Position Defined: Part 2

Position Defined:  Part 2

Part 1 explored how certain exercise techniques, cues, or improper prescription of stress can have consequences. The strength and conditioning professional or personal trainer, who is a stress manager, dictates exercise prescription. We discussed how appreciating the starting POSITION of the axial skeleton and pelvis is the foundation for movement of the entire system.  Appreciating the starting POSITION of the axial skeleton and pelvis can reduce stress, unnecessary wear and tear, allow for optimal length-tension relationship of muscles being targeted, and improve the range of motion at joints involved in the movement.

Part 2 will explore a summary of the steps involved in the process of appreciating how you are setting up an athlete or client during the start of an exercise and how to think about ways in which you can reduce unnecessary stress on a system.  We will then explore techniques for advanced POSITIONS you can consider with your athletes or clients when you are providing instruction. The conclusion will summarize our coaching principles and reasons and rationale for this article. Let’s finish up…

An Athlete’s Relationship With An Exercise Environment Via Afferentation & Energy

An Athlete’s Relationship With An Exercise Environment  Via Afferentation & Energy

Sensory information dictates our perception of the world around us-whatever world that may be to you. That world may be walking down the street feeling the sunlight on your face, holding a barbell in a gym, or sitting at a table holding a loved one’s hand. Our brain needs accurate sensory information from our environment, in order to connect. Sensory information includes the linkage of both the external environment (sensory) and internal environment (emotions). Representations of our environment can occur with both real and remembered stimuli (1). Human behavior and motor control is based upon ACCURATE sensory information (19,21,22). Vision, vestibular, and somatosensory (pain, touch, temperature, and proprioception) input provides our brain with the information it needs to make accurate motor and behavioral responses. The brain needs this afferent information in order to feel safe and know that it can protect itself against threat. You need the ability to sense and feel.

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.

Why Your Coach Might Be Wrong About Your Squat: Knees In For the Win

Whether you're an elite powerlifter, a strength and conditioning coach, a personal trainer, or a physical therapist, you've probably been versed in the concept that proper cueing for the squat with the lower extremities is, spread the floor with the feet, and push the knees out. Perhaps you've even gotten the tid bit about screwing the floor with your feet in the direction of external rotation as well. If you've learned that these particular cues are the way to go, then you've probably also learned that knees caving in towards midline, or valgus is the devil. You've probably seen the technique involving putting a band around the knees so that you reflexively push the knees outwards (varus) against the input of the band. The rationale for squatting this way usually involves the concept that you're going to utilize more gluteal tissues since the actions of the femur will feature external rotation, via the feet screwing, and abduction with the feet spreading the floor and the knees pushing laterally. This is the accepted way to teach the squat, and seems to be agreed upon by the people who are super strong with all the in the trenches experience in the world, as well as the people who understand how to get people out of pain and how to perform prehab to prevent people from doing things like tearing their ACL in the first place.

Despite all these recommendations and agreed upon findings, you'll still see elite weightlifters feature the rapid action of knees moving towards midline while squatting up massive weights that they just dove under and caught in positions that require incredible levels of mobility and stability to get into. Some of the most gifted athletes I've ever worked with who demonstrate great sports biomechanics and produce incredible amounts of force production also seem to show this action of knees going towards midline during the upward portion of heavy squatting. I'm here to say that I don't think I have any problem with highly athletic individuals who possess great joint biomechanics demonstrating knees towards midline during the upward portion of a squat. I'm also here to say that I think I have the answer as to why the strongest power lifters and strength coaches amongst us have fallen so deeply in love with the spread the floor, knees out approach. To explain my argument I'm going to walk you through concepts relating to natural femoral biomechanics, and what joint force moments have to do with this approach. I'll also give some recommendations on what to do with this thought process, and what measurements might be helpful with making objective determinations of what's optimal for people regarding squat biomechanics.

