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Athletes with Exercise-Associated Fatigue Have Abnormally Short Muscle DNA Telomeres
Abstract
Although the beneficial health effects of regular moderate exercise are well established, there is substantial evidence that the heavy training and racing carried out by endurance athletes can cause skeletal muscle damage. This damage is repaired by satellite cells that can undergo a finite number of cell divisions. In this study, we have compared a marker of skeletal muscle regeneration of athletes with exercise-associated chronic fatigue, a condition labeled the "fatigued athlete myopathic syndrome" (FAMS), with healthy asymptomatic age- and mileage-matched control endurance athletes.
Muscle biopsies of the vastus lateralis were obtained from 13 patients diagnosed with FAMS and from 13 healthy control subjects. DNA was extracted from the muscle samples and their telomeric restriction fragment (TRF) or telomere lengths were measured by Southern blot analysis.
All 13 symptomatic athletes reported a progressive decline in athletic performance, decreased ability to tolerate high mileage training, and excessive muscular fatigue during exercise. The minimum value of TRF lengths (4.0 +/- 1.8 kb) measured on the DNA from vastus lateralis biopsies from these athletes were significantly shorter than those from 13 age- and mileage-matched control athletes (5.4 +/- 0.6 kb, P < 0.05). Three of the FAMS patients had extremely short telomeres (1.0 +/- 0.3 kb). The minimum TRF lengths of the remaining 10 symptomatic athletes (4.9 +/- 0.5 kb, P < 0.05) were also significantly shorter that those of the control athletes.
These findings suggest that skeletal muscle from symptomatic athletes with FAMS show extensive regeneration which most probably results from more frequent bouts of satellite cell proliferation in response to recurrent training- and racing-induced muscle injury.
... As displayed in Table 1, 19 studies examined athletes from different sports, 1,2,[4][5][6][7][8][9]12,13,[15][16][17]20,24,29,36,37,[43][44][45]53,54,58,64,66,68,72 while 9 studies focused on 1 single sport. Two studies did not disclose the type of sport played. ...
... In total, 952 subjects were examined including 328 athletes diagnosed with OTS and 624 healthy control subjects. In 24 studies, the athletes were already previously affected by OTS, 2,[4][5][6][7][8][9]12,[15][16][17]20,24,29,30,34,36,37,[42][43][44][45]47,53,54,[56][57][58]64,65,68,72 while in 6 studies, OTS developed during the study. 1,27,60,61,66,71 A total of 7 studies were uncontrolled: 2 studies did not have any control group, 4,24 and 5 studies were case-reports with only 1 subject and no control. ...
... 53 As shown in Table 3, 14 studies included both men and women. 2,[4][5][6]20,24,36,37,42,45,53,64,66,68,72 Ten studies, of which 3 were case reports, focused on men only 1,[7][8][9]12,13,[15][16][17]27,30,34,54,56,60,61,71 and 2 studies, of which 1 was a case report, on women only. 47,57 Four studies did not specify participants' sex. ...
Context
Overtraining syndrome (OTS) is a condition characterized by a long-term performance decrement, which occurs after a persisting imbalance between training-related and nontraining-related load and recovery. Because of the lack of a gold standard diagnostic test, OTS remains a diagnosis of exclusion.
Objective
To systematically review and map biomarkers and tools reported in the literature as potentially diagnostic for OTS.
Data Sources
PubMed, Web of Science, and SPORTDiscus were searched from database inception to February 4, 2021, and results screened for eligibility. Backward and forward citation tracking on eligible records were used to complement results of database searching.
Study Selection
Studies including athletes with a likely OTS diagnosis, as defined by the European College of Sport Science and the American College of Sports Medicine, and reporting at least 1 biomarker or tool potentially diagnostic for OTS were deemed eligible.
Study Design
Scoping review following the guidelines of the Joanna Briggs Institute and PRISMA Extension for Scoping Reviews (PRISMA-ScR).
Level of Evidence
Level 4.
Data Extraction
Athletes’ population, criteria used to diagnose OTS, potentially diagnostic biomarkers and tools, as well as miscellaneous study characteristics were extracted.
Results
The search yielded 5561 results, of which 39 met the eligibility criteria. Three diagnostic scores, namely the EROS-CLINICAL, EROS-SIMPLIFIED, and EROS-COMPLETE scores (EROS = Endocrine and Metabolic Responses on Overtraining Syndrome study), were identified. Additionally, basal hormone, neurotransmitter and other metabolite levels, hormonal responses to stimuli, psychological questionnaires, exercise tests, heart rate variability, electroencephalography, immunological and redox parameters, muscle structure, and body composition were reported as potentially diagnostic for OTS.
Conclusion
Specific hormones, neurotransmitters, and metabolites, as well as psychological, electrocardiographic, electroencephalographic, and immunological patterns were identified as potentially diagnostic for OTS, reflecting its multisystemic nature. As exemplified by the EROS scores, combinations of these variables may be required to diagnose OTS. These scores must now be validated in larger samples and within female athletes.
... Exercise training prevents and manages age-related cardiometabolic diseases possibly through the regulation of telomere maintenance (Collins et al., 2003;Denham et al., 2013Denham et al., , 2016a. Alternatively, exercise training could prevent disease through a reduction in disease-related risk factors (blood pressure, lipid profile, adiposity, etc.) (Cassidy et al., 2017), systemic inflammation and oxidative stress (Floyd et al., 1999;Kaszubowska, 2008;Radak et al., 2008;Calle and Fernandez, 2010;Chilton et al., 2014;Steckling et al., 2016), or psychological stress to ultimately prevent telomere shortening. ...
... Critically short telomeres induce cellular senescence in vascular smooth muscle cells (Uryga and Bennett, 2016), which could also be prevented by exercise training. Several studies have demonstrated that muscle strength and function is related to telomere length in both peripheral leukocytes and skeletal muscle cells, in athletic and apparently healthy populations (Collins et al., 2003;Kadi et al., 2008;Bunout et al., 2009;Rae et al., 2010;Gardner et al., 2013). ...
... Endurance exercise does not appear to be detrimental to leukocyte or muscle TL maintenance, according to the current data on endurance exercise and resistance training. There could, however, be an upper limit to the protective effect of exercise depending on volume (duration and frequency) and intensity of training, considering shorter muscle telomeres were inversely correlated to maximal strength and training history (years and hours spent training) (Collins et al., 2003). ...
Exercise training is one of the few therapeutic interventions that improves health span by delaying the onset of age-related diseases and preventing early death. The length of telomeres, the 5′-TTAGGGⁿ-3′ tandem repeats at the ends of mammalian chromosomes, is one of the main indicators of biological age. Telomeres undergo shortening with each cellular division. This subsequently leads to alterations in the expression of several genes that encode vital proteins with critical functions in many tissues throughout the body, and ultimately impacts cardiovascular, immune and muscle physiology. The sub-telomeric DNA is comprised of heavily methylated, heterochromatin. Methylation and histone acetylation are two of the most well-studied examples of the epigenetic modifications that occur on histone proteins. DNA methylation is the type of epigenetic modification that alters gene expression without modifying gene sequence. Although diet, genetic predisposition and a healthy lifestyle seem to alter DNA methylation and telomere length (TL), recent evidence suggests that training status or physical fitness are some of the major factors that control DNA structural modifications. In fact, TL is positively associated with cardiorespiratory fitness, physical activity level (sedentary, active, moderately trained, or elite) and training intensity, but is shorter in over-trained athletes. Similarly, somatic cells are vulnerable to exercise-induced epigenetic modification, including DNA methylation. Exercise-training load, however, depends on intensity and volume (duration and frequency). Training load-dependent responses in genomic profiles could underpin the discordant physiological and physical responses to exercise. In the current review, we will discuss the role of various forms of exercise training in the regulation of DNA damage, TL and DNA methylation status in humans, to provide an update on the influence exercise training has on biological aging.
... The number of studies showing the association between PA and TL has been increasing from the past to the present (Collins et al. 2003;Cherkas et al. 2008;Ponsot, Lexell, and Kadi et al. 2008;Woo, Tang, and Leung 2008;Kadi et al. 2008;Rae et al. 2010;LaRocca, Seals, and Pierce 2010;Zhu et al. 2011;Soares-Miranda et al. 2015;Loprinzi, Loenneke, and Blackburn 2015;Loprinzi 2015;Saßenroth et al. 2015;Borghini et al. 2015;Dimauro et al. 2016;Diman et al. 2016;Denham et al. 2016;Dankel, Loenneke, and Loprinzi 2017;Zietzer et al. 2017;Ogawa et al. 2017;Shadyab et al. 2017;Fretts et al. 2018;Brandao et al. 2020). According to the studies, not only being physically active (Soares-Miranda et al. 2015;Loprinzi, Loenneke, and Blackburn 2015;Loprinzi 2015;Saßenroth et al. 2015;Dankel, Loenneke, and Loprinzi 2017;Fretts et al. 2018) but also the PA levels could be associated with TL (Cherkas et al. 2008;Woo, Tang, and Leung 2008;Zhu et al. 2011;Ogawa et al. 2017;Shadyab et al. 2017). ...
... According to the studies, not only being physically active (Soares-Miranda et al. 2015;Loprinzi, Loenneke, and Blackburn 2015;Loprinzi 2015;Saßenroth et al. 2015;Dankel, Loenneke, and Loprinzi 2017;Fretts et al. 2018) but also the PA levels could be associated with TL (Cherkas et al. 2008;Woo, Tang, and Leung 2008;Zhu et al. 2011;Ogawa et al. 2017;Shadyab et al. 2017). Besides, there may be an association between specific exercise types and TL (Collins et al. 2003;Kadi et al. 2008;Rae et al. 2010;LaRocca, Seals, and Pierce 2010;Borghini et al. 2015;Dimauro et al. 2016;Diman et al. 2016;Denham et al. 2016;Brandao et al. 2020). ...
... However, the association between endurance exercise and TL may be affected by skeletal muscle damage due to heavy training and racing carried out by endurance athletes (Collins et al. 2003). In a study, it was reported that endurance athletes with severe fatigue myopathic syndrome (FAMS) had excessive telomere shortening in skeletal muscle compared to athletes who were equivalent in terms of age and training levels (Collins et al. 2003). ...
The aging of the population has great social and economic effects because it is characterized by a gradual loss in physiological integrity, resulting in functional decline, thereby loss of ability to move independently. Telomeres, the hallmarks of biological aging, play a protective role in both cell death and aging. Critically short telomeres give rise to a metabolically active cell that is unable to repair damage or divide, thereby leading to aging. Lifestyle factors such as physical activity (PA) and nutrition could be associated with telomere length (TL). Indeed, regular PA and healthy nutrition as integral parts of our lifestyle can slow down telomere shortening, thereby delaying aging. In this context, the present comprehensive review summarizes the data from recent literature on the association of PA and nutrition with TL.
... Athletes suffering FAMS have history of high-volume training for many years and are chronically fatigued. Histological evidence indicates extensive muscle regeneration (Collins et al., 2003;490 Vihko et al., 1978490 Vihko et al., , 1979, which results in an elevated demand for satellite cell proliferation (Collins et al., 2003). Consequently, if muscles are damaged over an extended period of time, telomeres can be expected to be shorter in skeletal muscle of FAMS athletes. ...
... Athletes suffering FAMS have history of high-volume training for many years and are chronically fatigued. Histological evidence indicates extensive muscle regeneration (Collins et al., 2003;490 Vihko et al., 1978490 Vihko et al., , 1979, which results in an elevated demand for satellite cell proliferation (Collins et al., 2003). Consequently, if muscles are damaged over an extended period of time, telomeres can be expected to be shorter in skeletal muscle of FAMS athletes. ...
... Consequently, if muscles are damaged over an extended period of time, telomeres can be expected to be shorter in skeletal muscle of FAMS athletes. To prove this hypothesis, (Collins et al., 2003) compared TRF min and TRF mean values in vastus lateralis muscle from 13 athletes aged 42.0±10.2 years suffering from FAMS with 13 healthy controls matched for age and, according to the authors, also for training volume. ...
Based upon a comprehensive analysis of current literature and by combining a molecular biology and a sports science perspective, this review examines (1) if a correlation between physical activity load and telomere length (TL) exists, and (2) comprehensively analyses and integrates molecular pathways regulating exercise dependent TL dynamics. The focus is on TL in leukocytes and muscle tissue in middle to advanced aged subjects. Regarding item (1), a strong tendency for an increase in mean leukocyte TL was found for exercise energy expenditures up to about 2∙103 kcal/week, while for higher activity levels no conclusive statement can be made. Conversely, research on skeletal muscle TL so far is quite limited but suggests that physical exercise with prolonged eccentric muscle contractions rather acts to shorten telomeres, while sports with little eccentric contractions might rather act to lengthen telomeres. As to item (2), a model for hypothetical pathways for exercise dependent telomerase activity regulation is proposed by consolidating findings of different studies in different cells. Consistent with this pathway model, various studies report increased telomerase transcription or activation by exercise. Moreover, a qualitative overall model for endurance exercise related TL dynamics is presented. It considers telomeres as dynamic structures in equilibrium between telomere shortening (e.g., cellular turnover, oxidative stress, inflammation) and telomere lengthening (e.g., telomerase activity, telomerase recruitment) effects. A negative feedback-loop mediated by enhanced telomerase recruitment to short telomeres is assumed to counteract too excessive TL alterations. Finally, a proposal is put forth for future research on exercise dependent telomere dynamics by adopting a systems biology approach to develop mathematical models that properly integrate the complexity of the interacting variables.
