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One road to Rome: Exercise

24 Aug, 17 | by atarazia

By Dr Nicky Keay (@nickykfitness)

Metabolic syndrome comprises a cluster of symptoms including: hypertension, dyslipidaemia, fatty liver disease and type 2 diabetes mellitus (T2DM). The underlying pathological process is insulin resistance which distorts metabolism. Temporal and mechanistic connections have been described between hyperinsulinaemia, obesity and insulin resistance. Insulin levels rise, potentially stimulated by an excess intake of refined carbohydrates and in addition the metabolic actions of insulin are attenuated on target tissues such as the liver, skeletal muscle and adipose tissue. At a cellular level, inflammatory changes play a part in this metabolic dis-regulation. Mitochondrial action in skeletal muscle is impaired, compromising the ability to oxidise fat as a substrate, thus resulting in muscle glycolysis and a consequent rise in blood lactate.

Although much attention has been focused on restricting calories and treating elevated lipids with medication (statins), evidence is now emerging that this does not have the anticipated effect of reducing mortality from cardiovascular disease. In addition, it has been proposed that the gut microbiota plays a pivotal role in metabolism, inflammation and immunity.

Metabolic syndrome usually conjures an image of an overweight person with or on the verge of developing T2DM. However, there is an interesting group of slim people who are also are at risk of developing metabolic syndrome due to insulin resistance. The majority of women with polycystic ovary syndrome (PCOS) present with menstrual disturbance of some description. However not all display the textbook characteristics of Stein-Leventhal syndrome (overweight, hirsute and with skin problems). There is in fact of spectrum of clinical phenotypes ranging from the overweight to the slim. In all phenotypes of PCOS, the crucial uniting underlying metabolic disturbance is insulin resistance. The degree of insulin resistance has been shown to be related to adverse body composition with increased ratio of whole body fat to lean mass. Although this confuses the picture somewhat, it also simplifies the approach. In all cases one important lifestyle modification is exercise.

Exercise improves metabolic flexibility: the ability to adapt substrate oxidation to substrate availability. Endurance exercise training amongst athletes results in improved fat oxidation and a right shift of the lactate tolerance curve. Conversely metabolic inflexibility associated with inactivity is implicated in the development of insulin resistance and metabolic syndrome.

What about nutritional strategies that could improve metabolic flexibility? Ketogenic diets can either be endogenous (carbohydrate restricted intake) or exogenous (ingestion of ketone esters and carbohydrate). Low carbohydrate/high fat diets (terms often used interchangeably with all types of ketogenic diets) have been shown to improve fat oxidation and potentially mitigate cognitive decline in older people.

In the case of athletes, the benefits of a ketogenic or low carb/ high fat diet do not necessarily translate to better performance. Despite reports of such diets enhancing fat oxidation and favourable changes in body composition, a recent study demonstrates that this, in isolation, does not translate into improved sport performance. A possible explanation is the oxygen demand toincreas oxidation of fat needs to be supported by a higher oxygen supply. The intermediate group of endurance athletes in this study, on the periodised carbohydrate intake, fared better in performance terms. Another recent study, where the majority of participants were women, confirmed that a ketogenic diet failed to improve the performance of endurance athletes, in spite of improving fat metabolism and body composition.

In all likelihood, the reason that these type of diets (ketogenic, high fat/low carb)did not improve sport performance is that only one aspect of metabolism was impacted and quantified. Although fat oxidation, modified via dietary interventions, is certainly an important component of metabolism, the impact on the interactive network effects of the Endocrine system should be evaluated in the broader context of circadian rhythm. For athletes this goes further, to include integrated periodisation of nutrition, training and recovery to optimise performance, throughout the year.

