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

Authors

  • Laura C. Rall PhD, RD,

    1. Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts
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  • Clifford J. Rosen MD,

    1. Maine Center for Osteoporosis Research and Education, St. Joseph Hospital, Bangor
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  • Gregory Dolnikowski PhD,

    1. Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts
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  • Wilburta J. Hartman PhD,

    1. Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts
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  • Nancy Lundgren,

    1. Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts
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  • Leslie W. Abad,

    1. Jean Mayer USDA Human Nutrition Research Center, and Tupper Research Institute, Tufts University School of Medicine and New England Medical Center, Boston, Massachusetts
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  • Charles A. Dinarello MD,

    1. Tupper Research Institute, Tufts University School of Medicine and New England Medical Center, Boston, Massachusetts
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  • Ronenn Roubenoff MD, MHS

    Corresponding author
    1. Jean Mayer USDA Human Nutrition Research Center, and Tupper Research Institute, Tufts University School of Medicine and New England Medical Center, Boston, Massachusetts
    • JMUSDA-HNRCA at Tufts University, 711 Washington Street, Boston, MA 02111
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Abstract

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 ± SD age 25 ± 2 years) and 8 healthy elderly (70 ± 5 years) men and women, and in 8 adults with RA (42 ± 13 years). An additional 6 healthy elderly subjects (69 ± 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 ± 17.2 versus 60.3 ± 5.8 and 63.7 ± 12.4 μmoles/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 α (TNFα) (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 TNFα production.

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