ACL article for the sporting athlete.

Training to minimise the sporting knee complaint.

by LaRue Cook

Learning Objectives:

1. To create an awareness in the reader and general trainer population in what activities and ‘events’ are high-risk for non-contact ACL injuries.
2. To raise the awareness on the importance of a well-designed, multi-pronged training program designed to address the several components contributing to non-contact ACL injury prevention.
3. To challenge the reader to continue study and research in this oft-overlooked, but extremely important aspect of athletic training – particularly for female athletes.

An athlete makes a sharp cut on the soccer field as she approaches the ball, or lands after grabbing a rebound in basketball. Suddenly there’s a loud popping sound from her knee that any athlete dreads hearing, and she crumbles to the ground – she has torn her ACL! Every year, the press has several news reports of high-profile professional athletes, such as NBA Most Valuable Player Derrick Rose or perennial Major League Baseball All-Star Mariano Rivera, suffering one of these potentially career-changing non-contact ACL injuries. These injuries seem to be all too prevalent in the sports world today. Though perhaps not as prominently displayed, but just as devastating, is the same injury to our College-level athletes; here’s one such example as reported in the Washington Post on December 1, 2012, “The 11th ranked Maryland women’s basketball team will be without starting guard Laurin Mincy for the rest of the season after the junior tore the anterior cruciate ligament in her right knee during Wednesday night’s …[A]n MRI exam on Thursday revealed the tear, which is the second of her career and the third to befall a member of the women’s basketball team.” But what often flies under the radar of media coverage and public attention is the literally thousands of these injuries that occur each year at the Middle School, and High School level as well – those injuries to our typical training client.


The Big Three

While a select few sports – soccer, basketball and volleyball – are recognized and reported as being the primary culprits for this type of injury and have become known as ‘The Big Three,’ the truth is that an athlete playing any sport requiring quick stops, cuts or changes in direction, or landings can be at risk for this injury. According to the American Orthopaedic Society for Sports Medicine (AOSSM), 70 percent of all ACL tears are non-contact in nature, and most of those occur during a landing or quick deceleration such as cutting or stopping (AOSSM, 2008). These injuries can have a devastating negative impact not only in terms of medical costs (it has been reported that the annual medical cost associated with these types of injuries exceed $650 million per year), but can also have a long-lasting impact on the specific athlete’s ability to perform in their sport, and on their quality of life outside of sport.

With literally hundreds of thousands of these injuries occurring each year, and with statistics revealing that female athletes suffer this type of injury at a rate that’s between 2-10 times higher than their male counterparts, the need for more attention focused on helping our athletes --- particularly females --- reduce their risk for these injuries could not be more apparent.


The ‘Typical’ ACL Injury

So, what does a ‘typical’ non-contact ACL injury look like? And how can we help our athletes avoid or at least reduce their risk for these terrible injuries? While there may not be a ‘typical’ non-contact knee injury per se, here are some of the common elements for this type of injury, as noted by several researchers:

The Quadriceps versus the Hamstrings

According to some researchers, many non-contact ACL injuries appear to be associated with multi-plane knee loadings where the ACL is excessively loaded due to strong quadriceps muscle forces (Myer, Ford, Jensen & Hewett, 2007). These strong forces are combined with frontal-plane and/or transverse-plane knee loading, and insufficient hamstring muscle co-contraction forces. A fairly typical example of this type of scenario would be where an athlete lands from a jump in a stiff legged and valgus (knees collapsing inward) position resulting in strong contractions of their quads coupled with a much lesser involvement of their hamstrings.

Many researchers consider the quadriceps muscles as one of the major forces producing an anterior force on the tibia, and it’s this anterior tibia force that loads the ACL – sometimes to excess and failure (Barber-Westin, Noyes, Tutalo-Smith, & Campbell, 2009). Conversely, the hamstring muscles exert a force that is associated with protecting the knee from this type of injury by leading to knee stability when they co-contract with the quadriceps. This is because of the hamstrings’ function of exerting a counter – posterior-shear force at the tibiofemoral joint. Knowing how these two muscle groups function, leads to the simple conclusion that teaching our athletes proper techniques for landing, cutting and stopping would be instrumental in helping to reduce their risk of this injury.

By training our athletes on proper muscle recruitment patterns that involve contraction of their hamstrings; and by helping our athletes to improve their hamstrings-to-quadriceps strength ratio so that the hamstrings are strong enough to serve their protective function – we can take some important steps to help our athletes reduce their risk of non-contact knee injury.

There are many components to a well-designed training program targeted to reducing the risk of non-contact knee injuries. A cursory online review of research reveals that there are a number of ACL-injury prevention programs out there. While a review of each of these programs and the training techniques that they espouse is beyond the scope of this paper, I would highly recommend that the reader conduct their own research in this area to determine which, if any, of these programs satisfies their needs.

There are a few components that are common to most, if not all, of these programs and the remainder of this article will review 3 components you may wish to include in your training program designed to help your athletes.


Common Components of an Injury Prevention Program

Training and drills targeted at teaching and training our athletes to become safer on the field of play by reducing their risk of non-contact ACL knee injuries fall under several categories:

• Strength Development,
• Deceleration Technique, and
• Kinesthetic Awareness Training or Controlling the Center of gravity (COG).

As trainers and coaches, we can have a positive impact in each of these areas.

Strength Development

Research findings indicate that by improving the athlete’s hamstring strength in relation to the quadriceps, we can better prepare those muscles to perform their protective co-contraction function when our athletes decelerate, and thus help them protect their knees from these types of injuries. By improving or maintaining the athlete’s hamstring strength we can have a positive effect on reducing their risk of these injuries. Additionally, improving the strength of the entire lower body posterior chain musculature will help reduce the occurrence of contributing factors such as valgus - which is often cited as being exacerbated by having weak gluteus medius muscles.

Exercise suggestions: Russian hamstring curls, Single-Leg Deadlifts, Squats, Lunges, Ankle Cuff Lateral Walks and Leg Curls can each be effective in improving strength for these muscles.

Figure 1(a): Ankle Cuff Lateral Walk

Figure 1(a) above shows the athlete in the starting position before performing an Ankle Cuff Lateral Walk. This exercise is used to strengthen the glutes – specifically the gluteus medius, a muscle that is instrumental to helping reduce the risk of non-contact knee injury.

Figure 1(b): Ankle Cuff Lateral Walk

In Figure 1(b) the athlete has taken a lateral step against the resistance of the ankle cuff band. Although not reflected in this photo, have the athlete point their toes straight-ahead throughout the exercise, which will help focus the tube resistance work onto the gluteus medius as intended.


Deceleration Technique Training

The primary focus for many speed coaches and trainers is on improving speed and acceleration. Yet, it’s in teaching properdeceleration techniques where we as trainers can have a positive impact on non-contact knee injuries. Deceleration training is an important, and often overlooked, part of speed training and injury prevention. Not only will teaching our athletes how to decelerate properly have a positive impact on their risk of injury, but also this will help our athletes become effectively fast by teaching them to control their speed in a way that allows them to perform an athletic skill in conjunction with their speed.

The skill-sets of acceleration and deceleration are mirror images of each other and are not, and should not, be treated the same. For example, in the case of jumping and landing (i.e. vertical speed and power), jumping or vertical acceleration is about improving ground-force production, while landing or deceleration training is all about improving ground-force reduction. These two abilities go hand-in-hand and are opposite sides of the training coin. Yet much of what we do as coaches and trainers is spent on theproduction side of this equation.

Reducing our athletes’ risk of non-contact knee injury relies to a great extent on developing the ability to reduce the forces of landing or stopping. From a deceleration perspective, this means using exercises and cueing tips that raise our athlete’s awareness during deceleration. Cueing the athlete to produce a “soft landing,” or a “quiet landing,” while incorporating triple-flexion (flexed ankles, knees and hips) on their landings is just one example of this type of training tip or cue used to improve our athlete’s vertical deceleration technique. Figure 2(a) and Figure 2(b) below show one exercise that I use to teach triple flexion from a stationary position. Once the athlete has adequate experience with triple flexion from this position, I introduce a more dynamic exercise requiring the athlete to jump and land into triple flexion with the cueing for a “soft landing” (see Figure 2(c)).