... Athletes suffering FAMS have history of high-volume training for many years and are chronically fatigued. Histological evidence indicates extensive muscle regeneration (Collins et al., 2003;490 Vihko et al., 1978490 Vihko et al., , 1979, which results in an elevated demand for satellite cell proliferation (Collins et al., 2003). Consequently, if muscles are damaged over an extended period of time, telomeres can be expected to be shorter in skeletal muscle of FAMS athletes. ...
... Athletes suffering FAMS have history of high-volume training for many years and are chronically fatigued. Histological evidence indicates extensive muscle regeneration (Collins et al., 2003;490 Vihko et al., 1978490 Vihko et al., , 1979, which results in an elevated demand for satellite cell proliferation (Collins et al., 2003). Consequently, if muscles are damaged over an extended period of time, telomeres can be expected to be shorter in skeletal muscle of FAMS athletes. ...
... Consequently, if muscles are damaged over an extended period of time, telomeres can be expected to be shorter in skeletal muscle of FAMS athletes. To prove this hypothesis, (Collins et al., 2003) compared TRF min and TRF mean values in vastus lateralis muscle from 13 athletes aged 42.0±10.2 years suffering from FAMS with 13 healthy controls matched for age and, according to the authors, also for training volume. ...
Based upon a comprehensive analysis of current literature and by combining a molecular biology and a sports science perspective, this review examines (1) if a correlation between physical activity load and telomere length (TL) exists, and (2) comprehensively analyses and integrates molecular pathways regulating exercise dependent TL dynamics. The focus is on TL in leukocytes and muscle tissue in middle to advanced aged subjects. Regarding item (1), a strong tendency for an increase in mean leukocyte TL was found for exercise energy expenditures up to about 2∙103 kcal/week, while for higher activity levels no conclusive statement can be made. Conversely, research on skeletal muscle TL so far is quite limited but suggests that physical exercise with prolonged eccentric muscle contractions rather acts to shorten telomeres, while sports with little eccentric contractions might rather act to lengthen telomeres. As to item (2), a model for hypothetical pathways for exercise dependent telomerase activity regulation is proposed by consolidating findings of different studies in different cells. Consistent with this pathway model, various studies report increased telomerase transcription or activation by exercise. Moreover, a qualitative overall model for endurance exercise related TL dynamics is presented. It considers telomeres as dynamic structures in equilibrium between telomere shortening (e.g., cellular turnover, oxidative stress, inflammation) and telomere lengthening (e.g., telomerase activity, telomerase recruitment) effects. A negative feedback-loop mediated by enhanced telomerase recruitment to short telomeres is assumed to counteract too excessive TL alterations. Finally, a proposal is put forth for future research on exercise dependent telomere dynamics by adopting a systems biology approach to develop mathematical models that properly integrate the complexity of the interacting variables.
... Telomere length is an important marker of the regenerative potential of tissues and can be affected both by physical and psychological stress. For instance, telomere length has been found severely shortened in skeletal muscle of athletes suffering from exercise-associated chronic fatigue (Collins et al., 2003) and in leukocytes of mothers giving care to chronically ill children (Epel et al., 2004). ...
... The number of studies on the effect of regular training on telomeres is limited. Severely shortened telomeres have been discovered in a group of athletes suffering from overtraining symptoms (Collins et al., 2003). Kadi et al. (2008) evaluated telomere length in experienced power-lifters and reported no shortening of telomeres in this population. ...
... Mean telomere length represents the telomere length of a majority of the post-mitotic myonuclei which has been incorporated in muscle fibers since birth and therefore have undergone few divisions, while minimum telomere length represents the telomere length from satellite cells and the most recently incorporated myonuclei (). In this study mean and minimum telomere lengths are within the normal ranges previously reported in vastus lateralis muscle of untrained healthy individuals () and endurance runners (Collins, et al., 2003; Rae et al., 2010), and exceeds that of athletes suffering from overtraining symptoms (Collins et al. 2003). A significant difference in age between the ultra-endurance athletes and controls was found. ...
Degree project in sports physiology and medicine Second level, 45 higher education credits, Spring 2011, Master programme in sports physiology and medicine
... Despite these previous findings, the association between telomere length and physical activity is not unequivocal. Increasing physical activity has been shown to have a positive correlation with telomere length (Cherkas et al., 2008;Zhu et al., 2011), but the linear association has not been confirmed in all studies (Collins et al., 2003;Ludlow et al., 2008). Furthermore, no association between physical activity and telomere length was found in one previous study (Cassidy et al., 2010). ...
... In a study of 69 volunteers aged 50-70 yr, Ludlow et al. (2008) also reported that moderate physical activity levels were associated with longer LTLs compared to both the lowest and the highest quartiles of physical activity. Furthermore, Collins et al. (2003) supported these findings of endurance athletes by indicating that participants with fatigued athlete myopathic syndrome had a severe reduction in skeletal muscle DNA telomere length compared to 13 healthy athletes. ...
The aim of this study was to determine whether there is an association between leukocyte telomere length (LTL), and estrogen level, oxidative stress, cardiovascular disease (CVD) risk factors, and cardiorespiratory fitness (CRF) in pre- and postmenopausal obese women. Fifty-four obese women (premenopausal, n=25; postmenopausal, n=29) were selected to participate in this study. The outcome measurements in the pre- and postmenopausal groups were compared using independent t-tests and Pearson correlation analysis. The estrogen level (P<0.001), LTL (P<0.05), high-density lipoprotein level (P<0.05), and CRF (P<0.001) were higher in premenopausal women than in postmenopausal women. The body fat percentage (P<0.05) and triglyceride concentration (P<0.05) were lower in premenopausal women than in postmenopausal women. There were no significant associations between LTL, CVD risk, CRF, and oxidative stress and antioxidant enzyme activity in pre-menopausal women. The body mass index (BMI) and body fat percent-age in postmenopausal women were negatively associated with LTL (P<0.05). When all women were considered (i.e., both pre- and post-menopause), the BMI, percentage of fat, and waist circumference had a negative association with LTL (P<0.05), and estrogen levels were positively associated with LTL (P<0.05). Decreased estrogen levels after menopause, a pivotal factor in the biology of aging, and obesity were more associated with shorter telomere lengths in pre- and postmenopausal women than aerobic capacity and other CVD risk factors.
... Their threedimensional structure is stabilized by telomere-binding proteins (TBP), as telomeric repeat binding factors (TRF1 and TRF2) [9]. Studies have reported the relationship between regeneration events and telomere shortening in skeletal muscle [10], and satellite cell regeneration ability is indirectly determined by telomere length [11]. ...
... Although the proliferative capacity and initial telomere length of satellite cells decrease during the first two decades of life due to increase in muscle mass, telomeres remain stable during adult stage [36]. Rehabilitation capacity is related to telomere length in injured muscle [11]. ...
Infrared laser therapy is used for skeletal muscle repair based on its biostimulative effect on satellite cells. However, shortening of telomere length limits regenerative potential in satellite cells, which occurs after each cell division cycle. Also, laser therapy could be more effective on non-physiologic tissues. This study evaluated low-level infrared laser exposure effects on mRNA expression from muscle injury repair and telomere stabilization genes in myoblasts in normal and stressful conditions. Laser fluences were those used in clinical protocols. C2C12 myoblast cultures were exposed to low-level infrared laser (10, 35, and 70 J/cm2) in standard or normal (10 %) and reduced (2 %) fetal bovine serum concentrations; total RNA was extracted for mRNA expression evaluation from muscle injury repair (MyoD and Pax7) and chromosome stabilization (TRF1 and TRF2) genes by real time quantitative polymerization chain reaction. Data show that low-level infrared laser increases the expression of MyoD and Pax7 in 10 J/cm2 fluence, TRF1 expression in all fluences, and TRF2 expression in 70 J/cm2 fluence in both 10 and 2 % fetal bovine serum. Low-level infrared laser increases mRNA expression from genes related to muscle repair and telomere stabilization in myoblasts in standard or normal and stressful conditions.
... Prolonged, demanding, weight-bearing exercise has also been reported to cause both acute and more chronic muscle damage which may contribute to fatigued athlete myopathic syndrome (FAMS) [89]. In a study by Collins et al. [90], telomere lengths in muscle biopsies from athletes with exerciseassociated fatigue were compared with those from controls. Subjects were matched for age, gender, height, weight, and training history. ...
... It was demonstrated that these athletes had significantly shorter telomeres than their controls. The results suggested that in an attempt to repair repeated bouts of exerciseinduced muscle damage, the satellite cells of the patients had undergone more oxidative damage and more frequent rounds of replication, resulting in extensive shortening of the telomeres [90]. ...
... Regular exercise training within physiologically tolerable limits appears to attenuate telomere shortening through up-regulated telomerase, and possibly other supporting mechanisms (e.g., telomere repeat-containing RNA [TERRA] and shelterin), mainly in human leukocytes, buccal cells and skeletal muscle (42,43). For instance, endurance athletes experiencing overtraining syndrome possess shorter skeletal muscle telomeres (44), whereas healthy endurance athletes exhibit longer leukocyte telomeres (45,46) and up-regulated telomerase activity in PBMCs (47). Furthermore, healthy endurance athletes also show 2-fold higher TERT expression in leukocytes relative to controls (46). ...
Cancer remains a leading cause of death worldwide and although prognosis and survivorship after therapy has improved significantly, current cancer treatments have long-term health consequences. For decades telomerase-mediated telomere maintenance has been an attractive anti-cancer therapeutic target due to its abundance and role in telomere maintenance, pathogenesis and growth in neoplasms. Telomere maintenance-specific cancer therapies, however, are marred by off target side-effects that must be addressed before they reach clinical practice. Regular exercise training is associated with telomerase-mediated telomere maintenance in healthy cells, which is associated with healthy ageing. A single bout of endurance exercise training dynamically, but temporarily, increases TERT mRNA and telomerase activity, as well as several molecules that control genomic stability and telomere length (i.e., shelterin and TERRA). Considering the epidemiological findings and accumulating research highlighting that exercise significantly reduces the risk of many types of cancers and the anti-carcinogenic effects of exercise on tumour growth in vitro, investigating the governing molecular mechanisms of telomerase control in context with exercise and cancer may provide important new insights to explain these findings. Specifically, the molecular mechanisms controlling telomerase in both healthy cells and tumours after exercise could reveal novel therapeutic targets for tumour-specific telomere maintenance and offer important evidence that could refine current physical activity and exercise guidelines for all stages of cancer care.
... In an earlier study, M. Collins et al. found abnormally shortened DNA telomeres in muscle cells of athletes with excessive physical activity, resulting in excessive production of reactive oxygen species. In a study by Chirag M Vyas et al., Consistent with our results, individuals with high physical activity (> 30 + MET-hours/week) also had shorter telomere length.(32,33) The telomere length shortening induced by occupational exposure to environmental hazards may be caused by oxidative stress and gene regulation. ...
Objectives
Numbers of studies have shown that human aging is related to environmental factors, among which workplace is an important living environment in people's life. However, there is still a lack of causal exploration research on the effect of workplace factors on human aging. From the perspective of genetic polymorphism, we explore the association between human aging and risk factors in the workplace,and the possible pathways of aging caused by risk factors in the workplace.
Methods
To systematically explore the association between workplace risk factors and aging, we used a two-sample Mendelian randomization method to examine the association of nine common workplace risk factors with telomere length and accelerated DNA methylation GrimAge clock. We used the corresponding single nucleotide polymorphisms screened as instrumental variables to enable causal associations between exposing to workplace factors and aging.
Results
According to our tests, "Heavy physical work" and "Noise" are associated with telomere length, which shows statistics as OR [95% CI] = -0.136[-0.229, -0.043], p = 0.004 and the OR [95% CI] = 0.014 [0.002, 0.027], p = 0.025) respectively. Meanwhile, the P value of the phenotype "Asbestos" was close to 0.05 (P = 0.059), and the OR value was OR [95%CI] = -1.098[-2.241, 0.044].The factor "diesel exhaust"(ukb-d-22615_2) associated with GrimAge acceleration was OR [95%CI] = 8.238[-0.023, 16.450], p = 0.05.
Conclusions
Our finding suggests that there existing causal relationship between workplace exposure to risk factors (noise, heavy physical activity, fuel engine exhaust) and aging.
