Dataset Information

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

ABSTRACT: 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 (V?o_2max), 53?±?3 mL·kg^-1·min^-1; quadriceps area, 78?±?3 cm²; means?±?SE], old healthy nonexercisers (OH; n = 10; 75?±?1 yr; V?o_2max, 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; V?o_2max, 34?±?1 mL·kg^-1·min^-1; quadriceps area, 67?±?2 cm²). Resting serum IL-6, TNF-?, 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-?, IL-1?, IL-10, IL-4, interleukin-1 receptor antagonist (IL-1Ra), and transforming growth factor-? (TGF-?)], 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-?, TGF-?, and EP4 levels (P ? 0.05 vs. OH)]. In OH only, acute exercise increased expression of proinflammatory factors TNF-?, TGF-?, 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.

SUBMITTER: Lavin KM

PROVIDER: S-EPMC6985808 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

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

Lavin Kaleen M KM Perkins Ryan K RK Jemiolo Bozena B Raue Ulrika U Trappe Scott W SW Trappe Todd A TA

Journal of applied physiology (Bethesda, Md. : 1985) 20191121 1

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; V̇o<sub ...[more]

PMID: 31751180

Similar Datasets

Project description:Low muscle mass and frailty are especially prevalent in older women and may be accelerated by age-related inflammation. Habitual physical activity throughout the life span (lifelong exercise) may prevent muscle inflammation and associated pathologies, but this is unexplored in women. This investigation assessed basal and acute exercise-induced inflammation in three cohorts of women: young exercisers (YE, n = 10, 25 ± 1 yr, [Formula: see text]: 44 ± 2 mL/kg/min, quadriceps size: 59 ± 2 cm2), old healthy nonexercisers (OH, n = 10, 75 ± 1 yr, [Formula: see text]: 18 ± 1 mL/kg/min, quadriceps size: 40 ± 1 cm2), and lifelong aerobic exercisers with a 48 ± 2 yr aerobic training history (LLE, n = 7, 72 ± 2 yr, [Formula: see text]: 26 ± 2 mL/kg/min, quadriceps size: 42 ± 2 cm2). Resting serum IL-6, TNF-α, C-reactive protein (CRP), and IGF-1 were measured. Vastus lateralis muscle biopsies were obtained at rest (basal) and 4 h after an acute exercise challenge (3 × 10 reps, 70% 1-repetition maximum) to assess gene expression of cytokines (IL-6, TNF-α, IL-1β, IL-10, IL-4, IL-1Ra, TGF-β), chemokines (IL-8, MCP-1), cyclooxygenase enzymes (COX-1, COX-2), prostaglandin E2 synthases (mPGES-1, cPGES) and receptors (EP3-4), and macrophage markers (CD16b, CD163), as well as basal macrophage abundance (CD68+ cells). The older cohorts (LLE + OH combined) demonstrated higher muscle IL-6 and COX-1 (P ≤ 0.05) than YE, whereas LLE expressed lower muscle IL-1β (P ≤ 0.05 vs. OH). Acute exercise increased muscle IL-6 expression in YE only, whereas the older cohorts combined had the higher postexercise expression of IL-8 and TNF-α (P ≤ 0.05 vs. YE). Only LLE had increased postexercise expression of muscle IL-1β and MCP-1 (P ≤ 0.05 vs. preexercise). Thus, aging in women led to mild basal and exercise-induced inflammation that was unaffected by lifelong aerobic exercise, which may have implications for long-term function and adaptability.NEW & NOTEWORTHY 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.

