Football and team handball training postpone cellular aging in women

AbstractSeveral hallmarks of aging have been identified and examined separately in previous exercise studies. For the first time, this study investigates the effect of lifelong regular exercise in humans on two of the central aging hallmarks combined. This cross-sectional study involved 129 healthy, non-smoking women, including young elite football players (YF, n = 29), young untrained controls (YC, n = 30), elderly team handball players (EH, n = 35) and elderly untrained controls (EC, n = 35). From a resting blood sample, mononuclear cells (MNCs) were isolated and sorted into monocytes and lymphocytes. Telomere length, mitochondrial (mtDNA) copy number and key regulators of mitochondrial biogenesis and function (PGC-1α and PGC-1β expression) were measured using quantitative polymerase chain reaction (qPCR). Overall, young women showed significantly longer telomeres and higher PGC-1α and PGC-1β expression, but lower mtDNA copy number compared to elderly subjects. A multivariate analysis showed that YF had 22–24% longer telomeres in lymphocytes and MNCs compared to YC. In addition, YF showed 19–20% higher mtDNA copy number in lymphocytes and MNCs compared to YC. The two young groups did not differ in PGC-1α and PGC-1β expression. EH showed 14% lower mtDNA copy number in lymphocytes compared to EC, but 3.4-fold higher lymphocyte PGC-1α expression compared to EC. In MNCs, EH also showed 1.4–1.6-fold higher PGC-1α and PGC-1β expression. The two elderly groups did not differ in telomere length. Elite football training and lifelong team handball training are associated with anti-aging mechanisms in leukocytes in women, including maintenance of telomere length and superior mitochondrial characteristics.

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Football and Team Handball Training Postpone Cellular Aging in Women

10.21203/rs.3.rs-275962/v1 ◽

2021 ◽

Author(s):

Marie Hagman ◽

Bjørn Fristrup ◽

Rémi Michelin ◽

Peter Krustrup ◽

Muhammad Asghar

Keyword(s):

Telomere Length ◽

Mitochondrial Function ◽

Copy Number ◽

Mononuclear Cells ◽

Quantitative Polymerase Chain Reaction ◽

Cellular Aging ◽

Elderly Subjects ◽

Mtdna Copy Number ◽

Cross Sectional ◽

Team Handball

Abstract Aims: Several hallmarks of aging have been identified and examined separately in previous exercise studies. For the first time, this study investigates the effect of lifelong regular exercise in humans on two of the central aging hallmarks combined. Methods: This cross-sectional study involved 129 healthy, non-smoking women, including young elite football players (YF, n=29), young untrained controls (YC, n=30), elderly team handball players (EH, n=35) and elderly untrained controls (EC, n=35). From a resting blood sample, mononuclear cells (MNCs) were isolated and sorted into monocytes and lymphocytes. Telomere length, mitochondrial (mtDNA) copy number and mitochondrial function (PGC-1α and PGC-1β expression) were measured using quantitative polymerase chain reaction (qPCR). Results: Overall, young women showed significantly longer telomeres and higher mitochondrial function, but lower mtDNA copy number compared to elderly subjects. A multivariate analysis showed that YF had 22–24% longer telomeres in lymphocytes and MNCs compared to YC. In addition, YF showed 19–20% higher mtDNA copy number in lymphocytes and MNCs compared to YC. The two young groups did not differ in PGC-1α and PGC-1β expression. EH showed 14% lower mtDNA copy number in lymphocytes compared to EC, but 3.4-fold higher lymphocyte PGC-1α expression compared to EC. In MNCs, EH also showed 1.4-1.6- fold higher mitochondrial function. The two elderly groups did not differ in telomere length.Conclusion: Elite football training and lifelong team handball training are associated with anti-aging mechanisms in leukocytes in women, including maintenance of telomere length and upregulation of mitochondrial function.

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Sperm mtDNA copy number, telomere length, and seminal spermatogenic cells in relation to ambient air pollution: Results of a cross-sectional study in Jing-Jin-Ji region of China

Journal of Hazardous Materials ◽

10.1016/j.jhazmat.2020.124308 ◽

2020 ◽

pp. 124308

Author(s):

Lixiao Zhou ◽

Lipeng Li ◽

Guimin Hao ◽

Binghua Li ◽

Sujuan Yang ◽

...

Keyword(s):

Air Pollution ◽

Telomere Length ◽

Copy Number ◽

Ambient Air ◽

Cross Sectional Study ◽

Ambient Air Pollution ◽

Spermatogenic Cells ◽

Sectional Study ◽

Mtdna Copy Number ◽

Cross Sectional

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Born to be young? Prenatal thyroid hormones increase early-life telomere length in wild collared flycatchers

Biology Letters ◽

10.1098/rsbl.2020.0364 ◽

2020 ◽

Vol 16 (11) ◽

pp. 20200364

Author(s):

Antoine Stier ◽

Bin-Yan Hsu ◽

Coline Marciau ◽

Blandine Doligez ◽

Lars Gustafsson ◽

...

