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      The effects of 12 weeks of beta-hydroxy-beta-methylbutyrate free acid supplementation on muscle mass, strength, and power in resistance-trained individuals: a randomized, double-blind, placebo-controlled study

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          Abstract

          Introduction

          Studies utilizing beta-hydroxy-beta-methylbutyrate (HMB) supplementation in trained populations are limited. No long-term studies utilizing HMB free acid (HMB-FA) have been conducted. Therefore, we investigated the effects of 12 weeks of HMB-FA supplementation on skeletal muscle hypertrophy, body composition, strength, and power in trained individuals. We also determined the effects of HMB-FA on muscle damage and performance during an overreaching cycle.

          Methods

          A three-phase double-blind, placebo- and diet-controlled randomized intervention study was conducted. Phase 1 was an 8-week-periodized resistance-training program; Phase 2 was a 2-week overreaching cycle; and Phase 3 was a 2-week taper. Muscle mass, strength, and power were examined at weeks 0, 4, 8, and 12 to assess the chronic effects of HMB-FA; and assessment of these, as well as cortisol, testosterone, and creatine kinase (CK) was performed at weeks 9 and 10 of the overreaching cycle.

          Results

          HMB-FA resulted in increased total strength (bench press, squat, and deadlift combined) over the 12-week training (77.1 ± 18.4 vs. 25.3 ± 22.0 kg, p < 0.001); a greater increase in vertical jump power (991 ± 168 vs. 630 ± 167 W, p < 0.001); and increased lean body mass gain (7.4 ± 4.2 vs. 2.1 ± 6.1 kg, p < 0.001) in HMB-FA- and placebo-supplemented groups, respectively. During the overreaching cycle, HMB-FA attenuated increases in CK (−6 ± 91 vs. 277 ± 229 IU/l, p < 0.001) and cortisol (−0.2 ± 2.9 vs. 4.5 ± 1.7 μg/dl, p < 0.003) in the HMB-FA- and placebo-supplemented groups, respectively.

          Conclusions

          These results suggest that HMB-FA enhances hypertrophy, strength, and power following chronic resistance training, and prevents decrements in performance following the overreaching.

          Electronic supplementary material

          The online version of this article (doi:10.1007/s00421-014-2854-5) contains supplementary material, which is available to authorized users.

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          Most cited references33

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          Exercise-Induced Muscle Damage in Humans

          Exercise-induced muscle injury in humans frequently occurs after unaccustomed exercise, particularly if the exercise involves a large amount of eccentric (muscle lengthening) contractions. Direct measures of exercise-induced muscle damage include cellular and subcellular disturbances, particularly Z-line streaming. Several indirectly assessed markers of muscle damage after exercise include increases in T2 signal intensity via magnetic resonance imaging techniques, prolonged decreases in force production measured during both voluntary and electrically stimulated contractions (particularly at low stimulation frequencies), increases in inflammatory markers both within the injured muscle and in the blood, increased appearance of muscle proteins in the blood, and muscular soreness. Although the exact mechanisms to explain these changes have not been delineated, the initial injury is ascribed to mechanical disruption of the fiber, and subsequent damage is linked to inflammatory processes and to changes in excitation-contraction coupling within the muscle. Performance of one bout of eccentric exercise induces an adaptation such that the muscle is less vulnerable to a subsequent bout of eccentric exercise. Although several theories have been proposed to explain this "repeated bout effect," including altered motor unit recruitment, an increase in sarcomeres in series, a blunted inflammatory response, and a reduction in stress-susceptible fibers, there is no general agreement as to its cause. In addition, there is controversy concerning the presence of sex differences in the response of muscle to damage-inducing exercise. In contrast to the animal literature, which clearly shows that females experience less damage than males, research using human studies suggests that there is either no difference between men and women or that women are more prone to exercise-induced muscle damage than are men.
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            Developing maximal neuromuscular power: part 2 - training considerations for improving maximal power production.

