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Age (Dordrecht, Netherlands) Sep 2007Our purpose was to examine the effects of age and gender on physical performance. We assessed a one-hour swimming performance and participation of 4,271 presumably...
Our purpose was to examine the effects of age and gender on physical performance. We assessed a one-hour swimming performance and participation of 4,271 presumably healthy men and women, aged 19-91 years, from the 2001-2003 United States Masters Swimming long-distance (1 h) national competition. The decline in performance with increasing age was found to be quadratic rather than linear. The equation which best fit variation in 1 h swimming distance in meters (m) according to variations in age in years (y) in men was: distance (m) = 4058 + 2.18 age-0.29 age (http://www.acsmmsse.org/pt/re/msse/positionstandards.htm;jsessionid=DiRVACC7YS3mq27s5kV3vwpEVSokmmD1ZJLC7pdnol3KcfoSu0t!1096311956!-949856145!9001!-1), with the same equation for women except that 380 m needed to be subtracted from the calculated value at all ages (about a 10% difference). There was a large overlap in performance between men and women. The overall mean decline in performance with age was about 50% and was parallel in men and women. The mean difference in distance for a 1-year increment in age was -9.7 m at 21 y of age, -21.3 m at 40 y, and -44.5 m at 80 y. Far greater declines of about 96% in numbers participating with advanced age (80 y and over, 4% of peak numbers) were observed than in the 40-49 y age group. In conclusion, the declines in performance were parallel in men and women at all ages, and the 1-year age-related declines in performance were about twice as great at 40 y and more than four-times as great at 80 y than at 20 y of age, with even greater age-related declines in participation being noted for both men and women.
PubMed: 19424833
DOI: 10.1007/s11357-007-9034-z -
Age (Dordrecht, Netherlands) Apr 2016The differential characteristics of absolute power in the EEG theta (4-8 Hz) and gamma (30-45 Hz) frequency bands have been analysed in young (18-25 years old,...
The differential characteristics of absolute power in the EEG theta (4-8 Hz) and gamma (30-45 Hz) frequency bands have been analysed in young (18-25 years old, n = 14) and mature adults (45-65 years old, n = 12) during the incidental or intentional behavioural conditions of learning and recalling in a visuospatial task. A printed drawing of a maze including eight figures of common objects in specific placements, solved by connecting its entrance and exit points, allowed the subject's performance efficiency to be measured based on the number, position accuracy and/or identity of incidentally or intentionally learned and remembered objects. Meanwhile, EEG recordings from frontal, parietal and temporal derivations were obtained to determine the power values of the theta (4-8 Hz) and gamma (30-45 Hz) bands for each behavioural condition and derivation. Relative to the young adults, the mature adults generally showed lower absolute theta power values, mainly due to their low theta powers under the basal and incidental learning conditions, and higher absolute gamma power values in the frontal and temporal regions. Furthermore, higher theta band power in the frontal regions was related to higher performance efficiency in both incidental and intentional learning, regardless of the subjects' age. A significant negative correlation between the parameters of individual incidental or intentional learning performance and age was also found. Indeed, a differential accuracy of remembered information seems to be associated with age and incidental or intentional learning/memory testing conditions. These data support an increasing vulnerability of visuospatial learning abilities at mature ages and as ageing progresses.