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During movement, the human body has to absorb forces as well as create propulsive forces. The gait cycle is the most fundamental and stereotypical movement pattern for humans. Gait is comprised of stance and swing, each featuring early, mid, and terminal phases. Absorption of forces, as well as the creation of propulsive forces, are primarily rooted in the stance phase of gait. On a very basic level we could say that early stance is the absorption dominant part of stance, terminal stance is the propulsion dominant phase of gait, and mid-stance is the transitional period. Gait and squatting are certainly not the same movement pattern, therefore generalizations between the two movements should be looked at with skepticism; however, examining gait will help with the formation of the primary reasoning piece helping us understand the biomechanical argument being presented here.

While going through the gait cycle, the femur typically features alternating triads of movement. There are times during the cycle where the femur will group flexion with abduction and external rotation (mostly swing), and there are times when the femur will match extension with adduction and internal rotation (mostly stance). The first triad of flexion, abduction, and external rotation is the strategy the femur uses to prepare for force absorption and to absorb force, while the second triad of extension, adduction, and internal rotation is the strategy the femur uses to prepare for and execute propulsion. Ultimately I see the same sort of strategy used by the femur during the squat, and that is the central premise of this argument. The common link between gait and the squat in this context is that both rely on the femur and the femur ultimately has its preferred strategy for absorption of force and creation of propulsive force.

The descent into the deep squat position would be the force absorption portion, and pushing back up to standing would be the propulsive component of the squat pattern. The natural tendency of the femur during the descent would be to group flexion with abduction and external rotation. Conversely, during the concentric portion of the squat pattern, the natural tendency of the femur would be to group extension with adduction and internal rotation. This would be an intelligent strategy to use as an organism from an energy conservation standpoint because the actions of flexion, abduction, and external rotation would lead to lengthening the extensors, adductors, and internal rotators, which may both maximize the length-tension relationship of those tissues, and provide a stretch reflex to assist the forthcoming concentric phase of the movement.

So why do we cue knees out so hard? My first thought is that the coaches who have figured out that this helps in the ability to squat heavy weights are people who have done a significant amount of training. People with extensive resistance training backgrounds are usually fairly easy to spot. Their bodies have undergone fairly stereotypical adaptations. They've clearly undergone extensive amounts of tissue remodeling, and show demonstrable hypertrophy of skeletal muscle. Heavily resistance trained individuals also seem to move differently...you can spot them walking. These individuals seem to present with an anteriorly tilted pelvis more than the general population.

Pelvic-tilt.jpg

To understand the essence of what kinds of bodily relationships happen with an anterior tilted pelvis, let's use a thought experiment. If you were to prop up someone who was unconscious and you were to anteriorly tilt their pelvis, that individual's femurs would passively follow the anterior tilt of the pelvis, and those femurs would orient internally and towards midline. Ultimately, if you excessively anteriorly tilted an unconscious person's pelvis, they would simply fall on their face (aka, go into prone collapse).

With a conscious human being interacting with the world, things will change, particularly in regards to battling gravity and preventing prone collapse. The typical response of an individual's femurs to a pelvis that is going into anterior tilt, while standing, is that the femurs will reflexively start externally rotating and abducting to prevent prone collapse. This is the typical strategy that will be used by a heavily resistance trained individual, who has an anterior tilted pelvis, to deal with gravity and prevent prone collapse while standing. Where things get interesting is when we lay this person on a table and measure femoral ranges of motion. When the person lies down on the table, we are removing the need for them to fight prone collapse, and the femurs will stop their reflexive behavior of externally rotating and abducting. This individual's femurs will now simply exist in the passive state of adduction and internal rotation because they're simply in line with the orientation of the anteriorly tilted pelvis.

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When I test the person for femoral range of motion on the table, they will demonstrate reduced adduction and internal rotation...why? Because the femur is already internally rotated and adducted. The femur has less room to further internally rotate and adduct. So, when dealing with a heavily resistance trained individual who has an anteriorly tilted pelvis, what you're really dealing with is a situation where the more the pelvis anteriorly tilts, the more the femurs are internally oriented and adducted PASSIVELY, and the more the behavior of the femurs in a weight bearing situation will be one where they move by externally rotating and abducting ACTIVELY to prevent prone collapse. Regardless of how you slice it, the individual will demonstrate a lack of adduction and internal rotation from a testing perspective, and from a functional movement perspective. Yet this person needs to utilize the actions of adduction and internal rotation with extension of the femur to be able to create the concentric portion of a squat. How does one obtain that which they do not have?

