoraphobia, panic attack, specific phobias, and social phobia. The relationships persisted after controlling for several demographic and self-reported illness variables. Goodwin also reported a dose-response effect (i.e., as the level of physical activity decreased the frequency of reported anxiety disorders increased). Using panic attacks as an example, 3.32% of regular exercisers were shown to have panic attacks, this increased to 4.85% for occasional exercise, 7.33% for those who rarely exercised, and 8.52% for those who never exercised. A similar dose effect was shown for GAD: occurred in 2.26% of regular exercisers, 2.97% of occasional exercisers, 5.93% of those who rarely exercised, and 6.49% of those who never exercised. Goodwin concluded that these results supported the probable link between regular exercise and reduced risk for a number of anxiety disorders.

Ströhle et al. (2007), in a cross-sectional and prospective epidemiological study in adolescents and young adults (~2,500, ranging in age from 14–24 years), examined initial physical activity and 12-month and lifetime prevalence of mental disorders (using DSM-IV criteria); a four-year follow-up was obtained on the same individuals. At the initial assessment, those reporting regular physical activity had significantly less likelihood of any DSM-IV mental disorder, especially so for anxiety disorders. When examining incidence rates for mental disorders at the four-year follow-up, regular physical activity at baseline was associated with a greatly reduced risk of any mental disorder. This was true of anxiety disorders, where regular activity at baseline (compared to no activity) was associated with significantly reduced incidence of any anxiety disorder.

Overall, the bulk of the evidence is consistent with the hypothesis that regularly participating in physical activity buffers against anxiety symptoms and anxiety disorders (PAGAC, 2008). However, it is worth pointing out that those with higher levels of anxiety are also less likely to engage in physical activity/exercise (De Moor et al., 2006; Stonerock et al., 2015).

Exercise and Anxiety Reduction

One of the first and most comprehensive reviews of the literature examining the effects of exercise on anxiety reduction (Petruzzello et al., 1991) concluded that single bouts of exercise or exercise training resulted in anxiety reduction, but the effect was only seen for aerobic exercise. Mode of aerobic exercise (e.g., walking, jogging, running, swimming, or cycling) did not appear to differentially influence the anxiety-reducing effects. Anaerobic forms of exercise (e.g., resistance exercise), by contrast, either did not change anxiety or slightly increased anxiety responses, at least for a brief period following the exercise (see the section “Anaerobic Exercise and Anxiety” below). The anxiolytic effects for aerobic activity occurred for state anxiety following acute exercise and for trait anxiety following training programs (i.e., chronic exercise) and were independent of how the anxiety was operationalized (i.e., self-report measures [questionnaires], psychophysiological measures [EMG, HR, blood pressure, EEG activity]). More often than not, the majority of these studies were done with individuals who were not experiencing elevated levels of anxiety or were not diagnosed with clinical anxiety.

The anxiety reduction seen following acute exercise was a transient reduction. In studies examining this effect for an extended post-exercise period, the reduction has been shown to return to preexercise levels within about two to four hours (Martinsen & Raglin, 2007; Petruzzello et al., 1991), paralleling some physiological changes that have also been shown to occur following exercise (e.g., post-exercise hypotension). Because the post-exercise hypotension response and the anxiolytic response have been shown in numerous studies, speculation is that the two might be linked; such a relationship has yet to be definitively shown and may be too simple. Although the acute effect is transient, since participants in chronic exercise programs often show reductions in trait anxiety, levels of state anxiety prior to acute exercise could easily become reduced (i.e., a reset baseline is achieved). However, transient anxiety reduction still occurs following a single bout of aerobic activity.

To this point, the anxiolytic effect of exercise has not been shown to have any differential effect based on age or sex (Petruzzello et al., 1991), although Ensari et al. (2015) provide some evidence that the effects are somewhat larger in older adults (compared to college students) and in females (see also Strickland & Smith, 2014; Ströhle et al., 2007), but these require further examination.

