TNF-alpha and TNFR1 responses to recovery therapies following acute resistance exercise

    Authors

    J. R. Townsend; J. R. Hoffman; M. S. Fragala; A. R. Jajtner; A. M. Gonzalez; A. J. Wells; G. T. Mangine; D. H. Fukuda;J. R. Stout

    Comments

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    Abbreviated Journal Title

    Front. Physiol.

    Keywords

    muscle damage; immune function; cytokines; athletic training; TNF-alpha; NECROSIS-FACTOR-ALPHA; SKELETAL-MUSCLE; ECCENTRIC EXERCISE; INFLAMMATORY; RESPONSES; ELECTRICAL-STIMULATION; CYTOKINES; HUMANS; CONTRACTIONS; NEUTROPHILS; VOLUNTARY; Physiology

    Abstract

    The purpose of this investigation was to compare the effect of two commonly used therapeutic modalities (a) neuromuscular electrical stimulation (NMES) and (b) cold water immersion (CWI) on circulating tumor necrosis factor alpha (TNF-alpha) and monocyte TNF-alpha receptor (TNFR1) expression following intense acute resistance exercise and subsequent recovery. Thirty (n = 30) resistance trained men (22.5 +/- 2.7y) performed an acute heavy resistance exercise protocol on three consecutive days followed by one of three recovery methods (CON, NMES, and CWI). Circulating TNF-alpha levels were assayed and TNFR1 expression on CD14+ monocytes was measured by flow cytometry measured PRE, immediately post (IP), 30-min post (30M), 24h post (24H), and 48h post (48H) exercise. Circulating TNF-alpha was elevated at IP (p = 0.001) and 30M (p = 0.005) and decreased at 24H and 48H recovery from IP in CON (p = 0.015) and CWI (p = 0.011). TNF-alpha did not significantly decrease from IP during recovery in NMES. TNFR1 expression was elevated (p < 0.001) at 30M compared to PRE and all other time points. No significant differences between groups were observed in TNFR1 expression. During recovery (24H, 48H) from muscle damaging exercise, NMES treatment appears to prevent the decline in circulating TNF-alpha observed during recovery in those receiving no treatment or CWI.

    Journal Title

    Frontiers in Physiology

    Volume

    6

    Publication Date

    1-1-2015

    Document Type

    Article

    Language

    English

    First Page

    6

    WOS Identifier

    WOS:000352932200001

    ISSN

    1664-042X

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