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World population has been continuously increasing and progressively aging.

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Aging is characterized by a complex and intraindividual process associated with nine major cellular and molecular hallmarks, namely, genomic instability, telomere attrition, epigenetic alterations, a loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication.

This review exposes the positive antiaging impact of physical exercise at the cellular level, highlighting its specific role in attenuating the aging effects of each hallmark. Exercise should be seen as a polypill, which improves the health-related quality of life and functional capabilities while mitigating physiological changes and comorbidities associated with aging.

To achieve a framework of effective physical exercise interventions on aging, further research on its benefits and the most effective strategies is encouraged. Understanding the specific cellular and molecular mechanisms implicit in aging still represents one of the most complex and integral issues that biological research has yet to overcome.

Despite hundreds of explored and developed theories, not a single one fully and comprehensively explains the process of aging 6. Traditionally, aging was not seen as an adaptation or genetically programmed phenomenon.

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More recently, biologic currents point to two main theories: the programmed aging and the damage or error-based theories. The first suggests an intrinsic biologic programmed deterioration of the structural and functional capacity of the human cells 7.

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The latter highlights the cumulative damage to living organisms leading to intrinsic aging 8. Nonetheless, a combination of these theories is usually preferred. These hallmarks should be expressed during normal aging, with their experimental aggravation speeding up the aging process, and in contrast, their experimental amelioration retards the normal aging process, thus increasing a healthy life span.

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The world population has been progressively aging and thus raising the average life expectancy. Inan estimated 8. Within this line, the older population percentage is expected to keep increasing, with an average annual increase of With this life span increase and its associated aging comorbidities, a growing challenge has arisen to make older people physically active and functionally independent until the rest of their lives.

Along with the nine cellular and molecular hallmarks stated above, aging is known to be correlated with several cardiovascular, cardiorespiratory, musculoskeletal, metabolic, and cognitive impairments In this sense, regular physical activity in the older population—especially aerobic and resistance training—plays an important role at a multisystem level, preventing severe muscle atrophy, maintaining cardiorespiratory fitness and cognitive function, boosting metabolic activity, and improving or maintaining functional independence 10 — Within this line, Garatachea et al.

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In addition, physical exercise has a positive antiaging impact at the cellular level, and its specific role in each aging hallmark is described below. Genomic instability, caused by exogenous physical, chemical, and biological and endogenous factors [deoxyribonucleic acid DNA replication errors, spontaneous hydrolytic reactions, and reactive oxygen species ROS ], often in mutations, translocations, chromosomal gains and losses, telomere shortening, and gene disruption In this sense, several cellular events contribute to genomic instability and subsequently to aging, including somatic mutations of nuclear DNA, mutations and deletions in aged mitochondrial DNA mtDNAand defects in the nuclear lamina 1416 Increased genomic damage has been linked to aging, highlighted by the DNA repair deficits found in accelerated mice models, translated into many human progeroid syndromes 1518 Likewise, mtDNA mutations in aged subjects appear to be induced by early replication errors rather than later cumulative oxidative damage In addition, the mutation of the nuclear lamina protein gene encoding and disturbances on its maturation or dynamics le to a few progeria syndromes 21 — This premature aging is supported by the delayed onset of progeroid features and extended life span after decreasing prelamin A or progerin levels 24 — In the face of genomic instability, the organism has developed a panoply of DNA repair mechanisms that skirmish altogether to overcome DNA nuclear damage Within the same line, genomic stability systems hold specific mechanisms to maintain proper telomere length and function and mtDNA integrity 28 Pharmacological and biologic strategies mainly hormonal or genetic therapies have been developed 30 — 32 ; howbeit, further research is required to validate nuclear architecture reinforcement for delaying normal aging 1.

Exercise plays a role in maintaining genomic stability. In a meta-analysis comprising data of genetic elements unique genes associated with exercise from 1, individuals, out of genes decreased in DNA methylation percentage after physical exercise among older people. More specifically, the genes that presented DNA methylation decreases were associated with a cancer-suppressing micro-ribonucleic acid miRNA gene network Telomeres are ribonucleoprotein complex structures that protect the integrity of information-carrying Free lages cell phone chat lines throughout cell cycle, preventing the base pair loss of chromosomal DNA during cellular division.