Topics: Adult; Aged; Aging; Electroencephalography; Frontal Lobe; Humans; Male; Memory, Short-Term; Middle Aged; Spatial Learning; Young Adult
PubMed: 26961695
DOI: 10.1007/s11357-016-9896-z -
Age (Dordrecht, Netherlands) Apr 2016Autophagy is a molecular process essential for the maintenance of cellular homeostasis, which appears to (i) decline with age and (ii) respond to physical exercise. In... (Randomized Controlled Trial)
Randomized Controlled Trial
Autophagy is a molecular process essential for the maintenance of cellular homeostasis, which appears to (i) decline with age and (ii) respond to physical exercise. In addition, recent evidence suggests a crosstalk between autophagy and toll-like receptor (TLR)-associated inflammatory responses. This study assessed the effects of aerobic exercise training on autophagy and TLR signaling in older subjects. Twenty-nine healthy women and men (age, 69.7 ± 1.0 year) were randomized to a training (TG) or a control (CG) group. TG performed an 8-week aerobic training program, while CG followed their daily routines. Peripheral blood mononuclear cells were isolated from blood samples obtained before and after the intervention, and protein levels of protein 1 light chain 3 (LC3), sequestosome 1 (p62/SQSTM1), beclin-1, phosphorylated unc-51-like kinase (ULK-1), ubiquitin-like autophagy-related (Atg)12, Atg16, and lysosome-associated membrane protein (LAMP)-2 were measured. TLR2 and TLR4 signaling pathways were also analyzed. Peak oxygen uptake increased in TG after the intervention. Protein expression of beclin-1, Atg12, Atg16, and the LC3II/I ratio increased following the training program (p < 0.05), while expression of p62/SQSTM1 and phosphorylation of ULK-1 at Ser(757) were lower (p < 0.05). Protein content of TLR2, TLR4, myeloid differentiation primary response gen 88 (MyD88), and TIR domain-containing adaptor-inducing interferon (TRIF) were not significantly modified by exercise. The current data indicate that aerobic exercise training induces alterations in multiple markers of autophagy, which seem to be unrelated to changes in TLR2 and TLR4 signaling pathways. These results expand knowledge on exercise-induced autophagy adaptations in humans and suggest that the exercise type employed may be a key factor explaining the potential relationship between autophagy and TLR pathways.
Topics: Adult; Aged; Aging; Autophagy; Biomarkers; Blotting, Western; Female; Humans; Leukocytes, Mononuclear; Male; Middle Aged; Physical Fitness; Signal Transduction; Toll-Like Receptor 4; Young Adult
PubMed: 26940016
DOI: 10.1007/s11357-016-9897-y -
Age (Dordrecht, Netherlands) Mar 2010A postural vertical (PV) tilted backward has been put forward as a reason explaining the backward disequilibrium often observed in elderly fallers. This raises the...
A postural vertical (PV) tilted backward has been put forward as a reason explaining the backward disequilibrium often observed in elderly fallers. This raises the question of a possible ageing process of the PV involving a backward tilt of verticality perception increasing with age. We have explored this hypothesis by measuring PV in pitch using the wheel paradigm in 87 healthy subjects aged from 20 to 97 years. The possibility that this physiological ageing accelerated in the second part of life was also analysed. Two indices were calculated: the mean orientation (PV-orient) and the dispersion (PV-uncert). The correlation between age and PV-orient was r = -0.2 (p < 0.05). Added to the fact that PV was twice as shifted backward in the 38 seniors over 50 years (-1.15 degrees +/- 1.40 degrees ) as in the 49 young adults under 50 years (-0.45 degrees +/- 0.97 degrees ; t = 2.75, p < 0.01), this indicates the existence of a physiological ageing process on the direction perceived as vertical by the whole body, with a slight backward shift of PV throughout the life span. The correlation between age and PV-uncert was r = 0.35 (p < 0.001) in all subjects and r = 0.59 (p < 0.001) in seniors. This indicates that subjects get less and less accurate in their perception of the postural vertical with age, especially very old subjects who show great uncertainty in determining with their body the direction of the vertical. Taken together, these findings indicate that the internal model of verticality is less robust in elderly people. This may play a part in their postural decline.
Topics: Adult; Aged; Aged, 80 and over; Aging; Analysis of Variance; Chi-Square Distribution; Female; Humans; Middle Aged; Orientation; Postural Balance; Posture; Proprioception; Reproducibility of Results; Statistics, Nonparametric
PubMed: 19711197
DOI: 10.1007/s11357-009-9112-5 -
Age (Dordrecht, Netherlands) Sep 2011Aged canines naturally accumulate several types of neuropathology that may have links to cognitive decline. On a gross level, significant cortical atrophy occurs with...
