scholarly journals Effects of aging and lifelong aerobic exercise on basal and exercise-induced inflammation in women

2020 ◽  
Vol 129 (6) ◽  
pp. 1493-1504
Author(s):  
Kaleen M. Lavin ◽  
Ryan K. Perkins ◽  
Bozena Jemiolo ◽  
Ulrika Raue ◽  
Scott W. Trappe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Aerobic Exercise ◽  
Muscle Inflammation ◽  
Age Related ◽  
Aging Men ◽  
Anti Inflammatory ◽  
Exercise Induced ◽  
Effects Of Aging ◽  
Positive Effect ◽  
Lifelong Exercise

We previously reported a positive effect of lifelong exercise on skeletal muscle inflammation in aging men. This parallel investigation in women revealed that lifelong exercise did not protect against age-related increases in circulating or muscle inflammation and that preparedness to handle loading stress was not preserved by lifelong exercise. Further investigation is necessary to understand why lifelong aerobic exercise may not confer the same anti-inflammatory benefits in women as it does in men.

scholarly journals Effects of aging and lifelong aerobic exercise on expression of innate immune components in human skeletal muscle

2020 ◽  
Vol 129 (6) ◽  
pp. 1483-1492 ◽  
Author(s):  
Ryan K. Perkins ◽  
Kaleen M. Lavin ◽  
Ulrika Raue ◽  
Bozena Jemiolo ◽  
Scott W. Trappe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Aerobic Exercise ◽  
Acute Exercise ◽  
Innate Immune ◽  
Structural Components ◽  
Basal Expression ◽  
Age Related ◽  
Effects Of Aging ◽  
Insight Into ◽  
Lifelong Exercise

Findings from this investigation provide novel insight into the effect of aging and lifelong aerobic exercise on structural components of the innate immune system in skeletal muscle of humans. Data presented here suggest aging increases basal expression of select Toll-like receptors (TLRs), and lifelong exercise does not impact this age-related increase. Additionally, acute exercise stimulates gene expression of several TLRs, while the adaptor response is likely dysregulated with aging and maintained with lifelong exercise.

scholarly journals Protective effects of acute exercise preconditioning on disuse-induced muscular atrophy in aged muscle: a narrative literature review

2020 ◽  
Vol 70 (1) ◽  
Author(s):  
Toshinori Yoshihara ◽  
Hisashi Naito
Keyword(s):  
Skeletal Muscle ◽  
Acute Exercise ◽  
Muscular Atrophy ◽  
Protective Effects ◽  
Older Individuals ◽  
Age Related ◽  
Exercise Preconditioning ◽  
Narrative Literature Review ◽  
Exercise Induced ◽  
Effects Of Aging

AbstractAging is associated with a progressive loss of skeletal muscle mass and strength, resulting in frailty and lower quality of life in older individuals. At present, a standard of clinical or pharmacological care to prevent the adverse effects of aging does not exist. Determining the mechanism(s) responsible for muscular atrophy in disused aged muscle is a required key step for the development of effective countermeasures. Studies suggest an age-related differential response of genes and signalings to muscle disuse in both rodents and humans, implying the possibility that effective countermeasures to prevent disuse muscle atrophy may be age-specific. Notably, exercise preconditioning can attenuate disuse-induced muscular atrophy in rodent and human skeletal muscles; however, information on age-specific mechanisms of this exercise-induced protection remains limited. This mini-review aimed to summarize the protective effects of acute exercise preconditioning on muscular atrophy in aged muscle and provide potential mechanisms for its preventive effect on skeletal muscle wasting.

scholarly journals Effects of aging and lifelong aerobic exercise on basal and exercise-induced inflammation

2020 ◽  
Vol 128 (1) ◽  
pp. 87-99 ◽  
Author(s):  
Kaleen M. Lavin ◽  
Ryan K. Perkins ◽  
Bozena Jemiolo ◽  
Ulrika Raue ◽  
Scott W. Trappe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Acute Exercise ◽  
Prostaglandin E ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Exercise Induced ◽  
Cox 1 ◽  
Inflammatory Effect ◽  
Lifelong Exercise

