Physical activity recommendations for public health include typically muscle-strengthening activities for a minimum of 2 days a week. The range of interindividual variation in responses to resistance training (RT) aiming to improve health and well-being requires to be investigated. The purpose of this study was to quantify high and low responders for RT-induced changes in muscle size and strength and to examine possible effects of age and sex on these responses. Previously collected data of untrained healthy men and women (age 19 to 78 years, n = 287 with 72 controls) were pooled for the present study. Muscle size and strength changed during RT are 4.8 ± 6.1 % (range from −11 to 30 %) and 21.1 ± 11.5 % (range from −8 to 60 %) compared to pre-RT, respectively. Age and sex did not affect to the RT responses. Fourteen percent and 12 % of the subjects were defined as high responders (>1 standard deviation (SD) from the group mean) for the RT-induced changes in muscle size and strength, respectively. When taking into account the results of nontraining controls (upper 95 % CI), 29 and 7 % of the subjects were defined as low responders for the RTinduced changes in muscle size and strength, respectively. The muscle size and strength responses varied extensively between the subjects regardless of subject's age and sex. Whether these changes are associated with, e.g., functional capacity and metabolic health improvements due to RT requires further studies.

Leukocyte telomere length (LTL) is a heritable biomarker of genomic aging. In this study, we perform a genome-wide meta-analysis of LTL by pooling densely genotyped and imputed association results across large-scale European-descent studies including up to 78,592 individuals. We identify 49 genomic regions at a false dicovery rate (FDR) < 0.05 threshold and prioritize genes at 31, with five highlighting nucleotide metabolism as an important regulator of LTL. We report six genome-wide significant loci in or near SENP7 , MOB1B , CARMIL1 , PRRC2A , TERF2, and RFWD3 , and our results support recently identified PARP1, POT1 , ATM, and MPHOSPH6 loci. Phenome-wide analyses in >350,000 UK Biobank participants suggest that genetically shorter telomere length increases the risk of hypothyroidism and decreases the risk of thyroid cancer, lymphoma, and a range of proliferative conditions. Our results replicate previously reported associations with increased risk of coronary artery disease and lower risk for multiple cancer types. Our findings substantially expand current knowledge on genes that regulate LTL and their impact on human health and disease.

Waist circumference and skinfold thickness seem to reasonably assess changes in percent body fat during training. However, only DXA was capable to separate small differences between the groups in training-induced changes in lean body mass. Combined strength and endurance training is of greater value than either alone in optimizing body composition or improving physical fitness in older men.

In this study adaptations in body composition, physical fitness and metabolic health were examined during 21 weeks of endurance and/or strength training in 39- to 64-year-old healthy women. Subjects (n = 62) were randomized into endurance training (E), strength training (S), combined strength and endurance training (SE), or control groups (C). S and E trained 2 and SE 2 + 2 times in a week. Muscle strength and maximal oxygen uptake (VO(2)max) were measured. Leg extension strength increased 9 +/- 8% in S (P < 0.001), 12 +/- 8% in SE (P < 0.001) and 3 +/- 4% in E (P = 0.036), and isometric bench press 20% only in both S and SE (P < 0.001). VO(2)max increased 23 +/- 18% in E and 16 +/- 12% in SE (both P < 0.001). The changes in the total body fat (dual X-ray absorptiometry) did not differ between groups, but significant decreases were observed in E (-5.9%, P = 0.022) and SE (-4.8%, P = 0.005). Lean mass of the legs increased 2.2-2.9% (P = 0.004-0.010) in S, SE and E. There were no differences between the groups in the changes in blood lipids, blood pressure or serum glucose and insulin. Total cholesterol and low-density lipoprotein cholesterol decreased and high-density lipoprotein cholesterol increased in E. Both S and SE showed small decreases in serum fasting insulin. Both endurance and strength training and their combination led to expected training-specific improvements in physical fitness, without interference in fitness or muscle mass development. All training methods led to increases in lean body mass, but decreases in body fat and modest improvements in metabolic risk factors were more evident with aerobic training than strength training.