In addition to dietary interventions, medical researchers continue to explore the use of exercise mimetics and metabolic modulators, to address metabolic syndrome. Unfortunately, some have sought their use as a short cut to improved sport performance. Many of these substances appear on the WADA banned list for athletes. However the bottom line is that it is impossible to mimic, either through a dietary or pharmacological intervention, the multi-system, integrated interplay between exercise, metabolism and the Endocrine system.

There is only one road to Rome!

Whatever your current level of activity, whether reluctant exerciser or athlete, the path is the same to improve health and performance. This route is exercise, supported with periodised nutrition and recovery. Exercise will automatically set in motion the interactive responses and adaptations of one’s metabolic and Endocrine system.

For further discussion on Endocrine and Metabolic aspects of SEM come to the BASEM annual conference 22/3/18: Health, Hormones and Human Performance

 Dr Nicky Keay BA, MA (Cantab), MB, BChir, MRCP, Clinical and research experience in Endocrinology applied to Sport and Exercise Medicine


  1. Insulin action and resistance in obesity and type 2 diabetesNature Medicine 2017
  2. Inflammation: Why and How Much?Dr N. Keay, British Association of Sport and Exercise Medicine
  3. The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistanceClinical Pharmacist 2017
  4. Skeletal muscle mitochondria as a target to prevent or treat type 2 diabetes mellitusNature Reviews Endocrinology 2016
  5. The essential role of exercise in the management of type 2 diabetesCleveland Clinic Journal of Medicine 2017
  6. β cell function and insulin resistance in lean cases with polycystic ovary syndromeGynecol Endocrinol. 2017
  7. The many faces of polycystic ovary syndrome in Endocrinology. Conference Royal Society of Medicine 2017
  8. Association of fat to lean mass ratio with metabolic dysfunction in women with polycystic ovary syndromeHum Reprod 2014
  9. Sedentary behaviour is a key determinant of metabolic inflexibilityJournal of physiology 2017
  10. International society of sports nutrition position stand: diets and body compositionJ Int Soc Sports Nutr. 2017
  11. A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer’s diseaseExp Gerontol. 2017
  12. Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkersJ Physiol. 2017
  13. Ketogenic diet benefits body composition and well-being but not performance in a pilot case study of New Zealand endurance athletesJ Int Soc Sports Nutr. 2017
  14. Sports Endocrinology – what does it have to do with performance?Dr N. Keay, British Journal of Sports Medicine 2017
  15. Hormones and Sports Performance
  16. Endocrine system: balance and interplay in response to exercise training


Exercise and fitness in young people – what factors contribute to long term health?

14 Jul, 17 | by BJSM

Part-2 of the blog mini-series on youth

By Dr Nicky Keay

Recent reports reveal that children in Britain are amongst the least active in the world. At the other end of the spectrum there have been a cluster of articles outlining the pitfalls of early specialisation in a single sport.

Regarding the reports of lack of physical activity amongst young people in Britain, this is of concern not only for their current physical and cognitive ability, but has repercussions for health in adult life. Research demonstrates that young people with low cardiovascular fitness have an increased risk of developing cardiovascular disease in adult life. Conversely, the beneficial effects of weight bearing exercise in prepubescent girls has been shown to enhance bone mineral density accumulation, which will have beneficial impact on peak bone mass. However, as I found in my longitudinal studies, the level of exercise has to be in conjunction with an appropriate, well-balanced diet to avoid relative energy deficiency deficiency in sport (RED-S), which can compromise bone mineral density accumulation.

At the other end of the scale, early specialisation in a single sport does not necessarily guarantee long term success. Rather, this can increase the risk of overuse injury in developing bodies, which in turn has long term consequences. Ensuring that all elements of fitness are considered may be an injury prevention strategy. I agree that injury prevention can be viewed as part of optimising sports performance, especially in young athletes for both the present and in the long term.

Sleep is a vital element in optimising health and fitness, especially in young people who may be tempted to look at mobiles or screens of other mobile devices which delays falling asleep by decreasing melatonin production. Sleep promotes mental freshness and physical elements such as boosting immunity and endogenous release of growth hormone. As Macbeth put it, sleep is the “chief nourisher in life’s great feast”.