Figure 2(a):
Deceleration Training Technique – Step 1

Figure 2(a) shows Step 1 of a drill I use to teach athletes soft landing into ‘triple flexion.’ Here I stand on a 12 inch platform holding a light medicine ball. I instruct the athlete to ‘catch the ball when I drop it,’ and as she catches it to ‘drop into triple flexion.’

Figure 2(b):
Deceleration Training Technique – Step 2
Triple Flexion

Figure 2(b) shows the athlete after she catches the ball while simultaneously dropping into triple flexion from her stationary position. While admittedly this final position is not one that the athlete may normally use in a sport competition, this exercise teaches the athlete what triple flexion is and feels like, and gives her the biomechanical feedback necessary to recreate this feeling during athletic competition.

Figure 2(c):
Deceleration Training Technique
Jump prior to Triple Flexion

Figure 2(c) shows the athlete jumping – as if she has just grabbed a rebound – from her position in Figure 2(b). From this jump, the athlete will land again into triple flexion and with a soft landing.

Kinesthetic Awareness and Control of COG

Researchers have cited landing with stiff legs, and decelerating either vertically or horizontally in a valgus knee position, as two main contributors to non-contact knee injuries. Also, studies have shown that many of these types of injuries occur during what researchers call a perturbation event. This is where the athlete decelerates in an uneventful way, but then is suddenly or simultaneously perturbed or disturbed – meaning bumped or otherwise contacted physically in a way that throws them off balance.

Teaching our athletes to become more kinesthetically aware of what their bodies are doing and where their various body parts are in relation to one another during these types of athletic skills is vitally important to the safety of our athletes (Fitzgerald, Axe, & Snyder-Mackler, 2000).

Exercise suggestions: Chair Stand-ups (while looking for signs of valgus), Drop-landings with triple flexion (ankles, knees and hips), Single-leg Squats, Stork Stands with perturbations, and Speed Skaters, are a few of the exercises intended to teach the athlete this type of kinesthetic awareness. During these exercises, the athlete should be required to stop after each repetition and bring their center of gravity under control (i.e. not toppling over laterally).

Figure 3(a): Speed Skater exercise

Here’s an example of the Speed Skater exercise. In Figure 3(a) above, the athlete has performed the Speed Skater exercise with ‘controlled deceleration.’ By controlling her body position and center of gravity the athlete reinforces her ability to dynamically decelerate from a lateral acceleration --- a sport skill that oftentimes leads to non-contact knee injury.


Conclusion

ACL injuries of all types are devastating injuries when they occur. While little can be done in the way of preventing or reducing the risk of the contact ACL injuries typical to such sports as football, trainers can have a significant positive impact on reducing the risk of noncontact ACL injuries when using proper program design and planning. This article highlighted some of the components of effective non-contact ACL Injury Reduction Programs as a way to stimulate thinking in this important direction for any trainers working with athletes.

By designing a training program that incorporates these and other important components, we as trainers can play a significant role in helping to reduce the epidemic of non-contact knee injuries, and thus become instrumental in helping our athletes improve the quality of their athletic and everyday lives.


References

Hewett, T. E., Shultz, S. J., & Griffin, L. Y. (2007). Understanding and Preventing Noncontact ACL Injuries. Champaign, IL: Human Kinetics.

Dintiman, G., & Ward, B. (2003). Sports Speed. Champaign, IL: Human Kinetics.

Noyes, F. R. and Barber Westin, S. D. (2011). Anterior Cruciate Ligament Injury Prevention Training in Female Athletes: A Systematic Review of Injury Reduction and Results of Athletic Performance Tests, Sports Health: A Multidisciplinary Approach, 4(1), 36-46.

Cross, M. (1998). Anterior Cruciate Ligament Injuries: Treatment and Rehabilitation. Retrieved May 6, 2010, from http://www.sportsci.org/encyc/aclinj/aclinj.html/

Meyer, G. D., Ford, K. R., Jensen, B. L., and Hewett, T. E. (2007). Differential Neuromuscular training Effects on ACL Injury Risk Factors in “high-Risk” Versus “Low-Risk” Athletes, BMC Muscular Disorders, 8(39).

Barber-Westin, S. D., Noyes, F. R., Tutalo Smith, S. and Campbell, T. (2009). Reducing the Risk of Noncontact Anterior Cruciate Ligament Injuries in the Female Athlete, The Physician and Sportsmedicine, 3(37), 1-13.

Fleming, B.C., Oksendahl, H., Beynnon, B. D. (2005). Open or Closed-Kinetic Chain Exercises After Anterior Cruciate Ligament Reconstruction, Exercise Sport Science Review, American College of Sports Medicine, 33(3), 134-140.

Lephart, S. M., Pincivero, D. M., Giraido, J. L. and Fu, F. H. (1997). The Role of Proprioception in the Management and Rehabilitation of Athletic Injuries, American Journal of Sports Medicine, 25, 130-137.

Fitzgerald, G. K., Axe, M. J. and Snyder-Mackler, L., (2000). Proposed Practice Guidelines for Nonoperative Anterior Cruciate Ligament Rehabilitation of Physically Active Individuals, Journal of Orthopaedic & Sports Physical Therapy, 30(4), 194-203.

American Orthopaedic Society for Sports Medicine, Anterior Cruciate Ligament (ACL) Injury Prevention, (2008).

 

COMMENTS Add Comment

De Veirman, Lieven | 13 Feb 2013, 08:42 AM Not sure if we should teach our athletes to consciously avoid a valgus knee position. Pronation is the most natural movement and I would prefer teaching my athlete's muscles how to get into pronation/valgus, decelerate the movement and explode back to the other direction.

Cook, LaRue | 12 Feb 2013, 04:09 AM Hi Brian. Thanks for your comment. I agree that “discovering a pattern of weakness” is a key element of developing an effective program here. One such weakness is (or can be) the strength ratio gap between the quads and posterior chain musculature – a weakness that has been shown to be a potential contributing factor to non-contact knee injuries in sports. “Cleaning up movement patterns” (where such defective patterns exist) is necessary as well, and oftentimes one of the primary movement pattern defects in this area – improper deceleration - is related to this muscular imbalance. Learning proper deceleration technique is a key to reducing the risk of non-contact knee injuries in sports movement, and obtaining or maintaining the requisite strength to properly decelerate goes hand-in-hand with this technique. The article speaks of three components to the training program --- strength development, deceleration technique and kinesthetic awareness. Each of these components is an important part of the program, and forms an integral part of the whole. Thanks again for your comment and I hope that you found the article somewhat helpful.

Strachan, Gary | 11 Feb 2013, 01:57 AM I think training for function may be the best place to start. Replicate all the possibilities of where the knee may go, and train at different tempos, ROMs, under load, no load, different drivers etc. And look for mobility or lack of to structure.

Thurston, Brian | 08 Feb 2013, 18:36 PM My belief is that there seems to be a great value in discovering a pattern of weakness or tightness and then exploring how to improve this pattern of weakness or tightness. I think to say that targeting the glute medius as a stamped out program for all athletes may not be the best way to go. Additionally, hamstring strength (as co-contrators) may not be as important to preventing sheer on the tibia-femoral region as we think. By strengthening the hamstrings without first cleaning up movement patterns, we may be doing what Gray Cook calls "adding fitness to imbalance".

Dynamic Spinal Support

(Based on an independent study by Jo Rainsley)

Posture effects three properties of the back and abdominal muscles: their length, the angles at which they pull on the vertebrae, and their lever arms relative to centres of rotation (Adams et al, 2006). Poor posture and movement can lead to local mechanical stress on the muscles, ligaments and joints, resulting in complaints of the neck, back and other parts of the musculoskeletal system (Dul & Weerdmeester, 1993). However, it has been highlighted through literature that the spine is particularly susceptible to postural stress (Pheasant, 1988; Adams et al, 2006; McGill, 2007; Nachemson & Jonsson, 2007).

