Behavior Change and MotivationCal USports MedicineSports Performance

Psychoneuroimmunology in Sport Injury and Rehabilitation

The interaction of the psychological, neurological, endocrine and immune function and the influence on health is known as psychoneuroimmunology and has been studied since the mid-1970’s (Langley Fonseca, & Iphofen, 2006). Likewise, the stress-injury-stress model has been studied since the late 1980’s and includes the physical, environmental, sociocultural, and psychological factors associated with injury (Wiese-Bjornstal & Shaffer, 1999). The following is an attempt to expose and inform the reader to the specific interactions that can play an important role in injury, illness, and recovery.

One common component addressed with injury and illness is stress. Stress is a simple word with a complex meaning, which can be attributed to physiological (physical changes such as blood pressure and release of hormones), social (relationship with others and the environment), and psychological (daily hassles and life event stress) factors (Brown, 2016; Langley, et al., 2006; Spano, 2006; Williams, 2001). Individuals engaged with exercise may have a general understanding of the stress and adaptation response as described by Seyle (Lovallo, 2016; Seyle, 1950). In general, Seyle’s General Adaptation Syndrome (GAS) model suggests that there are 3 stages: 1) alarm, 2) resistance, and 3) exhaustion. Essentially, individuals who have been exposed to short-term stress will immediately react to stress, which is known as the fight-or-flight response and prepares the body to protect itself from harm and maintain homeostasis in the cardiovascular, musculoskeletal, and neuroendocrine systems (Dhabhar, 2014; Lovallo, 2016). Depending on the situation, stress will prepare the immune system for injury and illnesses such as wounds, allergies, cardiovascular disease, obesity, or depression (Dhabhar, 2014). Prolonged psychological distress initially causes the body to release adrenaline. During the alarm stage there is sympathetic adrenal medulla (SAM) outflow. As a direct link the sympathetic nervous system neurons will release epinephrine and norepinephrine to bind with catecholamines. As an indirect link the hypothalamic-pituitary-adrenal (HPA) axis or HPAC system will release adrenocorticotropic hormone (ACTH), which causes the adrenal gland to release cortisol (hydrocortisone) into the blood (Seyle, 1950; Torpy & Chrousos, 1997). Cortisol is a primary catabolic hormone vital for muscle breakdown, which increases protein breakdown, inhibits amino acid intake, impairs cell proliferation, inhibits muscle cell differentiation, and inhibits testosterone production (Florini, 1987). Cortisol will go to an injured area, clean out the debris, and prepare the body for new construction. If stress continues, the body begins to secrete more hormones to defend against the threat. Basically the prolonged defense causes the body to become more fatigued and unable to rest, relax, and fight off the stress. The hypothalamus signals to the adrenals to release cortisol (Florini, 1987). Cortisol suppresses the immune system further, and the body loses the ability to heal. Therefore, if the stress is long term, then cortisol will continue the catabolic response and deconstruction resumes, inhibiting reconstruction (Florini, 1987).

As the stress continues, then the body will try to resist the breakdown to protect itself from harm to survive (resistance stage). This stage can last for as long as necessary, days or weeks or until death (Florini, 1987). Once death of the tissue has occurred, then the individual has reached the stage of exhaustion (Lovallo, 2106). At this point the stress has been ongoing and the body’s immune system is severely impaired and can cause adverse health responses including athletic injury and emotional distress (Dhabbar, 2014; Perna & McDowell, 1995). Inflammation increases in response to the threat (Kendall-Tackett, 2015). Therefore, the immune system becomes suppressed and injury and illness ensue (Kendall-Tackett, 2015; Langley, et al., 2006; Lovallo, 2016).

On a positive note, if athletes are exposed to moderate stressors with repeated exposure and the body learns to adapt to the threat, without releasing cortisol for long periods of time, then the body will endure greater strength and endurance over time, and muscle cell differentiation will take place (Forlini, 1985; Lovallo, 2016).   It is when the athlete’s body is unable to adapt to the additional stressors that the body becomes susceptible to illness and injury (Forlini, 1985; Lovallo, 2016).

When an athlete has been exposed to extreme stress, whether physical, psychological, social, or a combination, and their system is unable to handle the amount of stress, then illness and injury can occur. The immune system is considered to be most unprotected or exposed 3-72 hours following an extreme workout. The window of susceptibility (WOS) is open and viruses and bacteria can settle into the cells and weaken the body (Nieman & Pederson, 1999). When the body is unable to adapt to the duration of the stress, recruitment of leukocytes, timing of the stress hormone exposure, or differential effects of glucocorticoids then the immune system become suppressed and injury or illness will transpire (Dhabha, 2014). Furthermore, repeated physical stress compounded with emotional stress sleep deprivation, malnutrition or body weight loss will make the individual more vulnerable to illness and prolong the recovery process (Nieman & Pederson, 1999).

