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Standard methodologies of heart rate variability analysis and physiological interpretation as a marker of autonomic nervous system condition have been largely published at rest, but not so much during exercise. A methodological framework for heart rate variability (HRV) analysis during exercise is proposed, which deals with the non-stationary nature of HRV during exercise, includes respiratory information, and identifies and corrects spectral components related to cardiolocomotor coupling (CC). This is applied to 23 male subjects who underwent different tests: maximal and submaximal, running and cycling; where the ECG, respiratory frequency and oxygen consumption were simultaneously recorded. High-frequency (HF) power results largely modified from estimations with the standard fixed band to those obtained with the proposed methodology. For medium and high levels of exercise and recovery, HF power results in a 20 to 40% increase. When cycling, HF power increases around 40% with respect to running, while CC power is around 20% stronger in running. [ABSTRACT FROM AUTHOR]

Most of the research in body composition of young soccer players has used anthropometric techniques as assessment methods. On the other hand, there is lack of data concerning bioelectrical impedance analysis (BIA) in young soccer players, a method which might provide more detailed information on body composition than the traditional anthropometric techniques. Purpose: Therefore, the aim of this study was to examine body composition assessed by BIA of young soccer players with regard to their age and playing position. Methods: We examined the body composition of 65 soccer players (age 15.2 ± 0.2 years, weight 63.3 ± 9.4 kg, height 171.5 ± 8.3 cm and training experience of 9.0 ± 1.5 years), classified into three age groups (U14, ~13 years; U16, ~15 years; and U18, ~17 years) and four playing positions (goalkeepers, defenders, midfielders and forwards). Results: U14 showed lower weight, BMI, intracellular and extracellular water, protein, mineral mass, basal metabolism and all parameters of body balance ( p < 0.001) than U16 and U18. Within each age group, there were differences between forwards and defenders ( p < 0.05). Also, we found differences between defenders of different age groups; defenders in the younger group had lower values in all parameters than their older counterparts and the same trend was noticed in midfielders. Conclusions: Our findings with regard to positional differences in weight, height, BMI and body fat percentage were in agreement with previous studies. However, what is novel is that we observed corresponding differences in the cellular level, which should be confirmed by future studies. [ABSTRACT FROM AUTHOR]

Although the number of centenarians is growing worldwide, the potential factors influencing the aging process remain only partially elucidated. Researchers are increasingly focusing toward biomarkers as tools to shed more light on the pathophysiology of complex phenotypes, including the ability to reach successful aging, i.e., free of major chronic diseases. We therefore conducted a case-control study examining the potential associations of multiple candidate biomarkers in healthy centenarians and sex-matched healthy elderly controls. Using a case-control study of 81 centenarians (aged ≥ 100 years) selected based on the fact that they were disease-free and 46 healthy elderly controls (aged 70–80 years), serum levels of 15 different candidate biomarkers involved in the regulation of metabolism, angiogenesis, inflammation, and bone formation were measured. Of the 15 biomarkers tested, four molecules (chemerin, fetuin-A, and fibroblast growth factors [FGF] 19 and 21) were found to be independently associated with successful aging regardless of sex. Logistic regression analysis confirmed that chemerin, fetuin-A, FGF19, and FGF21 were independently associated with successful aging [predicted probability (PP) = 1 / [1 + 1 / exp (11.832 − 0.027 × (chemerin) − 0.009 × (fetuin-A) + 0.014 × (FGF19) − 0.007 × (FGF21)]. The area under the curve (AUC) of predicted probability values for the four-biomarker panel revealed that it can discriminate between centenarians and elderly controls with excellent accuracy (AUC > 0.94, P < 0.001). Although preliminary in essence and limited by the low sample size and lack of replication in other independent cohorts, our data suggest an independent association between successful aging and serum chemerin, fetuin-A, FGF19, and FGF21, which may provide novel information on the mechanisms behind the human aging process. Whether the four-biomarker panel may predict successful aging deserves further scrutiny. [ABSTRACT FROM AUTHOR]

