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Effects of {beta}-Hydroxy-{beta}-methylbutyrate Free Acid and Cold Water Immersion on Expression of CR3 and MIP-1{beta} following Resistance Exercise

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AJP Regulatory Integrative and Comparative Physiology

Published online on

Abstract

The inflammatory response to muscle damaging exercise requires monocyte mobilization and adhesion. Complement receptor type 3 (CR3) and macrophage inflammatory protein (MIP)-1β enables monocyte recruitment, adhesion, and subsequent infiltration into damaged muscle tissue. The purpose of this study was to examine the effects of cold water immersion (CWI) and/or β-hydroxy-β-methylbutyrate free acid (HMB-FA) on CR3 expression and MIP-1β concentration following four sets of up to ten repetitions of squat, dead lift, and split squat exercises at 70-80% 1-repetition maximum. Thirty-nine resistance-trained men (22.2 ± 2.5 y) were randomly divided into four groups: 1)Placebo (PL); 2)HMB-FA; 3)HMB-FA-CWI; 4)PL-CWI. The HMB-FA groups ingested 3 g•d-1 and CWI groups submersed into 10-12°C water for 10 minutes following exercise. Blood was sampled at baseline (PRE), immediately post (IP), 30 minutes post (30P), 24 hours post (24P), and 48 hours post (48P) exercise. Circulating MIP-1β was assayed and CR3 expression on CD14+ monocytes was measured by flow cytometry. Without treatment, CR3 expression significantly elevated at 30P when compared to other time points (p=0.030-0.047). HMB-FA significantly elevated the percent of monocytes expressing CR3 between IP and 24P (p=0.046) and between IP and 48P (p=0.046). No time effect was observed for MIP-1β concentration. The recovery modalities showed to attenuate the rise in CR3 following exercise. Additionally, supplementation with HMB-FA significantly elevated the percent of monocytes expressing CR3 during recovery. Although the time course which inflammatory responses are most beneficial remains to be determined, recovery modalities may alter immune cell mobilization and adhesion mechanisms during tissue recovery.