Original Investigations

The Effects of Regular Strength Training on

Telomere Length in Human Skeletal Muscle
FAWZI KADI1, ELODIE PONSOT2, KARIN PIEHL-AULIN2, ABIGAIL MACKEY3, MICHAEL KJAER3,
EVA OSKARSSON2, and LARS HOLM3
1
Department of Health Sciences, Örebro University, Örebro, SWEDEN; 2Department of Clinical Medicine, Örebro
University, Örebro, SWEDEN; and 3Institute of Sports Medicine, Bispebjerg Hospital, Copenhagen, DENMARK

ABSTRACT
KADI, F., E. PONSOT, K. PIEHL-AULIN, A. MACKEY, M. KJAER, E. OSKARSSON, and L. HOLM. The Effects of Regular Strength
BASIC SCIENCES

Training on Telomere Length in Human Skeletal Muscle. Med. Sci. Sports Exerc., Vol. 40, No. 1, pp. 82–87, 2008. Purpose: The length
of DNA telomeres is an important parameter of the proliferative potential of tissues. A recent study has reported abnormally short
telomeres in skeletal muscle of athletes with exercise-associated fatigue. This important report raises the question of whether long-term
practice of sports might have deleterious effects on muscle telomeres. Therefore, we aimed to compare telomere length of a group of
power lifters (PL; N = 7) who trained for 8 T 3 yr against that of a group of healthy, active subjects (C; N = 7) with no history of strength
training. Methods: Muscle biopsies were taken from the vastus lateralis, and the mean and minimum telomeric restriction fragments
(TRF) (telomere length) were determined, using the Southern blot protocol previously used for the analysis of skeletal muscle. Results:
There was no abnormal shortening of telomeres in PL. On the contrary, the mean (P = 0.07) and the minimum (P = 0.09) TRF lengths in
PL tended to be higher than in C. In PL, the minimum TRF length was inversely correlated to the individual records in squat
(r = j0.86; P = 0.01) and deadlift (r = j0.88; P = 0.01). Conclusion: These results show for the first time that long-term training is not
associated with an abnormal shortening of skeletal muscle telomere length. Although the minimum telomere length in PL remains
within normal physiological ranges, a heavier load put on the muscles means a shorter minimum TRF length in skeletal muscle.
Key Words: RESISTANCE EXERCISE, HYPERTROPHY, MUSCLE DNA, MYONUCLEI, SATELLITE CELLS, REGENERATION

T
elomeres are noncodant repetitive sequences
(TTAGGG)n located at the end of chromosomes.
The length of telomeres is an important measure of
the replicative history of the cell and also an indicator of its
proliferative potential, because in cell cultures chromosomal
telomeres shorten with each round of cell division
(2,10,16,26). One reason for this shortening is the so-called
end replication problem attributable to the inability of the
DNA polymerase to completely replicate the ends of the
linear molecules. However, recent in vivo studies suggest
that cell replication is not the only factor accountable for the
regulation of telomere length, and that external factors also
can affect telomeres. In this respect, it has been shown that
telomere shortening is stress dependent and that it occurs at
higher rates in cells with low antioxidative defense (24).
Address for correspondence: Fawzi Kadi, Ph.D., Assistant Professor,
Department of Health Sciences, Örebro University, 70182, Örebro, Sweden;
E-mail: Fawzi.Kadi@hi.oru.se.
Submitted for publication June 2007.
Accepted for publication August 2007.
0195-9131/08/4001-0082/0
MEDICINE & SCIENCE IN SPORTS & EXERCISEÒ
Copyright Ó 2007 by the American College of Sports Medicine
DOI: 10.1249/mss.0b013e3181596695
The fact that telomeres are influenced by external factors
has recently been shown in a study on the effects of chronic
stress on telomere length (9). Caregiving mothers (mothers
of chronically ill children) with the highest levels of
perceived stress have a significantly lower telomere length
in peripheral blood mononuclear cells than do control
mothers (mothers of healthy children) (9). It has also been
shown that mood disorders are associated with accelerated
telomere shortening (25), and it is known that telomere
shortening is not an irreversible process, because of the
existence of telomerase, an enzyme capable of extending
telomeres. New evidence suggests that the regulation of
telomere and telomerase in vivo is more complex than what
has been described in cell culture systems (23). Telomerase
has been demonstrated in many tissues, including heart
myocytes and skeletal muscle (15,20). Thus, it now seems
likely that telomeres are subject to various regulations in
many body systems to maintain tissue integrity (23).
Skeletal muscle satellite cells are undifferentiated myo-
genic precursors able to reenter the cell cycle to 1) provide
new myonuclei during postnatal growth, 2) generate new
muscle fibers, or 3) produce new satellite cells (13). Recent
studies have demonstrated the important role played by
satellite cells in the adaptation of skeletal muscle to strength
training (13). Satellite cell proliferation can contribute to the