Introduction: Alzheimer's disease (AD) is the cause of more than two-thirds of all dementia cases. Although there is no effective treatment against this disorder, its association with neuroinflammation suggests that non-steroidal anti-inflammatory drugs (NSAIDs) might represent a potential therapeutic option. Objective: The objective of this study was to evaluate the efficacy of NSAIDs in the treatment of AD using a meta-analysis approach. Methods: MEDLINE, Web of Science, Science Direct, and the Cochrane Library were used to search all the randomized controlled trials that have evaluated the efficacy of NSAIDs as a treatment for AD (up to 1 October 2014). The overall effect of NSAIDs versus placebo was determined using a random effects model meta-analysis where we compared changes (i.e., mean differences pre- vs. post-treatment) between the two conditions in test scores indicative of cognition, disease severity, and related outcomes. Results: Seven studies were finally included in the meta-analysis. Diclofenac/misoprostol, nimesulide, naproxen, rofecoxib, ibuprofen, indomethacin, tarenflurbil, and celecoxib were the NSAIDs used in these reports. The results of the AD Assessment Scale-cognitive subscale (ADAS-cog), the Clinical Dementia Rating Scale sum-of-boxes (CDR-SOB), and the Mini-Mental State Examination (MMSE) showed no statistical or clinical significance of NSAIDs treatment compared with placebo, i.e., mean differences of −0.24 (95 % Confidence Interval (CI) −1.04 to 0.57; P = 0.52), −0.07 (95 % CI −0.7 to 0.56; P = 0.82), and 0.35 (95 % CI −0.34 to 1.04; P = 0.32), respectively. Conclusion: Current preliminary evidence suggests no beneficial effect of NSAIDs on cognition or overall AD severity. Thus, although more research is needed in the field, the evidence available does not support the use of NSAIDs for AD treatment. [ABSTRACT FROM AUTHOR]

Irisin might play an important role in reducing the risk of obesity, insulin resistance, or several related diseases, and high irisin levels may contribute to successful aging. Thus, the irisin precursor (FNDC5) gene is a candidate to influence exceptional longevity (EL), i.e., being a centenarian. It has been recently shown that two single-nucleotide polymorphisms (SNPs) in the FNDC5 gene, rs16835198 and rs726344, are associated with in vivo insulin sensitivity in adults. We determined luciferase gene reporter activity in the two above-mentioned SNPs and studied genotype distributions among centenarians (n = 175, 144 women) and healthy controls (n = 347, 142 women) from Spain. We also studied an Italian [79 healthy centenarians (40 women) and 316 healthy controls (156 women)] and a Japanese cohort [742 centenarians (623 women) and 499 healthy controls (356 women)]. The rs726344 SNP had functional significance, as shown by differences in luciferase activity between the constructs of this SNP (all P ≤ 0.05), with the variant A-allele having higher luciferase activity compared with the G-allele (P = 0.04). For the rs16835198 SNP, the variant T-allele tended to show higher luciferase activity compared with the G-allele (P = 0.07). However, we found no differences between genotype/allele frequencies of the two SNPs in centenarians versus controls in any cohort, and no significant association (using logistic regression adjusted by sex) between the two SNPs and EL. Further research is needed with different cohorts as well as with additional variants in the FNDC5 gene or in other genes involved in irisin signaling. [ABSTRACT FROM AUTHOR]