Project description:The purpose of this investigation was to evaluate the effects of aging and lifelong exercise on skeletal muscle components of the innate immune system. Additionally, the effects of an acute resistance exercise (RE) challenge were explored. Three groups of men were studied: young exercisers (YE: n = 10, 25 ± 1 yr; V̇o2max: 53 ± 3 mL/kg/min; quadriceps size: 78 ± 3 cm2), lifelong aerobic exercisers with a 53 ± 1 yr training history (LLE; n = 21, 74 ± 1 yr; V̇o2max: 34 ± 1 mL/kg/min; quadriceps size: 67 ± 2 cm2), and old healthy nonexercisers (OH: n = 10, 75 ± 1 yr; V̇o2max: 22 ± 1 mL/kg/min, quadriceps size: 56 ± 3 cm2). Vastus lateralis muscle biopsies were obtained in the basal state and 4 h after RE (3 × 10 reps, 70% of 1 repetition maximum) to assess Toll-like receptors (TLR)1-10, TLR adaptors (Myd88 and TRIF), and NF-κB pathway components (IκΒα and IKKβ) mRNA expression. Basal TLR3, TLR6, and TLR7 tended to be higher (P ≤ 0.10) with aging (LLE and OH combined). In general, RE increased expression of TLR1 and TLR8 (P ≤ 0.10) and TLR3 and TLR4 (P < 0.05), although TLR3 did not respond in OH. Both TLR adaptors also responded to the exercise bout; these were primarily (Myd88, main effect P ≤ 0.10) or exclusively (TRIF, P < 0.05) driven by the OH group. In summary, aging appears to increase basal expression of some innate immune components in human skeletal muscle, and lifelong aerobic exercise does not affect this age-related increase. An exercise challenge stimulates the expression of several TLRs, while the TLR adaptor response appears to be dysregulated with aging and maintained with lifelong exercise. Partially preserved muscle mass, coupled with a notable immunity profile, suggests lifelong exercisers are likely better prepared for a stress that challenges the immune system.NEW & NOTEWORTHY 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.

Project description:Key pointsThe results of the present study establish the temporal pattern of age-related vascular dysfunction across the adult lifespan in sedentary mice consuming a non-Western diet, and the underlying mechanisms The results demonstrate that consuming a Western diet accelerates and exacerbates vascular ageing across the lifespan in sedentary mice They also show that lifelong voluntary aerobic exercise has remarkable protective effects on vascular function throughout the lifespan, in the setting of ageing alone, as well as ageing compounded by Western diet consumption Overall, the results indicate that amelioration of mitochondrial oxidative stress and inflammation are key mechanisms underlying the voluntary aerobic exercise-associated preservation of vascular function across the lifespan in both the presence and absence of a Western dietary pattern ABSTRACT: Advancing age is the major risk factor for cardiovascular diseases, driven largely by vascular endothelial dysfunction (impaired endothelium-dependent dilatation, EDD) and aortic stiffening (increased aortic pulse wave velocity, aPWV). In humans, vascular ageing occurs in the presence of differences in diet and physical activity, but the interactive effects of these factors are unknown. We assessed carotid artery EDD and aPWV across the lifespan in mice consuming standard (normal) low-fat chow (NC) or a high-fat/high-sucrose Western diet (WD) in the absence (sedentary, SED) or presence (voluntary wheel running, VWR) of aerobic exercise. Ageing impaired nitric oxide-mediated EDD (peak EDD 88 ± 12% 6 months P = 0.003 vs. 59 ± 9% 27 months NC-SED), which was accelerated by WD (60 ± 18% 6 months WD-SED). In NC mice, aPWV increased 32% with age (423 ± 13 cm/s at 24 months P < 0.001 vs. 321 ± 12 cm/s at 6 months) and absolute values were an additional ∼10% higher at any age in WD mice (P = 0.042 vs. NC-SED). Increases in aPWV with age in NC and WD mice were associated with 30-65% increases in aortic intrinsic wall stiffness (6 vs. 19-27 months, P = 0.007). Lifelong aerobic exercise prevented age- and WD-related vascular dysfunction across the lifespan, and this protection appeared to be mediated by mitigation of vascular mitochondrial oxidative stress and inflammation. Our results depict the temporal impairment of vascular function over the lifespan in mice, acceleration and exacerbation of that dysfunction with WD consumption, the remarkable protective effects of voluntary aerobic exercise, and the underlying mechanisms.

Dataset Information

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

Publications

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets