Abstract
A reduction in aerobic capacity and the shortening of telomeres are hallmarks of the ageing process. We examined whether a lower aerobic capacity is associated with shorter TL in skeletal muscle and/or leukocytes, across a wide age range of individuals. We also tested whether TL in human skeletal muscle (MTL) correlates with TL in leukocytes (LTL). Eighty-two recreationally active, healthy men from the Gene SMART cohort (31.4±8.2 years; body mass index (BMI)=25.3±3.3kg/m2), and 11 community dwelling older men (74.2±7.5years-old; BMI=28.7±2.8kg/m2) participated in the study. Leukocytes and skeletal muscle samples were collected at rest. Relative telomere length (T/S ratio) was measured by RT-PCR. Associations between TL, aerobic capacity (VO2 peak and peak power) and age were assessed with robust linear models. Older age was associated with shorter LTL (45% variance explained, P<0.001), but not MTL (P= 0.7). Aerobic capacity was not associated with MTL (P=0.5), nor LTL (P=0.3). MTL and LTL were correlated across the lifespan (rs=0.26, P=0.03). In healthy individuals, age explain most of the variability of LTL and this appears to be independent of individual aerobic capacity. Individuals with longer LTL also have a longer MTL, suggesting that there might be a shared molecular mechanism regulating telomere length.
Highlights
Telomeres are highly conserved repetitive DNA sequences that cap chromosomes [1] and are important in maintaining genetic stability by protecting against genetic recombination, end-to-end fusion of the chromosome and cellular degradation [2, 3]
We investigated whether telomere length (TL) in human skeletal muscle is associated with TL in leukocytes
After adjustment for age, none of the fitness parameters (Supplementary Table 1) or the combined aerobic capacity score were associated with LTL (β= 0.06, P= 0.3; 95% CI= -0.1, 0.2) or MTL (β= 0.08, P= 0.5; 95% CI= -0.1, 0.2) (Figure 1)
Summary
Telomeres are highly conserved repetitive DNA sequences that cap chromosomes [1] and are important in maintaining genetic stability by protecting against genetic recombination, end-to-end fusion of the chromosome and cellular degradation [2, 3]. Somatic cell telomeres shorten with each round of mitotic division until they become too short to divide resulting in cellular senescence [4]. Telomere length (TL) is established early in life [5, 6], and shortens with older age [7, 8]. The length of telomeres varies considerably between individuals of the same chronological age and is indicative of biological age [8]. The inter-individual variability in TL www.aging-us.com is thought to be influenced by genetics, epigenetics and environ-mental factors including oxidative stress, and inflammation [9,10,11,12]
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