The rs1333049 (G/C) polymorphism located on chromosome 9p21.3 is a candidate to influence extreme longevity owing to its association with age-related diseases, notably coronary artery disease (CAD). We compared allele/genotype distributions of rs1333049 in cases (centenarians) and controls (younger adults, without (healthy) or with CAD) in two independent cohorts: Spanish (centenarians: n = 152, 128 women, 100-111 years; healthy controls: n = 343, 212 women, age <50 years; CAD controls: n = 98, 32 women, age ≤65 years) and Japanese (centenarians: n = 742, 623 women, 100-115 years; healthy controls: n = 920, 511 women, < 60 years; CAD controls: n = 395, 45 women, age ≤65 years). The frequency of the 'risk' C-allele tended to be lower in Spanish centenarians (47.0 %) than in their healthy (52.9 %, P = 0.088) or CAD controls (55.1 %, P = 0.078), and significant differences were found in genotype distributions ( P = 0.034 and P = 0.045), with a higher frequency of the GG genotype in cases than in both healthy and CAD controls as well as a lower proportion of the CG genotype compared with healthy controls. In the Japanese cohort, the main finding was that the frequency of the C-allele did not differ between centenarians (46.4 %) and healthy controls (47.3 %, P = 0.602), but it was significantly lower in the former than in CAD controls (57.2 %, P < 0.001). Although more research is needed, the present and recent pioneer findings ( Rejuvenation Res 13:23-26, 2010) suggest that the rs1333049 polymorphism could be among the genetic contributors to exceptional longevity in Southern European populations, albeit this association does not exist in the healthy (CAD-free) Japanese population. [ABSTRACT FROM AUTHOR]

The myostatin ( MSTN) gene is a candidate to influence extreme longevity owing to its role in modulating muscle mass and sarcopenia and especially in inhibiting the main nutrient-sensing pathway involved in longevity, i.e. mammalian target of rapamycin. We compared allele/genotype distributions of the exonic MSTN variants K153R (rs1805086), E164K (rs35781413), I225T and P198A, in Spanish centenarians ( cases, n = 156; 132 women, age range 100-111 years) and younger adults ( controls, n = 384; 167 women, age <50 years). No subject of either group carried a mutant allele of the E164K, I225T or P198A variation. The frequency of the variant R allele was significantly higher in centenarians (7.1 %) than in controls (2.7 %) ( P = 0.001). The odds ratio of being a centenarian if the subject had the R allele was 3.48 (95 % confidence interval 1.67-7.28, P = 0.001), compared to the control group, after adjusting for sex. The results were replicated in an Italian cohort (centenarians, n = 79 (40 women), age range 100-104 years; younger controls, n = 316 (155 women), age <50 years), where a higher frequency of the R allele in centenarians (7.6 %) compared to controls (3.0 %) ( P = 0.004) was independently confirmed. Although more research is needed, the variant allele of the MSTN K153R polymorphism could be among the genetic contributors associated with exceptional longevity. [ABSTRACT FROM AUTHOR]

Western populations are living longer. Ageing decline in muscle mass and strength (i.e. sarcopenia) is becoming a growing public health problem, as it contributes to the decreased capacity for independent living. It is thus important to determine those genetic factors that interact with ageing and thus modulate functional capacity and skeletal muscle phenotypes in older people. It would be also clinically relevant to identify 'unfavourable' genotypes associated with accelerated sarcopenia. In this review, we summarized published information on the potential associations between some genetic polymorphisms and muscle phenotypes in older people. A special emphasis was placed on those candidate polymorphisms that have been more extensively studied, i.e. angiotensin-converting enzyme ( ACE) gene I/D, α-actinin-3 ( ACTN3) R577X, and myostatin ( MSTN) K153R, among others. Although previous heritability studies have indicated that there is an important genetic contribution to individual variability in muscle phenotypes among old people, published data on specific gene variants are controversial. The ACTN3 R577X polymorphism could influence muscle function in old women, yet there is controversy with regards to which allele (R or X) might play a 'favourable' role. Though more research is needed, up-to-date MSTN genotype is possibly the strongest candidate to explain variance among muscle phenotypes in the elderly. Future studies should take into account the association between muscle phenotypes in this population and complex gene-gene and gene-environment interactions. [ABSTRACT FROM AUTHOR]

