«BOOK OF ABSTRACTS Edited by: Loland, S., Bø, K., Fasting, K., Hallén, J., Ommundsen, Y., Roberts, G., Tsolakidis, E. Hosted by: The Norwegian ...»
[Please note: This paper is part of the ECSS Position Statement: Prevention of Sport Injuries, K. Steffen, T.E. Andersen, T. Krosshaug, W. van Mechelen, G. Myklebust, E. Verhagen, R. Bahr and will be published in the European Journal of Sport Science (EJSS)]
PREVENTION OF SPORT INJURIES IV/IVKROSSHAUG, T.
THE NORWEGIAN SCHOOL OF SPORT SCIENCES, OSLO SPORTS TRAUMA RESEARCH CENTERTo maximize the health benefits of sports and exercise and minimize the direct and indirect costs associated with injuries, developing and adopting injury prevention strategies is an important goal. The aim of this ECSS consensus paper on injury prevention is to review current evidence on injury prevention methods and training programs aimed at reducing the most common or severe types of acute injuries. The target audience is everyone involved in protecting the health of the athlete, i.e. coaches, referees, medical staff, sports governing bodies, as well as athletes themselves. Effective sports injury prevention requires successful implementation of efficacious interventions. This paper reviews the main mechanisms and risk factors for acute injuries to the head, shoulder, elbow, hand/wrist, groin, thigh, knee and ankle, as well as the evidence supporting various strategies to prevent them. Approaches that have been proven successful include: 1) using equipment designed to reduce injury risk, 2) adopting the rules of play, and 3) specific exercise programs developed to reduce injury risk. Sports organizations should adopt available injury prevention strategies as part of their policies.
[Please note: This paper is part of the ECSS Position Statement: Prevention of Sport Injuries, K. Steffen, T.E. Andersen, T. Krosshaug, W. van Mechelen, G. Myklebust, E. Verhagen, R. Bahr and will be published in the European Journal of Sport Science (EJSS)] 14:00 - 15:30 Invited symposia IS-BC01 Satellite cells and regulation of muscle mass
THE BEHAVIOUR OF SATELLITE CELLS IN RESPONSE TO LOADING AND UNLOADING IN YOUNG AND OLDMACKEY, A.
BISPEBJERG HOSPITAL AND UNIVERSITY OF COPENHAGENOf the many different populations of cells residing in adult skeletal muscle, satellite cells are critical where processes of muscle growth, hypertrophy and repair are concerned. Increased life expectancy and associated sarcopenia have resulted in an increased effort to understand the function or dysfunction of satellite cells with ageing. It has now repeatedly been shown that heavy strength training and myofibre injury lead to proliferation of this cell population, in healthy young and old individuals, to varying extents. The purpose of these new myonuclei is to maintain an expanding cytoplasm or new muscle tissue in the case of hypertrophy or repair, respectively. Furthermore, it is apparent that satellite cells are subject to a strong regulatory influence by the niche in which they reside. Studying satellite cell activity with the aid of different markers, such as CD56 and Pax7, in the context of the local environment thus provides further insight into the behaviour of satellite cells in response to different stimuli. To provide some balance to the popular heavy loading models, muscle unloading is an interesting model for monitoring the behaviour of satellite cells. In addition, the ability to introduce pharmacological agents, such as anti-inflammatory medication and growth factors, directly into the muscle contributes further to the relatively limited selection of tools available for the study of satellite cells.
SATELLITE CELLS AND THE MYOGENIC RESPONSE TO DAMAGING EXERCISERAASTAD, T.
NORWEGIAN SCHOOL OF SPORT SCIENCESIt is well documented that satellite cells play an important role in the regeneration process after muscle damage in mammalian skeletal muscle . In animal models, severe muscle damage results in necrosis of muscle fibres and an inflammatory response is initiated. In the repair process the satellite cells are activated and start to proliferate. Later, a phase of differentiation and fusion of satellite cells leads to the formation of new myotubes that replace the once lost in necrosis. In the case of exercise-induced muscle damage, it is probably only segments of fibres that undergo necrosis and need to be replaced. The importance of satellite cells for full regeneration is demonstrated in studies where satellite cell activation is reduced .
Although the role of satellite cells in regeneration after damaging exercise is well described in animal models, the events of regeneration have so far not been shown in human muscles. The main reason is probably that necrosis rarely occurs after muscle-damaging exercise in humans. However, in a recent experiment we have observed extensive necrosis after high-force eccentric exercise with the elbow flexors . Analysis of repeated biopsies obtained in the days and weeks after exercise demonstrated a similar regeneration process as earlier described in animal models. The different phases of the satellite cell response can be followed by using markers for proliferation and differentiation. A number of different proliferation markers can be used, but so far the myogenic regulatory factors have been used most extensively to mark both proliferation and differentiation phases. Also in studies with no apparent fibre necrosis, activation of satellite cells has been indicated [3, 4]. The role of the satellite cells in recovery processes without necrosis is less clear, but addition of nuclei may help the reconstruction of damaged structures within surviving fibres as well.
The inflammatory process initiated after severe muscle damage seems to be important both for removing debris and in the activation of satellite cells . Consequently, administration of anti-inflammatory drugs may actually hamper regeneration after muscle damage. So far this potentially negative effect of anti-inflammatory drugs on the recovery processes is reported in animal models . In humans, administration of NSAIDs reduced the increase in satellite cells after running exercise . Surprisingly, in our recent study with extensive necrosis, the administration of a COX-2 inhibitor did not seem to affect the satellite cell response detectably . Consequently, more studies are needed to further explore the interaction between the inflammatory process, activation of satellite cells and the orchestration of the recovery processes in humans.