            This series of reviews focuses on the most important neuromuscular function in many sport performances: the ability to generate maximal muscular power. Part 1, published in an earlier issue of Sports Medicine, focused on the factors that affect maximal power production while part 2 explores the practical application of these findings by reviewing the scientific literature relevant to the development of training programmes that most effectively enhance maximal power production. The ability to generate maximal power during complex motor skills is of paramount importance to successful athletic performance across many sports. A crucial issue faced by scientists and coaches is the development of effective and efficient training programmes that improve maximal power production in dynamic, multi-joint movements. Such training is referred to as 'power training' for the purposes of this review. Although further research is required in order to gain a deeper understanding of the optimal training techniques for maximizing power in complex, sports-specific movements and the precise mechanisms underlying adaptation, several key conclusions can be drawn from this review. First, a fundamental relationship exists between strength and power, which dictates that an individual cannot possess a high level of power without first being relatively strong. Thus, enhancing and maintaining maximal strength is essential when considering the long-term development of power. Second, consideration of movement pattern, load and velocity specificity is essential when designing power training programmes. Ballistic, plyometric and weightlifting exercises can be used effectively as primary exercises within a power training programme that enhances maximal power. The loads applied to these exercises will depend on the specific requirements of each particular sport and the type of movement being trained. The use of ballistic exercises with loads ranging from 0% to 50% of one-repetition maximum (1RM) and/or weightlifting exercises performed with loads ranging from 50% to 90% of 1RM appears to be the most potent loading stimulus for improving maximal power in complex movements. Furthermore, plyometric exercises should involve stretch rates as well as stretch loads that are similar to those encountered in each specific sport and involve little to no external resistance. These loading conditions allow for superior transfer to performance because they require similar movement velocities to those typically encountered in sport. Third, it is vital to consider the individual athlete's window of adaptation (i.e. the magnitude of potential for improvement) for each neuromuscular factor contributing to maximal power production when developing an effective and efficient power training programme. A training programme that focuses on the least developed factor contributing to maximal power will prompt the greatest neuromuscular adaptations and therefore result in superior performance improvements for that individual. Finally, a key consideration for the long-term development of an athlete's maximal power production capacity is the need for an integration of numerous power training techniques. This integration allows for variation within power meso-/micro-cycles while still maintaining specificity, which is theorized to lead to the greatest long-term improvement in maximal power.
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              Minireview: the AMP-activated protein kinase cascade: the key sensor of cellular energy status.

              D Hardie (2003)
              All cells must maintain a high ratio of cellular ATP:ADP to survive. Because of the adenylate kinase reaction (2ADP ATP + AMP), AMP rises whenever the ATP:ADP ratio falls, and a high cellular ratio of AMP:ATP is a signal that the energy status of the cell is compromised. The AMP-activated protein kinase (AMPK) is the downstream component of a protein kinase cascade that is switched on by a rise in the AMP:ATP ratio, via a complex mechanism that results in an exquisitely sensitive system. AMPK is switched on by cellular stresses that either interfere with ATP production (e.g. hypoxia, glucose deprivation, or ischemia) or by stresses that increase ATP consumption (e.g. muscle contraction). It is also activated by hormones that act via Gq-coupled receptors, and by leptin and adiponectin, via mechanisms that remain unclear. Once activated, the system switches on catabolic pathways that generate ATP, while switching off ATP-consuming processes that are not essential for short-term cell survival, such as the synthesis of lipids, carbohydrates, and proteins. The AMPK cascade is the probable target for the antidiabetic drug metformin, and current indications are that it is responsible for many of the beneficial effects of exercise in the treatment and prevention of type 2 diabetes and the metabolic syndrome.
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                Author and article information

                Contributors
                +1-813-2576314 , jwilson06x@gmail.com
                ryan.lowery@spartans.ut.edu
                jordan.joy@spartans.ut.edu
                jcandersen@ut.edu
                stephanie.wilson@img.com
                Jeffrey.stout@ucf.edu
                nduncan@spartans.ut.edu
                fuller@mti-hmb.com
                baier@mti-hmb.com
                mnaimo@ut.edu
                rathmacher@mti-hmb.com
                Journal
                Eur J Appl Physiol
                Eur. J. Appl. Physiol
                European Journal of Applied Physiology
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                1439-6319
                1439-6327
                6 March 2014
                6 March 2014
                2014
                : 114
                : 1217-1227
                Affiliations
                [ ]Department of Health Sciences and Human Performance, The University of Tampa, Tampa, FL 33606 USA
                [ ]Department of Nutrition, IMG Academy, Bradenton, FL USA
                [ ]Institute of Exercise Physiology and Wellness, University of Central Florida, Orlando, FL USA
                [ ]Metabolic Technologies Inc, Iowa State University Research Park, Ames, IA USA
                [ ]Department of Animal Science, Iowa State University, Ames, IA USA
                Author notes

                Communicated by Michael Lindinger.

                Article
                2854
                10.1007/s00421-014-2854-5
                4019830
                24599749
                5db87bdf-23e0-40dc-8bc7-9c3cac966e1a
                © The Author(s) 2014

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                : 2 November 2013
                : 13 February 2014
                Categories
                Original Article
                Custom metadata
                © Springer-Verlag Berlin Heidelberg 2014

                Anatomy & Physiology
                leucine metabolite,resistance training,overreaching,recovery,sports supplements

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