Keyword(s):

Thyroid Hormones ◽

Telomere Length ◽

Early Life ◽

Copy Number ◽

Growth Period ◽

Mtdna Copy Number ◽

Cross Sectional ◽

Telomere Shortening ◽

Underlying Mechanisms ◽

Age At Birth

The underlying mechanisms of the lifelong consequences of prenatal environmental condition on health and ageing remain little understood. Thyroid hormones (THs) are important regulators of embryogenesis, transferred from the mother to the embryo. Since prenatal THs can accelerate early-life development, we hypothesized that this might occur at the expense of resource allocation in somatic maintenance processes, leading to premature ageing. Therefore, we investigated the consequences of prenatal TH supplementation on potential hallmarks of ageing in a free-living avian model in which we previously demonstrated that experimentally elevated prenatal TH exposure accelerates early-life growth. Using cross-sectional sampling, we first report that mitochondrial DNA (mtDNA) copy number and telomere length significantly decrease from early-life to late adulthood, thus suggesting that these two molecular markers could be hallmarks of ageing in our wild bird model. Elevated prenatal THs had no effect on mtDNA copy number but counterintuitively increased telomere length both soon after birth and at the end of the growth period (equivalent to offsetting ca 4 years of post-growth telomere shortening). These findings suggest that prenatal THs might have a role in setting the ‘biological' age at birth, but raise questions about the nature of the evolutionary costs of prenatal exposure to high TH levels.

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Telomere Shortening in Formerly Abused and Never Abused Women

Biological Research For Nursing ◽

10.1177/1099800411398479 ◽

2011 ◽

Vol 14 (2) ◽

pp. 115-123 ◽

Cited By ~ 64

Author(s):

Janice Humphreys ◽

Elissa S. Epel ◽

Bruce A. Cooper ◽

Jue Lin ◽

Elizabeth H. Blackburn ◽

...

Keyword(s):

Telomere Length ◽

Chronic Stress ◽

Partner Violence ◽

Molecular Mechanisms ◽

Mononuclear Cells ◽

Quantitative Polymerase Chain Reaction ◽

Cellular Aging ◽

Abused Women ◽

Peripheral Blood Mononuclear ◽

Convenience Sample

Recent studies suggest that chronic psychological stress may accelerate aging at the cellular level. Telomeres are protective components that stabilize the ends of chromosomes and modulate cellular aging. Women exposed to intimate partner violence (IPV) experience chronic stress and report worse health. The purpose of this exploratory study was to examine telomeric DNA length in women who have experienced chronic stress related to IPV. We hypothesized that IPV exposure would be associated with shorter telomere length. The investigation used a cross-sectional design to study telomere length in women with a history of IPV exposure and control women who reported no prior exposure to IPV. Advertisements and public notices were used to recruit a convenience sample of healthy women. Mean leukocyte telomere length was measured in DNA samples from peripheral blood mononuclear cells (PBMCs) by a quantitative polymerase chain reaction assay (qPCR). Telomere length was significantly shorter in the 61 formerly abused women compared to the 41 controls ( t = 2.4, p = .02). Length of time in the abusive relationship and having children were associated with telomere length after controlling for age and body mass index (BMI) ( F(2, 99) = 10.23, p < .001). Numerous studies suggest that women who experience IPV have poorer overall health. It is often presumed that the stress of IPV may be causing greater morbidity. Findings from this descriptive study suggest a link between IPV exposure, duration of IPV-related stress, and telomere length molecular mechanisms that regulate cellular aging.

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Fruit and Vegetable Intake and Telomere Length in a Random Sample of 5448 U.S. Adults

Nutrients ◽

10.3390/nu13051415 ◽

2021 ◽

Vol 13 (5) ◽

pp. 1415

Author(s):

Larry A. Tucker

Keyword(s):

Telomere Length ◽

Random Sample ◽

Vegetable Intake ◽

Quantitative Polymerase Chain Reaction ◽

Cellular Aging ◽

Fruit And Vegetable Intake ◽

Biological Aging ◽

Fruit And Vegetable ◽

Base Pairs ◽

Cross Sectional

The relationship between fruit and vegetable intake and telomere length was examined using a cross-sectional design and an NHANES random sample of 5448 U.S. adults. Fruit and vegetable (F&V) consumption was assessed using a 24 h recall, and telomere length, an index of cellular aging, was measured using the quantitative polymerase chain reaction method. Telomere length was linearly related to F&V intake when combined (F = 22.7, p < 0.0001) and also when separated as fruit (F = 7.2, p < 0.0121) or vegetables (F = 15.4, p < 0.0005), after adjusting for covariates. Specifically, telomeres were 27.8 base pairs longer for each 100 g (3.5 ounces) of F&V consumed. Because each additional year of chronological age was associated with telomeres that were 14.9 base pairs shorter, when women and men were analyzed together, results indicated that a 100 g (3.5 oz) per day increment in F&V corresponded with 1.9 years less biological aging. When the 75th percentile of F&V intake was compared to the 25th, the difference was 4.4 years of cellular aging. When separated by sex, fruits and vegetables were both related to telomere length in women, but only vegetable intake was predictive of telomere length in men. In conclusion, evidence based on a random sample of U.S. adults indicates that the more the servings of F&V, the longer telomeres tend to be.