Aged canines naturally accumulate several types of neuropathology that may have links to cognitive decline. On a gross level, significant cortical atrophy occurs with age along with an increase in ventricular volume based on magnetic resonance imaging studies. Microscopically, there is evidence of select neuron loss and reduced neurogenesis in the hippocampus of aged dogs, an area critical for intact learning and memory. The cause of neuronal loss and dysfunction may be related to the progressive accumulation of toxic proteins, oxidative damage, cerebrovascular pathology, and changes in gene expression. For example, aged dogs naturally accumulate human-type beta-amyloid peptide, a protein critically involved with the development of Alzheimer's disease in humans. Further, oxidative damage to proteins, DNA/RNA and lipids occurs with age in dogs. Although less well explored in the aged canine brain, neuron loss, and cerebrovascular pathology observed with age are similar to human brain aging and may also be linked to cognitive decline. Interestingly, the prefrontal cortex appears to be particularly vulnerable early in the aging process in dogs and this may be reflected in dysfunction in specific cognitive domains with age.
Topics: Aging; Amyloid beta-Peptides; Animals; Brain; Brain Chemistry; Cerebrovascular Circulation; Dogs; Female; Gene Expression; Inflammation; Male; Models, Animal; Neurobiology; Neurons; Neurotransmitter Agents; Oxidative Stress
PubMed: 20845082
DOI: 10.1007/s11357-010-9183-3 -
Age (Dordrecht, Netherlands) Apr 2014Declines in muscle size and strength are commonly reported as a consequence of aging; however, few studies have investigated the influence of aging on the rate of muscle... (Comparative Study)
Comparative Study
Declines in muscle size and strength are commonly reported as a consequence of aging; however, few studies have investigated the influence of aging on the rate of muscle activation and rapid force characteristics across the lifespan. This study aims to investigate the effects of aging on the rate of muscle activation and rapid force characteristics of the plantar flexors. Plantar flexion peak force (PF), absolute (peak, 50, and 100-200 ms), and relative (10 %, 30 %, and 50 %) rate of force development (RFD), the rapid to maximal force ratio (RFD/PF), and the rate of electromyography rise (RER) were examined during an isometric maximal voluntary contraction (MVC) in young (age = 22 ± 2 years), middle-aged (43 ± 2 years), and old (69 ± 5 years) men. The old men exhibited lower PF (30.7 % and 27.6 % lower, respectively) and absolute (24.4-55.1 %) and relative (16.4-28.9 %) RFD values compared to the young and middle-aged men (P ≤ 0.03). RER values were similar between the young and old men (P ≥ 0.30); however, RER values were greater for the middle-aged men when compared to the young and old men for the soleus (P < 0.01) and the old men for the medial gastrocnemius (P ≤ 0.02). Likewise, RFD/PF ratios were similar between young and old men (P ≥ 0.26); however, these ratios were greater for the middle-aged men at early (P ≤ 0.03), but not later (P ≥ 0.10), time intervals. The lower PF and absolute and relative RFD values for the old men may contribute to the increased functional limitations often observed in older adults. Interestingly, higher rates of muscle activation and greater early RFD/PF ratios in middle-aged men may be a reflection of physiological alterations in the neuromuscular system occurring in the fifth decade.