Age-associated chronic basal inflammation compromises muscle mass and adaptability, but exercise training may exert an anti-inflammatory effect. This investigation assessed basal and exercise-induced inflammation in three cohorts of men: young exercisers [YE; n = 10 men; 25 ± 1 yr; maximal oxygen consumption (V̇o2max), 53 ± 3 mL·kg−1·min−1; quadriceps area, 78 ± 3 cm2; means ± SE], old healthy nonexercisers (OH; n = 10; 75 ± 1 yr; V̇o2max, 22 ± 1 mL·kg−1·min−1; quadriceps area, 56 ± 3 cm2), and lifelong exercisers with an aerobic training history of 53 ± 1 yr (LLE; n = 21; 74 ± 1 yr; V̇o2max, 34 ± 1 mL·kg−1·min−1; quadriceps area, 67 ± 2 cm2). Resting serum IL-6, TNF-α, C-reactive protein, and IGF-1 levels were measured. Vastus lateralis muscle biopsies were obtained at rest (basal) and 4 h after an acute exercise challenge (3 × 10 repetitions, 70% 1-repetition maximum) to assess gene expression of cytokines [IL-6, TNF-α, IL-1β, IL-10, IL-4, interleukin-1 receptor antagonist (IL-1Ra), and transforming growth factor-β (TGF-β)], chemokines [IL-8 and monocyte chemoattractant protein-1 (MCP-1)], cyclooxygenase enzymes [cyclooxygenase-1 and -2 (COX-1 and COX-2, respectively), prostaglandin E2 synthases [microsomal prostaglandin E synthase 1 (mPGES-1) and cytosolic prostaglandin E2 synthase (cPGES)] and receptors [prostaglandin E2 receptor EP3 and EP4 subtypes (EP3 and EP4, respectively), and macrophage markers [cluster of differentiation 16b (CD16b) and CD163], as well as basal macrophage abundance (CD68+ cells). Aging led to higher ( P ≤ 0.05) circulating IL-6 and skeletal muscle COX-1, mPGES-1, and CD163 expression. However, LLE had significantly lower serum IL-6 levels ( P ≤ 0.05 vs. OH) and a predominantly anti-inflammatory muscle profile [higher IL-10 ( P ≤ 0.05 vs. YE), TNF-α, TGF-β, and EP4 levels ( P ≤ 0.05 vs. OH)]. In OH only, acute exercise increased expression of proinflammatory factors TNF-α, TGF-β, and IL-8 ( P ≤ 0.05). LLE had postexercise gene expression similar to YE, except lower IL-10 ( P ≤ 0.10), mPGES-1, and EP3 expression ( P ≤ 0.05). Thus, although aging led to a proinflammatory profile within blood and muscle, lifelong exercise partially prevented this and generally preserved the acute inflammatory response to exercise seen in young exercising men. Lifelong exercise may positively impact muscle health throughout aging by promoting anti-inflammation in skeletal muscle. NEW & NOTEWORTHY This study assessed a unique population of lifelong aerobic exercising men and demonstrated that their activity status exerts an anti-inflammatory effect in skeletal muscle and circulation. Furthermore, we provide evidence that the inflammatory response to acute exercise is dysregulated by aging but preserved with lifelong exercise, which might improve skeletal muscle resilience to unaccustomed loading and adaptability into late life.

Exercise and Mitochondrial Function: Importance and InferenceA Mini Review

2021 ◽  
Vol 21 ◽  
Author(s):  
Vaishali K. ◽  
Nitesh Kumar ◽  
Vanishree Rao ◽  
Rakesh Krishna Kovela ◽  
Mukesh Kumar Sinha
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Skeletal Muscles ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Present Review ◽  
Age Related ◽  
Exercise Induced ◽  
Mitochondrial Adaptations

: Skeletal muscles must generate and distribute energy properly in order to function perfectly. Mitochondria in skeletal muscle cells form vast networks to meet this need, and their functions may improve as a result of exercise. In the present review, we discussed exercise-induced mitochondrial adaptations, age-related mitochondrial decline, and a biomarker as a mitochondrial function indicator and exercise interference.

scholarly journals Cardiovascular and skeletal muscle health with lifelong exercise

2018 ◽  
Vol 125 (5) ◽  
pp. 1636-1645 ◽  
Author(s):  
Kevin J. Gries ◽  
Ulrika Raue ◽  
Ryan K. Perkins ◽  
Kaleen M. Lavin ◽  
Brittany S. Overstreet ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Aerobic Exercise ◽  
Muscle Biopsy ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Metabolic Phenotype ◽  
Vastus Lateralis Muscle ◽  
Metabolic Fitness ◽  
Lifelong Exercise

