Effects of progressive resistance training on immune response in aging and chronic inflammation

Rall, Laura C.; Roubenoff, Ronenn; Cannon, Joseph G.; Abad, Leslie W.; Dinarello, Charles A.; Meydani, Simin Nikbin

doi:10.1097/00005768-199611000-00003

Cited by 145 publications

(119 citation statements)

References 35 publications

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“…6). This compartmentalization of cytokine responses is similar to our previous observations in patients with HIV infection (1) and rheumatoid arthritis (38).…”

Section: Discussionsupporting

confidence: 91%

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Sacheck¹,

Cannon²,

Hamada³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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mediates many aspects of the exercise-induced acute-phase response, including upregulation of antioxidant defenses. Moreover, IL-6 synthesis is regulated in part by oxidative stress. This investigation tested the hypothesis that an IL-6-mediated acute-phase response after exercise provides negative-feedback protection against exerciseinduced oxidative stress. Healthy young (n ϭ 16, 26.4 Ϯ 1.8 yr) and older men (n ϭ 16, 71.1 Ϯ 2.0 yr) ran downhill for 45 min at 75% maximal oxygen consumption before and after a 12-wk period of supplementation with vitamin E (1,000 IU/day) or placebo. Circulating IL-6 and soluble IL-6 receptors, peripheral mononuclear cell production of IL-6, and IL-6 transcripts in muscle were measured before and within a 72-h time window after each acute exercise bout. At all time points plasma IL-6, IL-6 bioavailability, and C-reactive protein were higher in the older men; yet in response to exercise, young and older subjects experienced similar increases in these factors. Although the magnitude of postexercise changes in acutephase variables was independent of age, correlations among plasma, mononuclear cell, and muscle IL-6 and oxidative stress were evident only in young men (R 2 ϭ 0.64, 0.35, and 0.33, respectively). These changes in circulating IL-6 were closely associated with a prooxidant state (R 2 ϭ 0.47), whereas muscle IL-6 mRNA correlated with an antioxidant state (R 2 ϭ 0.65). Supplementation with vitamin E did not affect exercise-induced responses or differences between the young and old men in a consistent manner. Therefore, oxidative stress is linked to the acute-phase response after exercise in young men, but not in older men who had elevated acute-phase reactants, suggesting that further research is warranted to determine the basis for these differences.

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“…6). This compartmentalization of cytokine responses is similar to our previous observations in patients with HIV infection (1) and rheumatoid arthritis (38).…”

Section: Discussionsupporting

confidence: 91%

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Sacheck¹,

Cannon²,

Hamada³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…There were no changes in these parameters between baseline and followup among any of the subjects. Production of IL-lp, TNFa, and IL-6 did not change as a result of strength training (Table 2) (26). At baseline, however, elderly exercisers and subjects with RA produced -50% more total TNFa than did young subjects (S epidermidzs-stimulated) ( P < 0.03), and elderly control subjects produced -33% more than did young subjects (P not significant).…”

Section: Subject Characteristics Diet and Training Effectsmentioning

confidence: 88%

Protein metabolism in rheumatoid arthritis and aging. Effects of muscle strength training and tumor necrosis factor α

