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Artificial turf in elite soccer, new finding give rise to new questions ~ Karolina Kristenson, MD PhD

Does artificial turf (AT) affect injury rates in football (soccer)? It is a question widely debated. Robust data states that artificial turf does not affect the general injury rate for acute injuries. Few studies, however, have included overuse injuries when comparing injury rates with AT and natural grass (NT).  Also, the aspect of rapid change between surfaces is often discussed among football players, trainers and clinicians, but no previous studies have evaluated whether this actually affect injury rates.

With this background, our research group (Football Research Group, Linköping Sweden) and The Oslo Sports Trauma Research Group (Oslo, Norway) initiated a research project. We thought that a study setting in the Swedish and Norwegian first male leagues was appropriate since a) artificial turf is common in the Nordic countries, and b) the leagues are similar in climate and standards. In this way, we could collect a larger data set, which is a prerequisite to be able to analyze injury pattern, such as the injury rate for different specific muscle groups.

Photo by See-ming Lee. Used with permission. All rights reserved. Source: flickr

Photo by See-ming Lee. Used with permission. All rights reserved. Source: flickr

During two full football seasons (2010 and 2011), we recorded injuries that led to absence from football as well as player’s individual exposure to football on grass and AT. In November 2011, we could sum up that 32/37 clubs playing in the first leagues during this period had participated for the full study period. This resulted in 1063 match injuries and 1178 training injuries registered during 48,922 match and 318,568 training hours.

We compared the acute injury rates on AT and NG at the individual player level (to see if this study would replicate the findings from previous studies). Also, in this study setting we were able to compare acute and overuse injury rates between clubs that have artificial turf at their home venue (AT clubs) and clubs that have natural grass (NG clubs).

Interestingly, the result we found was that professional football clubs with AT installed at their home venue had a higher acute training injury rate and overuse injury rate compared to clubs with NG. In particular, AT clubs had a higher rate of overuse injuries to the hip/adductors (60% increase) and calf (four-fold increase).

Also, AT clubs had a higher match injury rate during the competitive season, while no differences between AT clubs and NG clubs were found during pre-season. Still, at the individual level, no differences in acute injury rates were found when playing on AT compared to NG in the total cohort analysis.

Consequently, our study replicated the findings from previous research that there is no difference in the acute injury rate at the two surfaces, yet clubs playing home matches on AT have a higher injury rate. Why is that?

Our hypothesis is that the AT clubs´ higher injury rates could be due to a rapid switching between playing surfaces and inadequate adaptation to a new surface. Since there were fewer AT clubs than NG clubs in this cohort, players from AT clubs had to alternate between surfaces more often when playing away matches.

It is possible that such frequent shifts between surfaces could lead to a greater load on musculoskeletal tissues and an increased overuse injury rate. This could explain why a higher match injury rate for AT clubs was only evident during the competitive season when switching between surfaces at away matches occurred frequently, while match injury rates were similar during the pre-season, when most friendly matches were played on AT.

Of course, many questions still remain to be answered. Sweden and Norway are located in the northern part of Europe and cross several climate zones. It is possible that clubs with AT installed at their home venue could have chosen this surface because of the rough climate conditions, i.e. a generally colder climate, which itself could influence injury rates. It is also possible that clubs chose AT turf at their home venue because of the saving in costs. Therefore, the role of climate and clubs economy as a potential risk factor needs to be addressed in future studies.

For more detailed information: Kristenson K, Bjørneboe J, Waldén M et. al. The Nordic Football Injury Audit: higher injury rates for professional football clubs with third-generation artificial turf at their home venue. Br J Sports Med. 2013 Aug;47(12):775-81.

Dr Karolina Kristenson is a PhD graduate in Football Research Group (FRG), Linköping University, Sweden. FRG has conducted injury studies since 2001 in cooperation with the Union of European Football Associations (UEFA). These cohorts include clubs playing in the UEFA Champions League, English Premier League and the Nordic top leagues. Her thesis focus on injury rate in elite football related to playing surface.

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“Do you even lift, Bro?” ~ Ann Gates @exerciseworks

The recent viral videos and ‘outtakes’ of the responses to this pertinent (and yes, hilariously funny) rhetorical question got me thinking… what a great question to trend in the fight against the type 2 diabetes epidemic.