Picture the following scenario. I am standing with my weight equally on both feet. Both feet are side by side and pointed straight ahead. I see something move to my left. Without moving my feet, I rotate/orient my entire center of mass to the left to look at it. I then hear something slightly to my right, so I adjust myself to examine what made the noise. To do so, I begin rotating back to the right. Interestingly, the noise that I heard was still to the left of my starting orientation in this scenario. Despite the fact that I was rotating back to the right, my center of mass still remained rotated and oriented to the left. This example illustrates the difference between true joint actions and joint action moments.

The true joint actions that took place were vertebral rotations left. When I heard the noise, I started rotating back to the right, but my vertebrae were still rotated left. I was creating the moment of right rotation, but I never got to the point where you could say I was rotated to the right...I was always rotated left. With the heavily resistance trained individual who is squatting, this person, while standing, has an anteriorly tilted pelvis, and their femurs are reflexively externally rotating and abducting. This person overall cannot reach the true joint actions of adduction and internal rotation, but what this person can do is utilize a strategy of further abducting and externally rotating, so that they can utilize the moment of adduction and internal rotation to group with extension to take advantage of the way the femur naturally creates propulsive force.

How would this person do this? They would spread the floor and externally screw the floor with their feet, and push the knees out during the descent to go further into the actions of abducting, and externally rotating their femurs. To reverse the squat and come back up, the person would then begin creating the moment of extending, adducting, and internally rotating...they may never reach the true joint actions of femoral extension, adduction, and internal rotation (likely because they lack those motions), but they can still utilize the propulsive force coming from the moment of that triad to execute the concentric portion of the squat. When watching these individuals squat, you may never see the knees crashing towards midline...because they likely can't...but they're still relying on the same muscular strategy as someone who is demonstrating medial translation or true adduction in their squat. This strategy may also get confused with some sort of pathological strategy where the femur is moving medially and rotating internally, but the tibia/calcaneus/foot complex remains lateral and externally rotated, which will be discussed more in a forthcoming paragraph.

When dealing with young athletes, these individuals likely haven't gone through many of the adaptations (or perhaps stress responses) that heavily resistance trained individuals have, and thus likely do not demonstrate as much anterior tilt of the pelvis. These individuals likely can get into the true joint actions of adduction and internal rotation, so when we see knees moving towards midline, we may just be seeing the manifestation of the true joint actions being driven by the muscular moment of those actions. With elite weightlifters, and other extremely athletic individuals who produce tremendous force during the squat they may also be showing the true joint actions of internal rotation and adduction, and we may be seeing people who have somehow avoided changes that drive a pelvis into anterior tilt that come along with extensive heavy resistance training. With these individuals we may be seeing the most resilient amongst us to consistent heavy resistance training/those who have survived and thrived in the selection process.

The tricky parts to this concept involve the areas that revolve around injury. The mechanism of injury for the ACL is when the knee moves medially and rapidly internally rotates. The catch though is that the injury to the ACL is based on the relationship of the femur to the tibia. There has to be torque, twist, and a difference in direction between the femur and the tibia for this particular knee injury to happen. Frequently you'll see a situation where the tibia, relative to the femur is translating laterally and externally rotating at that same time as the femur is rapidly translating medially and internally rotating. If people are squatting and maintaining a flat foot with the weight evenly distributed throughout the foot, and the foot/calcaneus/tibia complex is not externally rotating during the descent, then witnessing the true actions of adduction and internal rotation of a femur is probably not cause for concern. When we do start seeing the foot/calcaneus/tibia complex start to spin out with concomitant medial translation and internal orientation of a knee, then we are probably seeing torque between the femur and the tibia, which could be threatening to ligamentous and other soft tissue structures of the knee, particularly if the force and/or velocity of those divergent joint movements is high. Fully addressing the entire scope of injury mechanics is beyond the scope of this article; however, supposing that any observable movement of the knee towards midline is threatening, dangerous, likely wearing down soft tissues, and is undesirable is perhaps a rush to judgment on something that may be benign, so long as foot, calcaneus, tibia, and femur are synchronously working together in a fairly natural and stereotypical way for the human squat pattern.