Clinical and Biomechanical findings
Occupational epidemiology and ergonomics commonly highlight four risk factors inciting the event of LBP: perceived exertion within the workplace: discomfort or fatigue; occurrence of LBP; and sick leave due to LBP (Muller, 2007). One biomechanical factor contributing to patients with LBP is reduced lordosis; especially in the lower lumbar spine and a particular flat back is a risk factor for future low back pain (Jackson and McManus, 1994; Adams et al, 1999).
The vertebrae form the passive units of the lumbar spine while the intervertebral discs (IVDs) and the posterior ligamentous structures form an active unit (Palastanga et al, 2006). The IVD and cartilage end plate postulate to buffer against gravity and torsion and act as a shock absorber of forces transmitted into the spinal column. IVD compressive force load failure is 3000 Newton’s (N) with a torsional strength of 40kg/cm2. This end point is that similar to steel, however the IVD is able to retain some power after recovery, thereby retaining its properties of elasticity (Adams et al, 2006).
When gravity exerts a vertical force on the spine, depending upon the posture of the spine will depend upon which gravitation force is imposed i.e. in flexion and extension shear loading is higher segmentally in the spine than compressional force loading. The larger the angle in extension and flexion from neutral, the higher the shear force. Intervertebral compressive and shear force components rise when the spine is taken through flexion and extension.
Flexed posture stretches the intervertebral ligaments, and tension in these ligaments increases the compressive force acting on the intervertebral disc. Muscular contractions in excess of normal requirements may have a detrimental effect on the nutrition of the discs, as this is dependent on imbibitions of fluid, which occurs when the compression is reduced (Oliver and Middleditch, 1991). In a seated position with a slump, the pelvis is tilted forwards, the thoracic curvature is increased and the lumbar curvature flattened (Kapandji, 1988). Whilst standing the IVD compressive load of the lumbar spine is 500N (White et al, 1999), sitting with a slouched position IVD pressure is doubled (Nachemson & Jonsson, 2007).
When muscles are lengthened beyond their optimum length, overlap between actin and myosin filaments decreases and cross-bridge formation falls. Consequently, an increasing proportion of the force generated is due to tension in the stretched collegenous tissue sheaths of the muscle. During bending, compression and shear to stimulate flexion of the spine, the intervertebral ligaments provide most the resistance to movement. The tensile strength of the longitudinal ligaments is 200kg/cm2, after a few minutes ligaments creep substantially in whereas disc creep happens over longer distance (McGill and Brown, 1992; McMillan et al 1996) therefore sustained repetitive flexion will have a relatively greater effect on the posterior intervertebral ligaments and as a consequence of this reducing their protective duties of the IVDs. Just 5 minutes of this creep is enough to reduce the ability of the intervertebral ligaments to protect the discs in bending by 40% (Adams and Dolan, 1996). Most disc creep is due to the expulsion of water (Adams & Hutton, 1983; Kreamer et al, 1985; McMillan et al, 1996). Approximately 25% of the creep has attributed to viscoelastic deformation of the annulus (Broberg, 1993) as a result leaving the annulus tissue more elastic (Koeller et al, 1984; Smeathers, 1984). Therefore, if a forward bending task followed a prolonged duration of being sat in a flexed position, the impairment of the spinal stabilisers could be delayed therefore inciting the possibility of injury.
Posture is the position assumed by the body either by means of the integrated action of muscles working to counteract the force of gravity, or when supported during muscular inactivity. Many postures are assumed by an individual during a 24 hour period, and at any given moment posture compromises the positions of all the joints of the body (Kendall et al, 1993). Posture influences the water expulsion from the discs (Adams & Hutton, 1983) as well as load bearing by the zygzpophysial joints. Water loss from IVDs leads to stress concentrations in the disc itself. When a person stands in an upright position, the mass of the head, trunk and arms press vertically on the lumbar spine. Ruff (1950) discovered the compressive force loaded vertically in a human standing in an upright position was approximately 55% of their bodyweight. In a relaxed recumbent sitting position the compressive forces on the lumbar discs approximately double from the forces that are found in a superincumbant bodyweight (Nachemson & Jonsson, 2007). Postures are maintained or adapted as a result of neuromuscular coordination, the appropriate muscles being innervated by means of a complex reflex system. The efferent response is a motor one, the antigravity muscles being the principal effector organs (Oliver and Middleditch, 1991). Individuals, who have impaired proprioceptive or motor function, would be more likely to sustain fatigue damage to spinal tissues during repetitive bending and lifting tasks (Adams and Dolan, 1991).
During static effort the muscle does not change its length but remains in a state of heightened tension, with force exerted over the duration of the effort. This isometric state has a steady consumption of energy while it is supporting a given weight, but does not appear to be doing useful work (Kroemer & Grandjean, 2005). Therefore a muscle that is performing heavy static effort is receiving no fresh blood and no sugar or oxygen and must depend on its own reserves. More importantly no waste products are being removed, therefore the waste products are accumulating and producing the acute pain of muscular fatigue. However when the static effort is less than 20% of the maximum the blood flow should be normal (Kroemer & Grandjean, 2005). Liira et al (1996) suggested that static office workers are more exposed to LBP than those office workers who vary their work position.
Design of the Dynaspine
Seat design over the centuries has implemented backrests in chairs to assist in the maintenance of the lumbar concavity (Singleton, 1982). However, although these designs may assist in lumbar lordosis, therefore reducing the tensile forces on the posterior ligaments of the lumbar spine and IVDs. However, the issue still remains that innervation of spinal stabilisers has not been met. Research indicates power output of static effort restricts the flow of blood to a muscle where a series of physiological condition of muscle fatigue supervenes, whilst frequent shifts of posture are subjectively desirable (Pheasant, 1988; Liira et al, 1996; Kroemer & Grandjean, 2005; McGill, 2007). Kramer (1985) produced evidence that to keep the IVDs well nourished and in good condition, they need to be subjected to frequent changes of pressure, as a kind of pumping mechanism. From a medical point of view, therefore, an occasional change of posture from bent to erect, and vice versa, must be beneficial (Kelsey, 1975; Kroemer & Grandjean, 2005; McGill, 2002).
The design of the Dynaspine is such that it has considered the need to create a lumbar support product to alleviate unnecessary stress on the lower spine. However, the design has also considered the emergent data, from a scientific review, that a dynamic component of lumbar support is also necessary to ensure the integral health of the lumbar spine. Ergonomic evidence; angle of the backrest to optimal reduce pressure on the lumbar spine to be 120 degrees; lumbar pad should offer a height of 100-200mm above the lowest point of the seat surface; lumbar support of 5cm in depth from the front of the lumbar pad and the plane of the back rest to reduced the pressure on the IVD by 200N respectively (Andersson and Ortengren, 1974; Kroemer & Grandjean, 2007) are all contributed to the design of the Dynaspine.
Conclusion
In summary of the COST B13 Working Group on European Guidelines for the Prevention in Low Back Pain (DATE) states that lumbar supports or back belts are not recommended (Level A). However, although the Dynaspine has not had any experimental trials conducted on it, the theory behind the design appears to have met both ergonomic and biomechanical standards for preventing LBP from sitting (Andersson and Ortengren, 1974; Kappler, 1982; Kelsey, 1975; Kroemer & Grandjean, 2007; McGill, 2007)
Callagham and McGill (2001) suggested that no single, ideal sitting posture exists; rather a variable posture is recommended as a strategy to minimise the risk of tissue overload. Dynamically and statically, an efficient posture is one that is; stable, minimises stress and strain on the tissues and minimises energy cost (Oliver and Middleditch, 2005).
Dynaspine allows for a dynamic, ergonomically sound seated position, which reduces pressure on the spinal ligaments and discs.

Running Shoe or Minimalist Shoe?

By Fabio Comana, MA, MS, NASM-CPT, CES, PES

Director, Continuing Education, National Academy of Sports Medicine

Running shoe, minimalist shoe, or just taking it all off and going bare? Take a walk with us as we share how the type of footwear worn impacts running style and how to step into a minimalist transition training program.

