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I recently read the article Jamtvedt et al on whether pre and post
stretching prevents injury 1 with interest. I commend the authors for
their well-conducted study and would like to comment on two particular
issues.
First, the authors correctly point out that there was no difference in the
primary outcome of all injuries, and that the analysis showing an absolute
22% reduction in muscle, ligament a...
I recently read the article Jamtvedt et al on whether pre and post
stretching prevents injury 1 with interest. I commend the authors for
their well-conducted study and would like to comment on two particular
issues.
First, the authors correctly point out that there was no difference in the
primary outcome of all injuries, and that the analysis showing an absolute
22% reduction in muscle, ligament and tendon injuries with stretching
should be interpreted cautiously. However, they then continue to say
"Nonetheless, it is plausible that stretching reduces muscle, ligament and
tendon injuries, and it may be implausible that stretching increases other
injuries". Moreover, in the conclusion, they only mention the "probable
reduction in muscle, ligament and tendon injuries" and omit the absence of
an effect on the primary outcome of overall injuries. This type of
thinking appears to be gaining popularity. For example, Small et al (cited
by the current article) emphasized the decrease in musculo-tendinous
injuries they observed in their review of stretching and discounted the
associated increase in stress fractures and "shin splints" 2.
In other areas of medicine, we have already learned the difficult lesson
that "all-cause mortality" is generally a much more important outcome
compared to "disease-specific mortality" because interventions can cause
damage through unrecognized mechanisms. It would be a pity if the sport
medicine world has to go through the same lessons. Plausible reasons why
stretching would increase some types of injuries are already available
from a review of basic science evidence 3. Because Jamtvedt et al do not
actually detail the non muscle-tendon-ligament injuries, I will use the
example from Small et al. related to stress fractures and "shin splints"
(not defined, but presumably periostitis and compartment syndrome). An
acute bout of stretching causes weakness, 4 which is expected to lead to
1) an increased force transmission to the bone 5, 6, which would lead to
increased stress reaction and stress fractures and 2) a possible increase
in compensatory muscle use, which could theoretically cause shin splints
of any cause. Further, stretching-induced weakness would theoretically
also decrease proprioception, although this remains to be studied. Authors
who decide to report sub-group analyses need to show the same analyses for
all the sub-groups created by the categorization.
Second, "stretching" as an intervention is intricately related to the
timing of the stretch, and one expects different results from stretching
before exercise compared to stretching at other times 7. In their
conclusion, Jamtvedt et al suggest that "the results of this trial support
the decision to stretch" 1, with no mention of the timing; reviews by
Small et al 2, and Thacker et al 8 (cited by the current article) made the
same error. In brief, the effects of "stretching" are similar to those of
"weight lifting". An acute bout of weight lifting or stretching will cause
an immediate decrease in strength, power and endurance 4. However, if one
weight lifts or stretches for weeks, there is an increase in strength,
power and endurance 4. Based on this, one would expect that stretching
before every exercise session would increase the risk of injury due the
acute effects, but there would also be an expected decrease in injury risk
as the body adapts and strengthens over time. If the two effects were
relatively balanced, one would expect no effect on overall injury rate.
However, if one stretched regularly but not before exercise, then one
would expect only the benefits, with a decrease in overall injury rate.
Indeed, there have been three randomized trials prior to this study and a
meta-analysis of these (one study had subjects stretch before and after
exercise as in the current study 9) suggests regular stretching not before
exercise reduces injury risk [OR=0.68 (95%CI: 0.52, 0.88)] 7.
Given these previous studies, it would be interesting for the authors to
conduct a post-hoc analysis (with the appropriate cautious interpretation)
comparing the injury risk among those who stretched only before exercise,
those that stretched only after exercise, and those that stretched both
before and after exercise.
In summary, there should be little controversy about 1) post-exercise
stretching reducing acute muscle soreness, just as it reduces any chronic
musculoskeletal pain 10, presumably due to its well-studied effects on
stretch-tolerance (a form of analgesia) 11, 12, and 2) stretching not
before exercise reducing injury risk given that both basic science and
clinical science provide consistent evidence, although a couple more
confirmatory studies could be helpful. Future research priorities should
focus on questions where there is little to no evidence such as 1) whether
post-exercise stretching is as beneficial as stretching at other times, 2)
what are the effects for high intensity sports, 3) the effects of
stretching on rehabilitation of injuries, and 4) the effects on the
performance in injured athletes (all published studies examined healthy
subjects) 13.
Ian Shrier MD, PhD, Dip Sport Med, FACSM
Centre for Clinical Epidemiology and Community Studies
SMBD-Jewish General Hospital
3755 Cote Ste-Catherine Rd
Montreal, Qc H3T 1E2
Tel: 514-340-7563
Fax: 514-340-7564
References
1. Jamtvedt G, Herbert RD, Flottorp S, et al. A pragmatic randomised
trial of stretching before and after physical activity to prevent injury
and soreness. Br J Sports Med. 2010;44:1002-1009.
2. Small K, McNaughton L, Matthews M. A systematic review into the
efficacy of static stretching as part of a warm-up for the prevention of
exercise-related injury. Res Sports Med. 2008;16:213-231.
3. Shrier I. Does stretching help prevent injuries? In: MacAuley D, Best
T, eds. Evidence-based sports medicine. London: BMJ Publishing Group;
2007.
4. Shrier I. Does stretching improve performance: A systematic and
critical review of the literature. Clin J Sport Med. 2004;14:267-273.
5. Mizrahi J, Verbitsky O, Isakov E. Fatigue-related loading imbalance on
the shank in running: a possible factor in stress fractures. Ann Biomed
Eng. 2000;28:463-469.
6. Christina KA, White SC, Gilchrist LA. Effect of localized muscle
fatigue on vertical ground reaction forces and ankle joint motion during
running. Hum Mov Sci. 2001;20:257-276.
7. Shrier I. Meta-analysis on preexercise stretching. Med Sci Sports
Exerc. 2004;36:1832-1832.
8. Thacker SB, Gilchrist J, Stroup DF, et al. The impact of stretching on
sports injury risk: a systematic review of the literature. Med Sci Sports
Exerc. 2004;36:371-378.
9. Amako M, Oda T, Masuoka K, et al. Effect of static stretching on
prevention of injuries for military recruits. Mil Med. 2003;168:442-446.
10. Law RY, Harvey LA, Nicholas MK, et al. Stretch exercises increase
tolerance to stretch in patients with chronic musculoskeletal pain: a
randomized controlled trial. Phys Ther. 2009;89:1016-1026.
11. Magnusson SP, Simonsen EB, Aagaard P, et al. Mechanical and
physiological responses to stretching with and without preisometric
contraction in human skeletal muscle. Arch Phys Med Rehabil. 1996;77:373-
378.
12. Halbertsma JPK, Mulder I, Goeken LNH, et al. Repeated passive
stretching: acute effect on the passive muscle moment and extensibility of
short hamstrings. Arch Phys Med Rehabil. 1999;80:407-414.
13. Shrier I. Stretching perspectives. Curr Sports Med Rep. 2005;4:237-
238.
In response to the editorial- Physical activity in the UK: a unique
crossroad.Br J Sports Med 2010 vol44 no 13
I was delighted to read Dr Weilers editorial which eloquently
presents many of the issues currently faced in exercise medicine.
It is so important to debate this subject-particularly as we are in a
unique position in the U.K to effect permanent change.
I was interested in Dr Weilers' view that the intro...