Photo by "HIRAOKA,Yasunobu". Used with permission. All rights reserved. Source: flickr

Photo by “HIRAOKA,Yasunobu”. Used with permission. All rights reserved. Source: flickr

Type 2 diabetes is largely preventable and treatable with the right medicines, a healthy, balanced diet and regular daily exercise. Recent studies show that adding in resistance or ‘strength’ training confers significant results in the overall management and health outcomes of Type 2 diabetes. Two particular studies warrant highlighting:

  • The Umpierre, 2011 study clearly shows that a structured exercise plan including strength training, is associated with greater health outcomes including a significant HbA(1c) reduction in patients with type 2 diabetes than with exercise plans without strength training. Structured exercise training such as aerobic exercise, resistance training, or both combined of more than 150 minutes per week is associated with greater HbA(1c) declines and is also  a cost effective management approach in type 2 diabetes.However, the physical activity advice is associated with lower HbA(1c) only when combined with dietary advice. This adds even more weight to the question ‘do you even lift. Bro?’ The study clearly demonstrates that a combination of cardiovascular exercise and strength training improves the overall management and cost effectiveness of type 2 diabetes care.
  • The second study of interest showed that men who do strength (resistance) training regularly—for example, for 30 minutes per day, five days per week—may be able to reduce their risk of type 2 diabetes by up to 34 percent. In this new 2012 study, by Harvard School of Public Health (HSPH) and University of Southern Denmark researchers also combined strength training and aerobic exercise, such as brisk walking or running, and showed that men may be able to reduce their type 2 diabetes risk even further—up to 59 percent!

59 percent reduction of risk of type 2 diabetes is surely something that all health commissioners, doctors, sports and exercise specialists, allied health professionals and patients at risk of developing type 2 diabetes should be aiming for with structured exercise plans and lifestyle advice.

In fact, wouldn’t it be fantastic if patients actually knew this benefit of a regular exercise plan including strength exercises as part of routine exercise plans in the prevention and treatment of type 2 diabetes? Wouldn’t it be a great idea to use social media in this way, to get the message over to health professionals and their patients that yes … medically and scientifically……..strength training works!

So actually, as dangerous as asking the question is, ‘Do you even lift, Bro?’ (you have to watch the videos to really appreciate the risks of this scenario….!).

The enlightened answer is…

 “Bro….. I lift because it reduces my risks of type 2 diabetes by 39 percent, I run because it reduces those risks further by 25 percent, I also add in balance and flexibility training ‘cause man… that really helps you feel good in yourself…… I combine all of this with a healthy diet….”

And the outtakes may well result in better national, local and individual health in the management of type 2 diabetes!

Strength training support should be offered to all patients at risk of type 2 diabetes.

Ann Gates is the founder of Exercise Works! @exerciseworks

Disclosures: Many thanks to my ‘physiotherapy student’ son for enlightening his mum on what’s funny and cool in the world!

This post was originally published on the BJSM blog site. Used with permission.

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Post Traumatic Stress Disorder (PTSD) – An important co-morbidity in military athletes ~ BRIG Stephan Rudzki (Rtd) FACSP PhD

In western nations, military populations are required to achieve and maintain high levels of physical fitness in order to keep their jobs –hence the oft heard term “military athlete”. It doesn’t make them elite, but it does make them persistent and willing to endure pain and discomfort well beyond the threshold of civilian athletes.

The recent wars in Afghanistan and Iraq have left a legacy of psychological disruption, mainly Post Traumatic Stress Disorder (PTSD) that will be significant in the years ahead. But why should a Sports Physician have any interest in PTSD?

If you deal with military patients who have been at war or on peacekeeping missions, up to 20 percent (US and Australian Armies) will have symptoms of PTSD. Many soldiers who suffered injuries while deployed will have experienced trauma of various degrees in acquiring those injuries. The same applies to emergency response workers such as police, paramedics and firemen.

Photo Credit: The U.S. Army via Compfight cc

Photo Credit: The U.S. Army via Compfight cc

A key issue in the treatment of injured soldiers is diagnosis of co-morbid psychological conditions. Many soldiers are reluctant to come forward and seek psychological assistance and many military patients have symptoms, but have not been diagnosed or identified as symptomatic.

So the first thing a sports physician can do is ask about symptoms and if suspicious administer a simple screening tool called the Post-traumatic checklist or PCL. This form can be downloaded from the internet free of charge (1).  A PCL score above 50 is highly suggestive of a diagnosis of PTSD and need confirmation by a psychiatrist or a clinical psychologist. Patients will often confide in their doctor when asked specifically, but will rarely volunteer any information about symptoms.

A US Navy colleague of mine once told me that he relocated the mental health section into the physiotherapy department, because the physiotherapists were identifying so many cases of PTSD among the Marines they were treating. Having the mental health section co-located with physiotherapy automatically removed the stigma of being seen going to the mental health clinic and allowed the sports physicians to cross refer within the same building.

PTSD is an unusual disorder in that it is currently diagnosed purely upon the presence, severity and impact of symptoms only. To date there are no proven objective tests able to confirm the diagnosis. This leads to unsurprising controversy as to the validity of relying on symptoms alone, but that is a controversy I will not delve into.

From my perspective, the condition is real and early identification and effective treatment reduces symptoms significantly. This is important because if left untreated, PTSD symptoms progressively worsen leading to social and occupational impairment.