The debate continues and is perhaps becoming more spirited in light of the growing popularity of minimalist shoes. According to SportsOneSource, sales of minimalist or barefoot shoes (e.g., Nike Free^®, Vibram Five Fingers^®) represent at least 12% of all running shoes sold in a 2.5 billion dollar industry and continues to grow at a faster rate than regular running shoes (1). It comes as no surprise to learn that these shoes, originally introduced by Nike in 2004 (Nike Free) and Vibram in 2005 (Five Fingers) are now offered by over two dozen different shoe manufacturers.

But what is a minimalist shoe? Traditional running shoes generally position the heel 22 – 24 mm (0.87 – 0.94”) off the ground and position the forefoot approximately 10 – 15 mm (0.4 – 0.6”) off the ground. This creates a heel-to-forefoot differential of approximately 12 – 16 mm, whereas minimalist shoes have moved towards a ‘zero drop’ level with no differential. This is achieved by the removal of most, if not all of the shoe midsole (i.e., cushioning between the outsole and the insole). This creates a shoe that is lighter (generally less than 9 ounces or 255 grams) and offers less cushioning and lateral stability (control) – mandating the individual actively engage their own physiological systems to achieve both. However, the implications of ‘zero drop’ technology to the human body is significant, ranging from alterations in posture and movement (i.e., running mechanics), to injury and prevention strategies.

Many questions remain. Are there real benefits to this minimalist movement? Should we continue to run in running shoes? Are running shoes doing more harm than good? These arguments are fueled by minimalist popularity, but the debate is not new. It dates back to 1960 when Abebe Bikila of Ethopia won the Olympic Marathon in Rome running barefoot. Then Zola Budd, a South African distance runner, set the 5,000m world record and competed in the 1984 Los Angeles Olympics barefoot, demonstrating that barefoot running presented no barriers to performance.

Although researchers like Adam Daoud and Daniel Leiberman; and marathoners and medical experts like Mark Cucuzzella (2:24 marathon time) have long supported a return to a minimalist-style of running, perhaps the most influential person for this paradigm shift in thinking has to be Christopher McDougall, who authored the book ‘Born to Run: A Hidden Tribe, Superathletes, and the Greatest Race the World Has Never Seen’ in 2009 (2). What started as a quest to find answers to why his feet hurt after being repeatedly injured as a runner himself, became a journey of discovery. McDougall found the reclusive Tarahumara Indians of Mexico who practiced techniques that allowed them to run hundreds of miles without injury or breakdown. His book gained recognition for how he overcame his own injuries and the opinions from medical experts to stop running. In the process, he discovered his own inner ultra-athlete by completing a 50-mile run challenge using the Tarahumara running style and continues to run today.

This shift in thinking and opinion has certainly changed the mindset of many with respect to training and human movement science. For a Certified Personal Trainer (CPT), a Performance Enhancement Specialist (PES) or a Corrective Exercise Specialist (CES), a more thorough understanding of this trend and the science driving the arguments are certainly relevant and merited. Ultimately, we all share a consistent thread in training our clients, patients and athletes; namely to improve movement efficiency and avoid injury. Consequently, if running is an exercise component in your program, perhaps this debate needs to be considered.

Human Movement Science

The human foot is a complex and amazing structure with 33 joints, 26 bones, about 24 intrinsic muscles (not crossing the ankle joint), 10 extrinsic muscles (crossing the ankle joint), and countless sensory receptors; all designed to help move us efficiently by absorbing forces (on landing) and creating forces (during propulsion), all while offering dynamic stability and mobility throughout movement. Yet we keep it cradled in a shoe where the likelihood of losing strength and tactile responsiveness is increased. In a shoe we have greater sensory interference between the sole of the foot and the ground, and shift more responsibility for cushioning and stability into our footwear or our legs, hips and low back. This translates into a weaker, less aware platform for movement that relays less sensory feedback on spatial orientation and alignment, or more simply stated, this promotes poor posture and dysfunctional (compensated) movement.

During gait (walking) – our default movement pattern, the body prepares itself for heel strike by positioning the foot in a slightly supinated position. This position aims to invert the calcaneous (heel bone) on contact, compressing the bones of the feet together to increase stability within the structure as it accepts load (3). As the forefoot lowers to make contact with the ground, the foot pronates inward leading to eversion of the calcaneous (providing more mobility), whilst relying upon the elasticity within the longitudinal and transverse arches to act as springs and absorb some of the impact forces.

Try This

A common mistake made is to examine the wear patterns of shoes and assume it reflects how we stand. During gait the outside portion of the heel should strike first, undertaking a greater burden of load, thus should wear faster – this does not reflect standing posture. Furthermore, during running our mechanics change significantly as we spend 30% of our gait cycle in the air (2 x 15% float phases – one for each leg) and land with our stance (support) leg positioned directly under our center of mass (COM) (4). This implies moving the stance leg further under the body in the frontal plane to maintain balance and avoid falling. To better understand this explanation, perform a series of single steps, each time placing your right foot on the ground in front of you, but alter the foot position each time to progressively move it under your COM as you would when running. What you should notice is a more supinated position as the right foot moves inward in the frontal plane. Repeat this process while maintaining a flat foot each time and notice the increased amount of stress (valgus) placed at the knee. Supination on heel strike is critical to preserving your knees, thus running should wear down the outside of your shoes faster.

Drawing upon previous research where barefoot rear-foot or heel striking (RFS) increased impact forces (within 50 ms of striking the ground) between 1.9 – 3.0 times body weight in comparison to cushioned RFS where the forces were approximately 1.75 times body weight, Daniel Lieberman and colleagues examined differences between impact forces on RFS and mid-foot / forefoot striking (MFS / FFS) and discovered significant differences (5). With a MFS / FFS, these impact forces were reduced to approximately 0.6 times body weight.

So why use a RFS then when running? Part of this question can be explained by the original information on impact forces between barefoot and cushioned RFS that triggered the running shoe boom of the 1970s as an opportunity to reduce running-related injuries. Ironically, since then, the percentage of runners getting injured each year has remained rather consistent – recreational runner injury rates vary between 37 and 56%; long distance runner rates vary between 19.4 and 79.3% (6, 7). Although some argue inconsistencies in study methodology when comparing ‘then-and-now’ injury statistics; the general consensus appears to be one where the running shoe has not reduced the incidence of running-related injuries. One might even argue that a new series of musculoskeletal issues have emerged since the introduction of the elevated and cushioned heel that has changed standing, walking and running mechanics.

• Elevated heels produce poor posture, foot and joint pain throughout the kinetic chain.
• A padded outsole weakens the intrinsic muscles of the feet to support our arches.
• Enclosed shoes interfere with ground sensation resulting in a loss of proprioceptive feedback (tactile responses) from our feet.

More recently, Daoud and colleagues examined 52 cross-country runners where 36 subjects (69%) were primarily RFS while 16 subjects (31%) were primarily FFS. At the end of the study, it was estimated that approximately 74% of the runners experienced some form of moderate-to-severe injury each year, but the habitual RFS had about twice the incidence of repetitive stress injuries than individuals who habitually used FFS (8).

Impact Forces

In order to facilitate an understanding of the effect of impact forces, consider the following analogy. A steel bridge is designed to withstand many forces including vibrational forces (e.g., repeated waves or oscillations from earth movements). However, the rigid nature of steel makes it better suited to tolerating high frequency forces rather than low frequency forces which are characterized by large undulations (waves) in the force frequency. In the latter case, the bridge sways, placing tremendous stress within the steel beams that may result in failure (explaining why we build suspension bridges). In similar fashion, our hard structures (i.e. bones) are better suited to tolerate high frequency forces whereas our soft tissue is better suited to tolerate lower frequency forces that can absorb these larger undulations into elastic tissue. Considering how ground reactive forces fit the category of low frequency forces, soft tissue is better suited to absorb this force. In other words, rather than using a RFS when running with high impact forces (4 – 11x body weight) that transmits much of the force into the skeleton, a MFS or FFS involves an eccentric stretch into the calves as the heel drops (after contact), coupled with slight knee and hip flexion that helps dissipate forces more easily through the kinetic chain. Additionally, the elastic loading into the posterior chain, may also aid in propelling the body forward in recoil.