In response to the editorial- Physical activity in the UK: a unique
crossroad.Br J Sports Med 2010 vol44 no 13
I was delighted to read Dr Weilers editorial which eloquently
presents many of the issues currently faced in exercise medicine.
It is so important to debate this subject-particularly as we are in a
unique position in the U.K to effect permanent change.
I was interested in Dr Weilers' view that the introduction of the GGPAQ
into QOF would be a valuable place to start what will have to be a process
of cultural change. I would like to debate this opinion further.
It has been clearly established in the literature that changes in physical
activity levels in the long term are not easy to effect. The most
successful interventions involve patient centred, long term, well
supported, behaviourally based interventions delivered by highly motivated
and well trained medical professionals. I do not agree with your statement
that 'brief interventions (3-10min) can lead to substantial increases in
physical activity level (by around 30%)'. I am not aware of any evidence
to substantiate this claim, particularly in the long term. The studies
which have shown these sorts of results have used of a much more intense
intervention, not sustainable within the NHS, and most do not show
significant long term results (greater than 3 months).(1,2)
I agree that physical activity promotion to 'healthy' populations can only
be delivered by primary care. I feel, however, that we are not yet ready
for GGPAQ. The effect of creating another 'box to tick' in an already
target driven culture, I feel, at this stage would be counterproductive.
We have a long way to go in the process of educating G.P's and practice
nurses about the evidence base for the benefits of and the delivery of
exercise prescription. It will, rightly, take convincing evidence of
effectiveness to persuade G.P's to engage in this process. There is,
currently, no evidence that could possibly lead us to suppose that the
introduction of GGPAQ would lead to significant and sustained changes in
physical activity levels
?1million , to introduce a QOF point does not seem an enormous amount of
money until you consider that with that sum, per year, you could employ 10
SEM consultants. I feel this would be a very much more effective way of
spending the limited resources available at this stage. A single SEM
consultant could provide a comprehensive education programme from medical
school to primary and secondary care, could lead good quality,
translational research into cost effective ways of delivering exercise
interventions and could coordinate existing services for exercise in
chronic disease which are often non-existent or ineffective and poorly
evaluated. They could assess local needs, building on strengths of
existing structures and working on the weaknesses. They could improve
links with the fitness industry which in many cases are poorly supported
and therefore less effective.
I agree, clinical research is essential at this stage and funding is not
easy to come by. The N.H.S needs to address this through its own research
organisations. Partnerships with the tremendously powerful fitness
industry may also help to fund translational research as might charitable
foundations for chronic disease research.
Overall, I agree with much of the editorial, but feel that in the current
economic climate , we need to think very carefully before rolling out
blanket schemes which are open to criticism from the very people we are
hoping will deliver them.
1.Eakin EG, Glasgow RE, Riley KM. Review of primary care-based
physical activity intervention studies: effectiveness and implications for
practice and future research. J Fam Pract. 2000; 49: 158-168.
2. Lawlor D.A The Effect of physical activity advice given in primary care
consultations-a review. Journal of public Health Medicine.2001; 23:219-226
An article entitled "The challenge of low physical activity during
the school day: at recess, lunch and in physical education" was recently
published in the British Journal of Sport Medicine.[1] Briefly, Nettlefold
and colleagues used uniaxial accelerometers (Actigraph GT1M) to estimate
the level of physical activity (PA) over the school day in Canadian
children aged 8-11 years. One of their most striking findings was th...
An article entitled "The challenge of low physical activity during
the school day: at recess, lunch and in physical education" was recently
published in the British Journal of Sport Medicine.[1] Briefly, Nettlefold
and colleagues used uniaxial accelerometers (Actigraph GT1M) to estimate
the level of physical activity (PA) over the school day in Canadian
children aged 8-11 years. One of their most striking findings was that
only 1.8% of girls and 2.9% of boys in the compliant fraction (216 of 629
students recruited) met the U.S. guideline of performing moderate to
vigorous physical activity (MVPA) during at least 50% of their physical
education (PE) classes.[2] This troubling finding has important
implications regarding the quality of PE programmes.
All the PE classes in this study were taught by regular classroom
teachers, as it is commonly the case for primary students in British
Columbia and elsewhere.[1, 3] However, in interview data collected from
two different Manitoban primary schools, DeCorby and colleagues [4] found
normal classroom teachers were very uncomfortable in delivering PE
instruction, due to a lack of specific knowledge and appropriate training.
The principal of the school concerned commented: "I really feel sorry for
them [the kids] because we wouldn't ask teachers to teach music, for
example, with no training, but yet we do with phys. ed."[4] In the second
school that was examined, PE was taught by a specialist who developed a
programme that focused on the acquisition of developmentally appropriate
motor skills, a variety of physical activities performed in a non-
competitive environment, and positive social development. That programme
proved successful in stimulating participation and enjoyment, particularly
among the girls and the boys who had difficulty in undertaking PE.[4]
A small number of experimental, quasi-experimental and/or
longitudinal studies in various jurisdictions have compared the response
of primary school students to high quality, specialist taught PE
programmes with the response to a "normal" curriculum. In the Trois-
Rivieres study, conducted from 1971 to 1978, 546 Quebecois children were
assigned (on the basis of year of entry to a school) to either an
experimental programme (5 h of PE per week taught by a qualified physical
educator from Grades 1 through 6) or the standard curriculum (40 min of PE
once per week under the supervision of their home-room teacher).[5] The PE
classes for children in the experimental group were designed to ensure
that students spent most of the class performing vigorous exercise (heart
rate equal or greater than 160 beats per minute), and this was verified by
telemetry. Moreover, questionnaire data demonstrated that there was not a
compensatory reduction of PA level during the rest of the day.[5]
The CATCH intervention studied American children in grades 3 to 5;
the experimental group received a comprehensive intervention which
included modifications to school food services, enhanced PE classes and
use of health curricula in the classroom [6]. The proportion of MVPA
during PE for the experimental group gradually increased to over 50% of
class time; they also accumulated more intense PA than the controls (58.6
vs. 46.5 minutes daily).[6] Similarly, in the SPARK project, American
children who received PE from a specialist accumulated more minutes of
MVPA during their PE classes than those who were taught by a partially
trained or an untrained (e.g. control) classroom teacher (40 vs. 33 vs. 18
minutes respectively).[7]
More recently, a Swiss study of students in Grades 1 and 5 has
examined the effects of supplementing the regular PE curriculum (3 weekly
45 minutes PE lessons taught by a classroom teacher) by twice weekly 45
minutes specialist-taught PE lessons, several 5 minutes PA breaks
throughout the school day, and 10 minutes of daily PA homework in the
context of a cluster randomized control trial.[8] Accelerometry data
suggested that students in the experimental group accumulated more MVPA
and total PA than controls during school time, but unfortunately in this
study there was a compensatory reduction of PA during leisure hours, so
that the experimental group did not increase their total activity for the
day relative to controls.