Evidence based treatments for PTSD include various forms of Cognitive Behavioural Therapy and Prolonged Exposure therapy. They are essentially desensitisation approaches which teach the patient to change the way they respond to reliving the traumatic event (2).  Eye Movement Desensitisation Reprograming (EMDR) is a form of prolonged exposure therapy that also includes eye movement activities. A recent report from the Pakistani Army found that EMDR was more effective than the use of SSRI in relieving symptoms in a combat veteran cohort, with 90 percent of the EMDR group having a treatment response compared to 36 percent taking paroxetine (3).

Most treatment guidelines recommend the use of SSRI as first line treatment, primarily for their anxiolytic effect and the US DoD/VA clinical practice guidelines can be downloaded (4). The absence of a biological basis for PTSD results in therapeutic challenges, but there is some emerging evidence of a physiological basis to some of the symptoms of the disorder.

The possibility that the sustained threat environment of combat creates an abnormally sustained stress response resulting in the persisting symptoms seen in PSTD patients is not beyond the realms of probability.

One therapy that does not work is supportive counselling. If you refer a patient for psychological treatment it is important to ensure that an effective and evidence based treatment is being delivered.

In summary, if you treat injured soldiers, one in five will be suffering from symptoms of PTSD. The symptoms and associated co-morbidity may well inhibit a successful rehabilitation from injury. Doctor initiated diagnosis and treatment referral will be generally accepted by the soldier. Early identification and treatment offers the best possibility of recovery.

For more information on treating military athletes turn to Chapter 45 in Clinical Sports Medicine.

Dr Rudzki retired from the Australian Army in 2012 after 30 years of service. He was a Foundation Fellow of the Australian College of Sports Physicians. His main clinical interest is in the area of Injury Prevention and he has published a number of papers on this topic. Dr. Rudzki is currently a Regional Medical Advisor for the Australian Defence Force Joint Health Command in Canberra.


  2.  Ougrin D. Efficacy of exposure versus cognitive therapy in anxiety disorders: systematic review and meta-analysis. BMC Psychiatry. 2011; 11: 200.
  3.  EMDR versus Paroxetine in the treatment of PTSD – A Randomised Trial. International Congress of the Royal College of Psychiatrists (RCPsych) 2013. Poster 65. Presented July 3, 2013.
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Development of a Clinical Hypothesis for Patellofemoral Pain ~ Irene Davis, PhD, PT

Patellofemoral pain (PFP) is a common orthopedic condition and the number one injury in runners.  Though the exact cause of PFP is unknown, it is believed to be related to the interaction between patella and femur. As the patella has seven articular facets, subtle abnormalities in the movement between the patella and femur can create areas of high patellofemoral joint contact stress and cause PFP.  Abnormal movements can also lead to abnormal loads on the soft tissues that stabilize the patella, causing PFP.

Photo by diongillard. Used with permission. All rights reserved. Source: flickr

Photo by diongillard. Used with permission. All rights reserved. Source: flickr

Due to the closed chain nature of lower extremity motion during gait, movement at one joint can affect others in the kinetic chain.  Mechanics of the hip, the knee, and the foot –or some combination of these factors- can affect patellofemoral motion. Debate continues as to which of these factors are the most prevalent and most important.  Understanding which factors are related to PFP is critical to developing the optimal rehabilitative approach. All treatment approaches should be based upon a clinical hypothesis.

A clinical hypothesis is your theory as to the cause of a patient’s problem, developed from their history, physical exam, and gait assessment.  The history provides information as to whether the injury is acute perhaps from improper training, or a chronic problem, which may be related to mechanics.  The physical exam provides insights into contributing factors in strength, flexibility, and alignment.  The gait assessment reveals faulty hip, knee, or foot mechanics that may overload key musculoskeletal structures.

Different presentations of these factors lead to different hypotheses.  In one case, you may hypothesize that the patient’s abnormal hip mechanics and weak hip musculature is resulting in genu valgus and patellofemoral malalignment.  In another patient, you may theorize that their excessively pronated and weak feet are leading to genu valgus, patellofemoral malalignment, and PFP.  In a third case, you may believe it is the patient’s long stride and heavy heel strike that is increasing the loads and rate of loading to the patellofemoral joint.

Based upon these three clinical hypotheses, your interventions will be very different.  The first patient might receive hip strengthening and gait retraining to improve their hip mechanics.  The second patient would focus on foot strengthening and gait retraining to better their foot mechanics.  Finally, the third patient might reduce their stride length and land softer.

As with research hypotheses, clinical hypotheses are not always correct and are tested by the success of the intervention.  If you find that your approach is not working you must reassess and refine or alter your clinical hypothesis. This type of approach provides a well-justified framework for your intervention. However, this requires an understanding of the potential factors that can contribute to PFP.