82

Copyright @ 2007 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
acquisition of new myonuclei in hypertrophying muscle
fibers and to the repair of segmental muscle injuries caused
by excessive loading (1,11,14,17,18). It has also been shown
that the proliferation of satellite cells in response to exercise
allows the renewal of their own pool (3,5,8,12,14,18,22).
The increase in CyclinD1 mRNA levels, together with the
increase in the number of satellite cells during resistance
training, is indicative of the occurrence of extensive cell
divisions (14). Moreover, recent studies on the acute effects
of strength training demonstrate the capacity of satellite
cells to proliferate very rapidly in exercised muscle. Significant
increases in the proportion of satellite cells have been detected
in young men at 4 and 8 d after a single bout of maximal
exercise (5), and a remarkable increase in satellite cell
number (141% increase) has been observed as early as 24 h
after 92 maximal eccentric contractions in young men (8).
The significant recruitment of satellite cells in the adaptive
process of skeletal muscle to exercise raises the important
question of whether the regular practice of strength training
affects skeletal muscle DNA telomere length. To our
knowledge, the influence of regular strength training on
skeletal muscle telomere length of healthy athletes has never
been documented. There is only one report on skeletal
muscle DNA telomere length in endurance athletes suffering
from exercise-associated chronic fatigue, a condition labeled
fatigued athlete myopathic syndrome (FAMS) (4). A severe
reduction in skeletal muscle DNA telomere length has been
shown in FAMS patients compared with a healthy,
asymptomatic, age-matched control group.
Given the above discussion, the aim of the present study
was to assess whether the practice of strength training for
several years affects skeletal muscle DNA telomere length.
This was achieved by comparison of skeletal muscle
telomere length from a population of power lifters regularly
involved in strength training against that of a population of
healthy, active individuals.
METHODS
Our study aims to answer the question of whether long-
term practice of sports activities where muscles are put under
great strain affects the rate of telomere shortening in skeletal
muscle. To assess the effects of long-term power lifting on
telomere length in skeletal muscle, we have studied a
population of athletes who regularly trained for several
years, and we compared them with a population of healthy,
active individuals with no history of strength training.
Subjects
Seven power lifters (PL group) (28.5 T 6.6 yr, 100.2 T 15.5
kg, 178 T 5 cm) and seven healthy control individuals
(C group) (24.1 T 2.1 yr, 77.9 T 15.8 kg, 180 T 6 cm) with
no history of strength training participated in the study. All
power lifters participated in Swedish national competitions.
They practiced power lifting for a period of 8 T 3 yr and
TELOMERE LENGTH IN POWER LIFTERS
Copyright @ 2007 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
competitive power lifting for a period of 7 T 3 yr. They had
a training frequency of three to four sessions per week,
corresponding to a mean of 7 h of training per week.
Subjects in the control group did not participate in any
regular sport activities, and they exercised less than once a
week. They were active in that most did cycling and
walking for transportation. The study was approved by the
ethics committees of Uppsala and Copenhagen (M-255,
2003 and KF01-171/04), and written informed consent
conforming to the standards set by the Declaration of
Helsinki was obtained from all subjects.
Procedures
Evaluation of telomere length in skeletal muscle.
Mean and minimum telomere lengths were determined,
using the Southern blot protocol specifically adapted for the
BASIC SCIENCES
study of human skeletal muscle (19) and previously
described by Decary et al. (6,7), Collins et al. (4), and
Renault et al. (21).
Isolation of genomic DNA. Muscle biopsies were
obtained from the vastus lateralis muscle. The biopsies were
rapidly frozen in liquid nitrogen and stored at j80-C for
subsequent DNA extraction and telomere restriction
fragment (TRF)-length determination. For total genomic
DNA extraction, 8–10 mg of the muscle biopsy was
digested overnight at 55-C, with gentle agitation in
500 KL of digestion buffer (100 mM NaCl; 10 mM Tris-
Cl, pH 8.0; 100 mM EDTA, pH8; 1% Triton X-100)
containing 40 UImLj1 of proteinase K. The digest was
extracted with one volume of 25:24:1 (vol:vol:vol) phenol/
chloroform/isoamyl alcohol. The DNA was precipitated
with one volume of 0.5:2 (vol:vol) 7.5 M ammonium
acetate and ethanol 100%, washed with 70% ethanol,
resuspended in TE buffer (10 mM Tris-Cl, pH 8.0; 1 mM
EDTA, pH 7.5), and stored at 4-C (4,7).
Telomere length analysis. The intact genomic DNA
obtained from muscle tissue samples was digested for 4 h at
37-C with the restriction enzyme Hinf I (New England
Biolabs). A smear of DNA fragments containing TRF with
different lengths is generated (2). The undigested, extracted
DNA samples were resolved on agarose gels to verify the
absence of any DNA degradation. Mean and minimum TRF
lengths were determined, using Southern blot analysis (7).
Three micrograms of the digested DNA, together with two
DNA ladders (1 kb plus and high molecular weight, invi-
trogen), were resolved, using electrophoresis in 0.7%
agarose gels (+4-C, 90 V, 20 h), as previously described
(4,6,7,23). The gels were dried, denatured, and then neu-
tralized. TRF were detected by hybridization to a 32P-labeled
(TTAGGG)4 probe. Hybridization was performed directly on
the dried gels, which were then exposed to x-ray film
(BioMax MS, Kodak) with a BioMax transcreen (BioMax
MS, Kodak). A representative Southern blot of telomeric
skeletal muscle DNA is shown in Figure 1. The signals were
analyzed, using a computer-assisted system (Scion image
Medicine & Science in Sports & Exercised 83
 FIGURE 1VTelomere length assay. A, Representative autoradiogram showing the size distribution of TRF from skeletal muscle; molecular weight
standards are indicated in kilobase pairs. B, Determination of the mean TRF length (Lmean) and minimum TRF length (Lmini), using a sixth-degree
polynomial equation. Amax, maximal signal amplitude; I0, 2.5% of Amax added to baseline signal intensity. TRF length is then obtained by converting
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the migration distance (cm) into kilobase pairs, using the migration profile of low–molecular weight (range: 1–12 kb) and high–molecular weight
(range: 8–19 kb) ladders.