1. Bondesen. Am.J Physiol Cell Physiol 2004; 287:C475-C483
2. Charge. Physiol Rev. 2004; 84:209-238
3. Dreyer. Muscle Nerve 2006; 33:242-253
4. Mackey. J Appl Physiol 2007; 103:425-431
5. Paulsen. Scand J Med Sci Sports 2009 (In Press)
6. Tidball. Am.J.Physiol 2005; 288:R345-R353
THE BEHAVIOUR OF YOUNG AND OLD HUMAN MYOBLASTSHARRIDGE, S.
KING'S COLLEGE LONDONTwenty years ago Carlson and Faulkner (1989) made the interesting observation that if a muscle from an aged rat was transplanted into a young host the recovery potential of that muscle, in terms of mass and force production, was similar to that of a transplanted young muscle. Conversely, both young and old muscles recovered less well if they were transplanted into an aged as opposed to young host.
This study provided the first evidence of a negative of the systemic environment, rather than on the tissue itself, on skeletal muscle regenANNUAL CONGRESS OF THE EUROPEAN COLLEGE OF SPORT SCIENCE TH Wednesday, June 24th, 2009 eration. More recently these observations have been supported by work on parobiotic mice, animals which share a conjoined circulation.
Using this model, recovery to a damaged older muscle was markedly improved if the aged animal shared its circulation with a younger animal (Conboy et al. 2005). Recent studies (Carlson et al. 2008) suggest that this age related impairment to recovery from damage relates to changes in a number of signalling pathways (Notch, TGF-beta, pSmad3). These pathways regulate the proliferation and the myogenic commitment of satellite cells which are required not only for repair, but also for adaptation and hypertrophy. Whilst age-related impairments in the recovery of muscle from damage have been demonstrated in rodent studies, human exercise studies have shown that even the muscles of very elderly people are able to increase satellite cell number and hypertrophy in response to overload. We have recently used a primary cell / serum model to study the effects of the age of systemic environment on the behaviour of human cells extracted from muscle biopsies in culture. We have shown that committed myoblasts show similar abilities to both proliferate and differentiate when cultured in either a young or old serum. Furthermore, the cell itself (i.e. whether it originates from a young of elderly donor) shows no age-dependent behaviour. These findings would therefore suggest that a sufficient number of satellite cells are able to successfully progress through the myogenic lineage and can contribute to adaptation, even in an apparently hostile aged milieu.
Carlson BM & Faulkner JA. (1989) Muscle transplantation between young and old rats: age of host determines recovery. Am J Physiol.
Carlson ME, Hsu M & Con boy IM. (2008) Imbalance between pSmad3 and Notch induces CDK inhibitors in old muscle stem cells. Nature 454:528-32 Conboy IM, Con boy MJ, Wagers AJ, Girma ER, Weissman IL & Rando TA. (2005) Rejuvenation of aged progenitor cells by exposure to a young systemic environment. Nature.433:760-4.
THE REGENERATIVE POTENTIAL OF HUMAN SKELETAL: EFFECTS OF EXERCISE ON TELOMERES.PONSOT, E.
ÖREBRO UNIVERSITYThe length of DNA telomeres is an important parameter of the proliferative potential of tissues. Recent data also suggest that the rate of telomere shortening is accelerated by external factors such as oxidative stress. A recent study reported abnormally short telomeres in skeletal muscle of athletes with exercise-associated fatigue. This important report raises the question of whether long-term practise of exercise might have deleterious effects on muscle telomeres, and thus on skeletal muscle tissue regenerative capacity.
Recent data suggest that skeletal muscle telomere length is not altered during healthy aging as no significant differences in telomere are found between healthy active old men and women and young men and women with comparable physical activity level (Ponsot et al., 2008). In addition, in well-trained athletes with long history of strength training but free from symptoms of overtraining, there are no deleterious effects on telomeres, and on the contrary, telomere length in these subjects tend to be longer than in subjects with no history of strength training (Kadi et al., 2008). In accordance with data found in skeletal muscle, recent findings suggest that physical activity can be a positive regulator of telomere length in leukocytes (Cherkas et al., 2008; Ludlow et al., 2008). These results set the basis for a new hypothesis suggesting that, rather than being deleterious, well-designed exercise training may have a positive effect on in vivo regenerative capacity of skeletal muscle in healthy individuals.
References Cherkas LF, Hunkin JL, Kato BS, Richards JB, Gardner JP, Surdulescu GL, Kimura M, Lu X, Spector TD & Aviv A. (2008). The association between physical activity in leisure time and leukocyte telomere length. Arch Intern Med 168, 154-158.
Kadi F, Ponsot E, Piehl-Aulin K, Mackey A, Kjaer M, Oskarsson E & Holm L. (2008). The effects of regular strength training on telomere length in human skeletal muscle. Med Sci Sports Exerc 40, 82-87.
Ludlow AT, Zimmerman JB, Witkowski S, Hearn JW, Hatfield BD & Roth SM. (2008). Relationship between physical activity level, telomere length, and telomerase activity. Med Sci Sports Exerc 40, 1764-1771.
Ponsot E, Lexell J & Kadi F. (2008). Skeletal muscle telomere length is not impaired in healthy physically active old women and men.
Muscle Nerve 37, 467-472.