Stress works in a cyclic fashion; when stress injury or illness occur, then the injury or illness may create additional stress, thus causing a delay in the healing process, and the pattern continues (stress-injury-stress cycle). Research has shown that the interaction of personality, history of stressors, and the coping resources will determine the stress response (Albinson & Petrie, 2003; Wiese-Bjornstal & Shaffer, 1999; Wiese-Bjornstal, Smith, Shaffer, & Morrey, 1998). The body will appraise the stress and determine whether it is a threat or not (primary cognitive appraisal). Once the body makes that determination, then the body must decide whether the coping resources available can handle the stress (secondary cognitive appraisal). These cognitive appraisals will determine whether the individual is experiencing eustress (pleasant stress) or distress (unpleasant stress) and the ability to meet or overcome the demands of the stress (Albinson & Petrie, 2003; Williams, 2000). If one is unable to handle the stress, then injury is likely to occur (Weise-Bjornstal & Shaffer, 1999; Wiese-Bjornstal, et al., 1998).

If an athlete has experienced injury, then it is not unlikely that psychological stress will emerge. Commonly reported stress following injury includes anger, depression, anxiety, tension, fear, and decreased self-esteem (Appaneal, Levine, Perna, & Roh, 2009; Appaneal, Perna, & Larkin, 2007; Reese, Pittsinger, & Yang, 2012; Wiese-Bjornstal, 2010).

Wound healing, whether associated with acute injury or post surgery, can be delayed when stress continues or is increased (Broadbent, Petrie, Alley & Booth, 2003; Brown, 2016; Cole-King & Harding, 2001). For example, research has shown that wound healing was delayed with elevated levels of depression and anxiety (Cole-King & Harding, 2001). Likewise, greater worry about surgery decreased the matrix and collagen development, increased pain, and lower levels of interleukin-1, poorer wound and slower wound healing, thus preventing regulation of the immune and inflammation responses (Broadbent, et al., 2003; Brown, 2016). Moreover, caregivers of family members with Alzheimer’s disease took significantly longer for the wound to heal than control subjects (Kiecolt-Glaser, Marucha, Malarkey, Mercado, & Glaser, 1995); and medical students with punch biopsies exposed to an exam and non-exam conditions took an average of 40% longer to heal under exam conditions (Marcucha, Kiecolt-Glaser, & Favagehi, 1998). This latter research shows that even normal stresses such as an exam can delay the wound healing process.

Once injury happens, then it is important to recognize any stressful situation and consider intervening. Various interventions such as stress inoculation training (SIT; Ross & Berger, 1996), cognitive behavioral stress management (CBSM; Perna, Antoni, Baum, Gordon & Schneiderman, 2003), stress management, goal-setting (Johnson, 2000; Wayda, Armenth-Brothers, & Boyce, 1998), relaxation (Johnson, 2000), guided imagery (Cupal & Brewer, 2001; Johnson, 2000), and social support (Williams & Appaneal, 2011) have all had successful outcomes by reducing post injury stressors and increasing psychological coping resources. Many of these interventions are employed regularly by applied sport psychologists and should be considered for referrals to assist with the recovery (Reese et al., 2012).

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The Author

Joni L. Cramer Roh, EdD, LAT, ATC

Joni L. Cramer Roh, EdD, LAT, ATC

Joni L. Cramer Roh has been teaching at Cal U since 1991. Roh earned her undergraduate degree in Professional Physical Education with a minor in Athletic Training at WVU (1988); graduate degree in Sports Medicine at UNC-CH (1990); and doctoral degree in Sport Psychology with a minor in Counseling (2001). She received her NATA BOC certification in 1988 and started teaching in the undergraduate and graduate Athletic Training Education Programs (ATEP) in 1991. In 2005 she created four core classes for the Sport Psychology concentration in the Exercise Science and Health Promotions program. Since then she taught the PRF 715 (Special Topics in Sport Psychology), PRF 753 (Psychology of Sport Injury and Rehabilitation), PRF 783 (Psychological Perspectives of Sport Performance Enhancement and Interventions), and PRF 830 (Research in Sport Psychology). The PRF 753, PRF 783, and PRF 770 (Exercise Physiology: Assessment and Exercise Prescription) have been recognized as acceptable online courses to fulfill requirements for the Association for Applied Sport Psychology Certified Consultant (CC-AASP) certification.