Anaerobic Exercise and Anxiety

As noted earlier, more anaerobic forms of exercise (e.g., resistance) result in slight increases in anxiety (Petruzzello et al., 1991; Raglin, 1997). It is somewhat difficult to reconcile such findings with the fact that: (a) such a difference does not occur for depression and (b) resistance exercise is such a popular form of activity, having been ranked in the top five fitness trends since 2010 (Thompson, 2011, 2012, 2016). More recent reviews offer a slightly different picture. From a sample of six studies published after 1995, the PAGAC (2008) concluded that anxiety reduction is unaffected by exercise mode: resistance and aerobic exercise yielded anxiety reduction of a similar magnitude. Even more recently, Strickland and Smith (2014) concluded that resistance exercise does reduce anxiety, albeit with several caveats (see below).

In trying to offer explanations for the lack of change seen in anaerobic/resistance exercise studies, exercise intensity has been a recurring theme. Specifically, light- to moderate-intensity resistance exercise is often accompanied by reduced anxiety; more vigorous intensities either result in no change or in increased anxiety, for at least some period of time following the activity (e.g., Cassilhas et al., 2007). The increase in anxiety is often relatively brief, dissipating within 5–15 minutes after exercise completion. The increased anxiety may be explained by work-rest cycles used in the studies. One study that manipulated both intensity and rest durations between sets was conducted by Bibeau et al. (2010). They randomly assigned participants to one of five treatment conditions: a no-exercise control; low intensity (50%–55% of the individual’s 1-RM), short rest (30 seconds rest between sets); low intensity, long rest (90 seconds rest between sets); high intensity (80–85% of the individual’s 1-RM), short rest; high intensity, long rest. Each of the exercise conditions involved three sets each of four different lifts. State anxiety was assessed before and within five minutes following exercise as well as 20 and 40 minutes following exercise completion. Perusal of Figure 1 from that paper reveals that state anxiety was reduced immediately following each of the conditions, with the largest decreases occurring following the high-intensity, short-rest condition. Unfortunately, the results are not presented in such a way to allow determination of whether these reductions within 5 minutes post-exercise were significant. However, it is clear that there was not an increase in anxiety, even with high intensity exercise.

It is also entirely possible that the findings of unchanged or increased anxiety are “simply” a function of measurement problems. Rejeski, Hardy, and Shaw (1991) and Ekkekakis, Hall, and Petruzzello (1999) noted that using the state version (SAI) of the STAI to measure anxiety in response to acute exercise could indicate increased anxiety which is really more a function of increased activation or arousal (e.g., increased HR). Because several items in the SAI reflect perceived somatic activation (e.g., jittery, tense—items reflective of perceptions of activation that would be related to changes in anxiety), increases in scores on these items are interpreted as increased anxiety. However, changes in these perceptions following exercise may be more accurately reflecting changes in physiological activity consistent with the demands of the exercise. Thus immediately following exercise, heavy breathing or a pounding chest may result in a response to an SAI item like “jittery” with “somewhat,” “moderately so,” or “very much so.” Although this is a normal and expected outcome of activity-related exertion, this is reflected as increased anxiety on a measure such as the SAI. This issue certainly needs more careful attention. Again, given the available literature, and the fact that resistance and high-intensity exercise activities are popular, it is hard to reconcile that activities like these could cause anxiety increases.