A balanced approach to health and fitness should be promoted, with young people encouraged to take part in a range of sporting activities.


Young athletes’ optimal health: Part 3 Consequences of Relative Energy Deficiency in sports Dr N. Keay, British Association Sport and Exercise Medicine, 13/4/17

Sleep for health and sports performance Dr N. Keay, British Journal Sport Medicine, 7/2/17

Optimising health, fitness and sports performance for young people

Telegraph article

Active Healthy Kids global alliance

Poor cardiovascular fitness in young people risk for developing cardiovascular disease 

Sports Specialization in Young Athletes

IOC consensus statement on youth athletic development British Journal Sport Medicine






For the “Body Matters” MOOC (McGill University, Prof Ian Shrier): Exercise is medicine, for the body and the brain by Nagamatsu and colleagues.

9 Mar, 15 | by Karim Khan

YourBrainLovesTheGym Each week over 23,001 folks are learning about the power of exercise via a Massive Open Online Course (MOOC).

Generously, BJSM helps out Professor Ian Shrier by answering one question each week on this blog. Prof Shrier just has to answer the other 23,ooo students’ questions.

This week’s question is:

“What are the effects of exercise on the brain’s ability for computation and memory?”

You could ‘Google it’ and you will find that the past 2o years has seen an explosion of literature on this topic. Fueled by? You guessed it – the wonder of MRI (magnetic resonance imaging) that provides structural images to complement tests of brain function (formerly pen and paper tests, now largely converted to computer/tablet tests). I don’t fully understand it yet, but MRIs can also show us changes in brain FUNCTION. So if exercise improves brain performance (which it does), some of these changes can be seen during ‘functional’ MRI of the brain. Wow!!  It used to thought that one exercised ‘for the heart’ but my feeling is that ‘exercise for the brain’ is even more important.

So, down to the nitty-gritty! “Show me the money” or, in this case – Show me the evidence!

And here I take you to a 2014 BJSM article –

LiuExerciseExercise is Medicine for the Body and the Brain


It is by Lindsay S Nagamatsu, Leon Flicker, Arthur F Kramer, Michelle W Voss, Kirk I Erickson, Chun Liang Hsu and my hero, Teresa Liu-Ambrose.

Cognitive decline is one of the most pressing healthcare issues   of the 21st century. Worldwide, one new case of major cognitive decline (ie, dementia) is detected every 4 s. Given that no effective pharmacological treatment to alter the progress of cognitive decline exists, there is much interest in lifestyle approaches for preventing or treating dementia. Ideally, such strategies should be cost-efficient and widely accessible at a societal level to have the largest benefit for older adults with varying income and functional status levels.

One attractive solution is exercise. However, despite a large and consistent pool of evidence generated over the past five decades linking exercise to improved cognitive functions in older adults, there is a reluctance among academics, healthcare practitioners and the public alike to embrace exercise as a prevention and treatment strategy for cognitive decline. For example, the National Institutes of Health (NIH) consensus statement from 2010 concedes that there appears to be preliminary data to support the efficacy of exercise in improving cognitive function. However, they caution that there is currently no strong evidence to suggest that modifiable lifestyle factors can alter the trajectory of cognitive decline.

Adding fuel to the fire are publications such as a 2013 systematic review of randomised controlled trials (RCTs) (prior to 31 October 2011) reporting ‘weak’ evidence for the effects of exercise on cognition. However, the search strategy used in that systematic review failed to capture many pertinent papers providing evidence from RCTs that exercise promotes cognitive and brain plasticity not only in healthy older adults but also in those with cognitive impairment. Animal studies that provide insight into the molecular and cellular mechanisms by which exercise promotes neuroplasticity.

