Reaction time in healthy elderly is associated with chronic low-grade inflammation and advanced glycation end product

Arnold, Pauline; Njemini, Rose; Vantieghem, Stijn; Gorus, Ellen; Pool-Goudzwaard, Annelies; Buyl, Ronald; Bautmans, Ivan

doi:10.1016/j.exger.2018.04.002

Cited by 11 publications

(5 citation statements)

References 54 publications

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“…Aging is linked with low-grade chronic inflammation, which has been implicated in skeletal muscle health and sarcopenia [2]. Omega-3 (n-3) polyunsaturated fatty acids (PUFAs) are receiving increasing attention due to their antiinflammatory action in several conditions, such as cancer, diabetes, and metabolic syndrome.…”

Section: Nutritionmentioning

confidence: 99%

Mitochondrial ROS and Aging: Understanding Exercise as a Preventive Tool

Brunetta

Holwerda

Loon

et al. 2019

J. of SCI. IN SPORT AND EXERCISE

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Sarcopenia, which is characterized by reduction in muscle mass and strength, contributes to several age-related conditions, including insulin resistance and frailty. Despite the importance of maintaining muscle mass for healthy aging, the mechanisms contributing to sarcopenia are not fully elucidated. Nevertheless, mitochondria appear to play a key role in the underlying condition, and importantly, respond robustly to exercise interventions. Mitochondria are intracellular organelles largely attributed to maintaining ATP concentrations, however, the importance of this organelle in overall cellular homeostasis has been expanded in the last decades to include redox signaling, calcium homeostasis, inflammation, and apoptosis. Several lines of evidence suggest that mitochondrial bioenergetics are altered in aged skeletal muscle, resulting in an increase in reactive oxygen species (ROS) production, while conversely genetic/pharmacological approaches that attenuate mitochondrial ROS promote healthy aging and maintenance of muscle mass. These observations suggest that increased free radicals are one of the bases of the aging process and related sarcopenia. Here, we reviewed the current knowledge regarding mitochondrial function and redox balance in aged human skeletal muscle, highlighting the implications of redox unbalance on skeletal muscle mass maintenance and muscle health. Additionally, we describe the benefits of exercise and nutrition interventions in the context of improving mitochondrial bioenergetics and functional outcomes regarding skeletal muscle mass and function.

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Section: Nutritionmentioning

confidence: 99%

Mitochondrial ROS and Aging: Understanding Exercise as a Preventive Tool

Brunetta

Holwerda

Loon

et al. 2019

J. of SCI. IN SPORT AND EXERCISE

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“…Decreased voluntary muscle activation and increased antagonist co-activation may contribute to age-related muscle weakness. Arnold et al [ 261 ] investigated the relationship between the profile of chronic low-grade inflammation and AGE (pentosidine) and selected parameters of muscle activation, which are likely to contribute to slowing down muscle efficiency. There was a negative relationship between MIP-1β (CCL4) and coactivation of the antagonist muscle during an isometric maximal isometric voluntary contraction (MVC), muscle activity of the antagonist muscle during the pre-movement time (PMT) and movement time (MT) during a fast dynamic contraction.…”

Section: Age and Muscle Ageingmentioning

confidence: 99%

“…In addition, elevated levels of pentosidine correlated with prolonged PMT. Therefore, it can be argued that pentosidine exerts both a mechanistic and inflammatory effect on slowing down upper limb movement with age [ 261 ]. In vitro and in vivo studies also provide evidence that AGEs are involved in skeletal muscle ageing.…”

Section: Age and Muscle Ageingmentioning

confidence: 99%

A Role for Advanced Glycation End Products in Molecular Ageing

Zgutka

Tkacz

Tomasiak

et al. 2023

IJMS

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Ageing is a composite process that involves numerous changes at the cellular, tissue, organ and whole-body levels. These changes result in decreased functioning of the organism and the development of certain conditions, which ultimately lead to an increased risk of death. Advanced glycation end products (AGEs) are a family of compounds with a diverse chemical nature. They are the products of non-enzymatic reactions between reducing sugars and proteins, lipids or nucleic acids and are synthesised in high amounts in both physiological and pathological conditions. Accumulation of these molecules increases the level of damage to tissue/organs structures (immune elements, connective tissue, brain, pancreatic beta cells, nephrons, and muscles), which consequently triggers the development of age-related diseases, such as diabetes mellitus, neurodegeneration, and cardiovascular and kidney disorders. Irrespective of the role of AGEs in the initiation or progression of chronic disorders, a reduction in their levels would certainly provide health benefits. In this review, we provide an overview of the role of AGEs in these areas. Moreover, we provide examples of lifestyle interventions, such as caloric restriction or physical activities, that may modulate AGE formation and accumulation and help to promote healthy ageing.

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“…The observed correlation between peripheral AGEs and fracture risk in individuals with T2D may therefore be influenced by nonbone factors. PEN forms through oxidation and differences in the bone vs. peripheral AGEs may reflect differential effects of sources of oxidative stress including aging, T2D, osteoporosis, chronic kidney disease, and many other diseases with elevated inflammation [62][63][64].…”

Section: Serum and Urine Markers Of Advanced Glycation End Products A...mentioning

confidence: 99%

Advanced glycation endproducts and bone quality: practical implications for people with type 2 diabetes

Moseley

Sacher

et al. 2021

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

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Purpose of review Individuals with type 2 diabetes (T2D) are at increased risk of fracture, often despite normal bone density. This observation suggests deficits in bone quality in the setting of abnormal glucose homeostasis. The goal of this article is to review recent developments in our understanding of how advanced glycation end products (AGEs) are incorporated into the skeleton with resultant deleterious effects on bone health and structural integrity in patients with T2D. Recent findings The adverse effects of skeletal AGE accumulation on bone remodeling and the ability of the bone to deform and absorb energy prior to fracture have been demonstrated both at the bench as well as in small human studies; however, questions remain as to how these findings might be better explored in large, population-based investigations. Summary Hyperglycemia drives systemic, circulating AGE formation with subsequent accumulation in the bone tissue. In those with T2D, studies suggest that AGEs diminish fracture resistance, though larger clinical studies are needed to better define the direct role of longstanding AGE accumulation on bone strength in humans as well as to motivate potential interventions to reverse or disrupt skeletal AGE deposition with the goal of fracture prevention.

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Reaction time in healthy elderly is associated with chronic low-grade inflammation and advanced glycation end product

Cited by 11 publications

References 54 publications

Mitochondrial ROS and Aging: Understanding Exercise as a Preventive Tool

Mitochondrial ROS and Aging: Understanding Exercise as a Preventive Tool

A Role for Advanced Glycation End Products in Molecular Ageing

Advanced glycation endproducts and bone quality: practical implications for people with type 2 diabetes

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