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Over consecutive cellular divisions, telomere length naturally decreases till a minimum critical size, which precludes further cell division, causing cellular senescence or apoptosis, also known as the end replication problem Telomerase, as an enzyme with a catalytic unit, answers to the end replication problem, promoting telomere lengthening This enzyme deficiency in humans has been linked to premature manifestations of chronic diseases specially related to scarce tissue regenerative ability such as pulmonary fibrosis, congenital dyskeratosis, or aplastic anemia Telomere shortening is described during normal aging in human and mice cells 45 — The fact that telomere length decreases with aging, contributing to the normal cell senescence process, suggested that this could be a potential marker for biological aging Moreover, the leukocyte telomere length is also positively associated with a of healthy living years, associated with numerous chronic conditions and their complications and with the mortality risk mainly at younger ages 52 Interestingly, recent evidence supports that telomerase activation can revert aging, namely, in the premature aging of telomerase-deficient mice when the enzyme is genetically reactivated The relationship between physical activity and healthy aging is well recognized, but the association between physical activity and telomere length remains unclear.

Aging induces DNA damage accumulation, especially in some particularly sensitive chromosomal regions such as telomeres, and recent data suggest that physical activity may play a protective role against stress-related telomere attrition 28 Although the potential mechanism is unclear, exercise exhibits a favorable impact on telomere length, especially on a chronic pattern and particularly in older individuals antagonizing the typical age-induced decrements in telomere attrition.

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Several potential mechanisms have been discussed linking exercise and telomere length decrements to changes in telomerase activity, inflammation, oxidative stress, and decreased skeletal muscle satellite cell content Exercise has been associated with an upregulation of protective proteins such as telomeric repeat-binding factor 2 and DNA repair pathway proteins such as Ku proteins as well as a downregulation of negative regulator proteins of cell cycle progression such as p16 in middle-aged athletes supporting this relationship Additionally, although it increases oxidative stress, continuous physical exercise is associated with antioxidant activity and inferior levels of ROS, favoring the REDOX balance, protecting from DNA damage and subsequently shorter telomere attrition 62 — Satellite cells are specific skeletal muscle cell precursors activated during muscle regeneration processes or in response to muscle injuries.

A positive correlation exists between the of satellite cells and skeletal muscle telomere length in older adults This pool of cells decreases normally during aging and appears to connect physical activity and skeletal muscle preservation since both resistance and aerobic exercise act as satellite cell pool stimulators, equalizing the decline related to aging The relationship between epigenetic regulation and aging is controversial and complex 1.

Although epigenome refers to the combination of chemical changes to DNA and histone proteins free lages cell phone chat lines a cell, epigenetic changes include alterations in DNA methylation patterns, the posttranslational modification of histones, and chromatin remodeling such as miRNA expression changes A multiplicity of epigenetic modifications affects all tissues and cells throughout life Increased histone H4K16 acetylation, H3K4 trimethylation, or H4K20 trimethylation, as well as decreased H3K27 trimethylation or H3K9 methylation, make up age-associated epigenetic marks 69 For example, the transgenic overexpression of mammalian SIRT1 closest homolog to invertebrate Sir2 improves health aspects during aging despite not increasing longevity Losing the function of SIRT6 reduces longevity, and the gain extends longevity in mice 71 Actually, the literature clearly reveals that the epigenetic response is highly dynamic and influenced by different environmental and biological factors, such as aging, nutrient availability, and physical exercise.

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Regular aerobic exercise can change the human genome through DNA methylation Transient hypoxia conditions are a good example Thus, by using epigenetic mechanisms, aerobic exercise can induce the transcription of genes encoding telomere-stabilizing proteins and telomerase activity not only in animals 617778 but also in humans Losing promoter methylation and histone H4 deacetylation is associated with the changed gene expression profile in adaptation to aerobic exercise 63 — 6775 — Also, the class II HDACs 4 and 5 transcriptional repressors can translocate from the nucleus to the sarcoplasm of muscle fibers in response to aerobic exercise Exercise effects are blocked by the overexpression of HDAC5 in transgenic mice, suggesting that histones are important in the transcriptomic response to muscle contraction In turn, during the recovery period, this mRNA elevation enables protein synthesis and induces gradual structural remodeling and long-term functional modifications Also, calcium and insulin aling was recently found to be differentially methylated in skeletal muscle after aerobic exercise These adaptations can occur in at least the brain, muscle, or cardiovascular system and are intrinsic to the skeletal muscle response during exercise e.