In a previous commentary,(Liu-Ambrose, BJSM 2009)  we outlined studies that provided compelling evidence that exercise should undoubtedly be considered as a promising treatment strategy for cognitive decline. Our present commentary aims to provide a brief update, as well as to discuss factors that have continued to hinder the adoption of exercise as a legitimate medical strategy for the prevention of cognitive decline and dementia.

Since 2010, we have additional evidence from RCTs that exercise, both moderate-to-vigorous intensity aerobic and resistance training, promotes cognitive and brain plasticity and have gained further insight into underlying mechanisms. Notably, the behavioural and mechanistic outcomes converge and support a cohesive picture. In 2011, Erickson et al demonstrated that aerobic exercise resulted in increased hippocampal volume in healthy community-dwelling older adults. Furthermore, changes in hippocampal volume in the aerobic exercise group were significantly associated with increased levels of serum brain-derived neurotrophic factor and spatial memory performance. In the same RCT, Voss et al  demonstrated that aerobic exercise also improved the functional connectivity or temporal coherence of brain regions that are functionally related in a network known to decouple with ageing.

For resistance training, Liu-Ambrose et al  demonstrated increased functional plasticity after 12 months of training with corresponding improvement in selective attention and conflict resolution in healthy older women. Critically, the benefits of exercise extend to those with mild cognitive impairment (MCI) and dementia. Among older women with MCI, Nagamatsu et al  demonstrated that 6 months of resistance training led to improved executive functions, spatial memory and associative memory with concurring functional plasticity. In the same study, the authors also found that aerobic training improved verbal memory and learning. These findings indeed support the findings from a recent systematic review on exercise and cognition in those with dementia, although to our knowledge no such systematic reviews exist for those with MCI.

Despite these recent positive findings, scepticism remains. Enthusiasm for increased exercise as a prevention strategy is often tempered by the fact that no RCT until now has demonstrated that exercise can actually reduce the incidence of MCI or dementia. Is the absence of such a definitive trial reason enough to disregard the evidence until now? We contend that the answer to this question is a resounding ‘no’ when the following points are considered:

  • The number of individuals with dementia will exponentially increase in the next 20 years.

  • There is now a large and consistent pool of animal and human data demonstrating the cognitive benefit of exercise. Importantly, recent randomised studies show a convergence among behavioural, neuroimaging, and serum biomarker outcomes. Furthermore, large cohort studies have demonstrated significant associations between exercise and reduced risk of cognitive impairment and dementia.

  • Exercise has a multitude of established health benefits with minimal side effects and is cost-effective. Even in older adults, exercise increases the chance of survival and healthy ageing.

  • Exercise significantly reduces the key vascular risk factors (eg, hypertension, diabetes type II, hypercholesterolaemia, etc) for Alzheimer’s disease and vascular dementia—the two most common types of dementia.

In fact, exercise should be promoted as an essential component of healthy ageing given that reducing physical inactivity by 25% could prevent as many as one million cases of dementia worldwide.

Providing healthcare practitioners and seniors with specific and individualised recommendations regarding the type, intensity, and frequency of exercise for benefit is critical to successfully advocate exercise as a treatment for cognitive decline. (FOR MOOC STUDENTS, THIS IS WHAT PROF SHRIER WILL COVER NEXT WEEK – THE PRINCIPLES OF EXERCISE PRESCRIPTION)

However, we are limited by the fact that dose and type of exercise have been utilised in different studies with varying success. For example, Baker et al  found that older women with MCI who engaged in aerobic exercise four times per week exhibited improved cognitive function, whereas in a similar population, aerobic exercise twice per week did not yield the same benefits. Further, confusion centres around the type of exercise (eg, aerobic vs resistance training) and sex differences.

