Programs Coaching Courses Blog Take The Training Quiz Login

Allostatic Overload: Stress and Emotional Context Part 1

Jul 21, 2017

Okay, I get it... ‘Allostasis’ has become the new catch phrase. However, I think it places an emphasis and understanding on the consequences of training adaptations. No, not every adaptation we make to training is positive for health and well-being; training can be associated with a cost. Consequence can have both a positive and negative result, but cost is associated with a price to pay. Training is stress. Stress can change the way we think, process information, and behave. As a coach, you need to be a thoughtful stress manager and understand that everything you do has a consequence.

Before an adaptation to training can be acquired, the payment in stress is required. The consequence of that stress depends on how it is managed. As strength and conditioning coaches, we are stress managers. Stress is a bodily or mental tension resulting from factors that tend to alter an existent equilibrium (8). Exercise is planned stress (i.e. periodization). The same chemical response occurs if you break up with your significant other, have an upcoming exam, or are lifting 90% of your max for multiple repetitions.

“Scientific understanding of stress and adaptation, have changed a lot in the past century, but periodization has not changed with them” - Martin Bingisser

The chemical response to an acute PERCEIVED stressor/adversity is initiated by a stimulus which activates the hypothalamus-pituitary-adrenal (HPA) axis to globally effect the major organs of the body. The hypothalamus, specifically the paraventicular nucleus releases corticotrophin-releasing Hormone (CRH), this activates the anterior pituitary to release adrenocorticotrophin-releasing hormone (ACTH), which causes the Adrenal cortex to produce corticosteroids (cortisol in humans). The associated physiological responses are activated: sympathetic nervous system (SNS), release of catecholamines (epinephrine and norepinephrine) accelerate heart rate, vasoconstriction of blood vessels, mobilization of energy resources, increased ventilation, inhibition of digestion, growth systems, and reproductive systems. This response will also be anatomical, humans will increase muscle tone and increase recruitment of extensors.

An inverted U-shaped relationship exists between stressor exposure and adaptation. There is an interplay over time between current stressor exposure, internal regulation of bodily processes, and health outcomes (6). On the adaptive side: small to moderate amounts of stressor exposure (stimulation or challenge) leads to increased health and improved physiological (immune, skeletal, muscular) and mental function (cortical plasticity and executive function). A tipping point occurs when a healthy challenge becomes a progressively unhealthy stressor (chronic, repeated exposure) and can result in long term, negative health outcomes (compromised immune function, neurogenesis).

Figure A and B. Correspond to two different athletes reflecting how much stress they can handle with and without an associated cost. Some athletes may be better equipped to handle more stress without negative health outcomes than others.

Homeostasis is a term used to describe the regulation of internal settings or set points that the body likes to maintain within a certain range. For example, pH between 7.35-7.45, sodium between 135-145 mEq/L, total serum calcium concentration between 8.5-10.2 mg/dL, or blood glucose between 79.2-110 mg/dL). When homeostasis is disturbed due to a stressor/imposed challenge, the brain and the body do not immediately seek to return to homeostatic balance. “Homeostasis resets itself in response to stress exposure” (6). The resetting of set points is allostasis.

“Allostasis explains how regulatory events maintain organismic viability, or not, in diverse contexts with varying set points of bodily needs and competing motivations.”- Jay Schulkin


Allostasis means adapting to change. Allostatic accommodation is an acute imposed stressor which IS a microtrauma; for example, an acute stressor elevates blood pressure. An acute stressor will activate the SNS thus increasing cardiac output, blood volume, and vascular constriction. This will temporarily increase blood pressure (allostatic accommodation), which your body should be able to handle without a system cost (return to resting levels). However, if the arousal becomes chronic the brain will respond to the elevated blood pressure by creating vascular system changes such as thickening arteriolar smooth muscle and increasing vascular wall-to-lumen ratio (allostatic load). Allostatic load is the physiological change required to respond and adapt to a stressor or repeated accommodation. Allostatic load is the wear and tear of central and peripheral allostatic accommodation. Allostatic overload and pathophysiology occur when a high blood pressure is needed to maintain the same blood flow through a stiffer vascular system, which turns into a feedforward system. Allostatic overload is the expression of pathophysiology (abnormal physiology) by the chronic over activation of regulating systems (6). For our

example of blood pressure, an individual’s normal blood pressure can now be reset to a higher level which is hypertension= pathology.