While cushioning in the modern running shoe may reduce heel strike forces, it also encourages people to land on their heels when running and develop different biomechanical running strategies. Approximately 75% of shod runners heel strike and while we may not definitively know why, several explanations have been proposed (9):

• Comfort – shock-absorbing cushions. Walking incurs smaller impact forces versus running (4 – 11 x body weight) and walking naturally involves a heel strike. With the option of a cushioned heel, we now adopt our same biomechanical strategy of walking without great concern for injury. Upon striking the ground, the heel creates a momentary ‘brake’ which creates an instantaneous and large increase in impact forces, but with a cushioned heel this force is lowered by about 10% (5). Furthermore, a shoe occupies more surface area than the foot, helping distribute forces over a larger area, thus making heel striking more comfortable.
• Stability – the shoe prevents excessive movement within the joints of the foot (e.g., excessive pronation) which helps some runners feel more stable.
• Running economy for distance: Speed = Stride Length x Stride Frequency.
  • Some optimal combination between the two variables constitutes running economy and we are generally more efficient (i.e., energy conservation) when we reduce leg turnover (frequency), but in order to maintain speed we need to increase stride length which implies reaching the lead leg further in front, resulting in more heel striking. Thus, lengthening the stride to include a softer heel strike (with a cushioned heel) may improve running economy for some.
  • Running mechanics (and heel striking) however, is influenced by running speed (5). Sprinters attain high speeds without heel striking (‘eccentric braking’), relying more upon leg turnover for achieving their stride lengths, not through the leading leg reaching forward, but through explosive propulsions from the trailing leg. Furthermore, shorter contact times with the ground translate into faster speeds, thus a heel-strike to forefoot transition takes too long in comparison to a mid- or forefoot strike.
  • However, research also demonstrates that FFS appears to incur no additional metabolic cost compared to a RFS (10, 11).

Therefore, if we have the opportunity to simultaneously reduce impact forces and potential injury risks, and it comes at no additional cost to metabolism, should we consider a transition to a minimalist-type strategy that involves MFS or FFS during endurance running?

Transitioning to a Minimalist Approach:

Perhaps the most important guideline is to transition slowly – to build a solid foundation, develop good technique, and then build training volume. Too many people transition too quickly without first completing the necessary pre-requisites and end up getting hurt.

Similar to NASM’s OPT^® training stages, this transitional program should also follow a systematic progression whereby stability and mobility are addressed first, followed by any necessary conditioning (strengthening) training before attempting any explosive activities. Consequently, programming should initially address postural mechanics and corrective exercises as needed (i.e., inhibit, lengthen, activate then integrate).

If we plan to biomechanically prepare the body for this transition, then it should start with addressing how we stand (i.e., neutral, supination or pronation – more common). Various methodologies to assess pronation/supination exist, but here is one simple approach (12):

1. Kneeling in front of your client, position the palm of your hand (hand extended vertically) lightly brushing the inside of one ankle (medial malleolus).
2. Instruct your client to collapse their ankle inward (driving the ankle, not the knee) and mark this end-range position with your hand (Figure 1a).
3. Next, position the palm of your opposite hand (hand extended vertically) lightly brushing the outside of that same ankle (lateral malleolus).
4. Instruct your client to roll their ankle outward (driving the ankle, not the knee) and mark this end-range position with that hand (Figure 1b).
5. Cue your client to slowly adjust their ankle position until it is positioned midway between both palms (Figure1c).
6. On your command, ask your client to relax their foot.
   • Foot collapsing inward – indicative of more pronated standing.
   • Foot rolling outward – indicative of more supinated standing.
7. The overall goal is to consciously correct how we stand and slowly retrain our neural pathways while simultaneously lengthening and activating extrinsic and intrinsic foot and lower leg muscles. It is important to note that this system is not perfect and may not offer a solution to all individuals (e.g., structural issues in the foot).

Figure 1 (a-c): Ankle Evaluation.

Your progressive training program should first develop the foundational components of proprioceptive awareness, stability and mobility in the feet then systematically train to load the body vertically through the kinetic chain (hopefully maintaining neutral sub-talar position) before introducing more complex static and dynamic exercises to prepare the body for MFS / FFS running. Table 1 outlines a basic progressive program one can follow.

Table 1: Minimalist Transition Foundational Training Program

Step One: Proprioceptive Awareness:

• Goal: Increase proprioception (tactile awareness) in our feet.
• Methods: Improving stability and mobility within the intrinsic foot muscles and mobility across the ankle joint. 4 – 5 x / week.

Figure 2: Surface Proprioception.

 Step Two: Active Feet Exercises.

• Goal: Introduce integrated barefoot drills to improve balance, proprioception and ultimately gait.
• Methods: Various proprioceptively-enriched, integrated (whole-body) exercises.

Keys to consider if you plan to run in minimalist shoes with a MFS / FFS strategy.

Step Three: Calves and Hip Flexors (Strengthening and Recovery)

• Many people complain of muscle soreness in the poster lower leg complex (calves) once they transition to a MFS or FFS, given the eccentric loading into these muscles during the heel drop.
  • Develop a lower-leg conditioning program (calves, tibialis group) that includes both eccentric strengthening and recovery (i.e., myofascial release and stretching).
• Initially, with shorter strides, running speeds drop, but many attempt to compensate immediately by generating faster leg turnovers.  Individuals may often try driving their thighs higher as an attempt to lift and turn legs over faster, and overwork their hip flexors.
• Although not mechanically proficient, attempt to overcome associated muscle soreness by including hip flexor strengthening and recovery exercises.

Step Four: Running Mechanics

Generally, the transition from a RFS to a FFS / MFS involves specific biomechanical changes in running technique. While a PES skilled as a running coach can effectively instruct an individual to improve their running mechanics, a brief list is provided for your consideration:

• Coach an overall 5º forward lean throughout body linkages (ankle through hips)
  • You can help develop this forward lean through various exercises to shift COM forward
    • Static, staggered-stance forward leans
    • Uphill walking
• Light foot placements (MFS / FFS)
  • Backwards walking – increase MFS / FFS feel
  • Light running – greater hip flexion
• Faster leg turnover exercises
  • ABCs:
    • A: High-knee run, power skipping
    • B: High-knee marches
    • C: Butt kicks (‘pawing’ not ‘mule kicking’ – an exaggerated rear leg extension in which you alternate kicking yourself in the hind quarters.
  • Quick feet (20 – 25 yards strides with as many foot contacts as possible)
• Arm Drives
  • Short, compact arm swings from the shoulder, not the elbow

In closing, while concerns expressed within the medical community tell us that countless hours spent pounding the pavement leads to debilitating injuries, and wear and tear on our joints, more and runners continue to flock to the starting line for marathons and other distance runs (13). Given this trend, should we shift our focus to address a MFS / FFS approach to running to potentially preserve the body from chromic overuse and if doing so, is it time to address this transition through a slower, progressive and more effective approach?