Evidence strongly suggests that exercise does have benefits for cognition—and critically, the magnitude of the benefit can exceed that of pharmaceutical approaches. It is estimated that if the onset and progression of dementia could be delayed by a mere 1 year, there would be nearly 9.2 million fewer cases in 2050. Given that exercise can be promoted at a population level with relatively low risks and costs, we highly recommend that older adults should be encouraged to engage in regular exercise to boost cognitive function as further research is concurrently conducted, rather than wait until all the intricacies of the relationship between exercise and cognition have been resolved.

We recognise that a large proportion of the population is sedentary and that successfully changing behaviour to a more active lifestyle is challenging. To effectively advocate exercise, we emphasise the need for a cross-disciplinary collaborative effort among researchers and healthcare workers to develop consistent standards and a united message of the multiple benefits of exercise. In light of the recent support for exercise in preventing cognitive decline, we stress that endorsing exercise as an effective strategy for improving health and well-being among older adults should be indisputable. Given that it may potentially have a high impact for mitigating multiple health concerns, including dementia, exercise should therefore be considered as a leading treatment strategy to delay or prevent dementia.

Thanks to BJSM for allowing us to reproduce the paper:

Exercise is medicine, for the body and the brain.

Nagamatsu LS, Flicker L, Kramer AF, Voss MW, Erickson KI, Hsu CL, Liu-Ambrose T.

Br J Sports Med. 2014 Jun;48(12):943-4. doi: 10.1136/bjsports-2013-093224. Epub 2014 Mar 21.

Karim Khan (@BJSM_BMJ)
One of the 3 lead editors at the BJSM – along with Babette Pluim (@DocPluim) and Jill Cook (@ProfJillCook).

If you use Google+, consider joining the Sports and Exercise Medicine community for sports medicine updates. (Search in ‘communities’ or follow this link).

IOC partnership: Children and Sport BJSM theme issue

13 Aug, 11 | by Karim Khan

This issue of BJSM – one of the 16 annually – focuses on keeping young people healthy. Many readers are not aware that the IOC and BJSM partner to produce 4 issues of the BJSM annually. These issues focus on the IOC mission of ‘Athlete Protection and Health Promotion’. The special issues, generally appearing in March, June, September and December (issue numbers 3, 7, 11, 15) are tagged as Injury Prevention and Health Promotion (IPHP) issues.

The (IOC) recognises the health and fitness benefits of physical activity (PA) and sport as stated in recommendation #51 from the Olympic Movement in Society Congress  Everyone involved in the Olympic Movement must become more aware of the fundamental importance of Physical Activity and sport for a healthy lifestyle, not least in the growing battle against obesity, and must reach out to parents and schools as part of a strategy to counter the rising inactivity of young people.1

Read the consensus paper from the expert group meeting in Lausanne

The IOC expert group  discussed the role of PA and sport on the health and fitness of young people and to critically evaluate the scientific evidence as a basis for decision making. Specifically, the purpose of this consensus paper is to identify potential solutions through collaboration between sport and existing programmes and to review the research gaps in this field. The ultimate aim of the paper is to provide recommendations for those involved in young people’s sport.

We’ll highlight other papers from the issue this week – check out the table of contents.

Comment via the box below or to Send us a Guest Blog! You just email the word document and we do the rest! Follow BJSM on Twitter @BJSM_BMJ for updates to the blog and links to other interesting practical sports and exercise medicine for clincians.

Response to Ian Shrier

30 Nov, 10 | by Karim Khan

We agree with Ian Shrier that the finding of an effect of stretching on risk of muscle, ligament and tendon injuries should be interpreted with caution. That is why we wrote “The finding of an effect of stretching on muscle, ligament and tendon injury risk needs to be considered cautiously because muscle, ligament and tendon injury risk was a secondary outcome, and there was no evidence of an effect of stretching on the primary outcome of all-injury risk. If stretching had reduced the risk of muscle, ligament and tendon injuries without increasing the risk of other injuries, we would expect a reduction in all-injury risk.” Nonetheless, after a prolonged discussion of this issue we decided that the finding could not be totally dismissed. We believe that it was appropriate to report the observed effect on muscle, ligament and tendon injuries with an explicit acknowledgement of the uncertainty associated with this finding.