4.03 software, Scion Corporation) as previously described Statistical Analysis

(19). The intensity of the signal is plotted as a function of the
Data are presented as means T standard deviation (SD).
distance of migration, to determine the migration distances
The statistical analysis was performed by using the
corresponding to the mean and the minimum TRF lengths.
Sigmastat 3.0 software (SPSS, Chicago, IL). The statistical
TRF length is then obtained by converting the migration
power analysis was estimated according to MSSEÒ guide-
distance (cm) into kbp, using the migration profile of low–
lines. For an alpha level of 0.05, the power of the tests
molecular weight (range: 1–12 kb) and high–molecular
ranged between 0.62 and 0.67. Differences in skeletal
weight (range 8–19 kb) ladders. The signal obtained is made
muscle telomere length between groups were analyzed,
of an ascending slope up to the plateau intensity, followed by
using a one-way analysis of variance (ANOVA). Pearson
a descending slope down to the baseline signal intensity. As
linear regression analysis was used to study the relationship
shown in Figure 1, for each sample, both the ascending and
between two variables. Differences were considered to be
the descending parts were modelized, using a sixth-degree
significant for P G 0.05 and to be a tendency for P G 0.10.
polynomial equation with a coefficient of correlation of 0.99.
Using the equations of the ascending and the descending
slopes, several parameters were determined (Fig. 1):
RESULTS
1. Amax: maximal signal amplitude from the baseline
Mean personal records in squat, bench press, and deadlift
signal to the plateau intensity.
were 292.5 T 42, 184 T 25, and 292.5 T 34 kg, respectively.
2. I0: corresponds to 2.5% of Amax added to the baseline
The performance in squat was highly associated with
signal intensity.
deadlift (r = 0.97, P = 0.0002), whereas the association
3. Lmean: mean TRF length, which corresponds to the
between bench press and both squat (r = 0.84, P = 0.02) and
midpoint of the segment formed by the intersection of
deadlift (r = 0.82, P = 0.02) was slightly weaker.
the ascending and the descending linear slopes with the
The Lmean of skeletal muscle DNA in PL (11.7 T 1.5 kbp)
plateau intensity. Lmean comprises TRF of the majority
tended to be higher (P = 0.07) than in C (10.5 T 0.5 kbp)
of postmitotic myonuclei, which were incorporated
(Fig. 2). Similarly, the Lmean tended to be higher in PL
into muscle fibers from birth and, consequently, have
(5.3 T 0.7 kbp) compared with C (4.7 T 0.3 kbp) (P = 0.09)
undergone only few mitoses before differentiation.
(Fig. 2). Because there was variability in both Lmean and
4. Lmini: minimum TRF length, which corresponds to the
Lmini in PL, and because the personal records of the power
intersection point between the linear slope of the
lifters also varied, we reasoned that the performance in
descending part with I0. Lmini comprises TRF from
power lifting might have a stronger association with
satellite cells and also from the myonuclei newly
telomere length than simply belonging to the PL group.
incorporated during the last mitotic cycles.
Interestingly, within the PL group, the Lmini of vastus
To improve the precision of the measurements, we have lateralis DNA was inversely correlated to the individual
determined the Lmean and Lmini three times, on three records in squat (r = j0.86; P = 0.01) and deadlift (r =
independent gels, with a coefficient of variation of 3.6%. j0.88; P = 0.01) (Fig. 3). The heavier the load lifted, the

