homeostasis

Allostatic Overload: Stress and Emotional Context Part 2

What we have learned from Part 1 is that physiological adaptations during training are due to the planning of stress. As humans, we need the stress response to survive. Stress is training variables (i.e reps, sets, intensity, loads, velocities, etc.) and the cascade of the HPA axis is the window into performance. But we also need to be able to turn it off when it is not needed.

A chronic state of stress will limit adaptation and performance. A chronic state can lead to changes in environmental perception, behavior, and anxiety (level of tension). Allostatic overload is a term that reflects the pathophysiology that chronic over activation of the stress response of regulating systems can create. These changes can reflect compensation patterns for movement and be reflected physically, emotionally, and behaviorally. Part 2 will be dedicated to the physical adaptations to allostatic overload.

However, we need to appreciate that it is not just physical. Part 1 discussed emotional and behavioral overload such as heightened threat perception, anxiety, increased level of alertness and tension, and difficulty relaxing (parasympathetic access). “Hyperactivity of amygdala may be part of mechanism through which normal fear process translates into anxiety disorder in some individuals” (15). “Stress- related neuroplastic changes are associated with decreased behavioral flexibility” (4,5).

Everything is connected.

“Do whatever you want, just know that it has a consequence” - Chris Chase

What does this look like?

Wolff’s Law states that bone in a healthy human will adapt to the loads under which it is placed; if loading on a particular bone increases, the bone will remodel in order to support the increase in load over time. This law also applies to muscle, the muscle will hypertrophy if there is an increased demand on the muscle. For example, if the body is lateralized to the right, the vastus lateralis is eccentrically loaded to support body weight thus creating hypertrophy.

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The pictured athlete is lateralized TO THE RIGHT. Not only is it evident in this picture, but it was determined through testing.

Muscles are SUPPOSE to function in a specific way but the position that the muscle is in due to boney landmarks dictates the function. Function is dictated by position. Stress will pull athletes into an extended position due to an increase in muscle tone of spinal erectors, lats, traps, gastrocnemius, and superficial neck muscles. Performance can be effected due to overreliance on non-

oxidative energy systems in these muscles.

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Superficial neck muscles such as the sternocleidomastoid and traps will be recruited to pull clavicles up to create more space vertically when the diaphragm is not in the most efficient/correct POSITION to function. Both the tendon (attachment point) and belly of the superficial neck muscle will hypertrophy due to increased load. Hello, neck pain.

It doesn’t stop at physical properties of the muscle. Firing patterns can be altered, in which neural pathways for breathing are going to be normalized and directed to using superficial neck muscles instead of the diaphragm, internal obliques, and transverse abdominals to breathe. If the rib cage or pelvis positions are altered and pathophysiology develops, neural firing patterns needed for all three planes of movement (sagittal, frontal, and transverse) may be altered. This may lead to compensation patterns and limit function of major, powerful muscles such as the gluteus maximus.

Impingement may also be a symptom of allostatic overload. An athlete may experience impingement because of lack of anatomical afferent information of where the body is in space. Positional impingement is the instability from misaligned structural position or orientation. Often athletes who experience impingement symptoms (feeling of ‘pinching’ at a joint) lack sensation and resort to a safety pattern. Misaligned body structures can be the result of allostatic overload and impingement becomes the response to threat.

What to do?

Sensory processing will reduce emotional intensity and DE threaten the environment and/or task. A low- resourced environment due to a lack of sensory information is likely to result in high levels of stress. Use tempos to SLOW PEOPLE DOWN. Get people to think, find, feel, and process information. Can you feel this? Can you find that? Feel appropriate muscle working and utilize spatial and ground references to provide athlete with sensory information.

Ground and spatial references that provide perceptual feelings will provide brain with sensory information to respond with the appropriate motor signal. Finding and feeling creates stimulation and stabilization which will help assist symptoms of impingement.

We all need sensory processing for proper motor function; this in combination IS performance.

Consider the pelvic floor when you squat. Pelvic floor dysfunction can lead to pelvic floor pain, poor bladder control (adult diapers), vulvodynia, erectile dysfunction in males, and dyspareunia (painful sexual intercourse). “The pelvic floor muscles contribute to postural (control of lumbar spine and pelvis) and respiratory functions” (7). During periods of increased intra-abdominal pressure such as lifting pelvic floor muscle (puborectalis, puboccygeus, and iliococcygeus) activity is increased to prevent or limit rostral displacement (anterior tilt) of the floor, maintain bladder neck, and assist with urethral and anal closure. If the pelvic floor is not in a good position during activity, weakness and dysfunction may result.

If pelvic position is not restored after lifting (external load) and the pattern/position becomes normalized, it further leads to pelvic floor weakness and possible dysfunction. Improper consideration of the position of the pelvis and function (descent) of the pelvic floor during training can lead to allostatic overload. Improper consideration of the position of the pelvis and function of the pelvic floor muscles during external loading (lifting) OR the inability to return to a neutral position after loading may lead to weakness and dysfunction. Consider the health and function of the athlete years after they are done training with you. What are you leaving them with?

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Re-think and APPRECIATE how the athlete is anatomically positioned and how this position is allowing and creating movement. How do you do this? TEST. The most beneficial thing I have taken away from Postural Restoration Institute (PRI) course is a greater understanding of anatomy and exercise selection that provides the athlete with the most benefit and least amount of cost on the system. Let’s use the example of a kettlebell swing: The athlete (on right) demonstrated bilateral pelvic anterior tilt with testing. During the KB Swing, the athlete is not maintaining foot contact with the ground, externally rotating the femur into further ranges of external rotation without the ability to flex, adduct, and internally rotate (I know this via testing).