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To determine whether seeing a knee translate medially is acceptable or not, testing must be done. I would recommend using an Ober's test to determine if the individual has a femur that can extend and adduct. I would recommend using supine and seated femoral internal rotation to determine whether the individual possesses this joint action. I would also recommend using a Thomas test to confirm femoral extension or determine that the femur is extending through some compensatory/pathological method if it was unable to extend in the Ober's test. If the person passes all these tests, then they possess the true joint actions of extension, adduction, and internal rotation, and this person would probably be fairly safe with demonstrating medial translation of the knee during the ascent of a squat so long as weight bearing on the foot remained appropriate. If someone is lacking these true joint actions, based on test results, and demonstrates medial knee translation during the squat, it's likely that there are some aberrant joint actions that could be problematic.

 Thomas Test

Thomas Test

There are two other specific topics that should be discussed before wrapping up this article. The first is the topic of seeing medial translation during the eccentric portion of the squat. This, to me, would be indicative of someone who would be existing in the state of having an anteriorly tipped pelvis, but is not kicking their femurs into the actions of externally rotating and abducting as their anti-gravity strategy. This is probably a highly untrained person, who is probably going to be fairly unimpressive and lack most of the desirable force production capabilities you'd look for. During the descent of the squat when the femurs should be flexing, abducting, and externally rotating, the pelvis should also be using the moment involving posterior rotating (aka, pelvic inlet flexion). If the pelvis is struggling with this moment and stays in the position of excessive anterior tilt, and the individual is not utilizing compensatory actions of the femur, you'll see this incredibly unimpressive looking, melting candle, squat presentation. This is undesirable, but we should begin the coaching process by trying to get the individual to gain better pelvic control first before trying to coach the femur.

This brings us to our last topic in this article, which is coaching strategy. Where I would start giving recommendations is to quote Charlie Francis in regards to advice to coaches...think twice and speak once or not at all. When you start thinking that you're smarter than the millions upon millions of years of evolution that led to a human organism standing in front of you executing patterns that are the result of protein behavior that were coded for by a genome and wired up by a nervous system that has figured out the most effective way to guide someone through the complex and multi-faceted environment that they've lived in for their entire life, you're starting to border on being someone who is either way too ego driven, or ignorant of the depth of reality, that you could be problematic. Observe people for a while. Check your opinions. Provide the feedback that the person needs, but be careful about what you say and how you say it...be cautious and humble. Then let testing guide you. Find your algorithm that takes decision-making out of your mind. Use the previous tests to determine whether the person has authentic joint actions or if they're resorting to compensatory strategies. Second, if you want to figure out what the most energy/electrically/physiologically efficient and effective squat would be, I would recommend looking at it through EMG, but I wouldn't try to see what the highest EMG would be. In fact, I would look for how I could get the lowest EMG for a squat. If I keep the load constant, and I see that one strategy uses less electrical energy, that should be the least compensatory strategy possible, and theoretically, that would be the best approach. For more on why that is the appropriate thought process regarding EMG readings, see the explanation given in this article.

My concluding thought on coaching and optimal performance with the squat is that the most likely best way to perform the movement would feature performing the pattern in the mid zone of abduction and adduction, and internal and external rotation. If I want the least wear and tear over time, I would want to try to move through the middle of the pathway rather than forcing my way into the boundaries at each side. So I personally wouldn't start coaching a beginner who possesses the true joint actions of extension, adduction, and internal rotation with the cues of spread the floor, screw the floor out and push the knees out. I would cue them to find and feel the middle of their heels on the descent. I would cue them to keep their heels at the bottom and to find their big toe. To push back up, I would have them continue to find and feel their heels and big toes, and then find and feel their medial arch, and to push through the medial arch to drive back up. I would observe their femoral behavior with those cues for a while, continue to monitor joint actions through table tests, progress them with load and reps and sets over time, and not think I necessarily had the right answers. Lastly, I wouldn't treat everyone the same, and I'd be very careful about giving cookie cutter coaching cues to groups.