The purpose of this study was to examine the effects of aerobic lifelong exercise (LLE) on maximum oxygen consumption (V̇o2max) and skeletal muscle metabolic fitness in trained women ( n = 7, 72 ± 2 yr) and men ( n = 21, 74 ± 1 yr) and compare them to old, healthy nonexercisers (OH; women: n = 10, 75 ± 1 yr; men: n = 10, 75 ± 1 yr) and young exercisers (YE; women: n = 10, 25 ± 1 yr; men: n = 10, 25 ± 1 yr). LLE men were further subdivided based on intensity of lifelong exercise and competitive status into performance (LLE-P, n = 14) and fitness (LLE-F, n = 7). On average, LLE exercised 5 day/wk for 7 h/wk over the past 52 ± 1 yr. Each subject performed a maximal cycle test to assess V̇o2maxand had a vastus lateralis muscle biopsy to examine capillarization and metabolic enzymes [citrate synthase, β-hydroxyacyl-CoA dehydrogenase (β-HAD), and glycogen phosphorylase]. V̇o2maxhad a hierarchical pattern (YE > LLE > OH, P < 0.05) for women (44 ± 2 > 26 ± 2 > 18 ± 1 ml·kg−1·min−1) and men (53 ± 3 > 34 ± 1 > 22 ± 1 ml·kg−1·min−1) and was greater ( P < 0.05) in LLE-P (38 ± 1 ml·kg−1·min−1) than LLE-F (27 ± 2 ml·kg−1·min−1). LLE men regardless of intensity and women had similar capillarization and aerobic enzyme activity (citrate synthase and β-HAD) as YE, which were 20%–90% greater ( P < 0.05) than OH. In summary, these data show a substantial V̇o2maxbenefit with LLE that tracked similarly between the sexes, with further enhancement in performance-trained men. For skeletal muscle, 50+ years of aerobic exercise fully preserved capillarization and aerobic enzymes, regardless of intensity. These data suggest that skeletal muscle metabolic fitness may be easier to maintain with lifelong aerobic exercise than more central aspects of the cardiovascular system.NEW & NOTEWORTHY Lifelong exercise (LLE) is a relatively new and evolving area of study with information especially limited in women and individuals with varying exercise intensity habits. These data show a substantial maximal oxygen consumption benefit with LLE that tracked similarly between the sexes. Our findings contribute to the very limited skeletal muscle biopsy data from LLE women (>70 yr), and similar to men, revealed a preserved metabolic phenotype comparable to young exercisers.

Neuroendocrine rhythms and sleep in aging men

1991 ◽  
Vol 260 (4) ◽  
pp. E651-E661 ◽  
Author(s):  
A. van Coevorden ◽  
J. Mockel ◽  
E. Laurent ◽  
M. Kerkhofs ◽  
M. L'Hermite-Baleriaux ◽  
...  
Keyword(s):  
Young Male ◽  
Extended Period ◽  
The Elderly ◽  
Thyroid Stimulating Hormone ◽  
Temporal Organization ◽  
Elderly Subjects ◽  
Elderly Men ◽  
Age Related ◽  
Aging Men ◽  
Effects Of Aging

To delineate the physiological effects of aging on basal levels and temporal patterns of neuroendocrine secretions, the 24-h profiles of cortisol, thyroid-stimulating hormone (TSH), melatonin, prolactin, and growth hormone (GH) levels were simultaneously obtained at frequent intervals in eight healthy, active elderly men, age 67-84 yr and in eight young male adults, age 20-27 yr. The study was preceded by an extended period of habituation to laboratory conditions, and sleep was polygraphically recorded. Mean cortisol levels in the elderly were normal, but the amplitude of the circadian rhythm was reduced. Circulating levels of daytime and nighttime levels of both TSH and GH were greatly diminished in old age. In contrast, prolactin and melatonin concentrations were decreased during the nighttime only. The circadian rises of cortisol, TSH, and melatonin occurred 1-1.5 h earlier in elderly subjects, and the distribution of rapid-eye-movement stages during sleep was similarly advanced, suggesting that circadian timekeeping is modified during normal senescence. Despite perturbations of sleep, sleep-related release of GH and prolactin occurred in all elderly men. Age-related decreases in hormonal levels were associated with a decrease in the amplitude, but not the frequency, of secretory pulses. These findings demonstrate that the normal process of aging involves alterations in the central mechanisms controlling the temporal organization of endocrine release in addition to a reduction of secretory outputs.