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So my question is, why would I prescribe an exercise that forces them to greater ranges of external rotation when I know that they are stuck in external rotation? If I force them to go into a greater range of motion in this position, I am driving them into pathology (overlengthening of ligaments, etc.). Is this beneficial? No. Can I find other ways to work on hip hinging and explosive hip extension? Yes. Be creative and understand the individual.

Address anatomical stress patterns. Promote exhalation and systemic flexion to change entrenched and automatic extension position. Get people to EXHALE. IF your athlete is stuck in extension, is giving more extension the best for that athlete? OR is it leading them down a path of pathology? This doesn’t mean stop training? NO, it means manage the consequences. Are they performing exercises in a safety pattern? Then DE threaten. DE threatening the task and/or environment will reduce stress on the system. For individuals who test as pelvic forward/anterior tilt, trap bar deadlifting may be more beneficial in terms of position to strengthen the posterior chain than squatting under high loads. (Understand the context: I work with collegiate athletes how are not competing for money and will most likely not compete at a higher level, so future health and function is a consideration.)

Create a comfortable, welcoming, and positive environment. Positively influence environment, mitigate athlete’s perceptions of both security and risk (2), create quality relationships/social interactions, and educate/provide awareness. Consider psychological stress, just as much as physical stress; know that they are interrelated.

“We spend so much time and energy designing programs and arguing about ‘best’ exercises or ‘best’ session designs, and yet so little time reflecting on how best to positively manipulate training and competition contexts to optimally reduce the negative impacts of stress.” - John Kiely

As a strength and conditioning coach, the best way to manage cost in consideration of allostatic load is with exercise selection. We shouldn’t just modify exercises if an athlete is injured or has physical restrictions, we should modify exercises to avoid unnecessary wear and tear. Choose exercises that avoid pain, provide appropriate position while maintaining intensity. For example, safety bar squatting instead of back squat to avoid shoulder wear and tear and allow athlete to maintain proper position throughout movement. We all have a tendency to want the biggest and best results as fast as possible, however focus on achieving sustainable long-term returns with the overall health and future of the athlete in mind.

About the Author

5ea55417297579193ee8ebe8e1f443ba.jpeg

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: www.michelleboland-training.com

 

  • References
  1. 1. Anderson, A. K. (2005). Affective influences on the attentional dynamics supporting awareness. Journal of Experimental Psychology: General, 134, 258–281.
  2. 2. Bingisser, M. (2017). How your emotional state can be more powerful than your rep scheme. HMMR Media
  3. 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. 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. 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. 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. 7. Lovallo, W. (2016). Stress & Health: Biological and psychological interactions. Sage Publications: Thousand Oaks, CA.
  8. 8. McEwen, B. S. (2000). Allostasis and allostatic load: Implications for neuropsychopharmacology. Neuropsychopharmacology, 22, 108–124.
  9. 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. 10. McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87, 873–901.
  11. 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. 12. Samueloff, S. & Yousef, M.K. (1987). Adaptive physiology to stressful environments. CRC Press Inc: Boca Raton, FL.
  13. 13. Schulkin, J. (2003). Rethinking homeostasis: Allostatic regulation in physiology and pathophysiology. Cambridge, MA: MIT Press.
  14. 14. Schulkin, J. (2004). Allostasis, homeostasis, and the costs of physiological adaptation. Cambridge, England: Cambridge University Press.
  15. 15. Schulkin, J. (2011). Social allostasis: Anticipatory regulation of the internal milieu. Frontiers in Evolutionary Neuroscience, 2 (111), 1-15.
  16. 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. 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.

Allostatic Overload: Stress and Emotional Context Part I

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-beingg; 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).

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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

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Allostasis

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

5ea55417297579193ee8ebe8e1f443ba.jpeg

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: www.michelleboland-training.com

  • References
  1. 1. Anderson, A. K. (2005). Affective influences on the attentional dynamics supporting awareness. Journal of Experimental Psychology: General, 134, 258–281.
  2. 2. Bingisser, M. (2017). How your emotional state can be more powerful than your rep scheme. HMMR Media
  3. 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. 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. 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. 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. 7. Lovallo, W. (2016). Stress & Health: Biological and psychological interactions. Sage Publications: Thousand Oaks, CA.
  8. 8. McEwen, B. S. (2000). Allostasis and allostatic load: Implications for neuropsychopharmacology. Neuropsychopharmacology, 22, 108–124.
  9. 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. 10. McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain. Physiological Reviews, 87, 873–901.
  11. 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. 12. Samueloff, S. & Yousef, M.K. (1987). Adaptive physiology to stressful environments. CRC Press Inc: Boca Raton, FL.
  13. 13. Schulkin, J. (2003). Rethinking homeostasis: Allostatic regulation in physiology and pathophysiology. Cambridge, MA: MIT Press.
  14. 14. Schulkin, J. (2004). Allostasis, homeostasis, and the costs of physiological adaptation. Cambridge, England: Cambridge University Press.
  15. 15. Schulkin, J. (2011). Social allostasis: Anticipatory regulation of the internal milieu. Frontiers in Evolutionary Neuroscience, 2 (111), 1-15.
  16. 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. 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.