To progress an industry or advance the overall information available to practitioners within a discipline, professionals should avoid dogmatic thoughts and behaviors. Often times, the degree to which a concept is entrenched in the collective working body of accepted beliefs can blind everyone in that field. I'm not saying that I'm absolutely correct with my assertions in this article. I may be damn well wrong, and somebody may come along and prove it to me so bad that I feel like an enormous fool. I don't think I'm wrong though. In fact, I think I'm very right on this one. It may take you a minute to see what I'm saying here, particularly with all this junk about true joint actions, and moments, and the difference between being rotated and rotating, and all the other blah blah blah. So I ask you to consider what I'm saying here in this article before you blow it off and quickly say that I don't know what I'm talking about and I'm going to get people hurt, and the sun won't come up tomorrow, and stand outside my door with torches and pitchforks, because I'm saying that knees moving towards midline may be no big deal, and perhaps is even natural and appropriate...and if you can't do it, maybe you're stuck and there's a problem. I'm not questioning a long-held assumption because I'm looking to cause a controversy or anything else like that. I like trying to see a puzzle for what it actually is. Active human anatomy is a beautiful puzzle. It can be an extremely vexing puzzle, and often times, what you think you see isn't what you get...but the logic always works if you follow it long enough with the right starting assumptions. Perhaps my starting assumptions are off, in which case this whole thing is wrong, and you can commence throwing a pie in my face. But if my starting assumptions are correct, I believe my Bayesian reasoning throughout this is strong, and you may have to come around to this way of thinking regarding what's actually going on with the squat. Anyways, here's to questioning authority, thinking for yourself, being unafraid of backlash and criticism, and trying hard in the life you've got.

I'd like to thank the Postural Restoration Institute for providing the theoretical foundations for helping me think through the big ideas of this article. They teach the ideas of the differences between being rotated/oriented and rotating. They also teach the idea that if you can't express a joint action, like adduction, it's probably because you're already existing in that position, and therefore are limited in being able to get further into that position. Without the course work and learning I've done with PRI, I would not have been able to conceive of the ideas for this article.

about the author

d9ca6c07fc91bb289822a676849ad941.jpeg

pat Davidson

-Director of Training Methodology and Continuing Education at Peak Performance, NYC.

-Assistant Professor at Brooklyn College, 2009-2011

-Assistant Professor, Springfield College 2011-2014

-Head Coach Springfield College Team Ironsports 2011-2013

-175 pound Strongman competitor. Two time qualifier for world championships at Arnold Classic

-Renaissance Meat Head

Hormones and Training: What You Need to Know

There are two communication systems in the body, one wired, the nervous system, and the other non-wired, the endocrine system. Communication systems are used to decode the meaning of the environment that the organism finds itself in, and to communicate the environmental messages to the individual cells and DNA of the organism. Hormones do not make the cells do anything differently than what the cells normally do. Instead, hormones change the rate and the magnitude of physiological expression of cellular behavior. Hormones are released from a source cell, and make their way to a target cell where they exert their effect. Some hormones are released a great distance from their target cell, others are released from a neighboring cell, while others still are released in the same cell that ultimately is the target cell. The endocrine system utilizes glands, ducts, and the circulatory system to send its messages throughout the body. To exert its effects on the body, a hormone must bind to its receptor at the target cell. Hormone receptors are located either at the plasma membrane, the nuclear envelope, or inside the nucleus. Generally, peptide hormones have membrane bound receptors, steroid hormones have nuclear envelope receptors, and thyroid hormones have nuclear receptors.

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For all the types of hormones, the receptors are always proteins. Protein receptors are shaped in a way that makes them optimal for a specific class of hormones. When the hormone binds to the receptor, the receptor’s charge will be effected by the presence of the new hormone molecule, and the receptor will seek to change shape to find the shape associated with the next most stable charge. This changing of shape of the receptor protein will set off an intracellular/intranuclear physiological cascade effect that will ultimately effect one of the two phases of protein synthesis, transcription or translation.