Evidence for the Use of Exercise as a Treatment

It has long been of interest to determine the extent to which exercise could be a useful treatment for alleviating the symptoms of anxiety when these are experienced, either as part of a “normal” anxiety response or within clinically anxious individuals. As noted, most research on the anxiolytic effects of exercise has been done with individuals who are not unusually anxious. If individuals who partake in exercise-anxiety studies are not anxious to begin with (as reflected in low scores on an anxiety measure), does a lower score following exercise really indicate a reduction in anxiety? Does no change really mean that exercise did not work? In many studies, participants have preexercise levels of anxiety near the bottom of the range of the scale being used for assessing anxiety. It may even be the case that participants in laboratory-based studies report lower levels of anxiety when they arrive for testing than they report in their “normal” environments (Petruzzello, 1995). With preexercise anxiety levels being so low, there is little room for further decreases to take place. This can also leave the impression that exercise may not impact anxiety at all. Lacking access to clinically anxious samples of individuals, an alternative method to study the anxiolytic effect of exercise is the “biological challenge” model. Such an approach utilizes techniques to generate anxiety or anxiety symptoms, thereby “creating” anxious individuals and then examining whether exercise modifies those symptoms or anxious states.

Biological Challenge Models

There are several techniques/methodologies that have been shown to induce anxiety symptoms in non-anxious individuals. These include the use of caffeine, inhalation of a carbon-dioxide (CO2)-rich air mixture, and injecting cholecystokinin tetrapeptide (CCK4). The effectiveness of exercise for alleviating such induced anxiety symptoms (as well as insights into mechanisms) can then be evaluated. A number of studies have utilized such an approach.

Perhaps the “easiest” of the biological challenge approaches is the use of caffeine to generate anxiety symptoms. Motl and Dishman (2004) had participants with low/normal baseline state anxiety ingest either a large dose of caffeine (10 mg·kg−1 body weight) or a placebo. They then compared self-reported state anxiety responses to 30 minutes of moderate exercise (60% VO2peak) and quiet rest. Caffeine ingestion effectively increased self-reported anxiety symptoms (i.e., from ~23.5 to ~30 units2 on the 20-item SAI, ~1 standard deviation); exercise (cycle ergometry) resulted in a significantly greater reduction in state anxiety compared to quiet rest.

Inhalation of a CO2-rich gas mixture (35% CO2, 65% O2) has been used in several studies. Esquivel et al. (2002) used healthy volunteers randomly assigned to either 12 minutes of cycling exercise (@70 r·min−1) at a workload designed to increase blood lactate or at a light exercise intensity. Immediately after the exercise (in both conditions), a panic symptom list and a visual analog anxiety scale were completed. Participants did a vital capacity inhalation of the CO2 mixture and again completed the panic symptom list and visual analog anxiety scale. Both panic symptoms and anxiety were elevated as a result of the CO2 inhalation, but the increase for the panic symptoms was significantly less following the exercise condition (ES= 0.53) than the control condition (ES= 2.72). Esquivel et al. (2008) essentially replicated these findings with a slightly modified exercise protocol, but again panic symptoms following the CO2 inhalation resulted in a smaller panic reaction in the exercise group (panic symptoms decreased, little change in self-reported anxiety) compared to the control group (panic symptoms increased, self-reported anxiety increased markedly).

Similar studies have been conducted by others (Smits et al., 2009) with similar results. The reduction in reactivity has been suggested to be due, at least in part, to a reduced fear of the somatic sensations. Exercise could thus mediate the interoceptive sensations that accompany panic attacks.

A third biological challenge model utilizes the injection of cholecystokinin tetrapeptide (CCK4) to induce symptoms of panic attacks. Ströhle and colleagues (Ströhle et al., 2005, 2006, 2009) have demonstrated several times that exercise prior to CCK4 injection results in a significantly lower increase in panic (as assessed via the Acute Panic Inventory; Dillon et al., 1987) than in control conditions. In one within-subjects design study (Ströhle et al., 2009), patients with diagnosed panic disorder showed elevated somatic symptoms (e.g., palpitations, breathing, and nausea) but not anxiety (e.g., fear of dying and general fear) following exercise; for both measures, while increases were seen, there were significantly fewer somatic and cognitive anxiety symptoms following exercise than following a quiet rest control condition.