The goal of combined endurance and strength training--increasing both aerobic capacity and maximal strength simultaneously--was only achieved by some of the older subjects. New means are needed to personalize endurance, strength, and especially combined endurance and strength training programs for optimal individual adaptations.

Both strength and endurance training have several positive effects on aging muscle and physical performance of middle-aged and older adults, but their combination may compromise optimal adaptation. This study examined the possible interference of combined strength and endurance training on neuromuscular performance and skeletal muscle hypertrophy in previously untrained 40-67-year-old men. Maximal strength and muscle activation in the upper and lower extremities, maximal concentric power, aerobic capacity and muscle fiber size and distribution in the vastus lateralis muscle were measured before and after a 21-week training period. Ninety-six men [mean age 56 (SD 7) years] completed high-intensity strength training (S) twice a week, endurance training (E) twice a week, combined training (SE) four times per week or served as controls (C). SE and S led to similar gains in one repetition maximum strength of the lower extremities [22 (9)% and 21 (8)%, P<0.001], whereas E and C showed minor changes. Cross-sectional area of type II muscle fibers only increased in S [26 (22)%, P=0.002], while SE showed an inconsistent, non-significant change [8 (35)%, P=0.73]. Combined training may interfere with muscle hypertrophy in aging men, despite similar gains in maximal strength between the strength and the combined training groups.

Several clinical studies suggest the involvement of premature ageing processes in chronic obstructive pulmonary disease (COPD). Using an epidemiological approach, we studied whether accelerated ageing indicated by telomere length, a marker of biological age, is associated with COPD and asthma, and whether intrinsic age-related processes contribute to the interindividual variability of lung function.Our meta-analysis of 14 studies included 934 COPD cases with 15 846 controls defined according to the Global Lungs Initiative (GLI) criteria (or 1189 COPD cases according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria), 2834 asthma cases with 28 195 controls, and spirometric parameters (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC) of 12 595 individuals. Associations with telomere length were tested by linear regression, adjusting for age, sex and smoking status.We observed negative associations between telomere length and asthma (b5 -0.0452, p50.024) as well as COPD (b5 -0.0982, p50.001), with associations being stronger and more significant when using GLI criteria than those of GOLD. In both diseases, effects were stronger in females than males. The investigation of spirometric indices showed positive associations between telomere length and FEV1 (p51.07610 -7 ), FVC (p52.07610 -5 ), and FEV1/FVC (p55.27610 -3 ). The effect was somewhat weaker in apparently healthy subjects than in COPD or asthma patients.Our results provide indirect evidence for the hypothesis that cellular senescence may contribute to the pathogenesis of COPD and asthma, and that lung function may reflect biological ageing primarily due to intrinsic processes, which are likely to be aggravated in lung diseases. @ERSpublicationsTelomere length is decreased in asthma and COPD patients and positively associated with spirometric indices

Background Biological aging estimators derived from DNA methylation data are heritable and correlate with morbidity and mortality. Consequently, identification of genetic and environmental contributors to the variation in these measures in populations has become a major goal in the field. Results Leveraging DNA methylation and SNP data from more than 40,000 individuals, we identify 137 genome-wide significant loci, of which 113 are novel, from genome-wide association study (GWAS) meta-analyses of four epigenetic clocks and epigenetic surrogate markers for granulocyte proportions and plasminogen activator inhibitor 1 levels, respectively. We find evidence for shared genetic loci associated with the Horvath clock and expression of transcripts encoding genes linked to lipid metabolism and immune function. Notably, these loci are independent of those reported to regulate DNA methylation levels at constituent clock CpGs. A polygenic score for GrimAge acceleration showed strong associations with adiposity-related traits, educational attainment, parental longevity, and C-reactive protein levels. Conclusion This study illuminates the genetic architecture underlying epigenetic aging and its shared genetic contributions with lifestyle factors and longevity.