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The Effects of a Multi-Ingredient Performance Supplement on Hormonal Profiles and Body Composition in Male College Athletes

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      Periods of intense training can elicit an acute decline in performance and body composition associated with weakened hormone profiles. This study investigated the effects of a multi-ingredient performance supplement (MIPS) on body composition and hormone levels in college athletes following a six-week training protocol. Twenty male college athletes were equally assigned to MIPS and placebo (PLA) groups for supplementation (three pills, twice daily) in conjunction with resistance training and specialized sports training (e.g., nine total sessions/week) for six weeks. Dual Energy X-ray Absorptiometry determined body composition at weeks 0 and 6. Serum samples collected at weeks 0 and 6 determined free testosterone (FT), total testosterone (TT), IGF-1 and total estrogen (TE) levels. PLA experienced a significant decline in lean body mass (LBM) (−1.5 kg; p < 0.05) whereas the MIPS sustained LBM. The MIPS increased TT 21.9% (541.5 ± 48.7 to 639.1 ± 31.7) and increased FT 15.2% (13.28 ± 1.1 to 15.45 ± 1.3 ng/dL) ( p < 0.05). Conversely, PLA decreased TT 7.9% (554.5 ± 43.3 to 497.2 ± 39.1 ng/dL), decreased FT 17.4% (13.41 ± 1.8 to 11.23 ± 2.55 ng/dL), and decreased FT:E 12.06% ( p < 0.05). These findings suggest the MIPS can prevent decrements in LBM and anabolic hormone profiles during intense training periods.

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      Most cited references 31

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      The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men.

      Athletes often take androgenic steroids in an attempt to increase their strength. The efficacy of these substances for this purpose is unsubstantiated, however. We randomly assigned 43 normal men to one of four groups: placebo with no exercise; testosterone with no exercise; placebo plus exercise; and testosterone plus exercise. The men received injections of 600 mg of testosterone enanthate or placebo weekly for 10 weeks. The men in the exercise groups performed standardized weight-lifting exercises three times weekly. Before and after the treatment period, fat-free mass was determined by underwater weighing, muscle size was measured by magnetic resonance imaging, and the strength of the arms and legs was assessed by bench-press and squatting exercises, respectively. Among the men in the no-exercise groups, those given testosterone had greater increases than those given placebo in muscle size in their arms (mean [+/-SE] change in triceps area, 424 +/- 104 vs. -81 +/- 109 square millimeters; P < 0.05) and legs (change in quadriceps area, 607 +/- 123 vs. -131 +/- 111 square millimeters; P < 0.05) and greater increases in strength in the bench-press (9 +/- 4 vs. -1 +/- 1 kg, P < 0.05) and squatting exercises (16 +/- 4 vs. 3 +/- 1 kg, P < 0.05). The men assigned to testosterone and exercise had greater increases in fat-free mass (6.1 +/- 0.6 kg) and muscle size (triceps area, 501 +/- 104 square millimeters; quadriceps area, 1174 +/- 91 square millimeters) than those assigned to either no-exercise group, and greater increases in muscle strength (bench-press strength, 22 +/- 2 kg; squatting-exercise capacity, 38 +/- 4 kg) than either no-exercise group. Neither mood nor behavior was altered in any group. Supraphysiologic doses of testosterone, especially when combined with strength training, increase fat-free mass and muscle size and strength in normal men.
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        Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men.

        We aimed to determine whether exercise-induced elevations in systemic concentration of testosterone, growth hormone (GH) and insulin-like growth factor-1 (IGF-1) enhanced post-exercise myofibrillar protein synthesis (MPS) and phosphorylation of signalling proteins important in regulating mRNA translation. Eight young men (20 +/- 1.1 years, BMI = 26 +/- 3.5 kg m(-2)) completed two exercise protocols designed to maintain basal hormone concentrations (low hormone, LH) or elicit increases in endogenous hormones (high hormone, HH). In the LH protocol, participants performed a bout of unilateral resistance exercise with the elbow flexors. The HH protocol consisted of the same elbow flexor exercise with the contralateral arm followed immediately by high-volume leg resistance exercise. Participants consumed 25 g of protein after arm exercise to maximize MPS. Muscle biopsies and blood samples were taken as appropriate. There were no changes in serum testosterone, GH or IGF-1 after the LH protocol, whereas there were marked elevations after HH (testosterone, P < 0.001; GH, P < 0.001; IGF-1, P < 0.05). Exercise stimulated a rise in MPS in the biceps brachii (rest = 0.040 +/- 0.007, LH = 0.071 +/- 0.008, HH = 0.064 +/- 0.014% h(-1); P < 0.05) with no effect of elevated hormones (P = 0.72). Phosphorylation of the 70 kDa S6 protein kinase (p70S6K) also increased post-exercise (P < 0.05) with no differences between conditions. We conclude that the transient increases in endogenous purportedly anabolic hormones do not enhance fed-state anabolic signalling or MPS following resistance exercise. Local mechanisms are likely to be of predominant importance for the post-exercise increase in MPS.
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          Testosterone action on skeletal muscle.

          To highlight recent data demonstrating direct anabolic effects of androgens on the mammalian skeletal muscle and review the mechanisms by which testosterone regulates body composition. Testosterone increases lean body mass and decreases fat mass in young men; the magnitude of the changes induced by testosterone in lean and fat mass are correlated with testosterone dose and the prevalent testosterone concentrations. Older men are as responsive to the anabolic effects of testosterone on the muscle as young men, but have increased frequency of adverse events with higher testosterone doses. This reciprocal change in lean and fat mass induced by androgens is best explained by the hypothesis that androgens promote the commitment of mesenchymal pluripotent cells into myogenic lineage and inhibit adipogenesis through an androgen receptor mediated pathway. Resident muscle satellite cells increase in number with testosterone administration forming myoblasts leading to greater numbers of myonuclei in larger myofibers. Testosterone administration is associated with increased size of motor neurons. The roles of 5-alpha reduction and aromatization of testosterone into dihydrotestosterone and estradiol, respectively, in mediating testosterone effects on body composition are poorly understood. Testosterone induces skeletal muscle hypertrophy by multiple mechanisms, including its effects in modulating the commitment of pluripotent mesenchymal cells. These changes in skeletal muscle lead to improved muscle strength and leg power; however, further studies are needed to determine the effects of testosterone on physical function and health-related outcomes in sarcopenia associated with aging and chronic illness.

            Author and article information

            [1 ]Applied Science and Performance Institute, Tampa, FL 33607, USA; ryanplowery@
            [2 ]Department of Health Sciences and Human Performance, The University of Tampa, Tampa, FL 33606, USA; kevinshields31@ (K.A.S.); jacobrauch1@ (J.T.R.); edesouza@ (E.O.D.S.)
            [3 ]Maximum Human Performance, West Caldwell, NJ 07006, USA; sdurkee@ (S.E.D.); gwilson@ (G.J.W.)
            Author notes
            [* ]Correspondence: msharp2113@ ; Tel.: +1-813-257-6314

            These authors contributed equally to this work.

            Role: Academic Editor
            Sports (Basel)
            Sports (Basel)
            06 May 2016
            June 2016
            : 4
            : 2
            5968923 10.3390/sports4020026 sports-04-00026
            © 2016 by the authors.

            Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (



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