Such biological challenge models provide a useful substitute for examining the anxiolytic efficacy of exercise. While the best option would be to work directly with clinically anxious samples, these challenge models may provide unique insights when access to such samples is not readily available. Although most of the research has tended to focus on panic disorder, the findings may be applicable to other anxiety disorders as well.

Clinically Anxious Samples

Although the preventive effects of exercise on anxiety are important, it is also important to determine the extent to which exercise can be useful as a treatment for anxiety problems once they have manifested themselves. Although the literature using clinically anxious samples is relatively small, it is growing. This is due in part to earlier work showing that exercise can be useful in the treatment of anxiety disorders, and subsequent calls for more carefully examining exercise for that purpose (Callahan, 2004; Chung & Baird, 1999). Johnsgard (1989) cited numerous case study examples and more carefully controlled studies conducted with clinically anxious samples highlight the utility of such an “exercise prescription”—what deVries (1981) referred to as the “ultimate tranquilizer.” A sampling of these studies is presented in the following section.

Some of the earliest research with clinically anxious individuals was done by Egil Martinsen and colleagues. In two separate samples of inpatients (one with diagnosed anxiety disorders: Martinsen, Hoffart, & Solberg, 1989; one with nonpsychotic inpatients: Martinsen, Sandvik, & Kolbjornsrud, 1989), using either eight weeks of 30 to 60 minutes of combined aerobic (walking, jogging) and nonaerobic (muscular strength, flexibility) exercise or aerobic exercise only, Martinsen’s group showed significant reductions in number of anxiety symptoms, particularly in patients with unipolar depressive and anxiety disorders (GAD and agoraphobia). Physical fitness (i.e., increased physical work capacity) was also increased. Importantly, for those who responded to a follow-up 12 months post-intervention (84%), symptom scores were lower in individuals who had established regular exercise habits. Recall the similar findings from the eight-week exercise program (walking or jogging) with symptomatic neurotics, which resulted in significant reductions in anxiety and depression symptoms (Sexton et al., 1989).

Although the overall amount of research is relatively small, there have been enough studies done with clinical samples (i.e., individuals diagnosed with various anxiety disorders) that several reviews and meta-analyses have been published (Asmundson et al., 2013; Bartley, Hay, & Bloch, 2013; Herring et al., 2014; Jayakody, Gunadasa, & Hosker, 2013; Rosenbaum et al., 2015; Stonerock et al., 2015; Wipfli et al., 2008). These reviews (ranging from as few as four randomized controlled trials [RCTs] to as many as 49 studies, with most between 7–12 RCTs or studies) reach mixed conclusions, even when quantitative reviews are done: exercise is (Wipfli et al., 2008), seems to be, or may be, effective for treating anxiety disorders (Jayakody et al., 2013; Stonerock et al., 2015) or more specifically for patients with panic disorder (Herring et al., 2014) and PTSD (Rosenbaum et al., 2015); exercise training could be a useful alternative treatment for SAD, GAD, and OCD (Herring et al., 2014); exercise is less effective compared to medication (Jayakody et al., 2013); and exercise cannot be supported as a primary treatment for anxiety disorders (Bartley et al., 2013). These reviews generally conclude that there is a need for: (a) more rigorous methodological design (e.g., lack of adequate controls); (b) larger sample sizes; (c) greater attention to dose-response issues (i.e., intensity, duration combinations) and different modes of exercise (e.g., resistance vs aerobic); and (d) more attention to maintenance following treatment.