Topics: Adult; Aged; Aging; Electromyography; Follow-Up Studies; Healthy Volunteers; Humans; Isometric Contraction; Male; Middle Aged; Muscle Strength Dynamometer; Muscle, Skeletal; Young Adult
PubMed: 24338233
DOI: 10.1007/s11357-013-9605-0 -
Age (Dordrecht, Netherlands) Jun 2012We assessed whether melatonin administration would prevent the hyperoxidative status that occurs in lung mitochondria with age. Mitochondria from lungs of male and... (Comparative Study)
Comparative Study
We assessed whether melatonin administration would prevent the hyperoxidative status that occurs in lung mitochondria with age. Mitochondria from lungs of male and female senescent prone mice at 5 and 10 months of age were studied. Age-dependent mitochondrial oxidative stress was evaluated by measuring the levels of lipid peroxidation and nitrite, glutathione/glutathione disulfide ratio, and glutathione peroxidase and reductase activities. Mitochondrial respiratory chain and oxidative phosphorylation capability were also measured. Age induces a significant oxidative/nitrosative status in lung mitochondria, which exhibited a significantly reduced activity of the respiratory chain and ATP production. These manifestations of age were more pronounced in males than in females. After 9 months of melatonin administration in the drinking water, the hyperoxidative status and functional deficiency of aged lung mitochondria were totally counteracted, and had increased ATP production. The beneficial effects of melatonin were generally similar in both mice genders. Thus, melatonin administration, as a single therapy, maintained fully functioning lung mitochondria during aging, a finding with important consequences in the pathophysiology of lung aging. In view of these data melatonin, the production of which decreases with age, should be considered a preventive therapy against the hyperoxidative status of the aged lungs, and its use may lead to the avoidance of respiratory complications in the elderly.
Topics: Adenosine Triphosphate; Administration, Oral; Aging; Animals; Antioxidants; Disease Models, Animal; Electron Transport; Female; Lung; Male; Melatonin; Mice; Mitochondria; Oxidative Phosphorylation; Oxidative Stress
PubMed: 21614449
DOI: 10.1007/s11357-011-9267-8 -
Age (Dordrecht, Netherlands) Oct 2013Type 2 diabetes is characterized by a deficit in β-cell function and mass, and its incidence increases with age. Autophagy is a highly regulated intracellular process...
Type 2 diabetes is characterized by a deficit in β-cell function and mass, and its incidence increases with age. Autophagy is a highly regulated intracellular process for degrading cytoplasmic components, particularly protein aggregates and damaged organelles. Impaired or deficient autophagy is believed to cause or contribute to aging and age-related disease. Autophagy may be necessary to maintain structure, mass, and function of pancreatic β-cells. In this study, we investigated the effects of age on β-cell function and autophagy in pancreatic islets of 4-month-old (young), 14-month-old (adult), and 24-month-old (old) male Wistar rats. We found that islet β-cell function decreased gradually with age. Protein expression of the autophagy markers LC3/Atg8 and Atg7 exhibited a marked decline in aged islets. The expression of Lamp-2, a good indicator of autophagic degradation rate, was significantly reduced in the islets of old rats, suggesting that autophagic degradation is decreased in the islets of aged rats. However, protein expression of beclin-1/Atg6, which plays an important role in the induction and formation of the pre-autophagosome structure by associating with a multimeric complex of autophagy regulatory proteins (Atg14, Vps34/class 3 PI3 kinase, and Vps15), was most prominent in the islets of adult rats, and was higher in 24-month-old islets than in 4-month-old islets. The levels of p62/SQSTM1 and polyubiquitin aggregates, representing the functions of autophagy and proteasomal degradation, were increased in aging islets. 8-Hydroxydeoxyguanosine, a marker of mitochondrial and nuclear DNA oxidative damage, exhibited strong immunostaining in old islets. Analysis by electron microscopy demonstrated swelling and disintegration of cristae in the mitochondria of aged islets. These results suggest that β-cell and autophagic function in islets decline simultaneously with increasing age in Wistar rats, and that impaired autophagy in the islets of older rats may cause accumulation of misfolded and aggregated proteins and reduce the removal of abnormal mitochondria in β-cells, leading to reduced β-cell function. Dysfunctional autophagy in islets during the aging process may be an important mechanism leading to the development of type 2 diabetes.
