european college of sport science

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.
256:C1262-6.
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 UNIVERSITY
The 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.
EXERCISE TRAINING, SATELLITE CELLS AND THE REGENERATIVE POTENTIAL OF SKELETAL MUSCLE
KADI, F.
ÖREBRO UNIVERSITY
Human skeletal muscle is a dynamic tissue characterised by a remarkable ability to continuously respond to environmental stimuli.
Experiments in humans clearly show the great ability of skeletal muscle to regenerate after loading or injury or both. Satellite cells in
human skeletal muscle enter proliferation in response to light and heavy resistance training or endurance exercises both in young and
old individuals. Enhancement of satellite cell pool in response to training is another health benefit of exercise. The proliferative capacity of
skeletal muscle is influenced by the length of DNA sequences located at the end of chromosomes called telomeres. A dramatic shortening
of telomeres is associated with a reduction in tissue regenerative potential. Rather than considering skeletal muscle as a stable tissue
in term of regenerative events, muscle biologists start to learn that under harmful circumstances an abnormal shortening of telomeres
might occur and that when training is properly performed the telomere length can be positively regulated. No doubt that new mechanisms
relating the effects of exercise on the regenerative capacity of skeletal muscle and the regulation of telomere length will emerge in
the near future.
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