Petruzzello (2012) pointed out that little research had been done to examine the effects of exercise in individuals with clinical conditions involving high levels of anxiety sensitivity (e.g., posttraumatic stress disorder, PTSD). There has been some research examining the viability of exercise to treat individuals with confirmed clinical PTSD (i.e., meeting diagnostic criteria). Manger and Motta (2005) evaluated a 12-week exercise intervention in adults who met criteria for PTSD, showing symptom reduction post-intervention. Two other exercise intervention studies with adolescents (Diaz & Motta, 2008; Newman & Motta, 2007) showed reductions in PTSD symptom severity following the intervention. Rosenbaum et al. (2014) conducted an RCT assessing a 12-week resistance exercise (RE) training program in addition to usual care for PTSD. Adults with primary PTSD (diagnosed by DSM-IV-TR) were randomized into usual care or usual care plus augmentation with RE treatments. The RE consisted of one supervised session per week and two at-home sessions, using resistance bands. Usual care included psychotherapy, pharmacological interventions, and group therapy. The usual care plus RE augmentation group showed a significant improvement in PTSD symptoms, along with reductions in depressive symptoms, waist circumference, and improved sleep quality relative to the usual care only condition (Rosenbaum et al., 2014). Finally, Fetzner and Asmundson (2015) had adults with PTSD perform six exercise sessions (cycle ergometry) over a two-week period. The majority of participants showed significant reductions in anxiety symptoms at the end of the two-week period. PTSD symptom severity was reduced, consistent with other studies using a similar two-week intervention (e.g., Broman-Fulks & Storey, 2008). Each of these studies utilized multiple exercise sessions over a period ranging from 2 to 12 weeks, but research has not examined the effects of a single exercise session on PTSD symptoms in a population with PTSD (e.g., active military or veterans). Answering this question would address the issue of whether reduction in symptoms can be more immediate or whether such reduction only occurs following the accumulation of multiple acute bouts over several weeks.

There has also been relatively little research comparing exercise with the most common treatment for anxiety, namely pharmacotherapy (medication). In a classic study involving adults with self-reported problems of anxiety/tension (e.g., difficulty concentrating, excessive muscle tension, nervousness), deVries and Adams (1972) compared different “doses” of exercise to anxiolytic medication, utilizing muscle tension (i.e., EMG measures from the biceps) as a proxy for anxiety, assessed before each of five treatment conditions and 30 and 60 minutes after each condition. The five treatment conditions were: (a) a 400-mg capsule of meprobamate (then a commonly used tranquilizer medication); (b) a 400-mg placebo capsule containing lactose (a sugar pill); (c) treadmill walking for 15 minutes at a moderate intensity; (d) treadmill walking for 15 minutes at a more vigorous intensity; and (e) a control condition (quiet rest). Drug and placebo conditions were conducted in double-blind fashion to minimize expectancy effects. DeVries and Adams found significant reductions in muscle tension but only for the moderate intensity exercise condition (although near-significant reductions in muscle tension were also seen in the higher-intensity exercise condition). The control, drug, and placebo conditions did not reduce muscle tension and were not different from one another.

Broocks and colleagues have conducted several studies comparing exercise and medication, and in at least one instance, the combination of exercise and medication. In their initial work (Broocks et al., 1998; Meyer et al., 1998), in separate samples of patients with diagnosed panic disorder (with or without agoraphobia), the influence of a 10-week exercise program was compared with pharmacotherapy (clomipramine) or control. In one case (Meyer et al., 1998), the exercise group showed clinically significant improvement in anxiety compared to the control condition and similar improvement compared to the clomipramine group (i.e., exercise was as effective as anti-anxiety medication). In the second case (Broocks et al., 1998), a 10-week exercise treatment was compared to pharmacotherapy (112.5 mg·day−1 of clomipramine) or a placebo treatment. Exercise was again shown to be as effective as medication in reducing self-reported anxiety, with both being superior to the placebo. Although medication resulted in an earlier anxiety symptom improvement (after four weeks), the exercise treatment was equivalent by the end of the 10-week trial. Both were superior to placebo in reducing the frequency and intensity of anxiety symptoms. Finally, Broocks et al. (2003) showed that, in response to an ipsapirone challenge, a 10-week exercise intervention resulted in self-reported anxiety reductions that were comparable to medication.