Transcription is the copying of the genotype for a specific sequence of the genome, while translation is the construction of a protein from the genomic information at the ribosome. The post-translation folded protein is the ultimate phenotypic representation of the cascade effect featuring the cyclic effects of, environmental signal leading to organismal recognition, leading to secretion of a hormone, leading to migration of hormone to target cell, leading to binding of hormone to receptor, leading to intracellular messaging cascade, leading to change in the rate and/or magnitude of expression of DNA or ribosomal protein synthesis activity, leading to new proteins driving cellular behavior, leading to changes in organism behavior, leading to new interactions with the environment…and the cycle repeats again and again.

Due to the complexity of having a multitude of hormones being released from various source cells and reaching target cells simultaneously for a variable message that leads to an enormous number of concurrent intracellular effects, we need a working model to make sense of any of this concept, and to have a sense of what to do with it as a topic for exercise program design. In this article, we will focus on, what makes a specific cell a target cell, and what sort of internal environment is optimal for a robust anabolic hormone response. As with all models, they simplify complex topics to the point where there are occasions of inaccuracy. So the nit-picking evidence based troll may find several problems with this particular article; however, this article will generally serve as a strong guide for what conditions are appropriate to create on specific training days in a well-crafted training program.

A target cell is one that has the protein receptor for a specific kind of hormone. The attractiveness of a target cell to a circulating hormone becomes greater when the sensitivity and number of the receptors to that hormone is increased (upregulation). We are primarily interested in muscle cells in this article. Skeletal muscle cells are target cells for all of the major types of anabolic hormones. The sensitivity of receptors varies greatly depending upon the state of that particular skeletal muscle cell. Sensitivity of skeletal muscle cell hormone receptors is changed primarily by whether that cell has been recruited and fatigued. The greater the degree of recruitment and fatigue of that particular cell, the greater the upregulation of hormone receptors, and the more that cell becomes a highly attractive target cell for hormones. The next logical question is, how does one recruit and fatigue particular muscle cells.

The Henneman Size Principle is the guiding phenomenon regarding recruitment of skeletal muscle cells. The Size Principle states that at the lowest levels of force production, the slowest twitch muscle cells will be recruited to perform the task, and that as force increases within the task, faster and faster twitch cells will be recruited. At the highest levels of force production, the fastest twitch muscle cells will be recruited.

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Fatigue of muscle cells is based on repeatedly using the same cell for a task, and ultimately witnessing a drop off in performance from that cell. The greater the drop off in performance, the greater the overall fatigue. Not all of the mechanisms of what drives performance drop off are known, but some examples include substrate depletion and accumulation of metabolic byproducts. As a general rule of thumb, we can say that slow twitch cells are easy to recruit and difficult to fatigue, while fast twitch cells are difficult to recruit and easy to fatigue. The juxtaposition of responses between slow twitch and fast twitch cells to recruitment and fatigue creates an adaptable organism, but does present challenges to the exercise program design specialist. The program designer must determine what sorts of cells are necessary for modifying as target cells, and devise training schemes that maximize the receptor sensitivity for those cells to drive adaptive changes into them.

In his tour de force, Science and Practice of Strength Training, Zatsiorsky presents his fiber corridor concept. The corridor demonstrates methods that will lead to specificity of twitch type adaptations. Athletes who need to keep body weight low, and still display the highest levels of force production within their sport tend to employ training methods that systematically recruit and fatigue just the fast twitch cells. Athletes who are looking to put on as much mass as possible without caring too much for what cell type they are targeting can use methods that will recruit and fatigue slow, moderate, and fast twitch cells.

If you want to target just the fast twitch fibers for adaptation, you are generally going to choose resistance training methods involving the maximum effort method (repetitions using 90% or greater of 1RM), or the dynamic effort method (sub-maximal loaded repetitions performed at the greatest velocity possible stopping well short of failure). If you want to target moderate twitch fibers, you can start using the repeated effort method (loads under 90% with sets going to failure). Finally, if you want to target slow twitch cells, you can start using approaches like the stato-dynamic method (explained in greater depth later), which is low force, but high in duration for sets. There are many more methods, particularly when opening the playbook into realms such as plyometrics, change of direction, speed and agility related drills, and conditioning, but for simplicity sake in this article we will stick to resistance training drills only.

