The Association Between Physical Activity in Leisure Time and Leukocyte Telomere Length

Introduction: The aging process in children and adolescents is accelerated resulting in the premature development of “adult” diseases such as hypertension and diabetes. Telomere shortening plays a key role in human aging; identifying factors that regulate this process is important for developing effective lifestyle interventions so as to prevent and treat age-associated diseases. In vitro and in vivo studies demonstrate that high salt content markedly decreases life span, and accelerates cellular aging through increased DNA breakage. However, the effect of high salt diet on telomere length, a marker of biological aging, remains unknown. Therefore, we aimed to test the hypothesis that high dietary sodium intake is inversely associated with leukocyte telomere length, especially in the context of obesity. Methods: Leukocyte telomere length (T/S ratio) was assessed by a quantitative polymerase chain reaction method in 766 adolescents aged 14-18 years (50% female, 49% African Americans). Diet was assessed with three to seven 24-h recalls, and physical activity was determined by accelerometry. Participants were classified according to low vs. high sodium intake (below or above the median), and according to weight status (normal vs. overweight/obese). Analysis of covariance and linear regression analyses were used to determine the effects of sodium intake and weight status on leukocyte telomere length. Results: After controlling for age, sex, race, energy intake, Tanner stage, and vigorous physical activity, a statistically significant sodium intake by weight status interaction was observed, such that leukocyte telomere length was significantly shorter in the high sodium intake vs. low sodium intake subjects from the overweight/obese group (1.24 ± 0.22 vs. 1.32 ± 0.21, p=0.02), but not the normal weight group (1.29 ± 0.24 vs. 1.30 ± 0.24, p=0.69). Consistent with the low vs. high sodium intake group data, multiple linear regression analyses, adjusting for age, sex, race, energy intake, Tanner stage and vigorous physical activity, revealed that higher dietary sodium intake was associated with shorter leukocyte telomere length in the overweight/obese group (β=-0.37, p=.045), but not the normal weight group. Conclusion: High dietary sodium intake is associated with shorter telomere length in overweight and obese adolescents suggesting that high sodium intake and obesity may act synergistically to accelerate cellular aging. Longitudinal studies are warranted to determine the synergistic effect of high sodium intake and obesity on telomere shortening over time.

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Abstract P417: Physical Activity, Physical Fitness and Leukocyte Telomere Length: The Cardiovascular Health Study

Circulation ◽

10.1161/circ.127.suppl_12.ap417 ◽

2013 ◽

Vol 127 (suppl_12) ◽

Author(s):

Luisa Soares-Miranda ◽

Fumiaki Imamura ◽

David S Siscovick ◽

Nancy Swords Jenny ◽

Annette L Fitzpatrick ◽

...

Keyword(s):

Physical Activity ◽

Older Adults ◽

Telomere Length ◽

Test Performance ◽

Leisure Time ◽

Walking Distance ◽

Cross Sectional ◽

Time Activity ◽

Leisure Time Activity ◽

Over Time

Background The influence of physical activity (PA) and fitness (PF) at older ages on changes in telomere length (TL), repetitive DNA sequences that may mark biologic aging, are not well established. Prior studies in older adults were cross-sectional, and few evaluated PF. Aim To investigate both cross-sectional and prospective associations of PA and PF with Leukocyte TL in older adults. Methods Among 582 adults age 73±5 y at baseline in CHS having serial LTL measures (leucocyte mean terminal restriction length) in 1992 and 1997, PA (walking pace, blocks, combined walking score; leisure time activity) and PF (15-ft walk, chair stands, grip strength) were assessed multiple times from 1989 to 1997. Cross-sectional associations were assessed using multivariable repeated-measures regression of cumulative average serial PA and PF measures from 1989 to 1992 against LTL in 1992; and cumulative averaged PA and PF from 1993 to 1997 against LTL in 1997. Longitudinal analyses assessed cumulative averaged PA and PF from 1989-92 against later changes in LTL from 1992-97; and changes in cumulative averaged PA and PF from 1989-92 to 1993-97 against changes in LTL from 1992-97. We evaluated all subjects, those without poor/fair self-reported health, and those without limited ADLs. Results Cross-sectionally, greater walking distance and chair test performance, but not other PA and PF measures, each associated with longer LTL ( P trend 0.007, 0.04 respectively). Lab measures of DNA integrity suggested measurable degradation that markedly attenuates ability to detect differences in LTL changes over time, especially over only 5 y. For example, baseline PA and PF from 1989-92 were unassociated with later changes in LTL. In contrast, changes in leisure time activity and chair test performance from 1992-97 were each inversely associated with LTL shortening. Conclusions Even late in life, certain PA and PF metrics are associated with longer LTL cross-sectionally and, even with likely substantial measurement error, with less LTL shortening over time.

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