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      The effect of training volume and intensity on improvements in muscular strength and size in resistance-trained men

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          Abstract

          This investigation compared the effect of high-volume (VOL) versus high-intensity (INT) resistance training on stimulating changes in muscle size and strength in resistance-trained men. Following a 2-week preparatory phase, participants were randomly assigned to either a high-volume (VOL; =  14, 4 × 10–12 repetitions with ∼70% of one repetition maximum [1RM], 1-min rest intervals) or a high-intensity (INT; =  15, 4 × 3–5 repetitions with ∼90% of 1RM, 3-min rest intervals) training group for 8 weeks. Pre- and posttraining assessments included lean tissue mass via dual energy x-ray absorptiometry, muscle cross-sectional area and thickness of the vastus lateralis (VL), rectus femoris (RF), pectoralis major, and triceps brachii muscles via ultrasound images, and 1RM strength in the back squat and bench press (BP) exercises. Blood samples were collected at baseline, immediately post, 30 min post, and 60 min postexercise at week 3 (WK3) and week 10 (WK10) to assess the serum testosterone, growth hormone (GH), insulin-like growth factor-1 (IGF1), cortisol, and insulin concentrations. Compared to VOL, greater improvements ( <  0.05) in lean arm mass (5.2 ± 2.9% vs. 2.2 ± 5.6%) and 1RM BP (14.8 ± 9.7% vs. 6.9 ± 9.0%) were observed for INT. Compared to INT, area under the curve analysis revealed greater ( <  0.05) GH and cortisol responses for VOL at WK3 and cortisol only at WK10. Compared to WK3, the GH and cortisol responses were attenuated ( <  0.05) for VOL at WK10, while the IGF1 response was reduced ( <  0.05) for INT. It appears that high-intensity resistance training stimulates greater improvements in some measures of strength and hypertrophy in resistance-trained men during a short-term training period.

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          Quantifying test-retest reliability using the intraclass correlation coefficient and the SEM.

          Reliability, the consistency of a test or measurement, is frequently quantified in the movement sciences literature. A common metric is the intraclass correlation coefficient (ICC). In addition, the SEM, which can be calculated from the ICC, is also frequently reported in reliability studies. However, there are several versions of the ICC, and confusion exists in the movement sciences regarding which ICC to use. Further, the utility of the SEM is not fully appreciated. In this review, the basics of classic reliability theory are addressed in the context of choosing and interpreting an ICC. The primary distinction between ICC equations is argued to be one concerning the inclusion (equations 2,1 and 2,k) or exclusion (equations 3,1 and 3,k) of systematic error in the denominator of the ICC equation. Inferential tests of mean differences, which are performed in the process of deriving the necessary variance components for the calculation of ICC values, are useful to determine if systematic error is present. If so, the measurement schedule should be modified (removing trials where learning and/or fatigue effects are present) to remove systematic error, and ICC equations that only consider random error may be safely used. The use of ICC values is discussed in the context of estimating the effects of measurement error on sample size, statistical power, and correlation attenuation. Finally, calculation and application of the SEM are discussed. It is shown how the SEM and its variants can be used to construct confidence intervals for individual scores and to determine the minimal difference needed to be exhibited for one to be confident that a true change in performance of an individual has occurred.
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            Chi-Square Tests for Goodness of Fit and Contingency Tables

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              Glucocorticoid-induced skeletal muscle atrophy.

              Many pathological states characterized by muscle atrophy (e.g., sepsis, cachexia, starvation, metabolic acidosis and severe insulinopenia) are associated with an increase in circulating glucocorticoids (GC) levels, suggesting that GC could trigger the muscle atrophy observed in these conditions. GC-induced muscle atrophy is characterized by fast-twitch, glycolytic muscles atrophy illustrated by decreased fiber cross-sectional area and reduced myofibrillar protein content. GC-induced muscle atrophy results from increased protein breakdown and decreased protein synthesis. Increased muscle proteolysis, in particular through the activation of the ubiquitin proteasome and the lysosomal systems, is considered to play a major role in the catabolic action of GC. The stimulation by GC of these two proteolytic systems is mediated through the increased expression of several Atrogenes ("genes involved in atrophy"), such as FOXO, Atrogin-1, and MuRF-1. The inhibitory effect of GC on muscle protein synthesis is thought to result mainly from the inhibition of the mTOR/S6 kinase 1 pathway. These changes in muscle protein turnover could be explained by changes in the muscle production of two growth factors, namely Insulin-like Growth Factor (IGF)-I, a muscle anabolic growth factor and Myostatin, a muscle catabolic growth factor. This review will discuss the recent progress made in the understanding of the mechanisms involved in GC-induced muscle atrophy and consider the implications of these advancements in the development of new therapeutic approaches for treating GC-induced myopathy. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting. Copyright © 2013 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Physiol Rep
                Physiol Rep
                phy2
                Physiological Reports
                John Wiley & Sons, Ltd (Chichester, UK )
                2051-817X
                2051-817X
                August 2015
                13 August 2015
                : 3
                : 8
                : e12472
                Affiliations
                [1 ]Institute of Exercise Physiology and Wellness, University of Central Florida Orlando, Florida
                [2 ]Health & Exercise Science, The College of New Jersey Ewing, New Jersey
                Author notes
                Correspondence Jay R. Hoffman, Institute of Exercise Physiology and Wellness, University of Central Florida, 4000 Central Florida Blvd, Orlando, FL 32816-1250., Tel: 407-823-1272, E-mail: jay.hoffman@ 123456ucf.edu

                Funding Information No funding information provided.

                Article
                10.14814/phy2.12472
                4562558
                26272733
                ecfcb30f-3a46-49ea-8da8-20661e55158e
                © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 June 2015
                : 01 July 2015
                Categories
                Original Research

                anabolic hormones,hypertrophy,muscle activation,strength

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