Some investigators have noted quite strong relationships between
curricular time devoted to PE and health-related outcomes including: a
higher maximal aerobic power and muscular fitness, enhanced motor skills,
a reduction of adiposity, and enhanced academic achievement.[3, 7-9]
German researchers compared sixth grade children who were assigned to an
enhanced PE program for an entire school year (45 minutes of daily PE with
a particular emphasis on endurance training) to a control group which
received 45 minutes sessions of PE only twice per week.[10] ANCOVA
analyses revealed major increases in maximal aerobic power (a gain of 3.7
ml*kg-1*min-1) and circulating progenitor cells and a trend to a decrease
in the prevalence of overweight and obesity (from 12.8% to 7.3%, N.S.) in
the experimental group.[10]
These several investigations highlight the importance of specialist
PE training to the quality of PE programmes, and their resulting ability
to maximize the fraction of class time spent in MVPA. Key elements of a
quality programme include: 1) development of a full range of motor skills
during early primary school; 2) improvement of both aerobic and muscular
fitness through a wide variety of physical activities; 3) a reduced
emphasis on competition, in order to foster participation of less skilled
individuals, and 4) the development of skills that will encourage physical
activity throughout the individual's lifespan.[3, 4, 8] Nevertheless, the
age-related decline in PA points the need for further research on long
term outcomes.[3] Changes in the content of PE classes still seem needed
to encourage long term participation in a volume of physical activity that
is optimal for health.
The British Columbia PE curriculum specifies a wide range of learning
outcomes, from knowledge of the topic to active living, movement skills,
safety, fair play and leadership.[1] Possibly, the demands on the PE class
are too diverse, and the responsibility for teaching some of these topics
should be delegated to other school disciplines. This strategy was
effective in the CATCH intervention.[6]
REFERENCES
1. Nettlefold L, McKay HA, Warburton DER, et al. The challenge of low
physical activity during the school day: at recess, lunch and physical
education. Br J Sport Med. Published Online First 9 March 2010. doi:
10.1136/bjsm.2009.068072
2. United States Department of Health and Human Services. Healthy
people 2010: understanding and improving health. Washington, DC: U.S.
Government Printing Office 2000.
3. Trudeau F, Shephard RJ. Contribution of school programmes to
physical activity levels and attitudes in children and adults. Sports Med
2005;35(2):89-105.
4. DeCorby K, Halas J, Dixon S, et al. Classroom teachers and the
challenge of delivering quality physical education. J Educ Res
2005;98(4):208-220.
5. Lavallee H, Shephard RJ, Jequier J-C, et al. A compulsory physical
activity program and out-of-school free activities in the Trois-Rivieres
study [In French]. In: Lavallee H, Shephard RJ, eds. Child growth and
development. Trois-Rivieres, Qc: editions du Bien Public 1982:61-71.
6. Luepker RV, Perry CL, McKinlay SJ, et al. Outcomes of a field
trial to improve children's dietary patterns and physical activity: the
Child and Adolescent Trial for Cardiovascular Health (CATCH). JAMA
1996;275(10):768-776.
7. Sallis JF, McKenzie TL, Alcaraz JE, et al. The effect of a 2-year
physical education program (SPARK) on physical activity and fitness in
elementary school students. Am J Public Health 1997;87(8):1328-1334.
8. Kriemler S, Zahner L, Schindler C, et al. Effect of school based
physical activity programme (KISS) on fitness and adiposity in primary
schoolchildren: cluster randomized control trial. BMJ 2010;340:c785.
doi:10.1136/bmj.c785
9. Shephard RJ. Long-term studies of physical activity in children -
The Trois-Rivieres experience. In: Binkhorst RA, Kemper HCG, Saris WHM,
eds. Children and Exercise XI. Champaign, Ill.: Human Kinetics 1985:252-
259.
10. Walther C, Gaede L, Adams V, et al. Effect of increased exercise
in school children on physical fitness and endothelial progenitor cells: A
prospective randomized trial. Circulation 2009;120:2251-2259.
In the midst of the genetic/genomic medicine revolution, the Caster's controversy illustrates how human society is lacking in its ability to deal with Disorders of Sex Development (DSD) at either a social, competitive, legal or ethical level. Political fractionalization, by way of "protecting human rights" added fuel to the fire rather than defusing the situation. "We can't afford any mistakes, particularly as we...
In the midst of the genetic/genomic medicine revolution, the Caster's controversy illustrates how human society is lacking in its ability to deal with Disorders of Sex Development (DSD) at either a social, competitive, legal or ethical level. Political fractionalization, by way of "protecting human rights" added fuel to the fire rather than defusing the situation. "We can't afford any mistakes, particularly as we already face threats to be taken to the United Nations Human Rights Council and because it has become a political matter in South Africa," said The International Association of Athletics Federations (IAAF) spokesman Nick Davies.1 Controversial issue in gender verification in sport include failure to understand the complexities of DSD, screening tests lacking validity, the discriminatory singling out of women based only on laboratory results and the stigmatization and emotional trauma experienced by individuals screened positive.2 The debate spurred by Caster's demands reflection on the meaning and aims of sport, its ethics and philosophy.3
Foddy and Savulescu are absolutely on target when they note that any attempt to use genetic or functional biochemical information for gender identification purposes would be inappropriate.4 As the authors reviewed, the historical physical inspection could not determine gender in some conditions; e.g. 46, XY pure gonadal dysgenesis 'where the apparent female' might have complete female external genitalia, but genetically, 'she' has an X and a Y chromosome, effectively being classified 'male'. On buccal smears, it was decided that XX athletes (with two X chromatids) were female. In fact, a female athlete with Turner syndrome (45, XO) would "fail" the gender test. Paradoxically, the test would have permitted men with Klinefelter's syndrome (47, XXY) to compete. It was also difficult to use the DNA detection of SRY gene (sex determining region of the Y chromosome). An athlete with 46, XX true hermaphroditism, may have an advantage in sport from her higher level of testosterone in the presence of testicular tissue and negative SRY test.
DSD could be classified into three groups: 1) sex chromosome abnormalities (including abnormal numbers and abnormal structures), 2) gonadal abnormalities and 3) sex hormone abnormalities (including abnormal levels of androgen and receptor defects).5 In addition, some authors recently claimed that defining functional advantage, irrespective of the genetic sex, could be useful for gender verification in ensuring fairer Olympics.6 The 46, XX females with congenital adrenal hyperplasia (CAH), have a much higher level of testosterone that might be an advantage in sport. One could argue that such individuals should not compete in the female category because of possible advantages in sport. But which sport? Women with CAH are expected to be shorter than average7 and would not be able to use this "advantage" in basketball! Salt loss that can occur in the condition may lead to a degree of fatigability, a potential disadvantage. In addition, treatment with glucocorticoids that is directed at preventing adrenal crises and ensuring normal childhood growth by alleviating hyperandrogenism7 could trigger an enhancement issue. Moreover, a greater understanding of the genotype-phenotype correlation supports the view that 21-OH Deficiency is a continuum of phenotypes,8,9 with variable expression of CAH even within a family.10 Another case in point is the condition called androgen insensitivity syndrome. The phenotype in partial form is extremely variable and is rarely predicted by the androgen receptor genotype;11,12 it is fair to classify an athlete with this condition to compete in a male category? Probably not! There just isn't a simple answer! Foddy and Savulescu amply illustrate that functional classification will be inadequate, in as much as, numerous genetic factors explain the extremely high variation in serum testosterone between individuals and no routine functional test is available to measure the effect of hormones androgen receptors.4
It should be added that any genetic testing should be accompanied by adequate counseling, informed consent, and respect for confidentiality13. Before the competition in Berlin, an email exchange between Harold Adams, the team doctor, and Molatelo Malehopo, the Athletic South Africa (ASA) general manager, discussed and authorized gender testing, with South African athletics chief Leonard Chuene copied in. Semenya was tested before competing in Berlin. Chuene later admitted that he was aware of this, but had kept the information confidential to protect Semenya's privacy. Interestingly, Wilfred Daniels, the team coach, also confirmed Semenya was made to undergo tests without being fully aware of their nature, and that tests were undertaken on August 7, 2009.14 In Berlin, the IAAF reported that two things triggered the investigation: firstly, the 'incredible improvement in the athlete's performance and secondly the fact that a South African blog was alleging that she was a hermaphrodite athlete"15 It's clear that none of routinely accepted genetic test and genetic counseling principles were respected from the beginning. First, how could we explain that medical professionals in South Africa carried out such an important gender test not only without any prior genetic counseling for the patient, but more gravely, without informing the client of the nature of the tests? Where are the principles of full information, informed consent, autonomy and non-directiveness? Where are the principles of confidentiality when the entire ASA team of officials including the coach (all but Caster) was aware of the nature of the first gender test? Secondly, in Berlin, the IAAF stood its ground, saying it only made the gender test public after it had already been reported in the media. Where was the professionalism of their medical expert committee with a duty to care about the dignity, emotional distress and confidentially rights of Caster? Thirdly, if political officials were properly informed about the complexity of genetic issues, especially gender disorders, would the public have faced such ill informed passionate public pronouncements? Finally, was the media right to give so much attention to this gender testing issue?13
The number of genetic 'abnormalities' concerning gender together with variable expression, and their complexity infers that the current IAAF gender policy is inadequate to cope with such cases. Gender verification has potential or causing great psychological harm to women who may unknowingly have a DSD and is far more likely to bar unfairly from competition women with genetic abnormalities that confer no such advantage that safeguard fair competition. The results of the gender verification tests on Caster were awaited by the end of November 2009, but IAAF has decided not to disclose those results. Interestingly, Semenya returned to competition in July 2010 after receiving confirmation from the IAAF that she could compete as a woman.16
REFERENCES:
1. Anonymous. IAAF tell ASA to test Semenya (2009). Retrieved March 15, 2010 from http://www.sport24.co.za/Content/OtherSport/262/72b18690dd41494593c6a9b39e86f255/19-08-2009%2006-16/IAAF_tell_ASA_to_test_Semenya
