Physical activity has long been touted as a means of reducing susceptibility to age-related disease and multiple studies have shown reduced mortality rates in individuals with a lifestyle including regular exercise. A variety of mechanisms for how physical activity reduces age-related diseases have been explored and multiple, redundant explanatory mechanisms are likely to emerge. Evidence has emerged that physical activity may impact directly on telomere biology, one of the primary theories of cellular aging. Telomeres are located at the ends of chromosomes and as cells divide, incomplete DNA replication results in telomere shortening; once shortening reaches a critical threshold, cell senescence results. Investigators hypothesize that part of the favorable influence of physical activity on mortality rates and age-related disease occurs through a direct impact on telomere biology, including delaying rates of telomere shortening. The present review examines key recent findings in this area and explores some of the unanswered questions and future directions for the field.
Kiyoji Tanaka, Ryosuke Shigematsu, Masaki Nakagaichi, Hunkyung Kim, and Nobuo Takeshima
In Japan, 2 approaches have been adopted to assess health and functional status in older adults. One is a battery of physical-performance tasks. The other is estimation of physical vitality using biomedical risk factors. Previous research has examined strength and direction of the relationship between functional fitness and performance on activities of daily living. Vital-age tests have most often been used to assess risk for developing a variety of age-related diseases. The present study examined interrelationships among functional fitness and vital-age scores in Japanese women (N = 129, mean age = 71.9). The functional fitness test battery consisted of arm curls, walking around 2 cones, moving beans with chopsticks, and functional reach. The vital-age test battery consisted of 6 coronary heart disease risk factors (systolic blood pressure, total cholesterol, low-density lipoprotein cholesterol, triglycerides, abdominal girth, and hematocrit) and 5 physical-performance variables (oxygen uptake and heart rate at lactate threshold, side-to-side stepping, 1-leg balance with eyes closed, and forced expiratory volume).
Sarah Aldred, Manjit Rohalu, Kate Edwards, and Victoria Burns
Dehydroepiandrosterone (DHEA) and its sulfate (DHEAS) are hormones produced by the adrenal cortex that decline in concentration with age. Decreased DHEA levels are associated with age-related disease and oxidative stress but might be increased in younger adults by exercise. Studies are presented assessing the response of DHEA and DHEAS to varied-intensity exercise in older age. DHEA increased significantly in young adults (14.5 ± 6.1 ng/ml rising to 21.1 ± 7.5 ng/ml; p < .01), whereas DHEAS decreased significantly (2.56 ± 1.11 µg/ml falling to 1.90 ± 0.8 µg/ml; p < .05), after submaximal exercise. DHEA and DHEAS levels were significantly lower in older adults than in younger adults (p < .01), and there was no observed response of either hormone to exercise in older adults. Lipoprotein protein carbonylation is presented as a measure of oxidative status and significantly decreased in younger adults postexercise. Participants with higher DHEA postexercise had lower LDL protein carbonyl concentrations (Pearson’s coefficient –.409, p < .05).
Marcus Colon, Andrew Hodgson, Eimear Donlon, and James E.J. Murphy
, body mass, and percentage body fat. It is now widely accepted that regular physical activity reduces the risk of many age-related diseases and promotes a higher quality of life. More recently, it has been hypothesized that exercise can slow cellular aging by decreasing the rate of telomere shortening
Scott J. Dankel, Jeremy P. Loenneke, and Paul D. Loprinzi
telomere biology: exploring the link with aging-related disease prevention, physical activity and telomere biology: exploring the link with aging-related disease prevention . J Aging Res . 2011 ; 2011 : e790378 . doi:10.4061/2011/790378 10.4061/2011/790378 31. Chen L , Nelson DR , Zhao Y , Cui
Salih A. Salih, Nancye M. Peel, Di Enright, and Wendy Marshall
. ( 2017 ). ‘Age-related diseases and clinical and public health implications for the 85 years old and over population’ , Frontiers in Public Health, 5 , 335 . doi:10.3389/fpubh.2017.00335 10.3389/fpubh.2017.00335 Klenk , J. , Rapp , K. , Denkinger , M. , Nagel , G. , Nikolaus , T. , Peter
Emmanuel Gomes Ciolac, José Messias Rodrigues da Silva, and Rodolfo Paula Vieira
part, by its effects on the immune system (Figure 1 ). 3 , 4 , 8 Figure 1 —The cycle of aging, sedentary lifestyle, immunomodulation, and age-related disease, and the potential role of exercise training counteracting this cycle. The present review summarizes the clinical and experimental studies
André L. Estrela, Aline Zaparte, Jeferson D. da Silva, José Cláudio Moreira, James E. Turner, and Moisés E. Bauer
may lead to the development of aging characteristics of skeletal muscle and various aging-related diseases. In response to a single bout of aerobic exercise, the 8-oxoG level was lastingly elevated in sedentary young and old subjects, but returned rapidly to preexercise levels in the DNA of physically
Jesse Mala, Jennifer McGarry, Kristen E. Riley, Elaine C.-H. Lee, and Lindsay DiStefano
). Cumulative exposure to adversity (e.g., abuse, violence, neglect) including experiencing socioeconomic disadvantage during childhood is related to the many leading causes of death among adults ( Felitti et al., 1998 ) and is predictive of age-related disease risks including heart disease, diabetes, and
Yijian Ding and Xi Xu
double, from 900 million in 2015 to about 2 billion in 2050 ( World Health Organization, 2021 ). Along with the process of aging, people become more predisposed to a variety of age-related diseases such as cardiovascular diseases, neurodegenerative diseases, metabolic disorders, and cancer ( Luo et