References

1. Powell, M. (2012). First Quarter 2012 Sales Analysis, SportsOneSource. Retrieved 01/30/13.
2. Christopher McDougall (2009) Born to Run: A Hidden Tribe, Superathletes, and the Greatest Race the World Has Never Seen. New York, NY: Random House.
3. Gray, G. & Tiberio, D., (2007). Chain Reaction Function.  Gray Institute, Adrian, MI.
4. Bryant, C.X. & Green, D.J. (eds.) (2008). ACE Advanced Health and Fitness Specialist Manual. San Diego, CA. American Council on Exercise.
5. Lieberman, D.E., Venkadesan, M., Werbel, W.A., Daoud, A.I., D’Andrea, S., Davis, I.S., Mang’eni, R.O., & Pitsiladis, Y., (2010). Foot strike patterns and collision forces in habitually barefoot versus shod runners. Nature, 463: 531–535.
6. Van Mechelen, W. (1992).  Running injuries: A review of the epidemiological literature. Sports Medicine, 14(5):320 – 335.
7. Van Gent, R.N., Siem, D., Van Middelkoop, M., Van Os, A.G., Bierma-Zeinstra, S.M.A., & Koes, B.W. (2007). Incidence and determinants of lower extremity running injuries in long distance runners: a systematic review. British Journal of Sport Medicine, 41: 469 – 480.
8. Daoud, A.I., Geissler, G.J., Wang, E., Saretsky, J., Daoud, Y.A. & Lieberman, D.E. (2012). Foot Strike and Injury Rates in Endurance Runners: A Retrospective Study. Medicine and Science in Sports and Exercise, 44(7): 1325 – 1334.
9. Hasegawa, H, Yamauchi, T, Kraemer, W.J. (2007).  Foot strike patterns of runners at the 15-Km point during an elite-level half marathon.  Journal of Strength and Conditioning Research, 21(3): 888 – 893.
10. Cunningham, C.B., Schilling, N., Anders, C., & Carrier, D.R. (2010). The influence of foot posture on the cost of transport in humans. Journal of Experimental Biology, 213: 790 – 797.
11. Perl, D., Daoud, A.I., & Lieberman, D.E. (2012). Effects of footwear and strike type on running economy. Medicine and Science in Sports and Exercise, 44: 1335– 1343.
12. Kendall, F.P., McCreary E.K., Provance, P.G., Rodgers, M.M., Romani, W.A., (2005).Muscles Testing and Function with Posture and Pain (5^th ed.). Baltimore, MD., Lippincott, Williams and Wilkins.
13. Running USA’s Annual Marathon Report 2011, (2012). Retrieved 01/31/13.

Stress, Consequences and Overall Health

By Fabio Comana, MA, MS, NASM-CPT, CES, PES,

Director, Continuing Education, National Academy of Sports Medicine

Stress stimulates appetite, it increases abdominal fat, it increases risks for disease and it can even play a role in our intimate relationships. The list could keep going, but what exactly is stress and how is it connected to all these consequences? Examine the concept of stress and discover how chronic stress can negatively impact specific physiological systems within our body.

Stress can be is defined as a nonspecific response to any stimulus that overcomes, or threatens to overcome, the body’s ability to maintain homeostasis or allostasis (state of equilibrium of the body’s internal biological mechanisms) (1). In other words, when the body is exposed to, or anticipates a stress, regardless of the source of the stress (e.g., lack of sleep, starvation, financial or emotional hardship, exercise, fighting to survive), it initiates a response mechanism to help restore a state of equilibrium. However, it is important to remember that this biological response is essentially the same regardless of the type of stress we impose upon ourselves, and only differs by magnitude of the response needed. Furthermore, the term allostasis refers to the concept whereby the entire body is involved in this adaptive response and therefore it is our weakest response mechanism (i.e., from one particular system,) that can become problematic as the body attempts to cope with the stress (1).

Nonetheless, if we have this built-in, biological stress-response mechanism, then why is it that medical experts are expressing more concern over stress and its association with disease and pre-mature death?  One major explanation lies with the type of stress we are exposed. Our stress-response mechanism is designed to respond to acute physiological stresses – ones that place stress upon our body for only short periods of time (e.g., escaping a sabre-tooth tiger) where we respond with physical work. We often refer to this mechanism as our ‘fight-or-flight’ response. We either confront the stressor or remove ourselves from it (1). The stress is short-lived and allows ample time for the body to recover from the stress response.

Our lives have evolved. The creation of an industrialized world has dramatically altered the nature of the stress we experience. We face less physiological stress and now deal with a new stressor that has become more significant in our lives; namely smaller bouts of continual psychological stress (e.g., work schedule, responsibilities, traffic, finances, environmental toxins, etc.) that ordinarily do not require physical work. Though our stress has changed, but our biological stress-response mechanism has not (2). Growing concern is not necessarily with the stressing agents, but more so related to the cumulative effect of our stress-response mechanism and how the body recovers from this stress-response. In modern times we are exposed to frequent bouts of psychological stress (i.e., chronic stress), the answers medical experts and researchers seek revolve around recovery from these responses. If we are unable to fully recover, the body becomes weak and vulnerable. Stress therefore does not necessarily cause disease, but simply exacerbates the potential for disease (2).

Takeaway

Primary change associated with our stress-response mechanism is with the nature of the stressor where we have experienced a shift from less frequent, acute bouts of intense physiological stress to more frequent, smaller bouts of psychological stress from which the body struggles to recover.

To better understand this difference, it may be helpful to first review key stress-response mechanisms. Our biological stress response was designed for survival and is regulated by both the neural and endocrine (hormonal) systems. Fundamentally, both systems are communication systems that receive sensory information from various sources (eyes, ears, skin, blood, etc.) and transmit appropriate responses to specific targets once information has been processed to re-establish balance.

• The nervous system is a rapid-acting, but short-lived communication system that functions by transmitting nerve impulses – it reacts very quickly to stimuli, but its effects do not last very long (e.g., the sudden, short-lasting elevation of heart rate when startled).
• The endocrine system is a slower-acting, but longer-lasting communication system that functions by hormonal action – it is activated more slowly (sometimes by nerve activity) and its effects may last longer (e.g., the sustained elevation of heart rate during a 60-minute run).

Many of our nerve responses are governed by our autonomic (ANS) or involuntary nervous system, which forms part of our peripheral nervous systems (i.e., nerve system excluding the brain and spinal cord). As illustrated in Figure 1-1, the ANS is further sub-divided into the parasympathetic (PNS) and sympathetic (SNS) nervous systems that operate independently and cooperatively with each other. The SNS is considered a rapid-acting, mobilizing system aimed at helping the body prepare itself to tolerate stress (sometimes called excitatory) whereas the PNS is considered a slower, dampening system that dominates during periods of calm or recovery (3).

Figure 1-1: Neural Organization

When activated, the SNS triggers numerous responses intended to help the body optimize its chances for success during the ‘fight-or-fight’ response. Many of these are mediated by hormones listed in Table 1-1. These responses include:

• Increased cardiopulmonary responses (e.g., blood pressure, heart rate, dilation of breathing tubes to move more air).
• Increased mobilization of fuels (i.e., breakdown of stored fat and stored carbohydrates – glycogen to make more readily available for energy production).
• Increased vasodilation of vessels to the brain and exercising muscles – needed to increase attention, recall and memory; and increase nutrient and oxygen delivery.
• Increased blood clotting ability– needed to stop one from bleeding to death during a‘fight-or-flight’ response.
• Decreased pain perception (analgesia) – needed to tolerate discomfort during a‘fight-or-flight’ response.
• Decreased growth, repair and maintenance.
• Decreased reproduction capacity.
• Decreased salivary and digestive enzyme secretion and digestion – this may explain why one experiences dry mouth when nervous (i.e., public speaking).
• Decreased stomach and small intestinal contractility.
• Increased large intestinal contractility (evacuates bowels to help chances of survival during ‘fight-or-flight’ responses) – this explains why diapers are used on prisoners when executed.
• Increased bladder contractility (removes urine to help chances of survival during‘fight-or-flight’ responses) – this explains why people and animals urinate when scared.
• Increased immune function – needed to fight off pathogens.
• Increased sweat rates – stimulation of the eccrine and appocrine (primarily under the arms) to remove heat.

Table 1-1: Hormones Influenced by SNS Activation

Connect: A Difference in Women?

Research by Shelley Taylor, a psychology professor from the University of California, Los Angeles (UCLA) has explored differences in the female response-mechanism to stress that resulted in the creation of a ‘tend-and-befriend’ response model rather than ‘fight- or-flight’ response (4). This response involves protection of offspring (tending) and seeking out social groups for mutual defense (befriending) as a coping mechanism to stress.This unique response appears to be regulated by the female hormone oxytocin, which in turn is regulated by the hormone estrogen. Oxytocin has been connected to a variety of social relationships and activities, including peer bonding, breast feeding and affiliative behaviors – including maternal tending and social contact with peers. Researchers believe these social responses help reduce biological responses such as elevated heart rate and blood pressure, and the release of certain stress hormones like cortisol (5).