2. Reeser JC. Gender identity and sport: is the playing field level? Br J Sports Med 2005; 39: 695-9.
3. Camporesi S, Maugeri P. Caster Semenya: sport, categories and the creative role of ethics. J Med Ethics. 2010 Jun;36(6):378-9.
4. Foddy B, Savulescu J.Time to re-evaluate gender segregation in athletics? Br J Sports Med. 2010. DOI: 10.1136/bjsm.2010.071639.
5. Lee PA, Houk CP, Ahmed SF, Hughes IA. and in collaboration with the participants in the International consensus conference on intersex organized by the Lawson Wilkins pediatric endocrine society and the European society for paediatric endocrinology. Consensus statement on management of intersex disorders. Pediatrics 2006; 118: e488-e500.
6. Tian Q, He F, Zhou Y, Ge Q. Gender verification in athletes with disorders of sex development. Gynecol Endocrinol 2009; 25: 117-121
7. Tahirovic H, Toromanovic A, Grubic M, et al. Untreated congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Eur J Pediatr 2009; 168: 847-9
8. Huynh T, McGown I, Cowley D, et al. The clinical and biochemical spectrum of congenital adrenal hyperplasia secondary to 21-hydroxylase deficiency. Clin Biochem Rev 2009; 30: 75-86.
9. Goossens K, Juniarto AZ, Timmerman MA, et al. Lack of correlation between phenotype and genotype in untreated 21-hydroxylase-deficient Indonesian patients. Clin Endocrinol (Oxf) 2009; 71: 628-35.
10. Tardy V, Menassa R, Sulmont V et al. Phenotype-genotype correlations of 13 rare CYP21A2 mutations detected in 46 patients affected with 21-hydroxylase deficiency and in one carrier. J Clin Endocrinol Metab 2010; 95:1288-300.
11. Boehmer AL, Brinkmann O, Br?ggenwirth H, et al. Genotype versus phenotype in families with androgen insensitivity syndrome. J Clin Endocrinol Metab 2001; 86: 4151-60.
12. Deeb A, Mason C, Lee YS, Hughes IA . Correlation between genotype, phenotype and sex of rearing in 111 patients with partial androgen insensitivity syndrome. Clin Endocrinol (Oxf) 2005; 63: 56-6.
13. Wonkam A, Fieggen K, Ramesar R. Beyond the Caster Semenya Controversy: The Case of the Use of Genetics for Gender Testing in Sport. J Genet Couns. 2010. DOI : 10.1007/s10897-010-9320-2
14. Samuel M. Sorry Tale, probed south African Athlete Caster Semenya (2009). Retrieved March 15, 2010 from: http://www.dailymail.co.uk/sport/article-1214895/martin-samuel-europes-elite-left-pots-trouble.html .
15. Wilson N. Athletics: boy, That's some win! Golden girl Caster Semenya to face sex test (2009). Retrieved March
We read with interest the recent review by Bleakley and Davison (BJSM vol 44: 179-187)[1], which described the physiological and biochemical responses to cold water immersion (CWI) after exercise. The authors examined some of the acute cardiovascular responses that occur with CWI, such as changes in heart rate, blood pressure and cerebral blood flow. We noted, however, that they did not address the effec...
We read with interest the recent review by Bleakley and Davison (BJSM vol 44: 179-187)[1], which described the physiological and biochemical responses to cold water immersion (CWI) after exercise. The authors examined some of the acute cardiovascular responses that occur with CWI, such as changes in heart rate, blood pressure and cerebral blood flow. We noted, however, that they did not address the effects of CWI on heart rate variability (HRV), which provides an indication of cardiac autonomic nervous system (ANS) activity[2]. Exercise increases cardiac sympathetic activity and reduces cardiac parasympathetic activity[3]. But when multiple bouts of high-intensity exercise are performed without adequate recovery, the return of cardiac parasympathetic activity to resting levels is diminished[4, 5, 6]. There is evidence to suggest however, that CWI quickens the (post-exercise) return of cardiac ANS activity to pre-exercise levels, which may be indicative of an improved recovery state.
Water immersion on its own alters cardiac ANS activity. In thermoneutral water immersion, hydrostatic pressure is the primary factor that induces a mild compression of the peripheral vasculature[7], thereby increasing venous return[8] and baroreceptor loading[9], ultimately increasing cardiac parasympathetic activity. For example, cardiac and vasomotor sympathetic activity was suppressed [8], while cardiac parasympathetic activity was elevated [8,10] during thermoneutral water (30 - 34.5 degrees C) immersion and further elevated during cool water (26 - 27 deg C) immersion[9] compared with sitting out of the water. Collectively, these findings indicate that water immersion increases cardiac parasympathetic activity, and the effect is augmented with the addition of a cold stimulus[9, 12].
Extending the findings of Mourot et al.[9] at rest (i.e., without exercise), Al Haddad et al.[12] observed a greater increase in cardiac parasympathetic activity after immersion in cold (14 - 15 deg C) compared with warm (33 - 34 deg C) water following submaximal exercise. Thus, CWI (at ~14 deg C) provides a moderate cold stimulus that likely has an additive effect on the hydrostatic pressure, increasing peripheral vasoconstriction[7, 13], and also stimulating cold receptors in the skin, subcutaneous tissue and veins. Together, these responses likely augment cardiac parasympathetic stimulation[14].
