The prevalence of the frailty syndrome in older Spanish adults is high and similar to that reported in other populations in the Mediterranean basin.

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Background The associations between free‐living physical activity (PA) and sedentary behaviour (SB) and sarcopenia in older people and its determinants are controversial. Self‐reporting, the use of one‐size‐fits‐all cut‐points for intensity categorization when using accelerometers and the absence of a clear sarcopenia definition hampered explorations. The aim of this study is to describe the associations between objectively measured PA patterns and sarcopenia and its determinants. Methods Subjects aged >65 with valid accelerometry and sarcopenia‐related measures from Toledo Study of Healthy Aging (TSHA) were included. Muscle mass (MM) was estimated by dual‐energy X‐ray absorptiometry. Handgrip strength (HS) was measured by dynamometry. Physical performance assessment relied on gait speed (GS). Sarcopenia presence was ascertained using Foundation for the National Institutes of Health (FNIH) criteria. PA and SB were estimated by ActiTrainer worn for 1 week and classified into time spent in SB and different PA intensity bands [light PA (LPA) and moderate‐to‐vigorous PA (MVPA)] using age‐specific cut‐points. Different multivariate linear and logistic regression models [(i) single‐parameter, (ii) partition, and (iii) isotemporal substitution models] were used for estimating associations between PA, SB, and sarcopenia determinants and sarcopenia rates, respectively. All models adjusted for age, sex, co‐morbidities (Charlson index), and functional ability (Katz and Lawton indexes). Results Five hundred twelve subjects from the TSHA had available data (78.08 ± 5.71 years of age; 54.3% women). FNIH sarcopenia assessment was performed in 497 subjects (23.3% were sarcopenic). In the linear regression, the single‐parameter model showed an association between MVPA and all sarcopenia determinants. In the partition model, MVPA was associated with greater MM and GS. The isotemporal substitution showed that reallocating 1 h/day of MVPA displacing SB was associated with greater values in MM [ β = 0.014; 95% confidence interval (CI) = 0.004, 0.024; P < 0.01], GS ( β = 0.082; 95% CI = 0.054, 0.110; P < 0.001), and HS ( β = 0.888; 95% CI = 0.145, 1.631; P < 0.05). In the logistic regression, the single‐parameter model yielded a significant association between 1 h/day increase in MVPA and sarcopenia reduction [odds ratio (OR) = 0.522; 95% CI = 0.367, 0.726; P < 0.001], as did the partition model (OR = 0.555; 95% CI = 0.376, 0.799; P < 0.01). The reallocation of 1 h/day SB only yielded a significant lower sarcopenia risk by almost 50% when it was substituted with MVPA, whereas the substitution of 15 min/day yielded a significant lower sarcopenia risk by 15% ( P < 0.001) but did not show any association...

Circulating oxidative damage biomarkers, such as MDA and protein carbonylation, are related to frailty and not to age or sex. These parameters may be considered as potential biomarkers of frailty in the context of a multidisciplinary health-promoting approach for older adults.

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BackgroundLife expectancy at birth in the first world has increased from 35 years at the beginning of the 20th century to more than 80 years now. The increase in life expectancy has resulted in an increase in age-related diseases and larger numbers of frail and dependent people. The aim of our study was to determine whether life-long spontaneous aerobic exercise affects lifespan and healthspan in mice.ResultsMale C57Bl/6J mice, individually caged, were randomly assigned to one of two groups: sedentary (n = 72) or spontaneous wheel-runners (n = 72). We evaluated longevity and several health parameters including grip strength, motor coordination, exercise capacity (VO2max) and skeletal muscle mitochondrial biogenesis. We also measured the cortical levels of the brain-derived neurotrophic factor (BDNF), a neurotrophin associated with brain plasticity. In addition, we measured systemic oxidative stress (malondialdehyde and protein carbonyl plasma levels) and the expression and activity of two genes involved in antioxidant defense in the liver (that is, glutathione peroxidase (GPx) and manganese superoxide dismutase (Mn-SOD)). Genes that encode antioxidant enzymes are considered longevity genes because their over-expression may modulate lifespan. Aging was associated with an increase in oxidative stress biomarkers and in the activity of the antioxidant enzymes, GPx and Mn-SOD, in the liver in mice. Life-long spontaneous exercise did not prolong longevity but prevented several signs of frailty (that is, decrease in strength, endurance and motor coordination). This improvement was accompanied by a significant increase in the mitochondrial biogenesis in skeletal muscle and in the cortical BDNF levels.ConclusionLife-long spontaneous exercise does not prolong lifespan but improves healthspan in mice. Exercise is an intervention that delays age-associated frailty, enhances function and can be translated into the clinic.

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The development of animal models to study human frailty is important to test interventions to be translated to the clinical practice. The aim of this work was to develop a score for frailty in experimental animals based in the human frailty phenotype. We also tested the effect of physical inactivity in the development of frailty as determined by our score. Male C57Bl/6J mice, individually caged, were randomly assigned to one of two groups: sedentary (inactive) or spontaneous wheel-runners. We compared the sedentary versus the active lifestyle in terms of frailty by evaluating the clinical criteria used in humans: unintentional weight loss; poor endurance (running time); slowness (running speed); weakness (grip strength), and low activity level (motor coordination) at five different ages: 17, 20, 23, 26 and 28 months of age. Each criterion had a designated cut-off point to identify the mice with the lowest performance. Lifelong spontaneous exercise significantly retards frailty. On the contrary sedentary animals become frail as they age. Thus, physical inactivity is a model of frailty in experimental animals. Our frailty score provides a tool to evaluate interventions in mice prior to translating them to clinical practice.