Stress and Cardiovascular Responses

Each time we respond to stress, the release of epinephrine increases platelet adhesiveness to help blood clot.  Likewise, under stress the body aims to increase blood volume to offset any potential loss of blood volume from sweating or bleeding by increasing the release of antidiuretic hormone (ADH) from the anterior pituitary gland that re-absorbs fluid from the kidneys. However, without any loss of blood volume (i.e., no exercise-induced sweating), the end result is an increase in blood pressure. Higher blood pressure results in a gradual thickening of the arterial walls to withstand increased pressure, resulting in a loss of vessel elasticity needed for dilation and constriction, and increased damage to the vessel’s interior lining. This in turn increases vessel inflammation, as evidenced by increased levels of C-reactive protein (CRP) (an inflammatory marker) in the blood during periods of, and following stress (6). One adaptive response to elevated blood volume and pressure is that the body attempts to push fluid back to the kidneys, taking calcium with it, which increases calcium losses from the blood and increases the risk of osteoporosis.

Under stress, the mobilization of fats from fat cells elevates circulating levels within the blood, increasing the likelihood that these lipids will be deposited on the damaged vessel walls. This escalates risks for heart disease and stroke (6). Furthermore, if these fats, mobilized from all regions of the body, are not utilized by cells due to the psychological nature of the stress, many of these circulating fats are re-deposited in the abdominal region and not within subcutaneous fats cells. This shift of fat stores to the more dangerous abdominal region (visceral fat) also increases risk for heart disease.

Therefore, exposure to acute, shorter bouts of stress that reduce blood volume (i.e., sweating) and utilize circulating fats is tolerable to the body, but it is the repeated exposure of chronic stress that ultimately results in health issues.

Stress, Metabolism, Appetite and Intestinal Health

The body releases insulin, an anabolic (storage) hormone, in response to food or in anticipation of the arrival of food, but during periods of stress, the body will inhibit the release of insulin as it favors catabolic or breaking down processes. These specific functions provide fuel during periods of stress and then allow the body to restore energy reserves during periods of recovery or calm (PNS dominance). However, during periods of chronic stress where there is no increase of energy utilized, these mobilized fuels are not utilized (baring a small energy cost to breakdown and restore energy reserves), but our biological response mechanism kicks in to increase the desire for food although we really have no need to eat. This response may override our regulatory processes of hunger and may help explain why two thirds of people experience an increase in appetite when stressed. As the body strives to replace its primary fuel (carbohydrates), this offers some insight to why carbohydrates (e.g., sugars) are often desired (7).

With the onset of stress, the release of corticotropin-releasing hormone (CRH) from the hypothalamus (the body’s master gland) occurs within seconds. This activates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary to activate the release of glucocorticoids (GC) from the adrenal cortex gland (cortisol is the primary GC). Glucocorticoids, particularly cortisol are considered primary stress hormones.  Likewise, within seconds of the removal of an acute stress, levels of CRH and ACTH disappear quickly but GC levels may remain elevated for some time. The prime reason why GC levels remain elevated during recovery is to stimulate appetite to replenish lost energy stores, which in turn elevate insulin to help push food into the cells. Elevating blood glucose levels following food consumption (especially sugar) lowers GC levels, helping explain why eating sugar is sometimes viewed as an anti-stress or stress-coping mechanism (8). As some people release more GC or have a slower process to restoring GC levels back to baseline, appetite levels vary with stress. Furthermore, some people also undergo small adaptations where repeated exposure to chronic stress results in a blunted GC (cortisol) release (8).

Under stress, gastrointestinal (GI) function is reduced and while tolerable over shorter durations, it will compromise GI health and nutrient intake under conditions of chronic stress. Functional bowel disorders (e.g., spastic colon, irritable bowel syndrome – IBS) are all associated with prolonged exposure to stress. Similarly, stomach ulcers caused byHelicobacter pylori bacteria in the stomach are highly correlated with stress levels. Although 50% of adults harbor these bacteria in their upper GI, and 80% of people are asymptomatic, it is those exposed to higher levels of chronic stress that experience a greater incidence of ulcers. Normal GI function and our body’s natural immune response appear to control these bacteria, but with reduced stomach activity and compromised immune function under stress, these bacteria flourish.

The thyroid gland releases two important hormones called thyroxine (T4) and triiodothyronine (T3) that regulate our metabolism, accounting for 60 – 75 % of all calories expended in a day. Thyroid stimulating hormone (TSH) released by the pituitary gland acts to stimulate thyroid gland production of T3 and T4, but under increased levels of chronic stress, elevated GC levels hinder TSH production, which in turn reduces the quantities of T3 and T4 needed to regulate metabolism.

Takeaway

Our physiological stress-response is intended to replace lost energy reserves, but with the changing nature of stress where energy is not expended, it may trigger over-eating. Overall intestinal health and nutrient uptake are both directly impacted by repeated bouts of stress.

Stress and Immune Function

Moderate amounts of sustained stress and short term exposure to acute stress increase GC release. This is actually beneficial to our immune function because while it temporarily suppresses immune function during the stress-response, it helps restore baseline (normal) immune function after the stress has been removed. Concern exists with exposure to chronic stress where frequent and sustained levels of elevated GC result in immune system levels returning to sub-baseline levels (7). Chronic stress initially produces elevated GC levels, but prolonged exposure also decrease levels over time if the adrenal glands become chronically fatigued (known as adrenal insufficiency or adrenal fatigue).

Connect: Cortisol

Cortisol is the primary glucocorticoid hormone in the body and often referred to as the key ‘stress hormone’ that helps maintain homeostasis by mediating various physiological responses that include:

• Regulating blood sugar levels
• Influencing macronutrient utilization to maintain blood glucose levels (e.g., stimulating gluconeogenesis)
• Fat deposition
• Having anti-inflammatory and some immuno-stabilizing effects
• Influencing hormonal and nerve system responses

As cortisol is our primary stress hormone, it responds during periods of stress (e.g., exercise, missed meals or starvation, following insufficient sleep), but returns to baseline when the stress is removed. However, with our continual exposure to psychological stress, this recovery or return to baseline may not occur. Health concerns exist, as seen in Table 1-2, with elevated levels of cortisol associated with chronic stress or from suppressed levels of cortisol. Levels generally fluctuate throughout the day, usually reaching the lowest levels 2 – 4 hours after falling asleep (e.g., 2 – 4 am) as we transition into deep sleep and reaches the highest levels in the hours immediately prior to waking (e.g., 6 – 7 am) as the body enters a prolonged fasted state and prepares itself to wake-up and increase metabolism.

Table 1-2: Effects of Elevated or Suppressed Cortisol Levels

Stress in Females

Healthy fetal development is largely dependent upon the health of the mother and those exposed to higher levels of chronic stress may develop babies who are both physically and cognitively compromised (2). The stressed mother has elevated SNS activity and GC levels coupled with decreased levels of HGH (needed for bone and tissue growth), compromised nutrient intake, and lower calcium stores, all of which negatively impact fetal development. Increased GC levels are also associated with increased vulnerability to anxiety and decreased ability to recover from, or cope with, stressful events (2).

The hypothalamic-pituitary-ovarian (HPO) axis regulates estrogen and progesterone levels throughout life and the menstrual cycle. They hypothalamus releases luteinizing hormone releasing hormone (LHRH) to the anterior pituitary gland which in turn releases luteinizing hormone (LH) and follicle stimulating hormone (FSH) to the ovaries to manufacture and release estrogen and progesterone. Under chronic stress however, elevated GC levels negatively impact the hypothalamus, resulting in less LHRH release. Additionally, beta-endorphins (neurotransmitters that act as an analgesic to numb or dull pain sensations), secreted in the hypothalamus are also increased under stress and block the release of LHRH (Table 1-1) (7). Less LHRH results in less LH and FSH being released from the pituitary gland (as the gland becomes less responsive to smaller quantities of LHRH). This in turn:

• Reduces levels of estrogen, which when coupled with the additive effect of GC makes the ovaries less responsive to LH and FSH, decreasing chances for fertilization.
• Reduces levels of progesterone, which decreases uterine wall thickening that normally occurs after fertilization.
• Increases levels of prolactin, which decrease pituitary sensitivity to LHRH and thins the uterine wall. Interestingly, this thinning effect of the uterine wall acts as a natural contraceptive in breastfeeding mothers when prolactin levels are higher to assist with milk secretion (2).