Rall

Rosen

Dolnikowski

et al. 1996

Arthritis & Rheumatism

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Objective. To determine the effects of rheumatoid arthritis (RA) on whole-body protein metabolism.Methods. We examined protein metabolism and its hormonal and cytokine mediators before and 12 weeks after progressive resistance muscle strength training in 8 healthy young (mean k SD age 25 2 2 years) and 8 healthy elderly (70 rt 5 years) men and women, and in 8 adults with RA (42 2 13 years). An additional 6 healthy elderly subjects (69 k 3 years) served as a swimming-only control group.Results. Subjects with RA had higher rates of protein breakdown than did young or elderly healthy subjects (79.9 f 17.2 versus 60.3 f 5.8 and 63.7 2 12.4 pmoles/gm total body potassium/hour, respectively, P < 0.05), while there was no effect of age per se. Patients treated with methotrexate had normal rates of protein breakdown (P < 0.01 versus RA without methotrexate; P not significant versus healthy young subjects). Increased protein catabolism in RA was no longer evident after strength training. In multiple regression analysis, levels of tumor necrosis factor a (TNFa) (r = 0.47, P = 0.01) and growth hormone (r = -0.51, P = 0.006) were associated with protein breakdown, and plasma glucagon levels were inversely correlated with protein synthesis (r = -0.45, P =0.02). Growth hormone (r = -0.56, P = 0.002) and glucagon (r = 0.45, P = 0.04, levels were associated with protein oxidation.Conclusion. Adults with RA have increased whole-body protein breakdown, which correlates with growth hormone, glucagon, and TNFa production.Despite the many advances in our understanding of the disordered immune response that occurs in rheumatoid arthritis (RA), little information has been available about the effect of inflammation on metabolism and body composition in RA. Previous work from our laboratory has shown that body cell mass and physical activity are significantly reduced, and resting energy expenditure (REE) significantly increased, in patients with RA compared with healthy age-, sex-, race-, and weight-matched controls (1-3). This hypermetabolism of RA (defined as an increase in REE by >lo% above predicted levels) was directly associated with the production of tumor necrosis factor a (TNFa) and interleukin-lp (IL-1p) by peripheral blood mononuclear cells (PBMC) from these patients, which was approximately 2-fold higher than that in the control subjects. We have termed the cytokine-associated loss of lean body mass in RA rheumatoid cachexia, and have proposed that this cachexia is an important contributor to morbidity and mortality in RA, and offers insights into inflammatory mediators of cachexia (4).Understanding the mediators of the decline in body cell and protein mass is important because loss of more than -40% of baseline body cell mass is fatal, as shown in starvation, aging, and in acute illness (5). In

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“…These results indicate that endurance training in later life is associated with a smaller age-related decline in certain aspects of circulating T-cell function. Rall et al (1996) found no changes in PBMNC subsets, production of IL-1β, TNF-α, ΙL-6, IL-2 or prostaglandin (PG)E 2 production, lymphocyte proliferation or delayedtype hypersensitivity response after 12 weeks of highintensity progressive-resistance training in eight healthy young subjects (22-30 years) and eight healthy elderly subjects (65-80 years). Rincon et al (1996) investigated the effect of an exercise intervention programme of 60 min three times weekly for 3 months in six frail men aged 70 years or more who were at risk of a fall but not suffering from serious medical problems compared with seven controls having no intervention.…”

Section: Chronic Exercise Effects In the Elderlymentioning

confidence: 89%

Exercise and immune function: effect of ageing and nutrition

et al. 1999

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fax +45 3545 6648, email bkp@rh.dk Strenuous exercise is followed by lymphopenia, neutrophilia, impaired natural immunity, decreased lymphocyte proliferative responses to mitogens, a low level of secretory immunoglobulin A in saliva, but high circulating levels of pro-and anti-inflammatory cytokines. These exercise-induced immune changes may provide the physiological basis of altered resistance to infections. The mechanisms underlying exercise-induced immune changes are multifactorial and include neuroendocrinological and metabolic mechanisms. Nutritional supplementation with glutamine abolishes the exercise-induced decline in plasma glutamine, but does not influence post-exercise immune impairment. However, carbohydrate loading diminishes most exercise effects of cytokines, lymphocyte and neutrophils. The diminished neutrophilia and elastase (EC 3.4.21.37) responses to eccentric exercise in elderly subjects were enhanced to levels comparable with those of young subjects by fish oil or vitamin E supplements. However, although vitamin C supplementation may diminish the risk of contracting an infection after strenuous exercise, it is not obvious that this effect is linked to an effect of vitamin C on exercise-induced immune changes. In conclusion, it is premature to make recommendations regarding nutritional supplementation to avoid post-exercise impairment of the immune system.

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Effects of progressive resistance training on immune response in aging and chronic inflammation

Cited by 145 publications

References 35 publications

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress

Protein metabolism in rheumatoid arthritis and aging. Effects of muscle strength training and tumor necrosis factor α

Exercise and immune function: effect of ageing and nutrition

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