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-α) and monocyte TNF-α receptor (TNFR1) expression following intense acute resistance exercise and subsequent recovery. Thirty (n = 30) resistance trained men (22.5 ± 2.7 y) performed an acute heavy resistance exercise protocol on three consecutive days followed by one of three recovery methods (CON, NMES, and CWI). Circulating TNF-α levels were assayed and TNFR1 expression on CD14+ monocytes was measured by flow cytometry measured PRE, immediately post (IP), 30-min post (30M), 24 h post (24H), and 48 h post (48H) exercise. Circulating TNF-α 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-α 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-α observed during recovery in those receiving no treatment or CWI.
Highlights
Tumor necrosis factor-α (TNF-α) is a multifunctional cytokine involved in the regulation of inflammation and tissue injury
Participants assigned to the cold water immersion (CWI), neuromuscular electrical stimulation (NMES), and CON groups did not differ in in any physical characteristics
Muscle damage corresponded with significant elevations in Creatine Kinase (CK) from pre-exercise for baseline measurement (PRE) (103.4–166.3 U/L) to 24 h post (24H) (290%, 468.9–677.1 U/L) and 48 h post (48H) (271% 424.6–612.5 U/L) post-T2 and myoglobin from PRE (23.3–35.5 ng/mL) to immediately post (IP) (192%, 63.8–114.8 ng/mL) and 30P (357%, 89.3–180.6 ng/mL), as reported previously (Jajtner et al, 2014)
Summary
Tumor necrosis factor-α (TNF-α) is a multifunctional cytokine involved in the regulation of inflammation and tissue injury. As an early mediator in muscle damage, TNF-α can be synthesized by several immune and nervous cells and is rapidly released in the blood by circulating monocytes and in skeletal muscle by invading macrophages after exercise-induced muscle damage (Hirose et al, 2004; Zaldivar et al, 2006). TNF-α can induce both necrosis and apoptosis of myocytes through intracellular signaling pathways (Hardin et al, 2008) which accompanies a decline in muscle contractile properties and diminished performance (Cassatella, 1995; Hardin et al, 2008). Strenuous exercise often results in considerable muscle damage that may impact subsequent athletic performance (Crameri et al, 2007). Various recovery modalities are often used by athletes as a means to counteract the inflammatory response which accompanies the potentially damaging effects of intense exercise. Cold water immersion (CWI) is one of the most common recovery modalities used by athletes to expedite muscle repair and recovery (Barnett, 2006; Rice et al, 2008; Bleakley et al, 2012)
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