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FIGURE 2VMinimum (A) and mean (B) TRF length of vastus lateralis muscles from power lifters (PL) and controls (C).

shorter the power lifter_s skeletal muscle DNA minimum porated into the muscle fibers from birth and, consequently,
telomere length. The Lmean of vastus lateralis also tended to have undergone only few mitotic divisions before differ-

be inversely correlated to the personal records in deadlift
(r = j0.7; P = 0.07) but not to squat (r = j0.64; P = 0.1).
Skeletal muscle DNA TRF length was not associated with
the number of training sessions per week, the number of
years of power lifting practice, or the number of years of
competitive power lifting. When both groups were taken
together, we found no relationship between the age of the
subjects and skeletal muscle DNA TRF length.
BASIC SCIENCES
entiation. On the contrary, the minimum telomere length
comprises TRF from satellite cells and also from the
myonuclei newly incorporated during the last mitotic cycles
(7). Thus, the minimum telomere length gives information
on the low rate of telomere shortening, which occurs in

DISCUSSION
According to Collins et al. (4), a population of athletes
suffering from exercise-associated chronic fatigue had
extremely short skeletal muscle DNA Lmini. This important
report raises the question of whether the regular practice of
sports at a high level is accompanied by deleterious effects
on telomere length in skeletal muscle. To our knowledge,
the exact influence of regular strength training on skeletal
muscle telomeric DNA has never been addressed. Our study
shows for the first time that at a group level, regular power
lifting is not associated with an abnormal shortening of
skeletal muscle DNA telomere length. On the contrary,
skeletal muscle telomeres of power lifters tended to be
longer than those in a population of active subjects with no
history of strength training. We also have demonstrated, for
the first time, the existence of an inverse relationship
between skeletal muscle minimum telomere length and the
personal records in squat and deadlift.
In our study, the Lmean and Lmini of skeletal muscle DNA
in both PL and C were within the range of values previously
recorded in healthy populations (4,7,21). The mean telo-
mere length is a parameter frequently used to investigate
telomere length in many tissues under normal and patho-
logical conditions. However, in a postmitotic tissue such as
skeletal muscle, it has been shown that the Lmean is not an
appropriate parameter to evaluate the small loss of telomeric
FIGURE 3VRelationships between the minimum TRF length of
DNA. The mean telomere length comprises TRF of the skeletal muscle in power lifters and their personal records in squat
majority of postmitotic myonuclei, which had been incor- (A), deadlift (B), and bench press (C).