... With the proposed role of shorter telomere length in HAPE pathophysiology ( Figure 5), shorter telomere length among endurance athletes is observed as a stressor in their skeletal muscles [62]. On the contrary, reports have associated higher physical activity levels and exercise training with longer telomere length [23][24][25][26][27]. ...
The hypobaric-hypoxia environment at high-altitude (HA, >2500 m) may influence DNA damage due to the production of reactive molecular species and high UV radiation. The telomere system, vital to chromosomal integrity and cellular viability, is prone to oxidative damages contributing to the severity of high-altitude disorders such as high-altitude pulmonary edema (HAPE). However, at the same time, it is suggested to sustain physical performance. This case-control study, comprising 210 HAPE-free (HAPE-f) sojourners, 183 HAPE-patients (HAPE-p) and 200 healthy highland natives (HLs) residing at ~3500 m, investigated telomere length, telomerase activity, and oxidative stress biomarkers. Fluidigm SNP genotyping screened 65 single nucleotide polymorphisms (SNPs) in 11 telomere-maintaining genes. Significance was attained at p ≤ 0.05 after adjusting for confounders and correction for multiple comparisons. Shorter telomere length, decreased telomerase activity and increased oxidative stress were observed in HAPE patients; contrarily, longer telomere length and elevated telomerase activity were observed in healthy HA natives compared to HAPE-f. Four SNPs and three haplotypes are associated with HAPE, whereas eight SNPs and nine haplotypes are associated with HA adaptation. Various gene-gene interactions and correlations between/among clinical parameters and biomarkers suggested the presence of a complex interplay underlining HAPE and HA adaptation physiology. A distinctive contribution of the telomere-telomerase system contributing to HA physiology is evident in this study. A normal telomere system may be advantageous in endurance training.
... MIAT (40-60% HRR), however, is the most commonly used AERO modality, and different HF guidelines recommended it [28][29][30]. Physiologically, very-high intensity exercise can lead to decreased TL due to an imbalance between severe oxidative stress and reduced antioxidant mechanisms [31,32]. In contrast, MIAT can lead to a reduction in oxidative stress through higher antioxidant activity, which can have beneficial effects on TL [33][34][35][36][37]. ...
Background
Heart failure (HF) with reduced ejection fraction (HFrEF) is a syndrome that leads to fatigue and reduced functional capacity due to disease-related pathophysiological mechanisms. Aerobic exercise (AERO) plays a key role in improving HF outcomes, such as an increase in peak oxygen uptake (VO 2 peak). In addition, HF promotes cell senescence, which involves reducing telomere length. Several studies have shown that patients with a worse prognosis (i.e., reduced VO 2 peak) also have shorter telomeres. However, the effects of AERO on telomere length in patients with HFrEF are still unknown. In an attempt to fill this gap, we designed a study to determine the effects of 16 weeks of aerobic training (32 sessions) on telomere length in HFrEF patients.
Methods
In this single-center randomized controlled trial, men and women between 50 and 80 years old will be allocated into two different groups: a moderate-intensity aerobic training and a control grouTelomere length, functional capacity, echocardiographic variables, endothelial function, and walking ability will be assessed before and after the 16-week intervention period.
Discussion
Understanding the role of physical exercise in biological aging in HFrEF patients is relevant. Due to cell senescence, these individuals have shown a shorter telomere length. AERO can delay biological aging according to a balance in oxidative stress through antioxidant action. Positive telomere length results are expected for the aerobic training group.
Trial registration
ClinicalTrials.gov NCT03856736 . Registered on February 27, 2019
... Despite the links between relatively long leukocyte telomeres, aerobic fitness and exercise training, skeletal muscle telomeres do not appear to be preserved by exercise training in humans (Hiam et al., 2020;Ponsot et al., 2008;Rae et al., 2010), although some have shown positive findings (Osthus et al., 2012). They are, however, inversely correlated to exercise training volumes in healthy athletes and shorter in overtrained athletes (Collins et al., 2003;Kadi et al., 2008;Rae et al., 2010). ...
Telomeres protect genomic stability and shortening is one of the hallmarks of ageing. Telomerase reverse transcriptase (TERT) is the major protein component of telomerase, which elongates telomeres. Given that short telomeres are linked to a host of chronic diseases and the therapeutic potential of telomerase-based therapies as treatments and a strategy to extend lifespan, lifestyle factors that increase TERT gene expression and telomerase activity could attenuate telomere attrition and contribute to healthy biological ageing.
Physical activity and maximal aerobic fitness are associated with telomere maintenance, yet the molecular mechanisms remain unclear. Therefore, the purpose of this systematic review and meta-analysis was to identify the influence of a single bout of exercise and long-term exercise training on TERT expression and telomerase activity. A search of human and rodent trials using the PubMed, Scopus, Science Direct and Embase databases was performed.
Based on findings from the identified and eligible trials, both a single bout of exercise (n; standardised mean difference [95%CI]: 5; SMD: 1.19 [0.41–1.97], p = 0.003) and long-term exercise training (10; 0.31 [0.03–0.60], p = 0.03) up-regulates TERT and telomerase activity in non-cancerous somatic cells. As human and rodent studies were included in both meta-analyses both exhibited heterogeneity (I2 = 55–87%, p < 0.05). Endurance athletes also exhibited increased leukocyte TERT and telomerase activity compared to their inactive counterparts. These findings suggest exercise training as an inexpensive lifestyle factor that increases TERT expression and telomerase activity. Regular exercise training could attenuate telomere attrition through a telomerase-dependent mechanism and ultimately extend health-span and longevity.
... Thus, despite a lack of association between the average weekly training distance and buccal cell TL amongst swimmers in the present study, the high number of training hours they performed may potentially explain their shortened telomeres compared with the recreationally active controls. Furthermore, highly trained middle-aged endurance athletes experiencing 'exercise-associated chronic fatigue' or 'overtraining' report significantly shorter skeletal muscle TL compared with age-and training-matched athletes free from these symptoms (Collins et al., 2003). Although we did not specifically diagnose whether the swimmers were 'overtrained' in the present study, we can only speculate that some of them may have been in such a physical state based on their reportedly high weekly training hours and average swimming distance. ...
Purpose
Elite athletes are reported to possess longer telomeres than their less active counterparts. ACE gene (Insertion/Deletion) polymorphism has been previously associated with elite athletic performance, with the deletion (D) variant appearing more frequently in short distance swimmers. Additionally, the D allele has been reported to have a negative effect on telomere length. The aim of this study was to investigate the telomere length of elite swimmers and its potential association with ACE genotype.
Methods
Telomere length was measured by real-time quantitative PCR and ACE I/D genotypes analysed by standard PCR and electrophoresis in 51 young elite swimmers and 56 controls.
Results
Elite swimmers displayed shorter telomeres than controls (1.043 ± 0.127 vs 1.128 ± 0.177, p = 0.006). When split by sex, only elite female swimmers showed significantly shorter telomeres than their recreationally active counterparts (p = 0.019). ACE genotype distribution and allelic frequency did not differ between elite swimmers and controls, or by event distance among elite swimmers only. No association was observed between telomere length and ACE genotype in the whole cohort.
Conclusions
Elite swimmers possessed shorter telomeres than recreationally active controls. Our findings suggesting a negative effect of high-level swimming competition and/or training on telomere length and subsequent biological aging, particularly in females. However, this significant difference in telomere length does not appear to be attributed to the D allele as we report a lack of association between telomere length and ACE genotype frequency in elite swimmers and controls.
... Although several previous studies have evaluated the effects of physical activity on telomere length, the results remain controversial, both for analyses performed on muscle cells and leukocytes. Collins et al. (45) demonstrated a shortening of the telomeres of muscle cells in athletes and suggested a possible mechanism related to the impact of stress, promoted by physical exercise on the musculoskeletal system. On the other hand, Rae et al. (46) demonstrated that athletes and sedentary individuals presented similar telomere lengths in the cells of the musculoskeletal system. ...
OBJECTIVES:
Immunosenescence is an age-associated change characterized by a decreased immune response. Although physical activity has been described as fundamental for maintaining the quality of life, few studies have evaluated the effects of different levels of exercise on telomere length in aged populations. The present study aimed to analyze the effects of different levels of physical activity, classified by the Maximal oxygen consumption (VO2 max) values, on the telomere length of memory Cluster of differentiation (CD) CD4⁺(CD45ROneg and CD45RO⁺), effector CD8⁺CD28neg, and CD8⁺CD28⁺ T cells in aged individuals.
METHODS:
Fifty-three healthy elderly men (aged 65-85 years) were included in this study. Their fitness level was classified according to the American College of Sports Medicine (ACSM) for VO2 max (mL/kg/min). Blood samples were obtained from all participants to analyze the percentage of CD3, CD4, CD8, CD28⁺, naïve, and subpopulations of memory T cells by using flow cytometry. Furthermore, using the Flow-FISH methodology, the CD4⁺CD45RO⁺, CD4⁺CD45ROneg, CD8⁺CD28⁺, and CD8⁺CD28negT cell telomere lengths were measured.
RESULTS:
There was a greater proportion of effector memory T CD4⁺ cells and longer telomeres in CD8⁺CD28⁺ T cells in the moderate physical fitness group than in the other groups. There was a higher proportion of terminally differentiated memory effector T cells in the low physical fitness group.
CONCLUSION:
A moderate physical activity may positively influence the telomere shortening of CD28⁺CD8⁺T cells. However, additional studies are necessary to evaluate the importance of this finding with regard to immune function responses in older men.
... Although human athletes with overtraining syndrome have a higher frequency of critically short telomeres in their skeletal muscle (range: 0.7-5.8 kbp; Collins et al. 2003), individuals who regularly exercise without overtraining symptoms have longer muscle telomeres than their inactive peers and may have attenuated telomere shortening in middle age (Ponsot et al. 2008;Denham et al. 2016a). ...
Telomeres are genetically conserved nucleoprotein complexes located at the ends of chromosomes that preserve genomic stability. In large mammals, somatic cell telomeres shorten with age, owing to the end replication problem and lack of telomere‐lengthening events (e.g. telomerase and ALT activity). Therefore, telomere length reflects cellular replicative reserve and mitotic potential. Environmental insults can accelerate telomere attrition in response to cell division and DNA damage. As such, telomere shortening is considered one of the major hallmarks of ageing. Much effort has been dedicated to understanding the environmental perturbations that accelerate telomere attrition and therapeutic strategies to preserve or extend telomeres. As telomere dynamics seem to reflect cumulative cellular stress, telomere length could serve as a biomarker of animal welfare. The assessment of telomere dynamics (i.e. rate of shortening) in conjunction with telomere‐regulating genes and telomerase activity in racehorses could monitor long‐term animal health, yet it could also provide some unique opportunities to address particular limitations with the use of other animal models in telomere research. Considering the ongoing efforts to optimise the health and welfare of equine athletes, the purpose of this review is to discuss the potential utility of assessing telomere length in Thoroughbred racehorses. A brief review of telomere biology in large and small mammals will be provided, followed by discussion on the biological implications of telomere length and environmental (e.g. lifestyle) factors that accelerate or attenuate telomere attrition. Finally, the utility of quantifying telomere dynamics in horses will be offered with directions for future research.
... One possibility is that moderate amounts of regular activity may generate low levels of reactive oxygen species that induce adaptive increases in endogenous antioxidant defenses, while high amounts of activity may generate excess reactive oxygen species that counteract these defenses (Covas M, 2002;Poulsen HE, 1996;Powers S, 2008;Radak, Chung, & Goto, 2008). Although current evidence for this hypothesis is inconsistent, our results and those of others (Collins et al., 2003;Ludlow et al., 2008;Rae et al., 2010) may be consistent with this mechanism. Activity may also help to prevent insulin resistance (McTiernan, 2008), which has been associated with increased inflammation, oxidative stress, and telomere attrition (Al-Attas et al., 2010;Ceriello & Motz, 2004;Demissie et al., 2006;Gardner et al., 2005). ...
Telomeres are dynamic nucleoprotein structures at the ends of linear chromosomes that maintain the genomic integrity of a cell (Blackburn E, 2005). Telomere length (TL) shortens with age due to incomplete replication of DNA ends with each cell division. Telomere attrition can also occur through damage incurred by reactive oxygen species released in the inflammation process or by chemical alterations to purines and pyrimidines from oxidative stress. Once telomeres shorten to a critical length, the cell encounters a proliferation block where it either ceases to divide (cellular senescence) or undergoes programmed cell death (apoptosis). Thus, telomere length is considered a biological clock that limits the lifespan of a cell and an organism: people with short telomeres often have reduced lifespans.