In an applied setting with athletes, Buchheit et al.[4] and Parouty et al.[15] observed that 5 min of CWI during recovery between two supramaximal exercise bouts helped to restore cardiac parasympathetic activity. This response however, was not associated with improved 1-km cycling performance[4], and was detrimental to repeated 100-m sprint swimming times[15]. Currently, limited data exists on the relationship between parasympathetic activity and athletic performance; however, it appears that improved/faster post-exercise parasympathetic reactivation does not necessarily translate into better high-intensity exercise performance. Further study exclusively manipulating cardiac autonomic activity before exercise (e.g., through pharmacological means) might help clarify this question. Exercise performance in such short events (1 min) may be more closely related to the efficiency of the neuromuscular and anaerobic systems, with the cardiovascular and autonomic systems playing only minor roles. Furthermore, the increased parasympathetic background before a repeated high-intensity effort might compromise cardio-acceleration at exercise onset, limiting oxygen delivery and therefore performance[15]. Greater parasympathetic activity before exercise may be beneficial for longer events, when a blunted increase in heart rate together with the increased plasma volume as a consequence of fluid shift after immersion[16] can prevent excessive myocardial work and therefore maintain prolonged aerobic performance. Future work could address this concept.
To date, no study has examined the effect of CWI during consecutive days of exercise on cardiac ANS activity, however, CWI following exercise sessions, particularly high-intensity exercise, may help restore/maintain cardiac parasympathetic activity during consecutive days of training. A concurrent reduction in cardiac sympathetic and increase in parasympathetic activity may be related to perceptions of less stress[17, 18], and greater well-being or - - recovery [4, 15]. Together, these observations may also be associated with improved sleep quality (personal observations), thereby reducing the period required for full recovery. Finally, the recent findings by Lung et al.[11] also suggest that repeated CWI might accelerate acclimation to altitude by reducing sympathetic responses to hypoxic exposure, which could be of interest for sea-level athletes travelling to and competing at altitude. This cross-adaptive response highlights further potential benefits of CWI for athletes competing in various environments, and warrants future research.
In summary, in addition to the numerous physiological effects of CWI described by Bleakley and Davison (BJSM vol 44: 179-187)[1], the clear alterations of HRV and cardiac autonomic activity are also important to consider. The effects of CWI on cardiac parasympathetic activity and associated perceptions of recovery suggest that CWI may be most effective when used after the final session of the day, or at the end of the day, which could improve an athletes overall recovery process (i.e., perceived well-being and sleep quality). The effect of CWI on training program adaptation and recovery requires further investigation.
Authors and affiliations
Jamie Stanley1,2, Paul B. Laursen3,4, Jonathan M. Peake1,2, Martin Buchheit5
1The University of Queensland, School of Human Movement Studies, Brisbane, Australia
2Centre of Excellence for Applied Sport Science Research, Queensland Academy of Sport, Brisbane, Australia
3New Zealand Academy of Sport North Island, Auckland, New Zealand
4School of Sport and Recreation, Auckland University of Technology, Auckland, New Zealand
5Physiology Unit, Sport Science Department, Aspire, Academy for Sports Excellence, Doha, Qatar
Address for correspondence:
Jamie Stanley, School of Human Movement Studies, The University of Queensland, Brisbane, Queensland 4072, Australia; E-mail: j.stanley@uq.edu.au; Tel: +61 7 3365 6482; Fax: +61 7 3365 6877.
References
1. Bleakley CM, Davison GW. What is the biochemical and physiological rationale for using cold-water immersion in sports recovery? A systematic review. Br J Sports Med. 2010 March 2010;44:179-87.
2. Task-Force. Heart Rate Variability: Standards of Measurement, Physiological Interpretation, and Clinical Use. Circulation. 1996 March 1, 1996;93:1043-65.
3. Perini R, Orizio C, Baselli G, Cerutti S, Veicsteinas A. The influence of exercise intensity on the power spectrum of heart rate variability. Eur J Appl Physiol. 1990;61:143-8.
4. Buchheit M, Peiffer JJ, Abbiss CR, Laursen PB. Effect of cold water immersion on postexercise parasympathetic reactivation. Am J Physiol Heart Circ Physiol. 2009 February 1, 2009;296:H421-7.
5. Furlan R, Piazza S, Dell'Orto S, Gentile E, Cerutti S, Pagani M, et al. Early and late effects of exercise and athletic training on neural mechanisms controlling heart rate. Cardiovasc Res. 1993;27:482-8.
7. Wilcock IM, Cronin JB, Hing WA. Physiological response to water immersion: a method for sport recovery? Sports Med. 2006;36:747-65.
8. Miwa C, Sugiyama Y, Mano T, Iwase S, Matsukawa T. Sympatho-vagal responses in humans to thermoneutral head-out water immersion. Aviat Space Environ Med. 1997;68:1109-14.
9. Mourot L, Bouhaddi M, Gandelin E, Cappelle S, Dumoulin G, Wolf JP, et al. Cardiovascular autonomic control during short-term thermoneutral and cool head-out immersion. Aviat Space Environ Med. 2008;79:14-20.
10. Perini R, Milesi S, Biancardi L, Pendergast DR, Veicsteinas A. Heart rate variability in exercising humans: effect of water immersion. Eur J Appl Physiol. 1998;77:326-32.
11. Lunt HC, Barwood MJ, Corbett J, Tipton MJ. "Cross-adaptation" habituation to short repeated cold-water immersions affects the response to acute hypoxia in humans. J Physiol. Published Online First: 19 July 2010. 10.1113/jphysiol.2010.193458
12. Al Haddad H, Laursen P, Chollet D, Lemaitre F, Ahmaidi S, Buchheit M. Effect of cold or thermoneutral water immersion on post-exercise heart rate recovery and heart rate variability indicies. Auto Neurosci. Published Online First: 18 April 2010. doi:10.1016/j.autneu.2010.03.017
13. Vaile J, O'Hagan C, Stefanovic B, Walker M, Gill N, Askew CD. Effect of cold water immersion on repeated cycling performance and limb blood flow. Br J Sports Med. Published Online First: 16 March 2010. 10.1136/bjsm.2009.067272
14. Buchheit M, Laursen PB. Treatment of hyperthermia: is assessment of cooling efficiency enough? Exp Physiol. 2009;94:627-9.
15. Parouty J, Al Haddad H, Quod M, Lepretre PM, Ahmaidi S, Buchheit M. Effect of cold water immersion on 100-m sprint performance in well-trained swimmers. Eur J Appl Physiol. 2010;109:483-90.
16. Park KS, Choi JK, Park YS. Cardiovascular regulation during water immersion. Appl Human Sci. 1999;18:233-41.
17. Hjortskov N, Rissen D, Blangsted A, Fallentin N, Lundberg U, Sogaard K. The effect of mental stress on heart rate variability and blood pressure during computer work. Eur J Appl Physiol. 2004;92:84-9.
18. Jiang D, He M, Qiu Y, Zhu Y, Tong S. Long-range correlations in heart rate variability during computer-mouse work under time pressure. Physica A: Statistical Mechanics and its Applications. 2009;388:1527-34.
19. Hopkins WG, Marshall SW, Batterham AM, Hanin J. Progressive statistics for studies in sports medicine and exercise science. Med Sci Sports Exerc. 2009;41:3-13.
A study recently published in the British Journal of Sports Medicine
suggests that accidents are more commonly to blame for on-ice amateur-
hockey injuries than bodychecking. The findings were based on a five-year
study of 3,000 boys aged four to 18 in a youth hockey program in
Burlington, Ontario. The study, conducted by researchers from the
University of Buffalo, found that 66 per cent of overall injuries were the
resul...
