Acute and timing effects of beta-hydroxy-beta-methylbutyrate (HMB) on indirect markers of skeletal muscle damage

Jacob M Wilson,J Derek Kingsley,John A Rathmacher,Anssi H Manninen,Raz Saadat,Brett Dalmau,Sang-Rok Lee,Heather Koch,Lynn B Panton,Jeong-Su Kim

doi:10.1186/1743-7075-6-6

Abstract

BackgroundWhile chronic β-Hydroxy β-Methylbutyrate (HMB) supplementation (≥ 2 wk) lowers exercise induced muscle damage, its acute or timing effects have not been examined. The purpose of this study was to investigate the acute and timing effects of oral HMB supplementation on serum creatine kinase (CK), lactate dehydrogenase (LDH), muscle soreness, and maximal voluntary contraction (MVC).MethodsSixteen non-resistance trained men (22 ± 2 yrs) were assigned to HMB-Pre or HMB-Post groups. In a crossover design, all subjects performed 55 maximal eccentric knee extension/flexion contractions on 2 occasions on either the right or left leg. HMB-Pre (N = 8) randomly received 3 grams of either a placebo or HMB before and a placebo after exercise. HMB-Post (N = 8) received a placebo before and either 3 grams of HMB or a placebo after exercise. Muscle damage tests were recorded before, at 8, 24, 48, and 72 hrs post exercise.ResultsThere was a reduction in MVC and an increase in soreness in the quadriceps and hamstrings following exercise (p < 0.001). Although HMB-Pre approached significance in attenuating soreness for the quadriceps (p = 0.07), there was no time × group effect. Serum indices of damage increased, peaking at 48 hrs for CK (773%) (p < 0.001) and 72 hrs for LDH (180%) (p < 0.001). While there were no time × group effects of HMB on CK and LDH, post hoc analysis revealed that only HMB-Pre showed no significant increase in LDH levels following exercise.ConclusionOur findings suggest no clear acute or timing effects of HMB supplementation. However, consuming HMB before exercise appeared to prevent increases in LDH.

Highlights

Oral administration of the leucine metabolite, betahydroxy beta-methylbutyrate (HMB), has been associated with increased lean body mass (LBM) [1,2], isometric [1], isokinetic [1], and dynamic strength [3]
Hydroxy β-Methylbutyrate (HMB) is converted to 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) with a subsequent increase in the activity of the rate limiting enzyme for cholesterol synthesis HMG-CoA reductase [3,9]
This is evidenced by studies demonstrating that HMB leads to decreased markers of muscle damage following mechanically strenuous exercise included lower levels of creatine kinase (CK) [3,4], lactate dehydrogenase (LDH) [10], 3-methylhistidine (3-MH) [3], urine urea nitrogen and plasma urea [2], and muscular soreness [4]

Summary

Introduction

Oral administration of the leucine metabolite, betahydroxy beta-methylbutyrate (HMB), has been associated with increased lean body mass (LBM) [1,2], isometric [1], isokinetic [1], and dynamic strength [3]. The result is an overall reinforcement of the sarcolemma as well as the provision of valuable substrate for its repair following muscle damaging and or injurious exercise [3,9] This is evidenced by studies demonstrating that HMB leads to decreased markers of muscle damage following mechanically strenuous exercise included lower levels of creatine kinase (CK) [3,4], lactate dehydrogenase (LDH) [10], 3-methylhistidine (3-MH) [3], urine urea nitrogen and plasma urea [2], and muscular soreness [4]. The purpose of this study was to investigate the acute and timing effects of oral HMB supplementation on serum creatine kinase (CK), lactate dehydrogenase (LDH), muscle soreness, and maximal voluntary contraction (MVC)

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