Mutations in known telomere maintenance genes have been shown to cause inherited congenital disorders, such as dyskeratosis congenita, that typically exhibit very short telomeres (Savage S, 2010). Accelerated telomere shortening has also been implicated in complex diseases that cannot be wholly explained by genetics, e.g., cardiovascular disease, type 2 diabetes, and osteoarthritis (Aviv A, 2012; Kong C, 2013). Certain lifestyle factors, such as smoking, body mass index (Kim S, 2009; Valdes AM, 2005), and psychological stress (Epel ES, 2004), have been found to correlate with accelerated telomere shortening, likely because they increase DNA damage through oxidative stress. Recently, studies have identified lifestyle factors that can potentially protect telomeres. For example, people who lead a healthy lifestyle by increasing their physical activity (Du M, 2012), practicing meditation (Hoge EA, 2013), adhering to the Mediterranean diet (Crous-Bou M, 2014), and using multivitamins have been shown to have longer telomeres than those who do not adhere to such lifestyle changes.
Further, several studies show as an integration with geroprotective molecules such as quercetin, resveratrol and omega 3, positively interferes with aging processes by stimulating DNA repair and by inhibiting oxidative stress, inflammatory processes and telomeres shortening.
This review highlights the influence of lifestyle factors on key biological mechanisms of health and aging and the importance to preventative health.
... An explanation might be that moderate and regular exercise may confer positive adaptations providing a protective environment for telomeres. However, the positive effect of exercise is reduced when the training is too intense or prolonged (Collins et al., 2003;Kadi et al., 2008;Rae et al., 2010). It is conceivable that high-intensity bouts of both aerobic and resistance exercise cause telomere shortening by inducing muscle damage (Del Coso et al., 2017;Fernandez-Gonzalo et al., 2014) and increased cell proliferation and tissue turnover. ...
Satellite cells (SCs) form the resident stem cell population in the skeletal muscle tissue. While their function in mediating tissue regeneration after injury is well described, their role in the undamaged-, aging-, and exercising muscle is only starting to be unraveled. Although direct evidence linking the loss of SC function to the onset of age-related loss of muscle mass and function (i.e., sarcopenia) is currently lacking, satellite cells are increasingly seen as an important component for the decline of tissue function seen with aging. This is evident from the pertinent role of SCs in maintaining homeostasis, and in mediating remodeling- and repair-responses, in the skeletal muscle. This narrative review focuses on human studies, but includes cellular and animal models, to describe the role of SCs in different physiological scenarios relevant for human aging. The intrinsic and extrinsic mechanisms underlying age-induced alterations in the SC pool are discussed, with particular emphasis on the genomic modifications that accumulate in human SCs during a lifetime (i.e., somatic mutation-burden). Finally, the role of exercise as a potential countermeasure to age-induced SC alterations is explored in the different scenarios covered.
... This training has been shown to convey a host of physiological benefits including improvements in aerobic capacity and economy of motion (O'Toole & Douglas, 1995). But there is a growing body of evidence showing that the intense training and competition schedules carried out by endurance athletes can have negative effects at the cellular level (Collins et al., 2003). Accordingly, the hypothesis of this study was that TL is positively correlated with physiological parameters key to athletic performance and as such competitive triathlon training would preserve TL over regular moderate-intensity exercise. ...
Telomeres act as a mitotic clock and telomere-related senescence has been linked to age-related physiological decline. There is increasing evidence lifestyle factors can influence telomere length (TL). The purpose of this study was to determine the effect of competitive triathlon training on TL. Seven competitive male triathletes and seven recreationally active males participated in the study. Relative TL was measured using quantitative polymerase chain reaction. Physiological parameters key to athletic performance such as maximal oxygen intake, lactate threshold, and running economy were also measured. Triathletes had longer telomeres than the recreationally active (1.257 ± 0.028 vs. 1.002 ± 0.014; p < .0001). Positive association was found between TL and maximal oxygen intake, lactate threshold, and running economy (R2 = .677, .683, and .696, respectively). This study indicates that competitive triathlon training buffers against age-related telomere shortening, and there is a correlation between exercise behaviors, higher maximal oxygen intake, and TL.
... Leukocyte telomere length is a marker of biological age and accelerated telomere shortening occurs as a consequence of excessive psychological stress (Epel et al. 2004) and overtraining in humans (Collins et al. 2003). Leukocyte telomere length could serve as a sensitive biomarker of prodigious psychological stress, as it seems to accelerate telomere attrition across species (Bateson 2016). ...
Thoroughbred racehorses possess superior cardiorespiratory fitness levels and are at the pinnacle of athletic performance compared to other breeds of horses. Although equine athletes have undergone years of artificial selection for racing performance, musculoskeletal injuries and illnesses are common and concerns relating to animal welfare have been proposed. Leukocyte telomere length is indicative of biological age, and accelerated telomere shortening occurs with excess physical and psychological stress. This study was designed to explore the association between leukocyte telomere length, biological factors (age, sex and coat colour), training status, winnings and race history parameters. Blood was collected from 146 Thoroughbred racehorses from around Geelong, Victoria, Australia. DNA was extracted from leukocytes; telomere length was measured using qPCR and analysed in context with traits obtained from the Racing Australia website. Age was inversely correlated with telomere length (r = −0.194, P = 0.019). The oldest horses (≥11 years) in the highest age quartile possessed shorter telomeres compared to younger horses in the first, second and third quartiles (≤2, 3–5 and 6–10 years respectively; P < 0.05). No statistically significant associations were observed between telomere length and biological factors, training status, winnings or race history parameters in age‐adjusted analyses. The study findings suggest that Thoroughbred horses may undergo age‐related telomere shortening similar to other mixed breeds and humans. Despite concerns from some quarters regarding the welfare of racehorses, there was a lack of accelerated biological ageing observed in the present study, as indicated by leukocyte telomere length.
... Both strength and endurance trainings have been reported to have beneficial effect on muscle TL and/or TRFmin maintenance [21,22], even though the regular participation to sport appeared to show no marked association with muscle telomere length in young adults (22-27 years) [22] or even a detrimental effect in adult endurance athletes (mean age ¼ 42 ± 7 years) with respect age matched sedentary controls [23]. Differently from TL, that in skeletal muscle are considered to comprise TRF of the majority of postmitotic myonuclei incorporated into the fibres from birth, TRFmin has been proposed as a valuable parameter which includes TRF from satellite cells and from myonuclei newly incorporated [4,54], possibly indicating the extent of large exposure to training-induced muscle remodelling [23]. Several epidemiological and interventional studies have shown that physical activity may reduce telomere shortening in elderly and in patients by decreasing chronic inflammation and oxidative stress [19,20,55] and may be especially beneficial in term of protective effect on telomere length for those at risk for or living with chronic conditions with high oxidative stress and inflammation [8]. ...
In skeletal muscle, which mainly contains postmitotic myonuclei, it has been suggested that telomere length remains roughly constant throughout adult life, or shortens in response to physiopathological conditions in muscle diseases or in the elderly. However, telomere length results from both the replicative history of a specific tissue and the exposure to environmental, DNA damage-related factors, therefore the predictive biological significance of telomere measures should combine the analysis of the various interactive factors. In the present study we analysed any relationship between telomere length [mean and minimum terminal restriction fragment (TRF) length] chronological age, oxidative damage (4-HNE, protein carbonyls), catalase activity and heat shock proteins expression (αB-crystallin, Hsp27, Hsp90) in semitendinous muscle biopsies of 26 healthy adult males between 20 and 50 years of age, also exploring the influence of regular exercise participation. The multiple linear regression analysis identified age, 4-HNE, catalase and training status as significant independent variables associated with telomere length and jointly accounting for ~ 30–36% of interindividual variation in mean and/or minimum TRF length. No association has been identified between telomere length and protein carbonyl, αB-crystallin, Hsp27 and Hsp90, as well as between age and the variables related to stress response. Our results showed that skeletal muscle from healthy adults displays an age-dependent telomere attrition and that oxidized environment plays an age-independent contribution, partially influenced by exercise training.
... Lastly, this investigation has included seven genotype polymorphisms while other genes such as the chemokine ligand 2 (CCL2) and its receptor chemokine receptor 2 (CCR2; [43]), the LPIN1 [44], the IL1B gene and/or the osteopontin gene [31] have also been identified as candidate genes for an elevated CK response and an exaggerated damage response to exercise. Even, DNA telomere lengths can be associated to the level of exercise-induced muscle damage [45]. Thus, these and other genetic variants that are likely to appear in the foreseeable future can also help to explain variations in CK response. ...
Purpose
Exertional rhabdomyolysis can occur in individuals performing various types of exercise but it is unclear why some individuals develop this condition while others do not. Previous investigations have determined the role of several single nucleotide polymorphisms (SNPs) to explain inter-individual variability of serum creatine kinase (CK) concentrations after exertional muscle damage. However, there has been no research about the interrelationship among these SNPs. The purpose of this investigation was to analyze seven SNPs that are candidates for explaining individual variations of CK response after a marathon competition (ACE = 287bp Ins/Del, ACTN3 = p.R577X, CKMM = NcoI, IGF2 = C13790G, IL6 = 174G>C, MLCK = C37885A, TNFα = 308G>A).
Methods
Using Williams and Folland’s model, we determined the total genotype score from the accumulated combination of these seven SNPs for marathoners with a low CK response (n = 36; serum CK <400 U·L⁻¹) vs. marathoners with a high CK response (n = 31; serum CK ≥400 U·L⁻¹).
Results
At the end of the race, low CK responders had lower serum CK (290±65 vs. 733±405 U·L⁻¹; P<0.01) and myoglobin concentrations (443±328 vs. 1009±971 ng·mL⁻¹, P<0.01) than high CK responders. Although the groups were similar in age, anthropometric characteristics, running experience and training habits, total genotype score was higher in low CK responders than in high CK responders (5.2±1.4 vs. 4.4±1.7 point, P = 0.02).
Conclusion
Marathoners with a lower CK response after the race had a more favorable polygenic profile than runners with high serum CK concentrations. This might suggest a significant role of genetic polymorphisms in the levels of exertional muscle damage and rhabdomyolysis. Yet other SNPs, in addition to exercise training, might also play a role in the values of CK after damaging exercise.
... Sample weights were re-weighted to account for the use of combined NHANES cycles. 21 Information on the use of sample weights to generate population weighted estimates is available elsewhere. 22 Linear regression analysis was used to examine cholesterol (TC, HDL-C, TC/HDL-C and triglyceride) differences across the respective activity status groups (i.e., inactive vs. active across the different BMI/WC combinations), with results stratified by gender. ...
Background:
The purpose of this study was to investigate if those who are physically active,compared to physically inactive, have better cholesterol profiles across different combinations of body mass index (BMI) and waist circumference (WC).
Methods:
Data from the 1999-2006 National Health and Nutrition Examination Survey (NHANES) were used (N = 16 095). Cholesterol parameters included total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), TC/HDL-C ratio, triglycerides and at herogenic index(Log10 [triglycerides/HDL-C]). Physical activity (PA) was assessed via self-report, with BMI and WC objectively measured. Cholesterol concentrations of 6 combinations of BMI and WC were evaluated among active and inactive participants. Multivariable linear regression analysis was utilized.
Results:
Findings were not consistent across sex. There was little evidence to suggest an association of PA on TC across varying BMI and WC combinations. For example, among those who had an obese BMI and high WC, inactive participants did not have different TC level when compared to active participants (β = -1.2; 95% CI: -3.9-1.5, P = 0.38). There was evidence to suggest a favorable association of PA on HDL-C, triglycerides and at herogenic index across varying BMI and WC combinations. For example, among those who had an obese BMI and high WC, inactive (vs. active) participants had a lower HDL-C (βadjusted = -1.6, P < 0.01). When considering either gender, there was sufficient evidence to suggest a favorable association of PA on at least one of the evaluated cholesterol parameters for each of the BMI/WC combinations with the exception of normal BMI and high WC.
Conclusion:
Except for those having normal weight central obesity, PA is favorably associated with cholesterol parameters across various combinations of BMI and WC.
... Otherwise, habitually trained animals showed amelioration of glycaemic and lipidic dysmetabolism, accompanied by a remarkable reduction of inflammatory and oxidative markers [265]. Athletes performing high intensity physical training displayed a dysregulation of the inflammatory system that, in turn, led to an excessive delayed-onset muscle soreness, muscle stiffness, reduction in muscle strength and increased CK activity [266,267]. Uncontrolled proliferation of inflammatory cells and increased oxidative stress can exacerbate muscle damage and slow down muscle healing and regeneration [268]. Moreover, a repeated harmful stimulus on muscle cells may develop a state of low-grade chronic inflammation [268]. ...
Background:
Oxidative stress is involved in different pathophysiological states, such as aging, inflammatory, cardiovascular and neurodegenerative diseases, by damaging several cellular and tissue components including proteins, DNA and lipids. On the other hand, free radicals generated during physical activity are important modulators of muscle contraction, antioxidant protection, and oxidative damage repair. Indeed, ROS, generated during physical activity, are likely main mediators of antioxidant molecules upregulation, as reflected by increased glutathione reductase levels after exercise training.
Methods:
The aim of this review is to summarize the main mechanisms responsible for ROS-dependent adaptations to exercise training.