A study recently published in the British Journal of Sports Medicine
suggests that accidents are more commonly to blame for on-ice amateur-
hockey injuries than bodychecking. The findings were based on a five-year
study of 3,000 boys aged four to 18 in a youth hockey program in
Burlington, Ontario. The study, conducted by researchers from the
University of Buffalo, found that 66 per cent of overall injuries were the
result of accidents that happen during a game, such as colliding with
teammates, sliding into the boards or posts or getting hit with the puck.
The remaining 34 per cent were attributed to players checking each other.
The researchers only took into account injuries serious enough to cause
players to be off the ice for at least 24 hours. This begs the
question...how many of the injuries not taken into account may have been
concussions and not diagnosed? For the record, the findings of this study
conflict with those of another study mentioned below. Regardless of
whether most injuries are intentional or not, the sad and harsh reality is
that minor hockey is plagued with a serious injury factor and bodychecking
is responsible for a disproportionately large number of those injuries,
including concussions.
A landmark study released on June 8 revealed that 11- and 12- year
old hockey players in leagues that allow bodychecking are 2.5 times more
likely to get hurt and 3.5 times more likely to suffer a concussion. In
Quebec, players do not bodycheck until bantam ages (ages 13 to 14), and
even then it is only introduced at the elite levels of the game. Pee wee
(ages 11 and 12) is when bodychecking begins in Alberta. The joint
University of Calgary, McGill University, and the University of Laval
study tracked 2,200 pee wee hockey players from both provinces for the
entire 2007-2008 season to measure injury frequency. The findings of this
study were published in a recent edition of the Journal of the American
Medical Association. This study suggests a case can be made for raising
the bodychecking age and for limiting bodychecking leagues across the
board. One of the researchers for this study, Dr.Carolyn Emery from the
department of kinesiology at the University of Calgary has been quoted as
saying: "Having a concussion increases your risk significantly of another
concussion and some kids are dropping out of hockey because of
concussions, fractures and other severe injuries." Dr. Emery estimates
that if bodychecking was not permitted in peewee hockey this would reduce
the risk of injury by over 1,000 injuries and 400 concussions among the
nearly 9,000 peewee level children playing hockey in Alberta.
This study should serve as a wake-up call for those Canadians
concerned with the health and safety of all players, especially minor
leaguers, and the future of the game as we know it.
The consequences of traumatic hits to the head speak for themselves.
Research done by Dr. Shree Bhalerao, director, medical psychiatry, St.
Michael's Hospital, Toronto and Deborah Pink, resident in psychiatry,
University of Toronto reveals the following. Traumatic brain injuries, via
hits to the head or bodies colliding against the boards or other bodies
can cause: post-concussive symptoms, cognitive disorders, depression,
personality changes, and substance abuse.
Indeed, an emotional debate has been raging for years about our
national sport. Should body checking be allowed in minor hockey? According
to the Canadian Institute for Health Information, 8,000 people were
treated for hockey related injuries in Ontario hospital emergency rooms in
the 2002-2003 seasons. Based on this rate, more than 25,000 people were
injured across the country. In 93 cases of the 8,000, the casualty was
admitted to hospital, 15 directly to critical care units.
Among young hockey players (18 and under) 62 percent of the injuries
were a result of checking. Injuries caused by body checks were the most
common in the 14 to 16 age group, after players have been exposed to body
checking for several years.
The decision to allow body checking in minor hockey is unquestionably
jeopardizing this wonderful sport and favourite pastime by turning it into
our most dangerous game. It is easily argued this practice borders on
child abuse. It certainly flies in the face of public health, safety, and
injury prevention; it trumps medical science, commonsense, and civility.
Hockey is an inherently dangerous game. That said, when medical
experts and safety advocates say evidenced-based research show injury-
prevention and harm-reduction initiatives are good for the health and
safety of the game and the players, everyone-hockey organizations,
coaches, players, parents- should take note.
Emile Therien,
Public Health & Safety Advocate,
Past President, Canada Safety Council
Ottawa, Ontario.
I recently read an article in the Wall Street Journal regarding football/soccer injuries amongst boys and girls. It referenced your medical study concerning the prevalence of knee injuries to the strong leg of boys, but to the weak leg of girls. As a former player of 20 years and coach for the past eight, I have a theory on this divergence. If a player strikes strongly through a ball, he lands on his striking leg (which is the str...
I recently read an article in the Wall Street Journal regarding football/soccer injuries amongst boys and girls. It referenced your medical study concerning the prevalence of knee injuries to the strong leg of boys, but to the weak leg of girls. As a former player of 20 years and coach for the past eight, I have a theory on this divergence. If a player strikes strongly through a ball, he lands on his striking leg (which is the strong leg for most youth players). The knee may turn when the player lands on this striking/strong leg. Also, if a defensive player is going hard to the ball, he is more likely to hit the leg that is planted, which would be the striking/strong leg in my scenario. While this is not always true, my guess is that fewer girls strike through the ball strongly. If this is not done, the player is more likely to maintain her plant/weak leg on the ground, rather than leaving that leg and landing on the striking/strong leg. Again, the plant leg is more likely to twist, and a defensive player is more likely to create contact with the leg that is planted on the ground. For this reason, many girls may be more likely to injure their weak/plant leg.
Ryan et al (1) provide empirical evidence that standards for running
shoes in relation to foot posture are far from convincing. In particular,
a sophisticated and expensive motion-control design intended for highly
pronated feet was less effective than more basic shoes in minimizing
injuries and pain to all categories of foot. This outcome echoes Richards
et al's (2) recent negative review regarding the role of shoe desi...
Ryan et al (1) provide empirical evidence that standards for running
shoes in relation to foot posture are far from convincing. In particular,
a sophisticated and expensive motion-control design intended for highly
pronated feet was less effective than more basic shoes in minimizing
injuries and pain to all categories of foot. This outcome echoes Richards
et al's (2) recent negative review regarding the role of shoe design in
reducing injury.
I wrote a rapid response (3) to the latter paper suggesting that the
origin of the conundrum may not reside only in biomechanics, but rather
there may be a psychological element concerning the individual's
interpretation of risk. The extreme form of this conceptualisation is
"risk homeostasis", whereby it is argued that the individual "targets" a
fixed level of perceived risk to govern his/her performance on any given
activity (4,5). The psycholigical mechanisms by which risk is perceived
and affects behaviour remain speculative; one model is based on low-level
learning of the outcomes of competing tendencies in beviour (6). The
typical activity to which the conceptualisation is applied has been road-
travel and reflects the observation that may safety features do not
maintain their benefit over time: drivers squander safety benefits in less
careful driving, as reflected for example in greater and more erratic
speeds. Two examples concern seat-belts and ABS brakes (5,6,7).
As applied to running, the implication is that greater sophistication
in shoe design reduces the perceived likelihood of potential injury;
however, the consequence may be an increase in risky running behaviour.
For example, the runner may pay more attention to uneven surfaces when
wearing a less sophisticated design of shoe, but determine that a more
sophisticated design deals adequately in equivalent circumstances; if this
is not the case then more pain and injuries will result from the more
sophisticated design.
References
1. Ryan MB, Valiant GA, McDonald K, Taunton JE. The effect of three
different levels of footwear stability on pain outcomes in women runners:
a randomised control trial. Br J Sports Med doi:10.1136/bjsm.2009.069849.
2. Richards CE, Magin PJ, Callister R. Is your prescription of
distance running shoes evidence-based? Br J Sports Med 2009; 43: 159-162.