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Religiosity and Telomere Length: Moderating Effect of Religiosity on the Relationship Between High-Risk Polymorphisms of the Apolipoprotein E and TOMM40 Gene and Telomere Length

Journal of Applied Gerontology ◽

10.1177/0733464819865415 ◽

2019 ◽

Vol 39 (6) ◽

pp. 627-634 ◽

Cited By ~ 3

Author(s):

Liqun Wang ◽

Harold G. Koenig ◽

Zhiqiang He ◽

Xiaoya Sun ◽

Saad Al Shohaib ◽

...

Keyword(s):

High Risk ◽

Apolipoprotein E ◽

Telomere Length ◽

Cross Sectional Study ◽

Moderating Effect ◽

Community Dwelling ◽

Cellular Aging ◽

Cross Sectional ◽

Older Chinese ◽

The Relationship

Objective: The current study seeks to examine the relationship between religiosity and telomere length (TL) in an older Chinese Muslim sample and to explore the moderating effect of religiosity on the relationship between high-risk polymorphisms and TL. Methods: A cross-sectional study of 1,692 community-dwelling adults aged 55 or older was conducted. Apolipoprotein E and TOMM40 (rs2075650) gene polymorphisms and TL were determined using standard procedures. Ordinal logistic regression was used to examine the associations. Results: Religiosity was significantly and positively related to TL. A significant interaction emerged between religiosity and the rs2075650 G polymorphism in predicting TL. Stratified multivariate analyses demonstrated that the relationship between the rs2075650 G state and TL was particularly strong among those who were more religious, as hypothesized. Conclusion: The findings revealed that religiosity may influence cellular aging in part by modifying the effect that high-risk genes have on increasing vulnerability to dementia and cognitive impairment.

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Mitochondrial Biogenesis, Telomere Length and Cellular Senescence in Parkinson’s Disease and Lewy Body Dementia

10.21203/rs.3.rs-754233/v1 ◽

2021 ◽

Author(s):

Muhammad Asghar ◽

Amani Odeh ◽

Ahmad Jouni Fattahi ◽

Alexandra Edward Henriksson ◽

Aurelie Miglar ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Mitochondrial Dna ◽

Mitochondrial Dysfunction ◽

Telomere Length ◽

Cellular Senescence ◽

Mitochondrial Biogenesis ◽

Copy Number ◽

Cellular Aging ◽

Mtdna Copy Number

Abstract Background Progressive age is the single major risk factor for neurodegenerative diseases. Cellular aging markers during the course of Parkinson’s disease (PD) have been implicated in previous studies, however majority of these studies have investigated the association of individual cellular aging hallmarks with PD but not jointly. Method Here, we have studied the association of PD with three aging hallmarks (telomere attrition, mitochondrial dysfunction, and cellular senescence) in blood and the brain tissue. Telomere length and mitochondrial DNA ( mtDNA ) copy number was assessed by qPCR, while mitochondrial function ( PGC-1α and PGC-1β ) and expression of cyclin-dependent kinase inhibitor 2A ( CDKN2A ), cellular senescence marker was measured by RT-qPCR. Results Our results show that patients diagnosed with PD had 20% lower mitochondrial DNA copy number but 26% longer telomeres in blood compared to controls. Moreover, telomere length in blood was positively correlated with medication (Levodopa Equivalent Daily Dose). Similar results were found in brain tissue, where patients with Parkinson’s disease (PD), Parkinson dementia (PDD) and Dementia with Lewy Bodies (DLB) showed (46-95%) depleted mtDNA copy number, but (7-9%) longer telomeres compared to controls. Furthermore, when compared to controls, patients had lower mitochondrial biogenesis ( PGC-1α and PGC-1β ) and higher load of cellular senescent cells in postmortem prefrontal cortex tissue, where DLB showing the highest effect among the patient groups. Conclusion Our results show that mitochondrial dysfunction and cellular senescence but not telomere shortening is associated with PD, PDD and DLB. Our findings suggest that mitochondrial copy number and function could be used as viable biomarker in blood as an early indicator for the risk of neurodegenerative diseases.