In order to examine the potential combined effects of exercise with medication, Wedekind et al. (2010) again utilized a 10-week intervention design. Diagnosed panic disorder patients were assigned to either: exercise + medication (paroxetine), exercise + placebo, relaxation + medication, or relaxation + placebo. Sizable reductions in anxiety symptoms were seen in all four groups, but they were not differentially effective. Those receiving medication improved more than those receiving placebo, and those receiving exercise tended to respond somewhat better than those receiving relaxation.

Results from such studies suggest that exercise may be at least as effective as anxiolytic medication, and deVries (1981) has referred to this as the “tranquilizer effect of exercise.” Given the widespread use of anti-anxiety (i.e., tranquilizer) medications for individuals with elevated anxiety symptoms or anxiety disorders, such research is sorely needed to determine whether there are other effective non-medication alternatives (see Martinsen & Stanghelle, 1997).

Studies have also shown exercise to positively supplement psychological treatments (e.g., cognitive therapy). Merom et al. (2008) provided 8- to 10-weeks of group cognitive behavioral therapy (GCBT) to diagnosed panic disorder, social phobia, or generalized anxiety disorder outpatients, supplemented with either an exercise intervention (home-based walking) or educational sessions. Patients who completed the GCBT-exercise intervention had significant reductions in anxiety, stress, and depression scores compared to the education group. Smits et al. (2008) randomly assigned individuals with high anxiety sensitivity to either an exercise group (Ex), an exercise + cognitive restructuring group (Ex+C), or a wait-list control group (WL). For the exercise interventions, participants completed six 20-minute sessions of aerobic exercise over two weeks. Participants in the Ex+C group also received a description of the usefulness of cognitive restructuring. Both interventions involving exercise (Ex, Ex+C) showed large, clinically significant reductions in anxiety sensitivity, which were comparable to reductions in existing anxiety-modification protocols (Smits et al., 2008).

What Remains Unknown: Dose Response, Causality

In spite of what has been learned regarding exercise and anxiety reduction, there are still important unknowns. This is perhaps most striking when it comes to the relation between the exercise dose (i.e., intensity, duration) and response. At various times it has been the suggested that thresholds for both intensity and duration need to be met to achieve anxiety reduction. Dishman (1986) proposed an intensity of at least 70% of aerobic capacity and a duration of at least 20 minutes was necessary; Raglin and Morgan (1987) suggested a lower, more moderate threshold for intensity (greater than 60% of maximum aerobic capacity) was sufficient. The minimum intensity needed for anxiety reduction, if it exists, remains poorly investigated. Ekkekakis and Petruzzello (1999) summarized the evidence specifically examining dose-response issues and reached the conclusion that anxiety and tension are sensitive to exercise intensity effects: higher intensities led to increases in anxiety/tension; lower intensities resulted in no change or decreases (however, recall the caveat raised earlier regarding the potential measurement problems within the exercise context). Further work is certainly needed before any firm conclusions can be drawn and certainly before any recommendations about minimal exercise intensity levels can be made.

As for a minimum duration of exercise, Petruzzello et al. (1991) noted that exercise durations of less than 20 minutes were as effective as durations of greater than 20 minutes for reducing anxiety. The PAGAC report (2008) essentially concluded the same thing—minimal and optimal exercise durations or intensities for anxiety reduction remain unknown. Thus research at this point shows that the anxiety-reducing effect that is achieved by exercise is present regardless of the duration of that exercise. Again, more work is needed for a definitive answer, but reductions in anxiety can apparently be realized simply by exercising aerobically.

Another aspect of the exercise-anxiety relationship that is less well examined involves resistance exercise. Although the effects of resistance exercise have been examined, this aspect of the anxiety response requires much more attention. What has been done suggests that anxiety reductions do not occur in the same way as seen following aerobic exercise (Raglin, 1997). There has been some work examining resistance training and its effects on trait anxiety, with that work essentially showing significant, albeit modest, reductions in anxiety symptoms (Gordon et al., 2017). This work showed that there was no influence of dose (intensity, duration, frequency) or length of training program on the anxiety reductions. However, this is a modality of exercise that sorely needs more systematic research.