Results:
Regular moderate exercise seems to counteract oxidative stress-related detrimental changes and to promote a healthy lifestyle. Conversely, acute and strenuous exercise can generate an excess of free radicals production. Moreover, regular habitual physical activity is related to reduced risk of coronary heart disease and death, whereas vigorous exercise has been shown to favoursudden cardiac death in sedentary individuals with preexisting vascular disease. New specific markers of mitochondrial or ER dysfunction may be better clues of oxidative stress, and their application to clinical practice may help set up the optimal dose, intensity and modality of exercise training for every single subject.
Conclusion:
The relationship between exercise and oxidative stress is extremely complex, depending on the mode, intensity, and duration of exercise. These conflicting effects and outcomes may be explained by the hormesis theory, in which low doses of an agent that is detrimental at high doses, induces an adaptive beneficial effect on the cells or organism.
... In cultured satellite cells that were isolated from the skeletal muscle of young adults, a telomeric loss of 155 bp per population doubling was previously reported (29), and differences of 100-200 bp can be detected in whole muscle homogenate (25) as a reference for the mean (nonsignificant) change of ;500 bp observed in the current study. Abnormally short minimum telomere lengths have been found in the skeletal muscle of endurance athletes with exerciseassociated chronic fatigue (30), and an inverse relationship was found between the load imposed on muscles and minimum telomere length in the skeletal muscle of experienced powerlifters (31), which indicates that minimum telomere length could be a sensitive indicator of the regenerative capacity of muscle. However, in the latter study, no differences were found between powerlifters and controls, which suggests that in vivo telomere shortening does not occur in heavily loaded skeletal muscle (31,32) or even in the skeletal muscle of patients with ongoing cycles of degeneration and regeneration (33). ...
With this study we investigated the role of nonsteroidal anti-inflammatory drugs (NSAIDs) in human skeletal muscle regeneration. Young men ingested NSAID [1200 mg/d ibuprofen (IBU)] or placebo (PLA) daily for 2 wk before and 4 wk after an electrical stimulation-induced injury to the leg extensor muscles of one leg. Muscle biopsies were collected from the vastus lateralis muscles before and after stimulation (2.5 h and 2, 7, and 30 d) and were assessed for satellite cells and regeneration by immunohistochemistry and real-time RT-PCR, and we also measured telomere length. After injury, and compared with PLA, IBU was found to augment the proportion of ActiveNotch1(+) satellite cells at 2 d [IBU, 29 ± 3% vs. PLA, 19 ± 2% (means ± sem)], satellite cell content at 7 d [IBU, 0.16 ± 0.01 vs. PLA, 0.12 ± 0.01 (Pax7(+) cells/fiber)], and to expedite muscle repair at 30 d. The PLA group displayed a greater proportion of embryonic myosin(+) fibers and a residual ∼2-fold increase in mRNA levels of matrix proteins (all P < 0.05). Endomysial collagen was also elevated with PLA at 30 d. Minimum telomere length shortening was not observed. In conclusion, ingestion of NSAID has a potentiating effect on Notch activation of satellite cells and muscle remodeling during large-scale regeneration of injured human skeletal muscle.-Mackey, A. L., Rasmussen, L. K., Kadi, F., Schjerling, P., Helmark, I. C., Ponsot, E., Aagaard, P., Durigan, J. L. Q., Kjaer, M. Activation of satellite cells and the regeneration of human skeletal muscle are expedited by ingestion of nonsteroidal anti-inflammatory medication.
... Conversely, the increased oxidative stress associated with aging may facilitate telomere shortening, as older mobile adults have reduced ROS and longer leukocyte and thigh skeletal muscle telomeres than their immobile peers [158]. Endurance athletes, however, with exercise-associated fatigue, possess short muscle telomeres [159]. Healthy athletes have been documented to have longer [156] or comparable [160] muscle telomere lengths relative to sedentary controls. ...
Telomeres are tandem repeat DNA sequences located at distal ends of chromosomes that protect against genomic DNA degradation and chromosomal instability. Excessive telomere shortening leads to cellular senescence and for this reason telomere length is a marker of biological age. Abnormally short telomeres may culminate in the manifestation of a number of cardio-metabolic diseases. Age-related cardio-metabolic diseases attributable to an inactive lifestyle, such as obesity, type 2 diabetes mellitus and cardiovascular disease, are associated with short leukocyte telomeres. Exercise training prevents and manages the symptoms of many cardio-metabolic diseases whilst concurrently maintaining telomere length. The positive relationship between exercise training, physical fitness and telomere length raises the possibility of a mediating role of telomeres in chronic disease prevention via exercise. Further elucidation of the underpinning molecular mechanisms of how exercise maintains telomere length should provide crucial information on how physical activity can be best structured to combat the chronic disease epidemic and improve the human health span. Here, we synthesise and discuss the current evidence on the impact of physical activity and cardiorespiratory fitness on telomere dynamics. We provide the molecular mechanisms with a known role in exercise-induced telomere length maintenance and highlight unexplored, alternative pathways ripe for future investigations.
... Especially in early life, the impact of inheritance on telomere length is strong, but it seems to diminish by age (Svenson et al., 2011). Shorter telomeres have been associated with increased incidence of several chronic non-communicable diseases and with shorter life span (Ludlow and Roth 2011; Shammas, 2011; Salpea and Humphries, 2010; Wong and Collins 2003). Several factors including smoking , obesity and an unhealthy diet, all conditions associated with an increase in oxidative stress and inflammation, have been linked with telomere shortening (Crous-Bou et al., 2014; Ornish et al., 2013; Shammas, 2011; Tiainen et al., 2012; Woo et al., 2010;). ...
A career as an elite-class male athlete seems to improve metabolic heath in later life and is also associated with longer life expectancy. Telomere length is a biomarker of biological cellular ageing and could thus predict morbidity and mortality. The main aim of this study was to assess the association between vigorous elite-class physical activity during young adulthood on later life leukocyte telomere length (LTL). The study participants consist of former male Finnish elite athletes (n = 392) and their age-matched controls (n = 207). Relative telomere length was determined from peripheral blood leukocytes by quantitative real-time polymerase chain reaction. Volume of leisure-time physical activity (LTPA) was self-reported and expressed in metabolic equivalent hours. No significant difference in mean age-adjusted LTL in late life (p = 0.845) was observed when comparing former male elite athletes and their age-matched controls. Current volume of LTPA had no marked influence on mean age-adjusted LTL (p for trend 0.788). LTL was inversely associated with age (p = 0.004).Our study findings suggest that a former elite athlete career is not associated with LTL later in life. Key pointsA career as an elite-class athlete is associated with improved metabolic health in late life and is associated with longer life expectancy.A career as an elite-class athlete during young adulthood was not associated with leukocyte telomere length in later life.Current volume of leisure-time physical activity did not influence telomere length in later life.
... Potentially reflecting systemic oxidative stress and inflammation (10,51), short LTL is linked with various cardiometabolic diseases (2,4,13,18,19,21,46,47). Physical activity (PA) may help attenuate age-related diseases, as previous research (8,14,20,(23)(24)(25)34,37,39,44,49) demonstrates that physically active adults have longer mean LTL. However, some studies show no relation (22,32,33,40,45,48,52), with others reporting an inverted U relation (9,31,43) (review articles, see Ludlow (29,30)). ...
Short leukocyte telomere length (LTL) has become a hallmark characteristic of aging. Some, but not all evidence suggests that physical activity may play an important role in attenuating age-related diseases and may provide a protective effect for telomeres. The purpose of this study was to examine the association between physical activity and LTL in a national sample of U.S. adults from the National Health and Nutrition Examination Survey (NHANES).
NHANES data from the 1999-2002 (n = 6,503; 20-84 yrs) were used. 4 self-report questions related to movement based behaviors (MBB) were assessed. The 4 MBB included whether individuals participated in moderate-intensity physical activity (MPA), vigorous-intensity physical activity (VPA), walking/cycling for transportation, and muscle strengthening activities (MSA). A MBB index variable was created by summing the number of MBB each individual engaged in (range: 0-4).
A clear dose-response relationship was observed between MBB and LTL; across the LTL tertiles, respectively, the mean number of MBB was 1.18, 1.44, and 1.54 (Ptrend<0.001). After adjustments (including age), and compared to those engaging in 0 MBB, those engaging in 1, 2, 3, and 4 MBB, respectively, had a 3% (p=0.84), 24% (p=0.02), 29% (p=0.04), and 52% (p=0.004) reduced odds of being in the lowest (vs. highest) tertile of LTL; MBB was not associated with being in the middle (vs. highest) tertile of LTL.
Greater engagement in MBB was associated with reduced odds of being in the lowest LTL tertile.
... The research of Collins et al. (2003) describes the negative effect of excessive physical stress on telomere length. The study compared 13 athletes with the overtraining syndrome and 13 healthy athletes. ...
Telomeres are the chromosomal ends to preserve DNA integrity and chromosomal stability. Shortening of telomere length induces the cell damage. Human telomere length is influenced by both genetic and environmental factors and it is closely related to aging and the development of some diseases. The paper summarizes the results of the work focused on the impact of lifestyle, particularly exercise and diet, to change the length of telomeres. These works have shown that various forms of exercise and diet modify the length of telomeres. It is possible to prevent the mass aging of cells and the emergence of many diseases due to longer and more stable telomeres. Our study suggests that an appropriate exercise and a reasonable diet can be effective nonpharmacological tools to slow down the aging process. However, the evaluation of the efficacy of such approaches is extremely difficult because the measurement of effects on fitness and lifespan would require long lasting clinical studies. The development of molecular markers which not only indicate a biological age of the individual but are also sensitive to intervention and lifestyle factors would represent an important step for the future development of antiaging therapies.
... When satellite cells were heavily recruited for regenerative events, as in the skeletal muscle of athletes, telomere length was found to be either significantly shortened or maintained, and was even found to be longer compared to that in non-trained individuals. Evidence suggested that physical activity may preserve or lengthen telomeres, although exhaustive exercise, such as that performed by athletes, may shorten the telomeres in skeletal muscle (23). Moreover, exercise induces autophagy (24) also demonstrated that SRM may exert multiple effects on the body, including pain reduction, tissue regeneration, immune system modulation and possible telomere lengthening. ...
Adult stem cells are distributed throughout the human body and are responsible to a great extent for the body's ability to maintain and heal itself. Accumulating data since the 1990s regarding stem cells have demonstrated that the beneficial effects of stem cells are not restricted to their ability to differentiate and are more likely due to their ability to release a multitude of molecules. Recent studies indicated that ≤80% of the therapeutic benefit of adult stem cells is manifested by the stem cell released molecules (SRM) rather than the differentiation of the stem cells into mature tissue. Stem cells may release potent combinations of factors that modulate the molecular composition of the cellular milieu to evoke a multitude of responses from neighboring cells. A multitude of pathways are involved in cellular and tissue function and, when the body is in a state of disease or trauma, a multitude of pathways are involved in the underlying mechanisms of that disease or trauma. Therefore, stem cells represent a natural systems-based biological factory for the production and release of a multitude of molecules that interact with the system of biomolecular circuits underlying disease or tissue damage. Currently, efforts are aimed at defining, stimulating, enhancing and harnessing SRM mechanisms, in order to develop systems-based methods for tissue regeneration, develop drugs/biologics or other therapeutics and enhance the release of SRM into the body for natural healing through proper dietary, exercise and other lifestyle strategies.
Exercise transiently impacts the expression, regulation, and activity of TERT/telomerase to maintain telomeres and protect the genome from insults. By protecting the telomeres (chromosome ends) and the genome, telomerase promotes cellular survival and prevents cellular senescence. By increasing cellular resiliency, via the actions of telomerase and TERT, exercise promotes healthy aging.
The aim of this systematic review and meta-analysis was 1) to assess whether master athletes have longer telomeres than age-matched non-athletes and 2) discuss possible underlying mechanisms underlying telomere length preservation in master athletes. A literature search was performed in PubMed, Web of Science, Scopus and SPORTDiscus up to August 2020. Only original articles published in peer-reviewed journals that compared telomere length between master athletes and aged-matched non-athletes were included. Eleven studies fulfilled eligibility criteria and were included in the final analysis. Overall, 240 master athletes (51.9±7.5 years) and 209 age-matched non-athletes (50.1±9.1 years) were analyzed. Master athletes had been participating in high-level competitions for approximately 16.6 years. Pooled analyses revealed that master athletes had longer telomeres than aged-matched non-athletes (SMD=0.89; 95% CI=0.45 to 1.33; p<0.001). Master athletes showed lower pro-oxidant damage (SMD=0.59; 95% CI=0.26 to 0.91; p<0.001) and higher antioxidant capacity (SMD=-0.46; 95% CI=-0.89 to −0.03; p=0.04) than age-matched non-athletes. Further, greater telomere length in master athletes is associated with lower oxidative stress and chronic inflammation, and enhanced shelterin protein expression and telomerase activity. In conclusion, 1) master athletes have longer telomeres than age-matched non-athletes, which may be the result of 2) lower levels of oxidative stress and chronic inflammation, and elevated shelterin expression and telomerase activity.