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Dietary Exposure to Polychlorinated Biphenyls and Dioxins and Its Relationship to Telomere Length in Subjects Older Than 55 Years from the SUN Project

Nutrients ◽

10.3390/nu14020353 ◽

2022 ◽

Vol 14 (2) ◽

pp. 353

Author(s):

Lucia Alonso-Pedrero ◽

Carolina Donat-Vargas ◽

Maira Bes-Rastrollo ◽

Ana Ojeda-Rodríguez ◽

Guillermo Zalba ◽

...

Keyword(s):

Polychlorinated Biphenyls ◽

Telomere Length ◽

Quantitative Polymerase Chain Reaction ◽

Dietary Exposure ◽

Cross Sectional Study ◽

Total Pcbs ◽

Linear Regression Models ◽

Cross Sectional ◽

Toxic Equivalents ◽

Sun Project

Exposure to persistent organic pollutants (POPs) may influence telomere length (TL), which is considered as a marker of biological age associated with the risk of chronic disease. We hypothesized that dietary exposure to polychlorinated biphenyls (PCBs) and dioxins could affect TL. Our aim was to evaluate the association of dietary exposure to PCBs and dioxins with TL. In this cross-sectional study of 886 subjects older than 55 y (mean age: 67.7; standard deviation (SD): 6.1; 27% women) from the “Seguimiento Universidad de Navarra” (SUN) project. TL was determined by real-time quantitative polymerase chain reaction and dietary PCBs and dioxins exposure was collected using a validated 136-item Food Frequency Questionnaire. Multivariable linear regression models were used to control for potential confounding factors. Shorter TL was associated with dietary total PCBs (SD of T/S ratio/(ng/day) = −0.30 × 10−7; 95% CI, −0.55 × 10−7 to −0.06 × 10−7), dioxin-like PCBs (DL-PCBs) (SD of T/S ratio/(pg WHO TEQ (Toxic Equivalents)/day) = −6.17 × 10−7; 95% CI, −11.30 × 10−7 to −1.03 × 10−7), and total TEQ exposure (SD of T/S ratio/(pg WHO TEQ/day) = −5.02 × 10−7; 95% CI, −9.44 × 10−7 to −0.61 × 10−7), but not with dioxins (SD of T/S ratio/(pg WHO TEQ/day) = −13.90 × 10−7; 95% CI, −37.70 × 10−7 to 9.79 × 10−7). In this sample of middle-aged and older Spanish adults, dietary exposure to total PCBs and DL-PCBs alone and together with dioxins was associated with shorter TL. Further longitudinal studies, preferably with POPs measured in biological samples, are needed to confirm this finding.

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Leukocyte mitochondrial DNA copy number and built environment in Mexican Americans: a cross-sectional study

Scientific Reports ◽

10.1038/s41598-020-72083-7 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Hua Zhao ◽

Jie Shen ◽

Evan Leung ◽

Xueying Zhang ◽

Wong‐Ho Chow ◽

...

Keyword(s):

Built Environment ◽

Mexican Americans ◽

Copy Number ◽

Mexican American ◽

Cross Sectional Study ◽

Sectional Study ◽

Multivariate Logistic Regression ◽

Mtdna Copy Number ◽

Cross Sectional ◽

Household Density

Abstract Mitochondrial DNA (mtDNA) copy number in leukocytes has been regarded as a biomarker for various environmental exposures and chronic diseases. Our previous study showed that certain demographic factors (e.g. age, gender, BMI, etc.) significantly affect levels of leukocyte mtDNA copy number in Mexican Americans. However, the effect of the built environment on leukocyte mtDNA copy number has not been studied previously. In this cross-sectional study, we examined the association between multiple components of the built environment with leukocyte mtDNA copy number among 5,502 Mexican American adults enrolled in Mano-A-Mano, the Mexican American Cohort Study (MACS). Based on the median levels of mtDNA copy number, the study population was stratified into low mtDNA copy number group (< median) and high mtDNA copy number group (≥ median). Among all built environment exposure variables, household density and road/intersection ratio were found to be statistically significant between groups with low and high mtDNA copy number (P < 0.001 and 0.002, respectively). In the multivariate logistic regression analysis, individuals living in areas with elevated levels of household density had 1.24-fold increased odds of having high levels of mtDNA copy number [Odds ratio (OR) = 1.24, 95% confidence interval (CIs) 1.08, 1.36]. Similarly, those living in areas with elevated levels of road/intersection ratio had 1.12-fold increased odds of having high levels of mtDNA copy number (OR = 1.12, 95% CI 1.01, 1.27). In further analysis, when both variables were analyzed together in a multivariate logistic regression model, the significant associations remained. In summary, our results suggest that selected built environment variables (e.g. population density and road/intersection ratio) may influence levels of mtDNA copy number in leukocytes in Mexican Americans.

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