scholarly journals Metabolic Adaptations to Aerobic Exercise in Aged Mice

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 533-533
Author(s):  
Tyler Marx ◽  
Anastasiia Vasileva ◽  
Stephen Hutchison ◽  
Jennifer Stern
Keyword(s):  
Type 2 Diabetes ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Aerobic Exercise Training ◽  
Metabolic Function ◽  
Glucagon Receptor ◽  
Age Related ◽  
Exercise Induced

Abstract Aerobic exercise training is a potent intervention for the treatment and prevention of age-related disease, such as heart disease, obesity, and Type 2 Diabetes. Insulin resistance, a hallmark of Type 2 Diabetes, is reversed in response to aerobic exercise training. However, the effect of aerobic exercise training on glucagon sensitivity is unclear. Glucagon signaling at the liver promotes fatty acid oxidation, inhibits De novo lipogenesis, and activates AMP Kinase, a key mediator of healthy aging. Like humans, aging in mice age leads to a decline in physical and metabolic function. To understand the role of glucagon signaling in exercise-induced improvements in physical and metabolic function in the mouse, we implemented a 16-week aerobic exercise training protocol in young and aged mice. 16 weeks of exercise training initiated at 6 months of age increased markers of physical function (P&lt;0.01) and attenuated age-related weight gain (P&lt;0.05) and fat mass (P&lt;0.0001). Additionally, exercise training improved glucose clearance (P&lt;0.01), enhanced glucose-stimulated insulin secretion (P&lt;0.01) and decreased hepatic lipid accumulation (P&lt;0.05). Importantly, exercise training decreased hypoglycemia stimulated glucagon secretion (P&lt;0.01), with no effect on hepatic glucagon receptor mRNA expression or serum glucagon. Thus, we propose that aerobic exercise training enhances glucagon sensitivity at the liver, implicating glucagon as a potential mediator of exercise-induced improvements in aging. Studies initiating the same aerobic exercise training intervention at 18 months of age in the mouse are currently underway to establish the role of glucagon receptor signaling in exercise-induced improvements in aging.

scholarly journals Exercise-Induced Mitohormesis for the Maintenance of Skeletal Muscle and Healthspan Extension

Sports ◽  
2019 ◽  
Vol 7 (7) ◽  
pp. 170 ◽  
Author(s):  
Robert V. Musci ◽  
Karyn L. Hamilton ◽  
Melissa A. Linden
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Damage ◽  
Aerobic Exercise ◽  
Muscle Protein ◽  
Redox Homeostasis ◽  
Future Research ◽  
Skeletal Muscle Protein ◽  
Skeletal Muscle Function ◽  
Age Related ◽  
Nrf2 Signaling Pathway

Oxidative damage is one mechanism linking aging with chronic diseases including the progressive loss of skeletal muscle mass and function called sarcopenia. Thus, mitigating oxidative damage is a potential avenue to prevent or delay the onset of chronic disease and/or extend healthspan. Mitochondrial hormesis (mitohormesis) occurs when acute exposure to stress stimulates adaptive mitochondrial responses that improve mitochondrial function and resistance to stress. For example, an acute oxidative stress via mitochondrial superoxide production stimulates the activation of endogenous antioxidant gene transcription regulated by the redox sensitive transcription factor Nrf2, resulting in an adaptive hormetic response. In addition, acute stresses such as aerobic exercise stimulate the expansion of skeletal muscle mitochondria (i.e., mitochondrial biogenesis), constituting a mitohormetic response that protects from sarcopenia through a variety of mechanisms. This review summarized the effects of age-related declines in mitochondrial and redox homeostasis on skeletal muscle protein homeostasis and highlights the mitohormetic mechanisms by which aerobic exercise mitigates these age-related declines and maintains function. We discussed the potential efficacy of targeting the Nrf2 signaling pathway, which partially mediates adaptation to aerobic exercise, to restore mitochondrial and skeletal muscle function. Finally, we highlight knowledge gaps related to improving redox signaling and make recommendations for future research.

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