Topics: Aging; Animals; Autophagy; Autophagy-Related Protein 7; Blotting, Western; Diabetes Mellitus, Experimental; Disease Progression; Immunohistochemistry; Insulin-Secreting Cells; Male; Microscopy, Electron; Microtubule-Associated Proteins; Rats; Rats, Wistar; Ubiquitin-Activating Enzymes
PubMed: 22843415
DOI: 10.1007/s11357-012-9456-0 -
Age (Dordrecht, Netherlands) Dec 2012While overall DNA methylation decreases with age, CpG-rich areas of the genome can become hypermethylated. Hypermethylation near transcription start sites typically...
While overall DNA methylation decreases with age, CpG-rich areas of the genome can become hypermethylated. Hypermethylation near transcription start sites typically decreases gene expression. Klotho (KL) is important in numerous age-associated pathways including insulin/IGF1 and Wnt signaling and naturally decreases with age in brain, heart, and liver across species. Brain tissues from young and old rhesus monkeys were used to determine whether epigenetic modification of the KL promoter underlies age-related decreases in mRNA and protein levels of KL. The KL promoter in genomic DNA from brain white matter did not show evidence of oxidation in vivo but did exhibit an increase in methylation with age. Further analysis identified individual CpG motifs across the region of interest with increased methylation in old animals. In vitro methyl modification of these individual cytosine residues confirmed that methylation of the promoter can decrease gene transcription. These results provide evidence that changes in KL gene expression with age may, at least in part, be the result of epigenetic changes to the 5' regulatory region.
Topics: 5-Methylcytosine; Aging; Animals; Brain; Cell Line; Cytosine; DNA Methylation; Down-Regulation; Epigenesis, Genetic; Female; Gene Expression Regulation; Glucuronidase; Klotho Proteins; Macaca mulatta; Male; Promoter Regions, Genetic; RNA, Messenger; Transcription Factors
PubMed: 21922250
DOI: 10.1007/s11357-011-9315-4 -
Age (Dordrecht, Netherlands) Jun 2013Biological aging alters the metabolism and volume of adipose tissue depots. Recent evidence suggests that circadian mechanisms play a role in promoting adipogenesis,... (Comparative Study)
Comparative Study
Biological aging alters the metabolism and volume of adipose tissue depots. Recent evidence suggests that circadian mechanisms play a role in promoting adipogenesis, obesity, and lipodystrophy. The current study compared cohorts of younger (5-9 months) and older (24-28 months) C57BL/6 mice as a function of biological age and circadian time. Advanced age significantly reduced the weight of the brown, epididymal, inguinal, and retroperitoneal adipose depots but not total body weight. The older mice reduced their physical activity by >50% and delayed their activity initiation after light offset. The expressed transcriptome in brown and white adipose depots and liver of both cohorts displayed evidence of circadian rhythmicity; however, the oscillating mRNAs differed significantly between age groups and across tissues. The amplitude of Cry1, a component of the negative arm of the circadian apparatus, and downstream regulators such as Rev-erbα were elevated in the older relative to the younger cohorts as a function of circadian time. Overall, transcript levels differed significantly for 557 (inguinal adipose), 1,016 (liver), and 1,021 (brown adipose) expressed sequences between the cohorts as a function of age. These included transcripts encoding proteins within the canonical and non-canonical Wnt pathways. Since the Wnt pathway regulates adipose stem cell differentiation and shares a critical enzyme, glycogen synthase kinase 3β, with the circadian mechanism, the intersection between these two fundamental regulatory mechanisms merits further investigation with respect to biological aging of adipose tissues.
Topics: Adipogenesis; Adipose Tissue; Aging; Animals; Cell Differentiation; Circadian Rhythm; Disease Models, Animal; Follow-Up Studies; Male; Mice; Mice, Inbred C57BL
PubMed: 22411258
DOI: 10.1007/s11357-012-9389-7