Estrogen plays a role in helping deposit fat in the hips and thighs, and helps prevent deposition in the waist region, thereby reducing the risk of heart disease (10). However, in chronically stressed females, this functionality is reduced due to lowered estrogen levels and females increase their levels of abdominal or android fat (2). Females also make small amounts of testosterone (TST) in the adrenal glands and fat cells possess specific enzymes that can convert some of this TST to estrogen (2). However, under conditions of chronic stress, these enzymes become less active and therefore convert less TST to estrogen.

Lastly, chronic stress also decreases sexual libido. Elevated levels of the reproductive hormones increase a female’s tactile responsiveness (i.e., responsiveness to physical touch). Chronic stress reduces dopamine levels, thus reducing pleasurable experiences associated with sex. Dopamine is a neurotransmitter involved in controlling our reward and pleasure centers.

Stress in Males

The release of LH and FSH stimulate production of TST in the testes, but under stress, elevated GC levels decrease LHRH secretion and diminish the sensitivity of the testes to LH and FSH. Less TST in men leads to many physiological changes that include decreased muscle mass, osteoporosis (low bone density), lowered red blood cell count, and changes in body composition and fat distribution (TST helps oppose cortisol’s effect on depositing fat into the abdominal region).

During sex, where the SNS system generally dominates, it is the co-activation of the PNS that enables a man to have an erection, and continue to maintain that erection until his SNS overwhelms him, resulting in an ejaculation. However, under conditions of stress where a man has greater SNS activity, this interferes with his ability to gain an erection, leading to impotence.

Stress and Aging

One aging theory proposes the existence of telomeres, structures composed of repetitive nucleotide sequences located at the end of our chromosomes (11). They are believed to protect chromosomes from deterioration from various stressors and it is the function of the enzyme telomerase to constantly repair them to help keep cells healthy (12). However, under sustained stress, the activity levels of this enzyme decrease, shortening the telomere and promoting accelerated cellular aging (2).

Stress Management

Given the need to control stress and elevated GC levels, numerous stress-management and coping mechanisms exist, but much of the earlier research in this area examined animal responses to physiological stress that surprisingly still have applications to humans with psychological stress (2). Some proposed strategies include:

1. Developing an outlet.
   • Stress creates muscle tension. Much like the gazelle that has eluded the cheetah (under intense SNS activation), it proceeds to jump around after the stress is removed (i.e., cheetah leaves) to release muscle tension. In a similar manner, humans also need physical sources to remove our stress (e.g., exercise, punching).
   • Create opportunities to reprioritize matters. After a stressful day, time spent enjoying an activity or person(s) that holds a high priority in your life helps prioritize events and build perspective (e.g., a hug or time with your children after a stressful workday creates that perspective).
   • Displacement of aggression. While not suggested as a coping mechanism, it is a common response in animals and humans. Here, the stressed animal attacks another innocent bystander without provocation. Humans demonstrate similar behaviors by venting their frustrations on an innocent bystander or perhaps worse, by abusing a person as a result of a stressful situation (e.g., financial hardships).
2. Identify and utilize social supports. Animals bond with each other following bouts of stress, offering a social calming effect (e.g., grooming). Likewise, humans should also develop social support systems that offer this same calming effect.
3. Predictability or predictive information. Having awareness or anticipation of the type, magnitude and duration of a stress enables individuals to develop effective coping mechanisms (e.g., asking a dentist how much longer he / she will need to drill may help an individual cope with that stress). The information however, must be relevant (i.e., tied to the stressful event) and must also be time-appropriate (i.e., having information three weeks prior to a procedure or one second prior to a procedure does not offer much solace).
4. Develop a sense of control – creating the impression of, or having actual control of a stressful situation can help reduce stress. Generally, when one has low levels of control, yet perceives the stress (demands) placed upon them to be high or low, stress will prevail. On the other hand, if one has high levels of control, they are more adept to managing their stress. However, for mild-to-moderate levels of stress, increased feelings of control promote self-efficacy, whereas with high levels stress, one may benefit more from less control to avoid extreme pressure, desperation or blame should they not succeed.
5. Interpret things as getting better.
6. Cognitive flexibility, where you develop the ability to remove the stressors that you can, but also learn to adapt to the stressors that you cannot remove. This in essence mirrors the Serenity Prayer by twentieth century American theologian, Reinhold Niebuhr who said, “… grant me the serenity to accept the things I cannot change, the courage to change the things I can, and wisdom to know the difference.”

In closing, as the human body was never designed to tolerate continual psychological stressors, our inability to cope with the biological stress-response mechanism and to adequately recover has emerged as a major health concern. While this article only addressed specific systems and fundamental gender differences, it is clearly evident that the pressures associated with modern living are contributing to major disturbances to homeostasis (allostasis), which in turn exposes us to greater risks for morbidity and mortality. Considering how we all experience some degree of continual stress, the need for effective stress-management techniques and coping strategies is now perhaps bigger than ever.

References:

1. Cannon, W. B., (1926). Physiological regulation of normal states: some tentative postulates concerning biological homeostatics. IN: Pettit, A., & Richet, A.C., Ses amis, ses collègues, ses élèves, Paris, France, Éditions Médicales.
2. Sapolsky, R. (2010). Stress and Your Body. Chantilly, VA., The Teaching Company. http://www.thegreatcourses.com/tgc/courses/course_detail.aspx?cid=1585. Retrieved 2013-01-21.
3. Kenney, W.L, Wilmore, J. H., & Costill (2012). Physiology of Sport and Exercise (5^thEd). Champaign, IL, Human Kinetics.
4. Taylor, S.E., Klein, L.C., Lewis, B.P., Gruenewald, T.L., Gurung, R.A.R., & Updegraff, J.A. (2000). Biobehavioral responses to stress in females: Tend-and-befriend, not fight-or-flight. Psychological Review, 107, 411–429.
5. Tamres, L., Janicki, D., & Helgeson, V.S. (2002). Sex differences in coping behavior: A meta-analytic review. Personality and Social Psychology Review, 6, 2–30.
6. Danesh, J., Wheeler, J.G., Hirschfield, G.M., Eda, S., Eiriksdottir, G., Rumley, A., Lowe, G.D., Pepys, M.B., & Gudnason, V. (2004). C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. New England Journal of Medicine, 350(14): 1387 – 1397.
7. Sapolsky, R, Romero, M.L., & Munck, A.U. (2000). How do glucocorticoids influence stress responses? Integrating permissive, suppressive, stimulatory, and preparative actions”. Endocrine Reviews, 21(1): 55 – 89.
8. Tomiyama, J.A., Dallman, M.F., & Epel, E.S. (2011). Comfort food is comforting to those most stressed: Evidence of the chronic stress response network in high stress women. Psychoneuroendocrinology, 36(10):1513 – 1519.
9. Brown, L.M. (2000). Helicobacter pylori: epidemiology and routes of transmission.Epidemiological Reviews, 22 (2): 283 – 97.
10. Cooke, P.S., & Naaz, A. (2004). Role of Estrogens in Adipocyte Development and Function. Experimental Biology and Medicine, 229(11): 1127 – 1135.
11. Puterman, E. & Epel, E. (2012). An intricate dance: Life experience, multisystem resiliency, and rate of telomere decline throughout the lifespan. Social and Personal Psychological Compass, 6(11): 807 – 825.
12. Daubenmier, J., Lin, J., Blackburn, E., Hecht, F.M., Kristeller, J., Maninger, N., Kuwata, M., Bacchetti, P., Havel, P.J., & Epel, E. (2012). Changes in stress, eating, and metabolic factors are related to changes in telomerase activity in a randomized mindfulness intervention pilot study. Psychoneuroendocrinology, 37(7): 917 – 28.Stress, Consequences and Overall Health