3. Reinhardt-Rutland AH. Negating the safety advantage in running
shoe design: perceived risk affecting performance? Br J Sports Med 2009
[http://bjsm.com/cgi/eletters/43/3/159]
4. Wilde GJS, Robertson LS, Pless IB. Does risk homeostasis theory
have implications for road safety? BMJ 2002; 324: 1149-1152.
5. Adams JGU. Risk. London: UCL, 1995.
6. Reinhardt-rutland AH. Seat-belts and behavioural adaptation: the
loss of looming as a negative reinforcer. Safety Sci 2001; 39: 145-155.
7. Aschenbrenner M, Biehl B. Improved safety through improved
technical measures? Empirical studies regarding risk compensation
processes in relation to anti-lock brake systems. In RM Trimpop, GJS Wilde
(eds). Changes in accident prevention: The issue of risk compensation.
Groningen: Styx, 1994.
Dear Editor,
We read with interest the article from Hasler et al. (2009) "Are there risk factors in alpine skiing? A controlled multicentre survey of 1278 skiers". In general, the answer is: 'yes, there are internal (e.g. gender, age, fitness, skill level, risk taking) and external (equipment, environment) risk factors' according to comprehensive model for injury causation by Bahr and Krosshaug (1). However, we would like to comm...
Dear Editor,
We read with interest the article from Hasler et al. (2009) "Are there risk factors in alpine skiing? A controlled multicentre survey of 1278 skiers". In general, the answer is: 'yes, there are internal (e.g. gender, age, fitness, skill level, risk taking) and external (equipment, environment) risk factors' according to comprehensive model for injury causation by Bahr and Krosshaug (1). However, we would like to comment on the presented data and methods used because some results seem contrary to other studies in this research field. Firstly, Hasler et al. reported that skiers with new equipment have a higher risk of being injured. However, there seems a mistake in the presented data because in the abstract the Odds Ratio (OR) was 59 with a 95% confidence interval of 0.37-0.93 while in Table 1 the OR was 0.59. If the OR of 0.59 was correct, new equipment would decrease injury risk. In addition, what means new equipment? Did the authors compare carving skiers with traditional skiers as done by Burtscher et al. (2) showing a reduced injury rate since the introduction of carving ski? Where is the cut off between new and old equipment? In the discussion section, Hasler et al. stated that the results might be explained by a mismatch between the abilities of the skier and the equipment. Unfortunately, they did not include skill levels in their questionnaire. Several studies showed higher injury rates in less skilled skiers and snowboarders (3, 4) while more skilled skiers had a higher risk to sustain a more severe injury (5).
Secondly, there seem mistakes concerning the presented data about snow conditions. In Figure 3, artificial snow versus old snow and fresh snow versus powder snow show OR <1 while in Table 1 the same OR are presented vice versa (OR 0.21 for old snow vs. artificial snow and OR 0.31 for old snow vs. fresh snow, respectively). It is the same with slush snow versus powder snow which is not a snow condition but a skiing condition in Figure 3 and powder snow vs. slush snow in Table 1, respectively. In addition, old snow seems to be in contrast to fresh snow. Does fresh snow mean powder snow? However, can old snow not be also old artificial snow? Therefore, it is not clear which snow condition actually increases or decreases injury risk.
Thirdly, seasonal checking of skiing equipment showed a trend to decrease injury risk (OR: 0.46, p = 0.056). In our opinion, seasonal checking of skiing equipment includes primarily an adjustment of the bindings. In accordance, Burtscher et al. (2) showed that female carving skiers with a binding adjustment older than 1 year had a twofold knee injury rate compared to those with newly adjusted bindings. The release of a binding is primarily important in preventing injuries to the lower extremity. Therefore, it would be better to define risk factors with regard to the injured body location.
Fourthly, injured skiers showed a higher readiness for risk taking in this study. In contrast, other studies reported that injured skiers did not take more risk but were less skilled compared to uninjured skiers (6-8). Therefore, it would make sense to include skill level.
Fifthly, Hasler et al. showed a higher injury risk when skiing under bad weather conditions which is well in accordance with the study by Aschauer et al. (9). However, poor snow and weather conditions may be misjudged by injured skiers because they may look for an explanation as to why the injury occurred. In general, self-report to questions might lead to underreport or overreport of health-risk behaviours affected by cognitive and situational factors (10).
Sixthly, gender has not been found to be a significant risk factor in this study. That might be due to the fact that Hasler et al. did not differentiate between injured parts of the body, e.g. females have a higher knee injury risk (2) and males have a higher head injury risk (11) compared to the other gender.
Seventhly, Hasler et al. calculated that injury risk is higher when warming up. This result contrasts general preventive recommendations (12) and also the findings by Ruedl et al. (13) who demonstrated a twofold injury reduction in a cohort of 36.000 participants of 12 ski schools when warming up.
Eighthly, there seems a mistake concerning the presented data about drug consumption. Figure 3 shows an OR > 1 for abstinence from drugs while in Table 1 drug consumption was presented vice versa. In addition, in Table 1 an OR of 5.92 was presented while in the discussion the OR was 1.78 for drug consumption.
Since a case control design was used, the amount of exposure to the suggested risk factors was unknown which should be taken into account when interpreting the results (14). In the study by Hasler et al. the controls were interviewed when coming off slopes after skiing. This implies that controls skied probably more than 3 hours although other studies showed that most injuries to the lower extremity occurred within the first 2 or 3 hours of skiing (15, 16). A total of 782 patients were recruited over a period of 5 and a half month and 496 controls were interviewed in six different ski resorts. This means an average of about 83 controls per ski resort and an average of 15 uninjured skiers per month, respectively. However, Hasler et al. (2009) did not specify when controls have been recruited, e.g. every second day. A continuous recruitment of controls seems of utmost importance to compare prospectively potential external risk factors like snow, weather and slope conditions.
In general, a prospective study design concerning internal and external risk factors in relation to gender and type of injury should be used. However, at least a case-control-design should be applied matching controls according to gender, age and skill level.
References
1. Bahr R, Krosshaug T. Understanding injury mechanisms: a key component of preventing injuries in sport. Br J Sports Med 2005; 39: 324-329.
2. Burtscher M, Gatterer H, Flatz M et al. Effects of modern ski equipment on the overall injury rate and the pattern of injury location in Alpine skiing. Clin J Sport Med 2008; 18:355-357.
3. Langran M, Selvaraj S. Increased injury risk among first-day skiers, snowboarders, and skiboarders. Am J Sports Med 2004;32:96-103.
4. Hagel B. Skiing and snowboarding injuries. Caine DJ, Maffulli (eds.): Epidemiology of Pediatric Sports Injuries. Individual Sports. Med Sport Sci. Basel. Karger,2005;48:74-119.
5. Goulet C, Hagel BE, Hamel D, et al. Self-reported skill level and injury severity in skiers and snowboarders. J Sci Med Sport 2008; doi: 10.1016/j.jsams.10.002
6. Bouter LM, Knipschild PG, Feij JA, et al. Sensation seeking and injury risk in downhill skiing. Person. Individ. Diff. 1988;9:667-73.
7. Cherpitel CJ, Meyers AR, Perrine MW. Alcohol consumption, sensation seeking and ski injury: a case-control study. Journal of Studies on Alcohol 1998;59:216-21.
8. Goulet C, Regnier G, Valois P, et al. Injuries and risk taking in alpine skiing. ASTM STP 1397, Skiing Trauma and Safety: Thirteenth Volume, RJ Johnson, P Zucco, JE Shealy (eds.), ASTM International, West Conshohocken, PA, 2000:139-46.