Chronic moderate aerobic exercise increases the methylation levels of the pro-inflammatory apoptosis-associated speck-like protein caspase gene, which modulates IL and IL-1b in the aged leukocytes, thereby contributing to reduced age-related pro-inflammatory cytokines In addition, several myogenic regulatory factors—e.

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The effect of physical exercise on epigenetic changes is just the beginning. However, studies so far show that an important modulation of exercise exists on the epigenetics mechanisms, particularly in DNA methylation, specially of regular physical exercise. Aging and some aging-related diseases are linked to impaired protein homeostasis, also known as proteostasis The array of quality control is guaranteed through distinct mechanisms that involve location, concentration, conformation, and the turnover of individual proteins, such as autophagy, proteasomal degradation, or chaperone-mediated folding These functions prevent the aggregation of damage components and ensure the continuous renewal of intracellular proteins, degrading altered proteins.

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Aging impairs the autophagy—lysosomal and ubiquitin—proteasome systems, which play a central role in cellular proteostatic mechanisms 94 Conversely, physical activity induces brain, muscle, and cardiac autophagy A t program of moderate-intensity leg-resistance exercises and walking demonstrated to upregulate autophagy muscle markers in old women 97despite that these data are still free lages cell phone chat lines to aged subjects, and scarce evidence is still available in humans.

In mouse models, this effect seems to be mediated by the activation of BCL-2—beclin 1 complex Acute resistance exercise programs induced muscle protein synthesis and decreased protein degradation through the activation of class 3 phosphatidylinositol 3OH kinase Vps34 mVps34, which forms an autophagy regulator complex with beclin-1 99 Moreover, in transgenic mice, the beclin-1 disruption reduces autophagy, leading to neurodegeneration Similarly, the aging human brain exhibits a downregulation of beclin-1 Higher basal levels of autophagy were related to healthy human exceptional longevity, and healthy centenarians have higher serum levels of beclin-1 compared with young controls Atrogin-1 MAFbx is a muscle-specific ubiquitin ligase involved in muscle atrophy through FoxO aling The atrogin-1 upregulation is associated with cardiac and skeletal muscle atrophy, and atrogin-1 knockout mouse models corroborate its association with autophagy dysfunction, cardiomyopathy, and premature death Within the same line, comparing aged atrogin-1 knockout mice with age-matched controls, the former shows a reduced tolerance to treadmill exercise and shortened life span The synthesis of cytosolic and organelle-specific chaperones is impaired in aging In animal models, the upregulation of cochaperone of the heat-shock proteins HSPs was associated with prolonged life-span phenotypesand HSF-1 activation, the heat-shock response regulator, was linked to longevity and thermotolerance Despite limited comparison studies, evidence supports that acute endurance- and resistance-type exercise protocols are associated with increased HSPs transcription not only during activity but also immediately postexercise or several hours following exercise, which points out the possible favorable impact of physical activity on proteostasis The growth hormone GH is produced by the anterior pituitary gland and is regulated by the growth hormone-releasing hormone, acting mainly in the hepatocytes to induce insulin-like growth factor 1 IGF-1 secretion.

IGF-1 is also produced in distinct tissues, such as osteocytes, chondrocytes, and muscle, to act in an autocrine or paracrine pattern Insulin and IGF-1 share the same intracellular aling pathway, an important aging-controlling route highly conserved during evolution. In this sense, enhanced longevity has been associated with the reduced functions of GH, IGF-1, and insulin receptors and their intracellular effectors such as Akt and mTOR complexes — Within this scope, several authors associated dietary restriction with an increased life or health span probably mediated by an attenuation of insulin and IGF-1 aling pathway— Regarding the intracellular effectors downstream, in animal models, the transcription factor FOXO represents the most relevant alteration linked to longevity The tumor-suppressor gene PTEN has also been associated with an antiaging impact on this aling pathway, promoting energy expenditure and improving mitochondrial oxidative metabolism Aging is also physiologically associated with somatopause, which represents a progressive decline in the GH secretory rate starting in the third decade of life, as reflected in decreasing IGF-1 levels In mouse models of premature aging, this GH-IGF-1 axis decline is also noted, highlighting this common denominator in normal and sped-up aging processes This paradoxical observation can be integrated as a defensive response that downmodulates the GH-IGF-1 axis, promoting lower cell growth and metabolism, free lages cell phone chat lines cellular damage and aiming to extend life span Exercise plays an important role in not only the glucose-sensing somatotrophic axis but also the three nutrient-sensing systems referred above, promoting a beneficial anabolic cellular state —

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