In dogs, decreasing telomere length is a biomarker for cellular aging. On a systemic level, aging affects the locomotor system in particular, leading to restricted joint mobility. As aging is thought to be related to oxidative stress, it may be counteracted by a diet enriched with antioxidants, mitochondrial cofactors and omega-3 fatty acids. This randomized, blinded and placebo-controlled study examined the influence of an accordingly enriched diet compared to a control diet on 36 young and 38 old shepherd dogs. At the outset, after 3 and after 6 months, mean and minimum telomere lengths were measured. Furthermore, minimum and maximum joint angles and range of motion of the shoulder, elbow, carpal, hip, stifle and tarsal joints were measured by computer-assisted gait analysis. A positive influence of the enriched diet on old dogs could be verified for minimum telomere length and all three parameters of the shoulder joint on the side with the higher vertical ground reaction force after 6 months. In the other joints there were less significant differences; in some cases they indicated a contrary influence of the enriched diet on young dogs, probably due to its reduced protein content. The greater effect of the enriched diet on minimum than on mean telomere length may be due to the higher preference of telomerase for short telomeres. The greater effect on shoulder joint mobility is explained by the greater influence of musculature and connective tissue in this joint. For elderly dogs it is advisable to feed these nutritional supplements.
Aging has been intensely studied by scientists of all times. Although many theories
have been proposed to explain the causes and processes involved in aging, the
approach that aging takes place in four levels has lately gained attention. The theory
supports that each level represents a biological scale, and alterations of the functions
in each level lead to the phenotype of aging and age-related diseases (Zhang et al.,
2015). These four layers would be: (1) general physical deterioration of the organism;
(2) dysfunction of systems involved in regulation of body physiology, that is, the
immune, metabolic, and endocrine systems; (3) altered cellular function, including
increases in the number of senescent cells and in the production of reactive oxygen species (ROS), loss in the ability of endoplasmic reticulum response to misfolded proteins
and reduction in the ability to degrade specific molecules using the ubiquitinproteasome
and autophagolysosome systems; and (4) failure to maintain biomolecules
(Zhang et al., 2015). At cellular level, six factors have been considered responsible for
the process of cellular senescence, namely (1) telomere shortening, (2) DNA doublestrand
breaks and DNA damage response, (3) epigenetic alterations, (4) aneuploidy,
(5) oxidative stress and mitochondrial dysfunction, and (6) inflammation, energy sensing,
and altered metabolic regulation. In this chapter, we will
focus on the mechanisms associated with telomere shortening in aging and we will
describe the potentially beneficial effects of physical activity.
Telomeres are the heterochromatic repeat regions at the ends of eukaryotic chromosomes that maintain the genomic integrity of a cell. Telomere shortening with increasing age is a part of the normal ageing process. However, factors such as inflammation, oxidative stress and other genotoxic stressors may also increase the rate of telomere attrition, leading to telomere dysfunction-mediated cellular senescence and accelerating the ageing process. Once telomeres shorten to a critical length, the cell encounters a proliferation block where it either ceases to divide or undergoes programmed cell death. Thus, telomere length is considered a biological clock that limits the lifespan of a cell and an organism: people with short telomeres often have reduced lifespan. Certain lifestyle factors such as smoking, body mass index and psychological stress have been found to correlate with accelerated telomere shortening, likely because they increase DNA damage through oxidative stress. Recently, studies have identified lifestyle factors that can potentially protect telomeres. For example, people who lead a healthy lifestyle by increasing their physical activity, practising meditation, adhering to the Mediterranean diet and using multivitamins have been shown to have longer telomeres than those who do not adhere to such lifestyle changes. This chapter highlights the influence of lifestyle factors on key biological mechanisms associated with telomere maintenance.
Muscle injuries are common, especially in sports and cumulative trauma disorder, and their repair is influenced by free radical formation, which causes damages in lipids, proteins and DNA. Oxidative DNA damages are repaired by base excision repair and nucleotide excision repair, ensuring telomeric and genomic stability. There are few studies on this topic in skeletal muscle cells. This review focuses on base excision repair and nucleotide excision repair, telomere regulation and how telomeric stabilization influences healthy muscle, injured muscle, exercise, and its relationship with aging. In skeletal muscle, genomic stabilization and telomere regulation seem to play an important role in tissue health, influencing muscle injury repair. Thus, therapies targeting mechanisms of DNA repair and telomeric regulation could be new approaches for improving repair and prevention of skeletal muscle injuries in young and old people.
PURPOSE This study was performed to investigate the effect of maternal exercise on cardiac and skeletal muscle telomere length and telomere repeat binding factor 2 (TRF2) in rat offspring. METHODS Sprague-Dawley rats (10 wk, N=21) were randomly assigned into control (CON), exercise during pregnancy (ExD), and exercise before and during pregnancy (ExBD) groups. Maternal training was performed on a rodent treadmill for 1 hour at 60-75% VO2max for 3 weeks (5 d/w) before and during pregnancy respectively. The offspring were sacrificed at birth and telomere length and TRF2 expression were measured with cardiac and skeletal muscle samples. RESULTS CON group had significantly longer telomere length (p=.011, p=.049) and higher TRF2 expression (p=.011, p=.002) than other two groups in skeletal muscle of offspring. In the cardiac muscle, CON group showed longer telomere length compared with ExD group in offspring (p=.001). CONCLUSIONS Intense maternal exercise before or during pregnancy may negatively affect their new offspring’s cardiac and skeletal muscle telomere length and TRF2 expression.
Our understanding of satellite cells, now known to be the obligate stem cells of skeletal muscle, has increased dramatically in recent years due to the introduction of new molecular, genetic, and technical resources. In addition to their role in acute repair of damaged muscle, satellite cells are of interest in the fields of aging, exercise, neuromuscular disease, and stem cell therapy, and all of these applications have driven a dramatic increase in our understanding of the activity and potential of satellite cells. However, many fundamental questions of satellite cell biology remain to be answered, including their emergence as a specific lineage, the degree and significance of heterogeneity within the satellite cell population, the roles of their interactions with other resident and infiltrating cell types during homeostasis and regeneration, and the relative roles of intrinsic vs extrinsic factors that may contribute to satellite cell dysfunction in the context of aging or disease. This review will address the current state of these open questions in satellite cell biology.
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Telomeres are strands of non coding DNA at the ends of chromosomes that have the primary function to protect DNA from damage and maintain chromosomal stability. Physical exercise will increase the antioxidant activity can increase telomere proteins, lengthen telomeres and or protein networks associated with telomere so that the telomere remains long, or stopping telomere shortening. Telomere length was also associated with age. The purpose of the research was to determine telomere length of leukocyte cells in the KONI athletes in Jakarta,
The research method is descriptive, by measuring telomere length using quantitative PCR on leukocyte cells. Samples are KONI athletes from several sports, including men and women athletes, with ages between 15-20 years. Used a control group (not athletes) is students of the Faculty of Medicine, University of YARSI. The results showed that there was no significant difference (p> 0.05) between telomere length group of athletes with the control group in both sexes. Similarly, telomere length between athlete male with female athletes also showed no significant difference (p> 0.05). It was concluded that physical exercise in athletes KONI at the age of 15- 20 years had no effect on telomere length in leukocytes. The results of this study provide information about the telomere length in Indonesian athletes at an early age</p
Over the past 50 years scientists have made substantial progress in understanding the processes at the cellular and molecular levels. Yet many ongoing processes in the cell still remain unclear. Thanks to the unique properties of telomeres, end segments of chromosomes are at the forefront of research. Not all processes that take place in these structures have been explained, but they present possible potential to protect the cells against aging, as well as in the understanding and treatment of tumour growth. Telomeres are the chromosomal ends to preserve DNA integrity and chromosomal stability. Shortening of telomere length induces cell damage. Human telomere length is influenced by both genetic and environmental factors and it is closely related to aging and the development of certain diseases. The study summarizes the results of work focused on the impact of exercise and diet on the length of telomeres. These studies have shown that various forms of exercise and diet modify the length of telomeres.
Sportive performance may be describe as all of the efforts put forth to succeed during fulfilling an obligatory athletic duty. One of the most important factors that affect sportive performance is genetic differences. Among these, mutations, polymorphism, epigenetic factors and chimerism lead. Mutations are permanent changes in genetic build and seen less than 1% of population. On the other hand, polymorphisms are seen more than 1% of population and are the existence of two or more different phenotype in the same kind of population. Epigenetic factors in which there is no change in DNA chain, while at the same time, it can change gene activation. However, chimerism is a single organism that is composed of two or more different populations of genetically distinct cells that originated from different zygotes involved in pregnancy. As a conclusion, it is found out that sportive performance may change due to the individuals’ phenotype feature changes caused by differences in genetic substructure.
Background:
Physical activity is known to relieve the metabolic complications of polycystic ovary syndrome (PCOS), and exercise is also associated with telomere biology. We investigated the changes induced by progressive resistance training (PRT) in telomere content and metabolic disorder in women with PCOS and controls.
Participants and methods:
Forty-five women with PCOS and 52 healthy women aged 18 to 37 years were submitted to PRT. A linear periodization of PRT was prepared based on a trend of decreasing volume and intensity throughout the training period. The volunteers performed PRT 3 times a week for 4 months. The participants' physical characteristics and hormonal concentrations were measured before and after PRT, as telomere content that was measured using quantitative real-time polymerase chain reaction.
Results:
Briefly, Progressive resistance training reduced waist circumference, body fat percentage, plasma testosterone and sex hormone-binding globulin concentrations, glycemia, and free androgen index. Fasting insulin and insulin resistance index were greater in women with PCOS. Androstenedione and homocysteine increased after PRT. There were no differences in telomere content between controls (0.96 ± 0.3 before vs 0.85 ± 0.21 after) and women with PCOS (0.94 ± 0.33 before vs 0.88 ± 0.39 after). Adjusted analysis showed telomere shortening after PRT in all women (0.95 ± 0.31 before vs 0.86 ± 0.31 after; P = .03). In women with PCOS, increased homocysteine levels were related to telomere reduction and increased androstenedione was positively correlated with telomere content after PRT.
Conclusions:
Progressive resistance training had positive effects on the hormonal and physical characteristics of women with PCOS and controls, but telomere content was reduced and homocysteine level increased in all participants.
SOUHRN Během posledních 50 let věda významně pokročila v poznání procesů na buněčné a molekulární úrovni. I přesto zůstává celá řada dějů probíhajících v buňce stále neobjasněna. Do popředí zájmu mnoha vědců se díky jedinečným vlastnostem dostaly koncové úseky chromozomů neboli telomery. Zdaleka ne všechny pochody probíhající v těchto strukturách jsou vysvětleny, i tak ale představují možný potenciál v ochraně buněk před stárnutím, nebo také v poznání a léčbě nádorových bujení. Telomery jsou specializované struktury chromozomů, které chrání integritu DNA a stabilitu chromozomů. Zkracováním délky telomer se buňky poškozují. Délka telomer člověka je ovlivněna genetickými i environmentálními faktory a má těsný vztah ke stárnutí a rozvoji některých chorob. Studie shrnuje výsledky prací zabývajících se zejména vlivem pohybové aktivity a výživy na změnu délky telomer. Zahraniční studie naznačují, že lidé věnující se pravidelně pohybové aktivitě mají oproti svým vrstevníkům se sedavým způsobem života výrazně delší telomery. Také výzkumy s některými složkami stravy vyznačující se vysokou antioxidační aktivitou poukazují na možnost existence vztahu zdravé výživy a delších telomer. Díky delším a stabilnějším telomerám je možné předcházet hromadnému stárnutí buněk a zamezit vzniku celé řady nemocí.
Physical activity has long been touted as a means of reducing susceptibility to age-related disease and multiple studies have shown reduced mortality rates in individuals with a lifestyle including regular exercise. A variety of mechanisms for how physical activity reduces age-related diseases have been explored and multiple, redundant explanatory mechanisms are likely to emerge. Evidence has emerged that physical activity may impact directly on telomere biology, one of the primary theories of cellular aging. Telomeres are located at the ends of chromosomes and as cells divide, incomplete DNA replication results in telomere shortening; once shortening reaches a critical threshold, cell senescence results. Investigators hypothesize that part of the favorable influence of physical activity on mortality rates and age-related disease occurs through a direct impact on telomere biology, including delaying rates of telomere shortening. The present review examines key recent findings in this area and explores some of the unanswered questions and future directions for the field.