Understanding which factors are related to PFP is a large focus of the upcoming International Patellofemoral Pain Research Retreat.  Renowned scientists from across the globe will convene to discuss their most research in the area of PFP.  The Clinical Symposium Day will bring this research to the clinical arena. Along with keynote presentations on current topics, and debates on rehabilitation approaches, an expert panel will discuss difficult PFP cases. The consensus statement from the last International Patellofemoral Pain Research Retreat will be reviewed. Seldom do you have an opportunity to hear from this many scientific leaders in the area of PFP at one meeting -in one day.  Don’t miss it – Hope to see you there!

Dr. Irene Davis is the Director of the Spaulding National Running Center, Harvard Medical School. Dr. Davis’ research has focused on the relationship between lower extremity structure, mechanics and injury. Her interest in injury mechanics extends to the development of interventions to alter these mechanics through gait retraining.She has been featured on ABC World News Tonight, Good Morning America, Discovery, the New York Times, the Wall Street Journal, Parade, and Time Magazine.

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Determining the Etiology of Exercise-Associated Muscle Cramping: New Evidence Comes to Light ~ Kevin C. Miller, PhD, AT, ATC

Despite estimates that exercise-associated muscle cramps (EAMC) affect up to 95 percent of the general population [1], their cause is currently unknown.  The two prevailing theories are the dehydration and electrolyte loss theory [2] and the neuromuscular control theory [3].

Photo by kopretinka. Used with permission. All rights reserved. Source: flickr

Photo by kopretinka. Used with permission. All rights reserved. Source: flickr

Briefly, the dehydration theory postulates that exercise-induced sweating results in a contracture of the interstitium causing an increase in the pressure on select nerve terminals and EAMC ensue.  The neuromuscular control theory suggests EAMC occur when fatigue and other factors coalesce and cause disinhibition of golgi tendon organs and increased excitation of muscle spindles resulting in the hyperexcitability of the alpha motor neuron pool.

Finding the etiology of EAMC is difficult because they are spontaneous and unpredictable and no suitable animal model exists for inducing cramps in a laboratory setting.  As a result, scientists have primarily studied EAMC using quasi-experimental or case study research designs.  These experiments have usually sought to determine the etiology of EAMC by comparing some physiological characteristic (e.g., body mass loss, plasma sodium concentration) between crampers and non-crampers before and after an athletic competition.

While these experiments are valuable, it is difficult to identify a true etiology with these designs as multiple physiological changes are happening to athletes during exercise besides dehydration, electrolyte loss, or fatigue.

Recent controlled, experimental studies [4,5] indicate that mild to severe dehydration does not affect cramp risk when peripheral fatigue is minimized.  These studies [4,5] were the first to try and study cramp etiology by controlling for fatigue but still have subjects lose substantial amounts of body water.

The results are consistent with other scientists’ [6-8] observations that cramps are likely the result of neurological changes rather than dehydration.  Further research is needed to identify the factors that coalesce to elicit EAMC so specific strategies to treat and prevent EAMC can be developed.

Dr. Kevin C. Miller, AT, ATC is an Associate Professor in Athletic Training at Central Michigan University.  His research interests involve the causes, treatments, and prevention of exercise-associated muscle cramps.  He has published numerous articles on muscle cramps in several Tier 1 journals including the British Journal of Sports Medicine, Muscle and Nerve, Medicine and Science in Sports and Exercise, and the Journal of Athletic Training.


1. Norris F, Gasteiger E, Chatfield P. An electromyographic study of induced and spontaneous muscle cramps. Electroencephalogr Clin Neurophysiol 1956;9:139-47

2. Bergeron M. Muscle cramps during exercise–Is it fatigue or electrolyte deficit? Curr Sports Med Rep 2008;7:S50-S55

3. Schwellnus M. Cause of exercise associated muscle cramps (EAMC)-Altered neuromuscular control, dehydration, or electrolyte depletion? Br J Sports Med 2009;43:401-08

4. Miller K, Knight K, Mack G, et al. Three percent hypohydration does not affect the threshold frequency of electrically-induced muscle cramps. Med Sci Sports Exerc 2010;42:2056-63

5. Braulick K, Miller K, Albrecht J, et al. Significant and serious dehydration does not affect skeletal muscle cramp threshold frequency. Br J Sports Med 2012;47:710-14

6. Minetto M, Holobar A, Botter A, et al. Mechanisms of cramp contractions: peripheral or central generation. J Physiol 2011;23:5759-73

7. Ge H, Zhang Y, Boudreau S, et al. Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points. Exp Brain Res 2008;187:623-29

8. Merletti R, Botter A, Lanfranco F, et al. Spinal involvement and muscle cramps in electrically elicited muscle contractions. Artif Organs 2011;35:221-25



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