The Brain & Emotional Context

“The brain is the central mediator of ongoing system wide physiological adjustment to an environmental challenge.”  - McEwen, 2004, 2007; Schulkin, 2003; Sterling, 2004; Sterling & Eyer, 1988

The brain as the higher levels in the system modulate and coordinate the activity of lower levels (8). “Allostasis involves the whole brain and body rather than simply local feedback,” and this is “a far more complex form of regulation than homeostasis” (18). Stress can be physical and emotional events, such as pain, discomfort, injury, distress; however, stress can also be a sense of angst inside that you don’t know or understand (reflect for a second...I’ll wait). A stressed system on an unconscious level can create a cortical response that leads to states and resetting neural pathways.

Most of our behavior is dictated by an emotion or feeling, not a thought. We have to associate an emotion with a physical task via the brain in order to dictate the APPROPRIATE physiological response. “A stressor must have sufficient magnitude to activate the emotional circuitry of the brain or the stress response will not be invoked by the organism: conversely, stressors that are of a magnitude sufficient to overwhelm the mechanisms of allostatic accommodation will produce greater allostatic load” (6). Emotional context drives training adaptations. As stimulus functions as a stressor depending upon its emotional valence (whether it is judged to be harmful or beneficial), level of intensity (threat or challenge) and personal importance relative to environmental context and personal beliefs, goals, and coping resources (6).

Emotional regions of the brain include the amygdala and basal ganglia, combined to call the limbic system. Amygdala is associated with threat value and avoidance behavior. The basal ganglia is associated with reward value and approach behavior. These emotional areas are most likely to show evidence of allostatic load which can increase probability of injury and negative health outcomes (2). WHY? Emotions overlay the chemical consequences of the training stimulus. The chemical environment is not just based upon the emotional intensities of training, but also of life. If an individual is PERCIEVING stress from personal relationships and school then trains repeatedly with high stressors, the same chemical response is overlaid. “Load can accumulate from daily low levels of stress in the environment,” (6). Exercise input involves both context and the stressor itself. The context is the environment, such as the setting (i.e. color of the room, volume of the music, or behavior of the strength coach). In an exercise environment the stressor can be number of sets, repetitions, intensity, velocities, or load.

“If you are stressed about the session or some other aspect of your life- you are essentially OVERLAYING THE CHEMICAL CONSEQUENCES OF THE IMPOSED MECHANICAL TRAINING STRESSORS ON A SUBOPTIMAL CHEMICAL BACKDROP. As a consequence, adaptations are inevitably compromised and risks, of injury or illness, escalate.” - John Keily

“Under chronic or repeated stress, the short-term gains of allostatic accommodation dwindle over time, while its physiological adaptations, become entrenched and automatic.” - Sterling & Eyer, 1988

Chronic, repeated stress will cause overactivation of the HPA axis leading to dysfunction of the Hypothalamus- Pituitary-Thyroid (HPT) axis and Hypothalamus-Pituitary-Gonad (HPG) axis. In the words of Dr. Ben House, “axes that function together, dysfunction together,” so you are not just dealing with a dysfunctional HPA axis, chronic stress will lead to HPT and HPG dysfunction; hello thyroid and testosterone production issues.

“Factor in aging process is the ability to secrete more cortisol when necessary and terminate the elevated levels when not necessary” - Schulkin, 2011

Physiological changes lead to changes in environmental perception, behavior, and anxiety (level of tension). A stress can become perceived as a threat and chronic stress can create change in neural pathways facilitating heightened perceptual processing of threatening stimuli in the environment (6). This threatening stimulus will be associated with emotional significance. A feedforward system is created involving chemical response to stress, neural signaling pathways, perception of environment or task, and behavior.