During periods of intensified physical training, reactive oxygen species (ROS) release may exceed the protective capacity of the antioxidant system and lead to dysregulation within the inflammatory and neuroendocrinological systems. Consequently, the efficacy of exogenous antioxidant supplementation to maintain the oxidative balance in states of exercise stress has been widely investigated. The aim of this review was to (1) collate the findings of prior research on the effect of intensive physical training on oxidant-antioxidant balance; (2) summarise the influence of antioxidant supplementation on the reduction-oxidation signalling pathways involved in physiological adaptation; and (3) provide a synopsis on the interactions between the oxidative, inflammatory and neuroendocrinological response to exercise stimuli. Based on prior research, it is evident that ROS are an underlying aetiology in the adaptive process; however, the impact of antioxidant supplementation on physiological adaptation remains unclear. Equivocal results have been reported on the impact of antioxidant supplementation on exercise-induced gene expression. Further research is required to establish whether the interference of antioxidant supplementation consistently observed in animal-based and in vivo research extends to a practical sports setting. Moreover, the varied results reported within the literature may be due to the hormetic response of oxidative, inflammatory and neuroendocrinological systems to an exercise stimulus. The collective findings suggest that intensified physical training places substantial stress on the body, which can manifest as an adaptive or maladaptive physiological response. Additional research is required to determine the efficacy of antioxidant supplementation to minimise exercise-stress during intensive training and promote an adaptive state.
When human fibroblasts from different donors are grown in vitro, only a small fraction of the variation in their finite replicative capacity is explained by the chronological age of the donor. Because we had previously shown that telomeres, the terminal guanine-rich sequences of chromosomes, shorten throughout the life-span of cultured cells, we wished to determine whether variation in initial telomere length would account for the unexplained variation in replicative capacity. Analysis of cells from 31 donors (aged 0-93 yr) indicated relatively weak correlations between proliferative ability and donor age (m = -0.2 doubling per yr; r = -0.42; P = 0.02) and between telomeric DNA and donor age (m = -15 base pairs per yr; r = -0.43; P = 0.02). However, there was a striking correlation, valid over the entire age range of the donors, between replicative capacity and initial telomere length (m = 10 doublings per kilobase pair; r = 0.76; P = 0.004), indicating that cell strains with shorter telomeres underwent significantly fewer doublings than those with longer telomeres. These observations suggest that telomere length is a biomarker of somatic cell aging in humans and are consistent with a causal role for telomere loss in this process. We also found that fibroblasts from Hutchinson-Gilford progeria donors had short telomeres, consistent with their reduced division potential in vitro. In contrast, telomeres from sperm DNA did not decrease with age of the donor, suggesting that a mechanism for maintaining telomere length, such as telomerase expression, may be active in germ-line tissue.
The terminus of a DNA helix has been called its Achilles' heel. Thus to prevent possible incomplete replication and instability of the termini of linear DNA, eukaryotic chromosomes end in characteristic repetitive DNA sequences within specialized structures called telomeres. In immortal cells, loss of telomeric DNA due to degradation or incomplete replication is apparently balanced by telomere elongation, which may involve de novo synthesis of additional repeats by novel DNA polymerase called telomerase. Such a polymerase has been recently detected in HeLa cells. It has been proposed that the finite doubling capacity of normal mammalian cells is due to a loss of telomeric DNA and eventual deletion of essential sequences. In yeast, the est1 mutation causes gradual loss of telomeric DNA and eventual cell death mimicking senescence in higher eukaryotic cells. Here, we show that the amount and length of telomeric DNA in human fibroblasts does in fact decrease as a function of serial passage during ageing in vitro and possibly in vivo. It is not known whether this loss of DNA has a causal role in senescence.
Chronic fatigue in the athletic population is a common but difficult diagnostic challenge for the sports physician. While a degree of fatigue may be normal for any athlete during periods of high-volume training, the clinician must be able to differentiate between this physiological fatigue and more prolonged, severe fatigue which may be due to a pathological condition. As chronic fatigue can be the presenting symptom of many curable and harmful diseases, medical conditions which cause chronic fatigue have to be excluded. The clinician must then be able to differentiate between chronic fatigue associated with training or chronic fatigue from other medical causes, and also between the chronic fatigue syndrome and the overtraining syndrome. Once the clinician has excluded all of the above medical conditions which cause chronic fatigue in athletes, a significant proportion of fatigued athletes remain without a diagnosis. Novel data indicate that skeletal muscle disorders may play a role in the development of symptoms experienced by the athlete with chronic fatigue. The histological findings from muscle biopsies of athletes suffering from the 'fatigued athlete myopathic syndrome' are presented. We have designed a clinical approach to the diagnosis and work-up of the athlete presenting with chronic fatigue. The strength of this approach is that it hinges on the participation of a multidisciplinary team in the diagnosis and management of the athlete with chronic fatigue. The athlete, coach, dietician, exercise physiologist and sport psychologist all play an important role in enabling the physician to make the correct diagnosis.
Regeneration of muscle fibers following damage requires activation of quiescent satellite cells, their proliferation and finally their differentiation and fusion into multinucleated myotubes, which after maturation will replace the damaged fiber. The regenerative potential of human skeletal muscle will be determined, at least partly, by the proliferative capacity of the satellite cells. In this study, we have measured the proliferative life span of human satellite cells until they reach senescence. These analyses were performed on cell populations isolated from old and young donors as well as from one child suffering from Duchenne muscular dystrophy, where extensive regeneration had occurred. In order to see if there are any age-related changes in the myogenic program we have also compared the program of myogenic differentiation expressed by satellite cells from these subjects at different stages of their proliferative lifespan.
Ageing is characterised by progressive deterioration of physiological systems and the loss of skeletal muscle mass is one of the most recognisable, leading to muscle weakness and mobility impairments. This review highlights interactions between the immune system and skeletal muscle cells (widely termed satellite cells or myoblasts) to influence satellite cell behaviour during muscle regeneration after injury, and outlines deficits associated with ageing. Resident neutrophils and macrophages in skeletal muscle become activated when muscle fibres are damaged via stimuli (e.g. contusions, strains, avulsions, hyperextensions, ruptures) and release high concentrations of cytokines, chemokines and growth factors into the microenvironment. These localised responses serve to attract additional immune cells which can reach in excess of 1 × 10 5 immune cell/mm 3 of skeletal muscle in order to orchestrate the repair process. T-cells have a delayed response, reaching peak activation roughly 4 days after the initial damage. The cytokines and growth factors released by activated T-cells play a key role in muscle satellite cell proliferation and migration, although the precise mechanisms of these interactions remain unclear. T-cells in older people display limited ability to activate satellite cell proliferation and migration which is likely to contribute to insufficient muscle repair and, consequently, muscle wasting and weakness. If the factors released by T-cells to activate satellite cells can be identified, it may be possible to develop therapeutic agents to enhance muscle regeneration and reduce the impact of muscle wasting during ageing and disease.
In humans, the amount of terminal (TTAGGG)n, telomeric DNA decreases during aging of various somatic cell types in vitro and in vivo. While the factors accounting for telomere shortening have not been thoroughly established, the inability of the DNA replication machinery to completely copy chromosomal termini (the "end replication problem") and the absence in somatic cells of telomerase, the enzyme that synthesizes telomeric DNA de novo, is a likely mechanism. One prediction of this hypothesis is that telomere shortening should be dependent on cell division. Thus we analyzed telomere length in actively dividing and quiescent cells in vitro and in vivo . In circular outgrowths of cultured human diploid fibroblasts (HDF), cells at the outer periphery had a significantly lower mean terminal restriction fragment (TRF) length (P = 0.011) and telomeric signal intensity (P = 0.024) than cells at the center. Also, the rate of telomere shortening over time for HDFs held quiescent was not statistically significant (m = -12 bp/day, P = 0.16) while that for serially passaged cells was significant (m = -34 bp/day, P = 0.017). To examine the rate of telomere shortening for quiescent cells in vivo, we measured mean TRF length in brain tissue from adult donors ranging in age from 32-75 years. No significant decrease was observed as a function of donor age (P = 0.087), in contrast to the shortening of telomere length that occurs during in vivo aging of mitotically active cells (P = 0.0001). These observations show that telomere shortening is largely, if not entirely, dependent on cell division and support the end replication problem as a mechanism for this process and the use of telomere length as a biomarker for replicative capacity.
The activities of β-glucuronidase, β-N-acetylglucosaminidase, arylsulphatase, ribonuclease,p-nitrophenylphosphatase, and malate dehydrogenase together with protein content were assayed from representative mixed (m. rectus femoris), predominantly red (proximal heads ofm. vastus lateralis, m.v. medius andm. v. intermedius), and predominantly white (distal head ofm. vastus lateralis) muscle homogenates of mice during a two-week period following one single exposure to exhausting intermittent running on a treadmill. The activities of cathepsin D and β-glycerophosphatase were assayed from mixed muscle only. In all three muscle types, particularly in red muscle, the activities of β-glucuronidase, β-N-acetylglucosaminidase, arylsulphatase, and ribonuclease progressively increased between one to five days after the exercise; thereafter the activities began to decrease, being near the control values 15 days after the exercise. In mixed muscle, cathepsin D activity increased. No corresponding changes were observed in the activities of acid phosphatases.
The time course of the activity changes closely resembled that earlier found to be caused by ischaemia in rabbit muscles. It is tentatively concluded that the two treatments, exhaustive exercise and temporary ischaemia, cause similar cell injuries, and that the lysosomal system involved seems to function similarly in the post-stress recovery of the fibres from these injuries.
The activity of eight acid hydrolases and two energy metabolism enzymes were assayed from homogenates of predominantly red (proximal heads of m. vastus lateralis, m. vastus medialis, and m. vastus intermedius) and predominantly white (distal head of m. vastus lateralis) skeletal muscle of mice belonging to one of the following groups: 1) sedentary controls, never trained or exhausted; 2) exhausted controls, exhausted once by running on a treadmill 5, 10, or 20 days before killing; 3) trained mice, exercising until killed; 4) exhausted trained mice, exercising until exhausted 5, 10 or 20 days before killing, not exercising during that period; and 5) detrained mice, terminating training 5, 10, or 20 days before killing. In untrained but not in trained animals, exhaustive exercise caused, 5 days afterward, fiber necrosis and a marked increase in the activities of beta-glucuronidase, beta-N-acetylglucosaminidase, arylsulphatase, ribonuclease, deoxyribonuclease, cathepsin D, and cathepsin C, especially in red muscle fibers. Training increased the activities of citrate synthase, beta-glucuronidase, and cathepsin D in both muscle types and those of beta-N-acetylglucosaminidase, arylsulphatase, and cathepsin C in red muscle. Effects of detraining were minor. Exhaustive exercise causes lethal and evidently also sublethal fiber injuries manifesting themselves as an activation of the lysosomal system of muscle fibers 5 days later. Training affects cellular homeostasis by causing an apparent resistance to the damaging effects of exhaustive exercise. Moderately increased hydrolase activities may reflect increased turnover in endurance-trained muscles.
The ends of human chromosomes have been shown recently to resemble those of simple organisms. With this in mind, we discuss the nature and possible significance of rare chromosome fusion events thought to involve telomeres, particularly those fusion events found in some tumours. Also we argue that interstitial telomere-like stretches may be particularly prone to recombination, breakage and fragility.
