Muscle hypertrophy and increased expression of leptin receptors in the musculus triceps brachii of the dominant arm in professional tennis players

Department of Physical Education, University of Las Palmas de Gran Canaria, Campus Universitario de Tafira s/n, 35017 Las Palmas de Gran Canaria, Canary Island, Spain.
Arbeitsphysiologie (Impact Factor: 2.19). 03/2010; 108(4):749-58. DOI: 10.1007/s00421-009-1281-5
Source: PubMed


In rodents, endurance training increases leptin sensitivity in skeletal muscle; however, little is known about the effects of exercise on the leptin signalling system in human skeletal muscle. Thus, to determine whether chronic muscle loading increases leptin receptor (OB-R170) protein expression, body composition dual-energy X-ray absorptiometry was assessed in nine professional male tennis players (24 +/- 4 years old) and muscle biopsies were obtained from the dominant (DTB) and non-dominant (NDTB) arm triceps brachii (TB), and also from the right vastus lateralis (VL). In each biopsy, the protein content of OB-R170, perilipin A, suppressor of cytokine signalling 3 (SOCS3), protein tyrosine phosphatase 1B (PTP1B) and signal transducer and activator of transcription 3 (STAT3) phosphorylation were determined by western blot. The DTB had 15% greater lean mass (P < 0.05) and 62% greater OB-R170 protein expression (P < 0.05) than the NDTB. SOCS3 and PTP1B protein expression was similar in both arms, while STAT3 phosphorylation was reduced in the NDTB. OB-R170 protein content was also higher in DTB than in VL (P < 0.05). In summary, this study shows that the functional isoform of the leptin receptor is up-regulated in the hypertrophied TB. The latter combined with the fact that both SOCS3 and PTP1B protein expression were unaltered is compatible with increased leptin sensitivity in this muscle. Our findings are also consistent with a role of leptin signalling in muscle hypertrophy in healthy humans.