Our study purpose was to compare a disease-related polygenic profile that combined a total of 62 genetic variants among (i) people reaching exceptional longevity, i.e., centenarians ( n = 54, 100-108 years, 48 women) and (ii) ethnically matched healthy controls ( n = 87, 19-43 years, 47 women). We computed a 'global' genotype score (GS) for 62 genetic variants (mutations/polymorphisms) related to cardiometabolic diseases, cancer or exceptional longevity, and also specific GS for main disease categories (cardiometabolic risk and cancer risk, including 36 and 24 genetic variations, respectively) and for exceptional longevity (7 genetic variants). The 'global' GS was similar among groups (centenarians: 31.0 ± 0.6; controls 32.0 ± 0.5, P = 0.263). We observed that the GS for hypertension, cancer (global risk), and other types of cancer was lower in the centenarians group compared with the control group (all P < 0.05), yet the difference became non significant after adjusting for sex. We observed significant between-group differences in the frequency of GSTT1 and GSTM1 (presence/absence) genotypes after adjusting for multiple comparisons. The likelihood of having the GSTT1 low-risk (functional) allele was higher in centenarians (odds ratio [OR] 5.005; 95% confidence interval [CI], 1.810-13.839), whereas the likelihood of having the GSTMI low-risk (functional) allele was similar in both groups (OR 1.295; 95% CI, 0.868 -1.931). In conclusion, we found preliminary evidence that Spanish centenarians have a lower genetic predisposition for cancer risk. The wild-type (i.e., functional) genotype of GSTT1, which is associated with lower cancer risk, might be associated with exceptional longevity, yet further studies with larger sample sizes must confirm these findings. [ABSTRACT FROM AUTHOR]

We studied the single and combined influence of the ACE I/D and the ACTN3 R577X polymorphisms on muscle phenotypes (thigh muscles' cross-sectional area assessed with magnetic resonance imaging) and strength (maximal handgrip, 30-s chair stand test), functional ability during activities of daily living (Barthel index) and bone mineral density (proximal femur) in Caucasian (Spanish) community-dwelling old people [ n = 81, 59 women; mean age 82.8 ± 4.8 years (range 71-93 years)]. We found no significantly differences in the aforementioned phenotypes across ACE and ACTN3 genotypes (all P > 0.05), except for handgrip in the ACE I/D recessive model (DD 19.5 ± 6.7 kg, ID 24.0 ± 9.1 kg, II 22.1 ± 7.9; P = 0.047), yet statistical significance disappeared after correction for multiple comparisons. Likewise, the analyses of the combined effects between genotypes did not yield any significant difference (all P > 0.05) between the two 'extreme' genotypes [theoretically 'power or muscularity oriented' [( ACTN3 RR + RX & ACE DD) versus 'non-power' ( ACTN3 XX & ACE II + ID)]. The aforementioned analyses were adjusted by sex, age and physical activity levels as covariates. Logistic regression analysis revealed no significant association of single or combined effect of ACE and ACTN3 genotypes or genotype combination group ( ACE + ACTN3) with sarcopenia (i.e. being in the lowest 25th sex-specific percentile for a combined score of the muscle and functional phenotypes we measured). Though ACE I/D and ACTN3 R577X polymorphisms are candidates to modulate exercise-related phenotypes in adults, our data suggest that they do not exert a major influence in the muscle phenotypes of old people. More studies with larger sample sizes are needed. [ABSTRACT FROM AUTHOR]

Mitochondrial haplogroups could influence individual susceptibility to mitochondrial DNA (mtDNA) damage, and human longevity, as indicated by previous studies with Caucasian (European) or Asian cohorts. Here, we compared the frequency of mtDNA haplogroups in a group of Spanish (Caucasian) centenarians ( n = 65, aged 100-108 years, 58 women, most from the central part of Spain) and a group of healthy young adults ( n = 138, 62 women, aged 20-40 years) of the same ethnic origin. We did not find significant differences between centenarians and the control group ( P > 0.2). Only two centenarians (both women) had the haplogroup J, which hampered comparison with the control group ( n = 15, five women). Our data confirm that the potential effects of mitochondrial haplogroups on human longevity might be population/geographic specific, with important differences between studies (notably, with regard to the previously reported potential benefit brought about by the haplogroup J) arising from the different living environment and ethnic background of the study cohorts. [ABSTRACT FROM AUTHOR]