All of the methods described in the previous paragraph, perhaps with the exception of the dynamic effort method, have the ability to create dramatic hormonal responses to training through various pathways. The repeated effort method is the approach most commonly thought of for hormonal effects. Most classical research in the area of hormonal responses to exercise have focused on repeated effort method approaches, and have shown that multiple sets of approximately 10RM efforts with short rest periods seems to be the gold standard for highest possible endocrine responses to exercise. Performing 3 to 5 sets of 10RM with 60 to 90 seconds of rest between sets with compound exercises like the squat is one of the most stressful stimuli that you can impart on an organism. Such a protocol will stress every system in the human body to near maximal.

As was mentioned earlier in the article, the endocrine system is a communication system. What was not mentioned earlier is that the messages that the endocrine system primarily relays have to do with the maintenance of homeostasis. Homeostasis involves a select set of variables that cannot leave an acceptable range of values or the organism will likely die. Some variables considered homeostatic include temperature, blood pH, oxygen tension, and blood glucose. A protocol like 5 sets of short rest 10RM squats will threaten all of the homeostatic variables. In response to this, the body will mobilize defense strategies that will protect homeostasis. Activation of the endocrine system is one such response the body uses to ensure that homeostasis is not lost.

The primary purpose of the endocrine system is to return the body to optimal conditions that provide for the greatest safe haven wherein homeostatic variables remain unchallenged. Ultimately, with training approaches aimed at hormones, we can say that the best way to grow muscle tissue would be to recruit and fatigue the maximal number of muscle cells (now target cells), and threaten homeostatic variables to the greatest possible degree to magnify the absolute hormonal response to the highest possible level. Multiple repeated effort method sets are like a shotgun blast to the systematic steps of maximal protein synthesis. A huge number of cells within the Zatsiorsky fiber corridor are recruited and fatigued, a tidal wave of multiple organ systems stress is unfurled within the organism, and the enormous threat to a variety of homeostatic variables forces the creature’s hand to mobilize massive endocrine responses.

The hormonal response to the multiple bouts of repeated effort method work described previously is a mixed bag. This protocol will cause the highest cortisol and growth hormone responses to any regular training method. Catecholamines will also be powerfully elevated due to the massive sympathetic response to this protocol. The elevation of the catecholamines seems to be related to a downstream testosterone response. The growth hormone response will trigger an increase in insulin-like growth factor (IGF) through downstream mechanisms. In short, you see all of the hormones involved with cellular remodeling all at once in massive amounts. For some athletes, this mixed bag is not optimal. Greater specificity of hormonal responses can be achieved with some of the other methods.

Repeated bouts of short rest between sets maximal effort method training are very effective approaches for driving a significant testosterone response. Loads generally have to be at or above 85% of the 1RM in order to witness this testosterone response. In the past I have devised blocks that have been testosterone specific blocks. One such block featured a 3 week build-up. I would pair compound exercises, such as front squat and bench press (A day), and deadlift and incline bench press (B day). 60 seconds of rest would exist between the two exercises. Week 1 would feature 6 sets of 3 reps performed at 85% 1RM. Week 2 would feature 8 sets of 2 at 88% 1RM. Week 3 would feature 12 sets of 1 at 92% 1RM. Structuring the training week could be variable, but generally speaking, you want to get at least 3 training sessions in per week, and preferably 4.

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This seems aggressive, but I’ve personally done it, and witnessed many individuals perform it with extremely impressive responses. I caution participants to avoid getting fired up for sets. Remain neutral emotionally as much as possible. Such a testosterone specific block generally targets fast twitch cells. I recommend not doing more than 2 of these testosterone specific blocks in an annual training cycle. I believe that this is primarily a neural oriented testosterone specific block. In short, this is because neural cell bodies contain an abundance of androgen receptors, and testosterone exerts profound effects on neural cellular remodeling physiology. The three week build up is a good timing element. Synaptic neuroplastic changes will take place within this time period. Neural cell bodies generally take approximately one month to remodel, but a full month of this protocol borders on what I would consider dangerous, and my hope is that the hormonal surge speeds up the remodeling process at the neural cell body.