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Available from: C. Borja Guerra Hdez.
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    • "We have recently shown that OB-rb protein expression is reduced in deltoid and vastus lateralis muscles of humans with obesity (Fuentes et al. 2010), but it is increased in the dominant triceps brachii of professional tennis players compared with the non-uploaded triceps (Olmedillas et al. 2010). A down-regulation of OB-rb protein expression in skeletal muscle could account for some of the peripheral leptin resistance typical of sedentarism and obesity (Fuentes et al. 2010). "
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    ABSTRACT: This study aimed at determining the effects of bed rest on the skeletal muscle leptin signaling system. Deltoid and vastus lateralis muscle biopsies and blood samples were obtained from 12 healthy young men (mean ± SD, BMI 22.8 ± 2.7 kg/m(2)) before and after 7 days of bed rest. Leptin receptor isoforms (OB-Rs), suppressor of cytokine signaling 3 (SOCS3) and protein tyrosine phosphatase 1B (PTP1B) protein expression and signal transducer and activator of transcription 3 (STAT3) phosphorylation were analyzed by Western blot. After bed rest basal insulin concentration was increased by 53 % (P < 0.05), the homeostasis model assessment (HOMA) by 40 % (P < 0.05), and serum leptin concentration by 35 % (P < 0.05) with no changes in body fat mass. Although the soluble isoform of the leptin receptor (s-OBR) remained unchanged, the molar excess of leptin over sOB-R was increased by 1.4-fold after bed rest (P < 0.05). OB-Rs and SOCS3 protein expression, and STAT3 phosphorylation level remained unaffected in deltoid and vastus lateralis by bed rest, as PTP1B in the deltoid. PTP1B was increased by 90 % with bed rest in the vastus lateralis (P < 0.05). There was a linear relationship between the increase in vastus lateralis PTP1B and the increase in both basal insulin concentrations (r = 0.66, P < 0.05) and HOMA (r = 0.68, P < 0.05) with bed rest. One week of bed rest is associated with increased leptin levels without augmenting STAT3 phosphorylation indicating some degree of leptin resistance in skeletal muscle, which can be explained, at least in part, by an elevation of PTP1B protein content in the vastus lateralis muscle.
    Full-text · Article · Feb 2014 · Arbeitsphysiologie
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    • "In agreement with published data, endurance exercise could also increase gene expression of the hypothalamic leptin receptor and activation of the JAK2-STAT3 signaling pathway, reducing leptin and insulin levels [48]. Increased expression of the leptin receptor was found in hypertrophied triceps of professional tennis players [49]. "
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    ABSTRACT: To investigate the effects of acute and chronic exercise on glucose and lipid metabolism in liver of rats with type 2 diabetes caused by a high fat diet and low dose streptozotocin (STZ). Animals were classified into control (CON), diabetes (DC), diabetic chronic exercise (DCE), and diabetic acute exercise (DAE) groups. Compared to CON, the leptin levels in serum and liver and ACC phosphorylation were significantly higher in DC, but the levels of liver leptin receptor, AMPK α 1/2, AMPK α 1, and ACC proteins expression and phosphorylation were significantly lower in DC. In addition, the levels of liver glycogen reduced significantly, and the levels of TG and FFA increased significantly in DC compared to CON. Compared to DC, the levels of liver AMPK α 1/2, AMPK α 2, AMPK α 1, and ACC phosphorylation significantly increased in DCE and DAE. However, significant increase of the level of liver leptin receptor and glycogen as well as significant decrease of the level of TG and FFA were observed only in DEC. Our study demonstrated that both acute and chronic exercise indirectly activated the leptin-AMPK-ACC signaling pathway and increased insulin sensitivity in the liver of type 2 diabetic rats. However, only chronic and long-term exercise improved glucose and lipid metabolism of the liver.
    Full-text · Article · Dec 2013 · Journal of Diabetes Research
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    • "Leptin is secreted from fat cells (adipocytes), but skeletal muscle is also a source of leptin [3], and serum leptin levels increase with increased muscle mass [4]. Leptin receptors have been identified in human skeletal muscle [5] and their expression is elevated with disuse atrophy [6] as well as with exercise [7]. On the other hand, leptin-deficiency increases expression of the muscle-wasting protein myostatin in myocytes [8], and the functional characteristics of skeletal muscle in leptin-deficient ob/ob mice have been noted to resemble those of aged rodents [9]. "
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    ABSTRACT: Leptin receptors are abundant in human skeletal muscle, but the role of leptin in muscle growth, development and aging is not well understood. Here we utilized a novel mouse model lacking all functional leptin receptor isoforms (POUND mouse, Lepr(db/lb)) to determine the role of leptin in skeletal muscle. Skeletal muscle mass and fiber diameters were examined in POUND mice, and primary myoblast cultures were used to determine the effects of altered leptin signaling on myoblast proliferation and differentiation. ELISA assays, integrated pathway analysis of mRNA microarrays, and reverse phase protein analysis were performed to identify signaling pathways impacted by leptin receptor deficiency. Results show that skeletal muscle mass and fiber diameter are reduced 30-40% in POUND mice relative to wild-type controls. Primary myoblast cultures demonstrate decreased proliferation and decreased expression of both MyoD and myogenin in POUND mice compared to normal mice. Leptin treatment increased proliferation in primary myoblasts from muscles of both adult (12 months) and aged (24 months) wild-type mice, and leptin increased expression of MyoD and myogenin in aged primary myoblasts. ELISA assays and protein arrays revealed altered expression of molecules associated with the IGF-1/Akt and MAPK/MEK signaling pathways in muscle from the hindlimbs of mice lacking functional leptin receptors. These data support the hypothesis that the adipokine leptin is a key factor important for the regulation of skeletal muscle mass, and that leptin can act directly on its receptors in peripheral tissues to regulate cell proliferation and differentiation.
    Full-text · Article · Aug 2013 · PLoS ONE
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