“The body is an entry point to the mind and the mind is an entry point to the body.” – Dr. Mike T. Nelson

What should you do with this information? STICK AROUND FOR PART 2...

ABOUT THE AUTHOR:  Michelle Boland


– Strength and Conditioning Coach at Northeastern University (Boston, MA)

– PhD. Exercise Physiology, Springfield College

– M.S. Strength and Conditioning, Springfield College

– B.S. Nutrition, Keene State College

– Follow on Instagram: mboland18

– Visit:


  1. Anderson, A. K. (2005). Affective influences on the attentional dynamics supporting awareness. Journal of Experimental Psychology: General, 134, 258–281.
  2. Bingisser, M. (2017). How your emotional state can be more powerful than your rep scheme. HMMR Media
  3. Bingisser, M. (2017). Training, Fast and Slow. HMMR Media Cerqueira, J. J., Mailliet, F., Almeida, O. F., Jay, T. M., & Sousa, N. (2007). The prefrontal cortex as a key target of the maladaptive response to stress. Journal of Neuroscience, 27, 2781–2787.
  4. Cerqueira, J. J., Pego, J. M., Taipa, R., Bessa, J. M., Almeida, O. F. X., & Sousa, N. (2005). Morphological correlates of corticosteroid-induced changes in prefrontal cortex-dependent behaviors. Journal of Neuroscience, 25, 7792–7800.
  5. Ganzel, BL, Wethington, E, & Morris, PA (2010). Allostasis and the human brain: Integrating models of stress from social and life sciences. Psych Review 117(1): 134-174
  6. Hodges, P.W., Sapsford, R., & Pengel, L.M. (2007). Postural and respiratory functions of the pelvic floor muscles. Neurourology and Urodynamics 26: 362-371.
  7. Lovallo, W. (2016). Stress & Health: Biological and psychological interactions. Sage Publications: Thousand Oaks, CA.
  8. McEwen, B. S. (2000). Allostasis and allostatic load: Implications for neuropsychopharmacology. Neuropsychopharmacology, 22, 108–124.
  9. McEwen, B. S. (2004). Protective and damaging effects of the mediators of stress and adaptation: Allostasis and allostatic load. In J. Schulkin (Ed.), Allostasis, homeostasis, and the costs of physiological adaptation (pp. 65–98). Cambridge, England: Cambridge University Press
  10. McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87, 873–901.
  11. Öhman, A., & Mineka, S. (2001). Fears, phobias, and preparedness: Toward an evolved module of fear and fear learning. Psychological Review, 108, 483–522.
  12. Samueloff, S. & Yousef, M.K. (1987). Adaptive physiology to stressful environments. CRC Press Inc: Boca Raton, FL.
  13. Schulkin, J. (2003). Rethinking homeostasis: Allostatic regulation in physiology and pathophysiology. Cambridge, MA: MIT Press.
  14. Schulkin, J. (2004). Allostasis, homeostasis, and the costs of physiological adaptation. Cambridge, England: Cambridge University Press.
  15. Schulkin, J. (2011). Social allostasis: Anticipatory regulation of the internal milieu. Frontiers in Evolutionary Neuroscience, 2 (111), 1-15.
  16. Sterling, P. (2004). Principles of allostasis: Optimal design, predictive regulation, pathophysiology, and rational therapeutics. In J. Schulkin (Ed.), Allostasis, homeostasis, and the costs of physiological adaptation (pp. 17–64). Cambridge, England: Cambridge University Press.
  17. Sterling, P., & Eyer, J. (1988). Allostasis: A new paradigm to explain arousal pathology. In S. Fisher & J. Reason (Eds.), Handbook of life stress, cognition, and health (pp. 629 – 649). Chichester, England: Wiley.

50% Complete

One More Step...