The stato-dynamic effort method uses loads of approximately 50% or less, and witnesses the participant moving the load at slow velocities. 2 to 4 second eccentric and concentric motions are typically used for this method. The low load and slow tempo makes this approach target the slow twitch fibers due to the very low forces. While the force variable is low, the duration of the set should be large. Slow twitch fibers are easy to recruit, but difficult to fatigue, and the longer duration sets are ideal for setting the stage to turn these slow twitch fibers into target cells. Sets are typically performed for 40 to 60 seconds, and participants can build up to performing multiple rounds of 3 to 5 sets. Typically the rest period is kept in a 1 to 1 ratio with the work duration.

The stato-dynamic effort method fits into the broader category of occlusion based training approaches. Occlusion techniques were made popular by the Japanese, Katso approach, also called Blood Flow Restricted Training (BFR). The overall findings from the various protocols that have been used in BFR approaches is that a substantial increase in growth hormone is typically seen, even when loads of approximately 30% 1RM are used. The thought behind this approach is that occlusion of venous vessels prevents the removal of metabolic byproducts from the local tissue area for an extended period of time, creating a larger than normal level of waste products and heat trapped in the blood that cannot escape until the occlusion is released. Once the occlusion is released, the blood that is loaded with waste products ultimately is circulated back to central regions, such as the heart and neck. Chemoreceptors in the carotid body and arch of the aorta register the high concentrations of metabolic byproducts in the blood, send an afferent signal to the nucleus tractus solitarius, which relays the message to the hypothalamus. The hypothalamus perceives the internal environment of the body to be one that would threaten homeostasis. The hypothalamus then begins a signaling cascade to the anterior pituitary that unleashes a potent growth hormone pulse.

The stato-dynamic effort method asks the participant to never completely lock out the joints during performance of the tempo based exercise. Such an approach keeps the muscle tissue actively creating tension throughout the time period that the exercise is being performed. When muscle tissue is actively creating tension, it mechanically compresses the blood vessels that supply and drain the tissue, thus creating an occlusal effect. Eventually the set ends, and the occluded blood is sent back into circulation, leading to the mechanism of hormonal signaling described in the previous paragraph. Since only the slow twitch muscle was recruited and fatigued with this approach, only the slow twitch tissue is the target cell for the hormonal cascade.

Creating appropriate training templates for athletes of various types could easily be considered an act of cellular remodeling specificity. The wise coach is the one who determines the fiber type that primarily needs to be developed, the rate at which that fiber type needs to be developed, and how much of a hormonal driver for increasing rate and magnitude of adaptations needs to be imparted on the athlete at any point in time. All of the approaches listed in this article are considered to be advanced methods. Such methods may not be necessary for young athletes; however, once athletes are reaching advanced years in college or have been involved with professional sports and intensive training for several annual cycles, these approaches need to be considered. When sport specific skill and technical and tactical knowledge have reached their highest levels in advanced athletes, those with more specific fitness for the physiological demands of the game will have an advantage over their peers. At the highest levels, differences are measured with the edge of the razor. The thought that goes into the focus of training blocks should be just as exacting. If alterations in body composition need to be accomplished, we ultimately come to the concept that the morphology of the organism is largely a hormonally driven phenomenon. Those with the knowledge of specific hormones, and the techniques to create specific target cells will be better suited to help individuals with that need.

about the author

d9ca6c07fc91bb289822a676849ad941.jpeg

pat davidson

-Director of Training Methodology and Continuing Education at Peak Performance, NYC.

-Assistant Professor at Brooklyn College, 2009-2011

-Assistant Professor, Springfield College 2011-2014

-Head Coach Springfield College Team Ironsports 2011-2013

-175 pound Strongman competitor. Two time qualifier for world championships at Arnold Classic

-Renaissance Meat Head