This study was designed to examine the interrelationships between performance in endurance running events from 10 to 90 km, training volume 3-5 weeks prior to competition, and the fractional utilization of maximal aerobic capacity (%VO2max) during each of the events. Thirty male subjects underwent horizontal treadmill testing to determine their VO2max, and steady-state VO2 at specific speeds to allow for calculation of %VO2max sustained during competition. Runners were divided into groups of ten according to their weekly training distance (group A trained less than 60 km X week-1, group B 60 to 100 km X week-1, and group C more than 100 km X week-1). Runners training more than 100 km X week-1 had significantly faster running times (average 19.2%) in all events than did those training less than 100 km X week-1. VO2max or %VO2max sustained during competition was not different between groups. The faster running speed of the more trained runners, running at the same %VO2max during competition, was due to their superior running economy (19.9%). Thus all of the group differences in running performance could be explained on the basis of their differences in running economy. These findings suggest either that the main effect of training more than 100 km X week-1 may be to increase running economy, or that runners who train more than 100 km X week-1 may have inherited superior running economy.(ABSTRACT TRUNCATED AT 250 WORDS)
In this paper we describe our studies on the mutagenic consequences of oxidative DNA damage introduced by radiation-induced OH radicals (.OH) and by exposure to singlet oxygen (1O2), released by thermo-dissociation of the endoperoxide 3,3'-(1,4-naphthalidene) dipropionate (NDPO2). We have made use of M13mp10 bacteriophage and pUC18 plasmid DNA, containing a 144 base pair (bp) insert in the lacZ alpha gene. This 144 bp insert was used as a mutational target sequence. When dilute aqueous solutions of double-stranded (ds) M13mp10 (plus 144 bp insert) were gamma-irradiated in the presence of oxygen (O2; 100% .OH) or nitrous oxide (N2O; 90% .OH, 10% .H), very specific mutation spectra were found. Mainly bp substitutions were observed, of which C/G to G/C transversions are the predominant type. Moreover, the mutations are for the most part concentrated into two mutational hot spots: a minor and major one. Differences between the oxic (O2) and anoxic (N2O) mutation spectra could also be observed. Under N2O-1 bp deletions were detected, which are absent in the presence of O2, and in the anoxic spectrum more C/G to A/T transversions are present. To investigate whether these differences were due to the small amount of H radicals, which are formed under N2O, ds M13mp10 (plus 144 bp insert) was exposed to gamma-rays in phosphate buffer under nitrogen (55% .H, 45% .OH). Under these conditions a remarkable shift was observed from C/G-->G/C to C/G-->A/T transversions, while the mutations were far more scattered along the 144 bp sequence and no -1 bp deletions were detected. These results strongly suggest that H radicals do not cause -1 bp deletions, but may be responsible for the observed C/G to A/T transversions. The kind of bp substitution not only appeared to be dependent on the type of the water radicals, but also appeared to be strongly influenced by the replicon in which the target sequence is incorporated. When an oxygenated solution of pUC18 plasmid DNA (plus 144 bp insert) is irradiated, mainly C/G to A/T transversions were found at the same major hot spot instead of C/G to G/C transversions when the 144 bp sequence is part of M13mp10 DNA. Finally, in agreement with the observation that 1O2 reacts preferentially with guanine in DNA, a guanine is involved in most of the mutations scored after exposure of single-stranded (ss) M13mp10 DNA to NDPO2-generated 1O2.(ABSTRACT TRUNCATED AT 400 WORDS)
We have studied the effect of adding extra satellite cells or soluble factors from crushed muscle on regeneration of minced fragments from rat tibialis muscle. The muscle mince was wrapped in an artificial epimysium to prevent adhesions and cell immigration from adjacent muscles. Regeneration was quantitatively assessed by electrophoretic determination of the muscle-specific form of creatine kinase. Control minces exhibited three periods of change in creatine kinase activity during a 7-week regeneration period. Activity fell rapidly during the first week, then rose gradually from 1-3 weeks and increased more rapidly from 3-7 weeks. To augment the original complement of myogenic cells, satellite cells were isolated from the contralateral muscle, purified by density gradient centrifugation, and expanded in culture for 3 days before adding to the muscle mince. The added cells resulted in a 3-fold enhancement of creatine kinase activity throughout the regeneration period. Soluble muscle extract incorporated into a collagen matrix also stimulated regeneration when added to muscle mince. The extract accelerated the rate of creatine kinase increase during the 1-3 week period beyond that observed in the control or cell augmented mince, suggesting that factors in the extract may facilitate revascularization or reinnervation. The specific activity of creatine kinase was increased in regenerates augmented with both cells and extract, indicating that the effects enhance primarily myogenic processes.
The telomere hypothesis of cellular aging proposes that loss of telomeric DNA (TTAGGG) from human chromosomes may ultimately cause cell-cycle exit during replicative senescence. Since lymphocytes have a limited replicative capacity and since blood cells were previously shown to lose telomeric DNA during aging in vivo, we wished to determine: (a) whether accelerated telomere loss is associated with the premature immunosenescence of lymphocytes in individuals with Down syndrome (DS) and (b) whether telomeric DNA is also lost during aging of lymphocytes in vitro. To investigate the effects of aging and trisomy 21 on telomere loss in vivo, genomic DNA was isolated from peripheral blood lymphocytes of 140 individuals (age 0-107 years), including 21 DS patients (age 0-45 years). Digestion with restriction enzymes HinfI and RsaI generated terminal restriction fragments (TRFs), which were detected by Southern analysis using a telomere-specific probe (32P-(C3TA2)3). The rate of telomere loss was calculated from the decrease in mean TRF length, as a function of donor age. DS patients showed a significantly higher rate of telomere loss with donor age (133 +/- 15 bp/year) compared with age-matched controls (41 +/- 7.7 bp/year) (P < .0005), suggesting that accelerated telomere loss is a biomarker of premature immunosenescence of DS patients and that it may play a role in this process. Telomere loss during aging in vitro was calculated for lymphocytes from four normal individuals, grown in culture for 10-30 population doublings. The rate of telomere loss was approximately 120 bp/cell doubling, comparable to that seen in other somatic cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Cell-mediated gene therapy requires an in vitro amplification of modified cells prior to their injection into target tissue. Since the proliferative capacity of normal human cells is limited, we have tested a method to follow in vitro the proliferative potential of human satellite cells. Our results show that telomere length can be used to predict the proliferative potential of human satellite cells. In this short communication, the telomere shortening and the limited replicative potential are discussed in the context of the possible use of human satellite cells for gene transfer and why cell-mediated gene therapy has been less successful in humans than in mice.
Extreme exercise increases oxygen uptake with a potential for increased formation of reactive oxygen species. Damage to biomolecules may occur if such an increase exceeds the protective capacity of antioxidant defence mechanisms. Vigorous exercise amounting to approximately 10 h a day for 30 days increased the rate of oxidative DNA modification by 33% (95% confidence limits, 3-67%; P < 0.02) in 20 men owing to the urinary excretion of 8-oxo-7,8-dihydro-2'-deoxyguanosine, an oxidatively modified deoxynucleoside originating from nuclear DNA repair, oxidation of the nucleotide pool from mitochondrial DNA and/or from cell turnover. Oxidative stress to DNA points to a risk for the development of cancer and premature ageing from extreme exercise.
In 12 moderately trained subjects reduced glutathione (GSH) and oxidized glutathione (GSSG) as well as thiobarbituric acid reactive substances (TBARS) were measured in the blood before and during the first two hours and first two days after a 2.5-h run. The participants covered between 19 and 26 km (20.8 +/- 2.5 km, mean +/- SD). The running speed was between 53 and 82% of the speed at which blood lactate concentration reached 4 mmol/L lactate (67.9 +/- 8.2%, mean +/- SD) assessed during a previously performed treadmill test. Blood samples were collected 1 h before, immediately before, immediately after, 1 and 2 h after, as well as 1 and 2 days after the run. Immediately after exercise GSH was significantly decreased (p < 0.01) and GSSG significantly increased (p < 0.01). In all subjects the ratio of GSH to GSSG showed a marked decline to 18 +/- 4% (mean +/- SD) of the pre-exercise values (p < 0.01). One hour later the mean GSH and GSSG values returned to baseline. However, there were considerable inter-individual differences. In some subjects the GSH/ GSSG ratio overshot the pre-exercise levels, in others the ratio remained low even two hours after exercise. Compared with the pre-exercise values TBARS concentrations did not change significantly at any time point after exercise. The findings suggest that after prolonged exercise in moderately trained subjects a critical shift in the blood glutathione redox status may be reached. The changes observed were generally short-lived, the duration of which may have depended on the relative importance of reactive oxygen species generation by the capillary endothelial cells and neutrophil and eosinophil granulocytes after the end of exercise.
In this study, we have evaluated the ability of human satellite cells isolated from subjects aged from 5 days to 86 years to proliferate in culture. Cells were cultivated until they became senescent. The number of cell divisions was calculated by counting the number of cells plated in culture compared to the number of cells removed following proliferation. Telomere length, which is known to decrease during each round of cell division, has been used to analyze the in vitro replicative capacity and in vivo replicative history of human satellite cells at isolation. The rate of telomere shortening in myonuclei of these muscle biopsies was also examined. Our results show that both proliferative capacity and telomere length of satellite cells decreases with age during the first two decades but that the myonuclei of human skeletal muscle are remarkably stable because telomere length in these myonuclei remains constant from birth to 86 years. The lack of shortening of mean terminal restriction fragments (TRF) in vivo confirms that skeletal muscle is a stable tissue with little nuclear turnover and therefore an ideal target for cell-mediated gene therapy. Moreover, our results show that it is important to consider donor age as a limiting factor to obtain an optimal number of cells.
Muscular dystrophies are characterised by continuous cycles of degeneration and regeneration resulting in an eventual diminution of the muscle mass and extensive fibrosis. In somatic cells chromosomal telomeres shorten with each round of cell division and telomere length is considered to be a biomarker of the replicative history of the cell. We have previously shown that human myoblasts have a limited proliferative capacity, and that normal skeletal muscle has a very low level of nuclear turnover. However, in patients suffering from muscular dystrophy the satellite cells will be forced to make repeated rounds of cell division, driving the cells towards senescence. In this study we have used the telomere length to quantify the intensity of the muscle cell turnover in biopsies from dystrophic patients of different ages. Our results show that as soon as the first clinical symptoms become apparent the muscle has already undergone extensive regeneration and the rate of telomere loss is 14 times greater than that observed in controls. This confirms that the decline in regenerative capacity is due to the premature senescence of the satellite cells induced by their excessive proliferation during muscle repair.
To establish whether there was a relationship between the total accumulated distances of racing in veteran runners and the neuromuscular efficiency of the quadriceps muscles before and after a downhill run.
University of Cape Town, Sports Science Institute of South Africa.
Twenty male veteran long distance runners (45-50 years of age) with a range of training (1,300 km to 111,280 km) and racing (0 km to 9,737 km) experience.
A 40-minute downhill run (-10% decline) on a treadmill, at a speed corresponding to 70% of the subject's peak treadmill running speed.
The difference between integrated electromyography (IEMG)/mean force over a 5 s maximal voluntary isometric contraction before and after the downhill run was calculated as the delta (delta) neuromuscular efficiency. This was related to the total kilometers trained, current training distance, total kilometers raced, and number of races > 56 km. The difference in drop jump height before and after the downhill run was measured as well as changes in heart rate throughout the run.
There was a significant curvilinear relationship between the delta neuromuscular efficiency and total kilometers raced (R2 = 0.53, p < 0.05), and a significant inverse relationship between delta neuromuscular efficiency and the number of races > 56 km (r = -0.50, p < 0.05). Drop jump height decreased after the downhill run, and heart rate increased during the run.
Runners who have raced an accumulated distance of > 5,000 km show a significant dissociation in the delta neuromuscular efficiency after a downhill run, compared with less experienced runners. Although possible causes for the dissociation are discussed, further research is needed.
In this study, we have investigated the consequences of aging on the regenerative capacity of human skeletal muscle by evaluating two parameters: (i) variation in telomere length which was used to evaluate the in vivo turn-over and (ii) the proportion of satellite cells calculated as compared to the total number of nuclei in a muscle fibre. Two skeletal muscles which have different types of innervation were analysed: the biceps brachii, a limb muscle, and the masseter, a masticatory muscle. The biopsies were obtained from two groups: young adults (23 +/- 1.15 years old) and aged adults (74 +/- 4.25 years old). Our results showed that during adult life, minimum telomere lengths and mean telomere lengths remained stable in the two muscles. The mean number of myonuclei per fibre was lower in the biceps brachii than in the masseter but no significant change was observed in either muscle with increasing age. However, the number of satellite cells, expressed as a proportion of myonuclei, decreased with age in both muscles. Therefore, normal aging of skeletal muscle in vivo is reflected by the number of satellite cells available for regeneration, but not by the mean number of myonuclei per fibre or by telomere lengths. We conclude that a decrease in regenerative capacity with age may be partially explained by a reduced availability of satellite cells.
Chronic exercise activity and the fatigued athlete myopathic syndrome (FAMS)
- St Clair
- A Gibson
- M I Lambert
- M Collins
ST CLAIR GIBSON, A., M. I. LAMBERT, M. COLLINS, et al. Chronic
exercise activity and the fatigued athlete myopathic syndrome
(FAMS). Int. SportMed. J. 1:1-7, 2000.
Fatigue, aging and the neuromuscular system
- St Clair
- A Gibson
ST CLAIR GIBSON, A. Fatigue, aging and the neuromuscular system.
M.D. Thesis, University of Cape Town, 2000, pp. 1-446, 2002.
Regeneration after ultra-endurance exercise
- A St Clair
- E W Gibson
- T D Derman
- Noakes
LAMBERT, M. I., A. ST CLAIR GIBSON, E. W. DERMAN, and T. D.
NOAKES. Regeneration after ultra-endurance exercise. In: Overload,
Performance Incompetence and Regeneration in Sport, M. Lehmann,
C. Foster, U. Gastmann, H. Keizer, and J. M. Steinacker (Eds.). New
York: Kluwer Academic/Plenum Publishers, 1999, pp. 163–172.
Regeneration after ultra-endurance exercise In: Overload, Performance Incompetence and Regeneration in Sport
- A St
- Clair Gibson
- E W Derman
- T D Noakes
LAMBERT, M. I., A. ST CLAIR GIBSON, E. W. DERMAN, and T. D.
NOAKES. Regeneration after ultra-endurance exercise. In: Overload,
Performance Incompetence and Regeneration in Sport, M. Lehmann,
C. Foster, U. Gastmann, H. Keizer, and J. M. Steinacker (Eds.). New
York: Kluwer Academic/Plenum Publishers, 1999, pp. 163–172.
Regenerative potential of human skeletal muscle during aging
- V Renault
- L-E
- P-O Thornell
- G Ericksson
- V Butler-Browne
- Mouly
RENAULT, V., L-E. THORNELL, P-O. ERICKSSON, G. BUTLER-BROWNE,
and V. MOULY. Regenerative potential of human skeletal muscle
during aging. Aging Cell 1:132-139, 2002.