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.
von Willebrand's disease is an inherited bleeding disorder which can
affect the quantity /- the quality of von Willebrand factor. It is more
common than haemophilia and there are 3 main types.
Type 1 (by far the most common and accounting for > 70% of cases)
is usually associated with mild bleeding symptoms (epistaxis, easy
bruising, menorrhagia etc) and may be diagnosed later in life.
von Willebrand's disease is an inherited bleeding disorder which can
affect the quantity /- the quality of von Willebrand factor. It is more
common than haemophilia and there are 3 main types.
Type 1 (by far the most common and accounting for > 70% of cases)
is usually associated with mild bleeding symptoms (epistaxis, easy
bruising, menorrhagia etc) and may be diagnosed later in life.
Type 2 is the second commonest and has several different sub-types.
It is associated with qualitative changes in von Willebrand factor (unlike
Type 1 which is associated with deficiency but normal quality vWF).
The rarest but most severe type is Type 3 and this behaves similarly
to severe haemophilia.
von Willebrand disease is different disease from haemophilia and not
X-linked like haemophilia. It can occur in boys or girls and can be
inherited in an autosomal recessive or dominant manner depending on the
type.
This article is totally wrong. Vonwillebrands' disease is not a mild
form of Haemophilia. It is a totally separate and, at my level, life
threatening bleeding disorder. Haemophilia is found in the sex linked X
chromosomes while Vonwilliebrands' disease is in the autosomes and not sex
linked the male or female can be hit with this disease. My great Aunt bled
to death from it. It has no comparison to Haemophilis. Haemophilia...
This article is totally wrong. Vonwillebrands' disease is not a mild
form of Haemophilia. It is a totally separate and, at my level, life
threatening bleeding disorder. Haemophilia is found in the sex linked X
chromosomes while Vonwilliebrands' disease is in the autosomes and not sex
linked the male or female can be hit with this disease. My great Aunt bled
to death from it. It has no comparison to Haemophilis. Haemophilia come in
type A factor 8 and type B factor 9. Vonwilliebrands disease is
Vonwilliebrand and platelet connected. In my case (rare for it's severity)
I have no detectable vonwilliebrands factor. This means that the first
step in clotting, the plug formed by the VWF and the platelets cannot take
place. Also since the VWF plays a part in bringing factor 8 into play I
also have low (11%) factor 8. To say that this disease is a mild form of
haemophilis shows the author has no working knowledge on bleeding
disorders and is, in my mind, criminal. Please remove that article from
you site ASAP.
My colleagues and I read with great interest your Editorial proposing
a new paradigm of inactivity physiology. This would be useful. In order
to properly discuss all aspects of any problem it clearly is necessary to
be able to name each precisely.
There is a clear distinction between not exercising and prolonged
sitting, though I would suggest that "seated immobility" as advocated by
Bea...
My colleagues and I read with great interest your Editorial proposing
a new paradigm of inactivity physiology. This would be useful. In order
to properly discuss all aspects of any problem it clearly is necessary to
be able to name each precisely.
There is a clear distinction between not exercising and prolonged
sitting, though I would suggest that "seated immobility" as advocated by
Beasley et al [1] describes the latter more precisely than "sedentary
behaviour", and could include the concept of muscular physio- and
pathophysiology.
Never before in the history of mankind have we been faced with such
an abrupt change of behaviour on such a global scale as that following the
advent of cars, TV, and notably the PC. Society, whilst very concerned
about viruses and worms damaging their computers, is seemingly heedless of
the health risks PCs pose their users.[2]
Long periods of seated immobility have become the norm, apparently
bringing in their train a multitude of serious health problems, even
death. A 20 year old Korean is reported of dying of a thromboembolism
after 80 hrs of sitting at a computer display station.[2] Interestingly,
during the London Blitz the introduction of bunk beds to air raid shelters
reduced this form of death in elderly females who had previously had to
sit for long hours.[3] But it will take considerable time for this
anecdotal material to be proved at a scientific level so overwhelmingly as
to compel changes in human behaviour.
I work in the field of rehabilitation of musculoskeletal disorders.
Cardiovascular, metabolic, even mental health are all related to
musculoskeletal health which, to be maintained, needs regular motion.
You alluded to the need for mechanistic studies. Some years ago
computer operators began presenting with neck and shoulder pain. I
hypothesized that this might be related to seated immobility. But it is
difficult to demonstrate what is happening in a body held immobile for
long periods.