It is also certainly worth noting that the question of causality has not been definitively answered. As De Moor et al. (2008) pointed out: “The evidence from these prospective and experimental studies makes it tempting to interpret the association at the population level as reflecting a causal effect of exercise on the symptoms of anxiety and depression. This explanation fits folk wisdom.” (p. 898). Examining causality in nearly 6,000 twins, approximately 1,500 of their siblings, and nearly 1,300 parents, De Moor et al. (2008) showed that in identical twins, the more frequently exercising twin did not have fewer anxiety symptoms, nor did increasing exercise activity result in decreased anxiety when examined longitudinally. De Moor et al. (2008) stated that despite the absence of a causal effect of voluntary exercise on anxiety symptoms, exercise may still be useful in alleviating such symptoms. However, it does mean that such an association should not be the sole justification for using exercise as a treatment for clinical anxiety (or depression). In spite of the claim by Wipfli et al. (2008) that solid evidence (i.e., RCTs) exists for using exercise as an anxiety treatment, the relative paucity of data with clinically anxious samples does not warrant such a conclusion yet. As clearly articulated by De Geus and De Moor (2008), incorporating “genetic sensitivity” into our research models would also help in better understanding the mental health benefits of exercise. Randomized controlled trials are a first necessary step in making such recommendations.

Mechanisms of Change

More than 30 years after the NIMH called for greater understanding of the mechanisms responsible for the anxiety-reducing effect of exercise, such explanation remains elusive. Many of the same mechanisms that have been proposed to explain the anxiolytic effect remain viable, if for no other reason than they have not been adequately examined and either refuted or supported. These include the thermogenic (Morgan & O’Connor, 1988), distraction/time-out (Bahrke & Morgan, 1978), endorphin (Dishman & O’Connor, 2009), neurotransmitter (Herring et al., 2014), and mastery (Asmundson et al., 2013) hypotheses. Rather than rehash these, it would seem worthwhile to present some more recent additions to the list of potential explanations exercise-related for anxiety reduction.

Core Affect Hypothesis

Although it is a related but different area of research, study of affective responses to exercise have shown that core affective responses (i.e., changes in the dimensions of valence [pleasant, unpleasant] and activation) are influenced by exercise and in relation to intensity of that exercise (Ekkekakis et al., 2011). Rebar, Faulkner, and Stanton (2015) proposed the core affect hypothesis, namely that physical activity “enhances affect by increasing the pleasantness of valence and increasing activation.” This in turn would “lead to large increases in pleasant-activated states and smaller effects on pleasant-deactivated states” (p. 56). As such, they proposed that those with anxiety disorders may respond to physical activity with increased pleasantness, or at least a shift from unpleasant to pleasant, with activation remaining higher. In a small sample study, individuals with a diagnosed anxiety disorder performed 20 minutes of cycle ergometry and 20 minutes of resistance exercise and were then asked to rate their effect (valence and activation) immediately before and immediately upon completion of the exercise. For the group, there was an increase in valence (ES=0.70) with no change in activation (ES= 0.00; it should be noted that half of the participants reported increased valence and half reported no change; activation increased, decreased and remained unchanged in roughly the same number of participants). Rebar et al. (2015) essentially supported the core affect hypothesis for those with anxiety disorders in that there was a change only in the valence dimension of affect while activation remained the same. They outline next steps to further establish the utility of the core affect hypothesis, but it appears to be a useful potential explanation.