Regardless of whether one accepts the finding that stretching reduces risk of muscle, tendon and ligament injuries, the implications would appear to be the same. Even if the effect is real, it is quite small in absolute terms (even in this population, at quite a high risk of injury, only “one injury to muscle, ligament or tendon was prevented for every 20 people who stretched for 12 weeks”). For this reason the data from this study do not appear to provide support for the practice of stretching, at least in so far as the aim is to reduce injury risk. The stronger justification for stretching, though still a marginal one in our view, is provided by the clear evidence of a very small effect of stretching on soreness. For other outcomes, such as performance or range of motion our study did not provide any data.

It is not yet known whether stretching is best carried out before exercise, after exercise, or both before and after exercise. We were surprised, when planning this study, to learn that most Australian stretch before exercise but not after, and most Norwegians stretch after exercise but not before! It was for that reason we designed a trial in which participants stretched both before and after exercise. We do not agree with Ian Shrier’s suggestion to conduct an unplanned post-hoc comparison of the non-randomised subgroups that chose to stretch only before, only after, or both before and after exercise. Such an analysis would almost certainly be seriously confounded and would probably be uninterpretable; at any rate it hardly seems consistent with his disapproval of our much more disciplined pre-planned secondary comparison between randomised groups. The only truly satisfactory way to resolve the issue of whether it is better to stretch before or after exercise is to conduct a further randomised trial in which participants are randomised to those two conditions.

Conflict of Interest: None declared

Achoooooo! Exercise in the cold season.

12 Nov, 10 | by Karim Khan

Yes, it’s the sound of a sneeze.

This month BBC news health reporter, Michelle Roberts wrote a feature on the  BJSM article titled,  Upper respiratory tract infection is reduced in physically fit and active adults.

David Nieman at the Human Performance Laboratory in North Carolina shows that exercise can prevent a cold. Their study on more than 1000 adults was undertaken over 12 weeks of fall/winter. During this time period, the odds of having a URTI were significantly reduced in those who exercised more and perceived themselves to be healthier.

For a link to the BBC report (which featured earlier this week  as the most shared article!), click here.

Does stretching reduce injury?

1 Nov, 10 | by Karim Khan

Stretching, or not, has been a controversial issue.

This month’s BJSM helps to unravel (or add to) this puzzle.

In an entirely web-based study (that gained awareness through media coverage), 2377 physically active adults were recruited in an effort to determine whether stretching modifies injury risk and soreness.

The verdict? In the short-medium term stretching reduces the risk of soreness and does not reduce the all-injury risk.

For a link to this article and to make up your own mind, see the November  BJSM.

E-letter: Are we ready for GGPAQ?

7 Oct, 10 | by Karim Khan

The following E-letter is a response to Physical activity in the UK: a unique crossroad (Br J Sports Med 2010; 44: 912-914). The original article can be read here.

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.

Natasha S. Jones
ST6 in SEM


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

Exercise alone won’t cut it for Canada’s obese

16 Mar, 10 | by Karim Khan

A recent Vancouver Sun article discusses new findings in the role of diet and exercise in obesity. Click here to read the story.

Photo by Tony Alter

CASM to include “Exercise” in their title

10 Mar, 10 | by Karim Khan

The sports medicine association formerly known as the Canadian Academy of Sport Medicine (CASM) voted to change their name to the Canadian Academy of Sport and Exercise Medicine (CASEM). This will come into effect on June 9th 2010. It is interesting that this follows the BASEM name change in the UK. Given the broad mandate of health professionals in our field, and the unfortunate association of the term ‘sports medicine’ with elite athletes in the mind of the general public, is it time for national societies of ‘sports medicine’ to follow the trend set by BASEM, CASEM, and others that preceded them.

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