9. Aschauer E, Ritter E, Resch H et al. Injuries and injury risk in skiing and snowboarding. Unfallchirug 2007; 110: 301-306. (in German)
10. Brenner ND, Billy JOG, Grady WR. Assessment of factors affecting the validity of self-reported health-risk behavior among adolescents: evidence from the scientific literature. J Adolesc Health 2003;33:436-457.
11. Mueller BA, Cummings P, Rivara FP, et al. Injuries of the head, face, and neck in relation to ski helmet use. Epidemiology 2008;19:270-76.
12. Koehle MS, Lloyd-Smith R, Taunton JE. Alpine ski injuries and their prevention. Sports Med 2002; 32 (12): 785-793.
13. Ruedl G, Sommersacher R, Woldrich T et al. A structured warm-up program to prevent injury in recreational skiers. Senner V, Fastenbauer V, Boehm H (eds.): Book of Abstracts of the 18th Congress of the International Society for Skiing Safety, Garmisch-Partenkirchen, Germany, April 26 to May 02 2009, 77.
14. Vandenbroucke JP, von Elm E, Altman DG et al. Strengthening the reporting of observational studies in epidemiology (STROBE): explanation and elaboration. Epidemiology 2007;18 (6): 805-835.
15. Ungerholm S, Engkvist O, Gierup J et al. Skiing injuries in children and adults: a comparative study from a 8-year period. Int J Sports Med 1983; 4 (4): 236-240.
16. Ruedl G, Schranz A, Fink C et al. Are ACL injuries related to perceived fatigue in female skiers? ASTM International 2010; 7 (4), Paper ID JAI102747
I read with appreciation Cook and Purdam's article, as this continuum
model is probably quite helpful in determining treatment choices. Where
the article falls short though is the unproved presumption that the key
initiating factor is over load. In perpetuating this oft quoted
presumption the article fails to acknowledge the large population who
develop tendon pain without overload/ overuse.
I read with appreciation Cook and Purdam's article, as this continuum
model is probably quite helpful in determining treatment choices. Where
the article falls short though is the unproved presumption that the key
initiating factor is over load. In perpetuating this oft quoted
presumption the article fails to acknowledge the large population who
develop tendon pain without overload/ overuse.
I suggest that other factors are far more important precipitants of
the pathological changes in this continuum, and propose that hypoxia is a
far better fit as to a key initiating factor.
Hypoxia explains a number of key features of tendinopathy that are
inexplicable from an overload model. Examples include:
- The location of pathology in the athlete appears primarily in the
stress shield area of the tendon: the area subject to compression with
use. There is no doubt the blood flow will be interrupted by this
compression. If the frequency of compression is sufficient to prevent
adequate blood flow restoration a relative hypoxic status even temporarily
may initiate the onset of what Cook and Purdam term reactive tendinopathy.
- Hypoxia certainly explains the neovascularisation that is one of
the primary pathological findings, likely through an upregulation of VEGF
in the hypoxic state.
- Microvascular disease may explain the prevalence of tendon
pathology in those with diabetes
- The success of sclerosing treatment may have more to do with the
short term increase in vascularity after treatment, the eventual sclerosis
an unfavourable side effect.
- The success of Glyceryl trinitrate may simply be due to a local
vasodilatory effect of the drug.
- That surgery is less successful in non athletic individuals
compared with athletes may be explained by a lack of collateral
circulation in the non athlete, where the remaining tendon remains under a
relative hypoxia, compared with the improved collateral circulation and
oxygenation via collateral arterial supply in the remaining tendon that
likely occurs in the athletic population.
- That exercise therapy remains a mainstay of treatment, may be one
factor that increases blood flow, improves circulation to the tendon in
general and hence reduces the hypoxic effect.
- Pain, may simply be due to ischaemia.
I suggest Cook and Purdam's paper makes more sense if the word
"hypoxia" is substituted for "overload" then there is no difficulty
explaining why exercise is the prime prescription for tendinopathies, and
why rest is not helpful as a therapeutic model.
In future publications about tendon pathology, I would like to see
less thoughtless presumption that overload is a primary initiating factor,
as this oversimplifies what is no doubt a multi-factorial condition. Cook
and Purdam acknowledged intrinsic factors such as genetics, sex, body
composition; but neglected to mention circulatory disturbance, and
attrition age related, disuse or arthritic. Factors proposed as early as
1966 in "The Standard Nomenclature of Athletic Injuries, 1966". While a
hypoxic model may not be perfect, I propose that a biochemical model
deserves consideration as the overload model has out lived it's
usefulness.
In summary, I challenge the prevailing presumption of overload as a
primarily initiating factor for development of tendon pathology and
suggest in fact the exact opposite. I challenge that despite the rare
excessive compressive loads experienced in a high level athlete, by far
the majority of tendon pathology is due to under use, not overuse; due to
inadequate exercise not overload; due to inadequate tissue oxygenation not
hypervascularity.
Editor,
I recently read the article Jamtvedt et al on whether pre and post stretching prevents injury 1 with interest. I commend the authors for their well-conducted study and would like to comment on two particular issues.
First, the authors correctly point out that there was no difference in the primary outcome of all injuries, and that the analysis showing an absolute 22% reduction in muscle, ligament a...
In response to the editorial- Physical activity in the UK: a unique crossroad.Br J Sports Med 2010 vol44 no 13
I was delighted to read Dr Weilers editorial which eloquently presents many of the issues currently faced in exercise medicine. It is so important to debate this subject-particularly as we are in a unique position in the U.K to effect permanent change. I was interested in Dr Weilers' view that the intro...
An article entitled "The challenge of low physical activity during the school day: at recess, lunch and in physical education" was recently published in the British Journal of Sport Medicine.[1] Briefly, Nettlefold and colleagues used uniaxial accelerometers (Actigraph GT1M) to estimate the level of physical activity (PA) over the school day in Canadian children aged 8-11 years. One of their most striking findings was th...
In the midst of the genetic/genomic medicine revolution, the Caster's controversy illustrates how human society is lacking in its ability to deal with Disorders of Sex Development (DSD) at either a social, competitive, legal or ethical level. Political fractionalization, by way of "protecting human rights" added fuel to the fire rather than defusing the situation. "We can't afford any mistakes, particularly as we...
We read with interest the recent review by Bleakley and Davison (BJSM vol 44: 179-187)[1], which described the physiological and biochemical responses to cold water immersion (CWI) after exercise. The authors examined some of the acute cardiovascular responses that occur with CWI, such as changes in heart rate, blood pressure and cerebral blood flow. We noted, however, that they did not address the effec...
A study recently published in the British Journal of Sports Medicine suggests that accidents are more commonly to blame for on-ice amateur- hockey injuries than bodychecking. The findings were based on a five-year study of 3,000 boys aged four to 18 in a youth hockey program in Burlington, Ontario. The study, conducted by researchers from the University of Buffalo, found that 66 per cent of overall injuries were the resul...
Ryan et al (1) provide empirical evidence that standards for running shoes in relation to foot posture are far from convincing. In particular, a sophisticated and expensive motion-control design intended for highly pronated feet was less effective than more basic shoes in minimizing injuries and pain to all categories of foot. This outcome echoes Richards et al's (2) recent negative review regarding the role of shoe desi...
I read with appreciation Cook and Purdam's article, as this continuum model is probably quite helpful in determining treatment choices. Where the article falls short though is the unproved presumption that the key initiating factor is over load. In perpetuating this oft quoted presumption the article fails to acknowledge the large population who develop tendon pain without overload/ overuse.
I suggest that othe...
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