Anxiety Symptom Interpretation

Distress intolerance (Moshier et al., 2013) has been implicated as an individual difference factor for psychopathology. The most studied measure of distress intolerance is anxiety sensitivity (AS), a “propensity to fear anxiety sensations” (Asmundson et al., 2013, p. 367) with the judgment that such sensations will result in disastrous outcomes; it is characteristic of many anxiety disorders. As described by Asmundson et al. (2013), one way that exercise can help with anxiety reduction may be through the exposure it provides to the somatic sensations that lead to fear and anxiety—what some refer to as interoceptive exposure (e.g., Sabourin et al., 2015). Aerobic exercise has been shown to reduce the various aspects of anxiety sensitivity (e.g., lack of cognitive control, fear of somatic sensations), and it is possible that aerobic fitness may help explain this effect. For example, Williams et al. (2016) demonstrated that higher aerobic fitness was associated with less overall anxiety as well more positive perceptions of anxiety symptoms experienced during an acute stress task. AS has also been shown to be negatively associated with physical activity/exercise (e.g., Sabourin et al., 2011), particularly when the exercise is vigorous in nature (Moshier et al., 2013). The work of Broman-Fulks and colleagues (Broman-Fulks et al., 2004; Broman-Fulks & Storey, 2008) demonstrated that exercise could influence the perception of anxiety symptoms and AS.

Selecting individuals with high AS scores, Broman-Fulks et al. (2004) showed that six 20-minute bouts of both low-intensity (60% of age-adjusted predicted HRmax) and high-intensity (90% of age-adjusted predicted HRmax) aerobic exercise over a two-week period effectively reduced AS, with the high-intensity exercise yielding faster decreases in AS and a greater treatment response (52% of participants) compared to the lower-intensity exercise treatment (20%) immediately following the treatment; by a one-week follow-up, responders had increased to 62% and 28% for the high- and low-intensity exercise groups, respectively. The follow-up work (Broman-Fulks & Storey, 2008) again showed that AS could be reduced by brief (i.e., 20-minute) bouts of aerobic exercise, with the reduced AS being maintained throughout the two weeks of brief exercise bouts and for at least one week after. Broman-Fulks and Storey suggested that exercise could effectively reduce AS in individuals with high levels of AS, which could be especially helpful if a rapid reduction in that sensitivity was needed.

Conclusion and Future Directions

As Petruzzello (2012) noted in his earlier review, it is sensible to suggest that exercise can be a useful technique for anxiety reduction, both in an acute sense as well as for more general tension, nervousness, and worry over the longer term. Exercise has also been shown to assist in the treatment of clinical manifestations of anxiety (e.g., panic disorder, phobias, generalized anxiety disorder, PTSD), although more research with clinically anxious populations is needed. The state of research as it stands in the early 21st century is summarized in Table 2. There remains much to do, including the determination of whether exercise actually causes the change in anxiety and, if so, what that mechanism is and what “doses” of exercise reliably yield such effects. It is also important to continue the examination of the utility of exercise as a potential treatment for individuals suffering from clinical levels of anxiety. Related to this will be the important task of determining whether exercise can be a useful treatment for all forms of anxiety disorders or whether only certain types can be positively influenced by exercise protocols. The coin of the realm in this regard would be randomized controlled trials, but given the paucity of research with clinical samples, all well-designed studies would be warranted at this point.

Table 2. Consensus Statements Regarding Exercise and Anxiety


Exercise is associated with reduced state anxiety.


Chronic exercise is usually associated with reductions in emotionality and trait anxiety.


Exercise can result in the reduction of various stress indices.


Exercise can have beneficial emotional effects across all ages and both genders.

Note. Adapted from Exercise and Mental Health (p. 156), by W. P. Morgan & S. E. Goldston (Eds.), 1987, Washington, DC: Hemisphere.


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(1.) Although PTSD is now classified as a trauma and stress-related disorder and no longer as an anxiety disorder, it will still be treated as an anxiety disorder in the present work. This is largely because most of the relevant research was conducted prior to the 2013 release of the DSM-5.

(2.) It should be noted that although caffeine ingestion did increase self-reported anxiety, a score of ~30 on the SAI is still well within the “non-anxious” range.