Until recently the chief tool used to study tension in muscle has
been electromyography (EMG), giving data on that part of muscle behaviour
mediated by the neural system. But in order to fully characterise muscle
in responding to gravitational forces on the human body we also need to
take into account its spring-like behaviour in relation to lever-like
bones, as well as its viscoelasticity. Such full characterisation needs
to be based on direct measurement of the physical state of the muscle
itself.
Simpson's report was intriguing. Could changing from sitting to
lying make a significant difference in the tension in a muscle? The simple
method to demonstrate any difference is by palpation of the relevant
muscle, the upper trapezius (UT) in this case, which did affirm the
supposition. But we needed to be able to report and replicate our
findings, and for that new technology was required. With the Myoton
device and myometry [4] we demonstrated up to 20% decrease of both tension
(Hz) and stiffness (N/m) in the UT.[5-7] It would seem that the force of
gravity makes greater demand of muscle tension to maintain the seated
position.
High muscle tension is associated with a higher risk of developing
neck pain.[8] Could declining to the horizontal be crucial to recover from
excessive muscle tension associated with seated immobility as Simpson
suggested? We found that quick relief was obtained by lying down supine
with flexed knees for two minutes each working hour, alternately
simulating rhythmical walking movements with simple rotations of the
shoulder girdle.
If our results could be verified in a larger study there would be
good grounds for encouraging this kind of motional activity. In the
workplace only a mat and roster would allow 10 people per hour this
simple, effective, and cheap quick respite from excessive sitting.
Similar things could be encouraged at home.
Even before all the scientific evidence describing the harmful
effects of excessive immobility is in, might this not be a useful first
step in reversing current behaviour? We owe this to our children. They
learn from example.
References:
1. Beasley R, Heuser P, Raymond N. SIT (seated immobility
thromboembolism) syndrome: a 21st century lifestyle hazard. N Z Med J.
2005;118(1212):U1379. http://www.nzma.org.nz/journal/118-1212/1376/
2. Lee H. A new case of fatal pulmonary thromboembolism associated with
prolonged sitting at computer in Korea. Yonsei Med J 2004;45:349-351.
3. Simpson K. Shelter deaths from pulmonary embolism. Lancet 1940;2:744.
4. Vain A. A method and device for recording mechanical oscillations in
soft biological tissues, United States Patent No. 6132385, 2000.
5. Viir R, Vain A, Virkus A, et al. Skeletal muscle tone characteristics
in upright, supine and partial water immersion conditions. 57th
International Astronautical Congress 2006;1:132-141.
6. Viir R, Virkus A, Laiho K, et al. Trapezius muscle tone and
viscoelastic properties in sitting and supine positions. SJWEH Supplements
2007;3:76-80.
7. Viir R, Ranna L, Rajaleid K, et al. Lying back gives prompt tension
decrease in upper trapezius muscle but not applied relaxation technique in
fibromyalgia patients [abstract]. Scand J Rheumatol 2008;37 (suppl
123):P36.
8. Wahlstrom J, Hagberg M, Toomingas A, et al. Perceived muscular tension,
job strain, physical exposure, and associations with neck pain among VDU
users; a prospective cohort study. Occup Environ Med. 2004;61:523-8.
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...
von Willebrand's disease is an inherited bleeding disorder which can affect the quantity /- the quality of von Willebrand factor. It is more common than haemophilia and there are 3 main types.
Type 1 (by far the most common and accounting for > 70% of cases) is usually associated with mild bleeding symptoms (epistaxis, easy bruising, menorrhagia etc) and may be diagnosed later in life.
Type 2 is...
This article is totally wrong. Vonwillebrands' disease is not a mild form of Haemophilia. It is a totally separate and, at my level, life threatening bleeding disorder. Haemophilia is found in the sex linked X chromosomes while Vonwilliebrands' disease is in the autosomes and not sex linked the male or female can be hit with this disease. My great Aunt bled to death from it. It has no comparison to Haemophilis. Haemophilia...
Dear Editor,
My colleagues and I read with great interest your Editorial proposing a new paradigm of inactivity physiology. This would be useful. In order to properly discuss all aspects of any problem it clearly is necessary to be able to name each precisely.
There is a clear distinction between not exercising and prolonged sitting, though I would suggest that "seated immobility" as advocated by Bea...
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