TELOMERE LENGTH IN POWER LIFTERS Medicine & Science in Sports & Exercised 85

Copyright @ 2007 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
 normal muscle as a result of satellite cell recruitment and
myonuclear replacement or during muscle regeneration (7).
For instance, using the Lmini, dramatic shortening of
telomeres has been shown to occur in children suffering
from muscular dystrophies (j187 bp per year) (6).
Our findings indicate that at a group level, the Lmini
tended to be higher in the power lifters compared with the
subjects with no history of regular strength training. This
observation clearly shows that long-term practice of power
lifting is not associated with an abnormal shortening of
telomeres such as that seen in the athletes suffering from
exercise-associated chronic fatigue, or FAMS (4). It is
noteworthy that the minimum telomere length in highly
trained subjects actually tended to be longer than in subjects
with no history of strength training. Although outside the
scope of this study, both genetic and nongenetic factors
might explain this observation. First, the existence of
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particular performance genes or the occurrence of genetic
predispositions to sports-related injuries has been frequently
discussed in the field of sports. In this respect, the
possibility that the higher telomere length in the athlete
population is part of their genetic predispositions cannot be
excluded. Second, the existence of in vivo regulatory
mechanisms able to influence the length of telomeres also
cannot be excluded. In this respect, recent studies clearly
have demonstrated the disparity between the regulation
of telomere length in vivo and in vitro (23). Third, the extent
of injury/regeneration cycles in skeletal muscle of these
athletes might be much lower than that seen in pathological
conditions. Finally, the handling of the biopsy includes the
removal of surrounding fat and connective tissue. However,
the occurrence of segmental fibrosis within the muscle fiber
cannot be ruled out. Therefore, it should be emphasized
that the possible occurrence of connective tissue cells in
skeletal muscle of athletes who might suffer from inflam-
mation/fibrosis might also affect telomere length in vastus
lateralis.
Interestingly, our findings also indicate that the perfor-
mance in power lifting (squat and deadlift) is inversely
correlated to the Lmini in vastus lateralis. This suggests that
the achievement of a high level of performance in power
lifting is associated with a higher level of satellite cell
recruitment. Thus, although the minimum telomere length
in the athlete population remains within normal physiolog-
ical ranges, it seems that the heavier the load put on
muscles, the shorter the Lmini of the muscles in question.
Thus, it can be hypothesized that when the exercise-induced
satellite cell recruitment exceeds a given threshold, the
telomere length positive regulation becomes ineffective.
Interestingly, the number of years of practice and the
number of years of competitive power lifting were not
associated with minimum telomere length.
It is suggested that within a muscle fiber, each myonucleus
is responsible for protein synthesis over a finite volume of
cytoplasmVa concept named the myonuclear domain.
Repeated bouts of resistance exercise induce increases in
86 Official Journal of the American College of Sports Medicine
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the number of domains (enhancement of the myonuclear
number) as existing myonuclei become unable to sustain
further enlargement of the cytosolic area (1,12,13,17,18).
As for the Lmini, the Lmean of skeletal muscle in PL was
within normal physiological ranges and tended to be
inversely correlated to the personal records in power lifting.
However, contrary to the strong associations found between
Lmini and performance level, Lmean was only weakly
associated with personal records. This might be explained
by the fact that a skeletal muscle fiber is a multinucleated
syncytium, where the newly incorporated myonuclei during
the course of muscle adaptation to strength training are
drowned within the thousands of myonuclei already present
in the muscle fiber.
Our results might indicate that the newly recruited
myonuclei are beginning to have an influence on the Lmean
of vastus lateralis in this population of power lifters.
Practical application. An alarming report has
indicated that endurance athletes with exercise-associated
fatigue have abnormally short skeletal muscle DNA
telomeres (4). This would suggest a dramatic decrease in
the capacity to repair severe or mild muscle injuries that
would occur during training or in daily activities. Our data
clearly show that the practice of regular strength training for
several years is not associated with abnormal telomere
shortening. For coaches and athletes, our data indicate that
the regular practice of strength training would not impair
the capacity of muscle repair, despite the regular
occurrence of cycles of muscle fiber injury/repair during
training. However, the question of whether the
occurrence of an overtraining syndrome negatively affects
telomere length remains to be assessed. Finally, it should
be emphasized that the data in this study were obtained
in young males performing strength training for a period
of 7 T 3 yr. Therefore, the results may not be applicable
to a longer period of strength training, older individuals,
or females.
In conclusion, at a group level, skeletal muscle DNA
telomere length in power lifters remains within the range of
values found in subjects with no history of regular strength
training. Thus, well-designed strength training protocols
where athletes are free from symptoms of overtraining do
not lead to deleterious effects on telomeres. The inverse
relationship between Lmini and personal records indicates
that the maximum load that can be sustained by skeletal
muscle, rather than the total amount of training, is an
important factor influencing satellite cell recruitment in the
course of skeletal muscle adaptation to strength training.
The existence of regulatory mechanisms allowing the
control of telomere length in vivo cannot be excluded.
Further investigations are needed to better understand the
regulation of telomere length in vivo under normal
physiological conditions.
This study was supported by grants from the Swedish National
Center for Research in Sports (74/06, 101/07, and 159/07).
http://www.acsm-msse.org
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