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      Effects of whole-body cryotherapy on 25-hydroxyvitamin D, irisin, myostatin, and interleukin-6 levels in healthy young men of different fitness levels

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          Abstract

          Skeletal muscle and adipose tissue play an important role in maintaining metabolic homeostasis and thermogenesis. We aimed to investigate the effects of single and repeated exposure to whole-body cryotherapy in volunteers with different physical fitness levels on 25-hydroxyvitamin D (25(OH)D) and myokines. The study included 22 healthy male volunteers (mean age: 21 ± 1.17 years), who underwent 10 consecutive sessions in a cryogenic chamber once daily (3 minutes, −110 °C). Blood samples were collected before and 30 minutes and 24 hours after the first and last cryotherapy sessions. Prior to treatment, body composition and physical fitness levels were measured. After 10 cryotherapy treatments, significant changes were found in myostatin concentrations in the low physical fitness level (LPhL) group. The 25(OH)D levels were increased in the high physical fitness level (HPhL) group and decreased in the LPhL group. The HPhL group had significant changes in the level of high-sensitivity interleukin-6 after the first treatment. The LPhL group had significant changes in 25(OH)D, irisin, and myostatin levels after the tenth treatment. Our data demonstrated that in healthy young men, cryotherapy affects 25(OH)D levels, but they were small and transient. The body’s response to a series of 10 cryotherapy treatments is modified by physical fitness level.

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          Most cited references 39

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          Interleukin‐6 myokine signaling in skeletal muscle: a double‐edged sword?

          Interleukin (IL)‐6 is a cytokine with pleiotropic functions in different tissues and organs. Skeletal muscle produces and releases significant levels of IL‐6 after prolonged exercise and is therefore considered as a myokine. Muscle is also an important target of the cytokine. IL‐6 signaling has been associated with stimulation of hypertrophic muscle growth and myogenesis through regulation of the proliferative capacity of muscle stem cells. Additional beneficial effects of IL‐6 include regulation of energy metabolism, which is related to the capacity of actively contracting muscle to synthesize and release IL‐6. Paradoxically, deleterious actions for IL‐6 have also been proposed, such as promotion of atrophy and muscle wasting. We review the current evidence for these apparently contradictory effects, the mechanisms involved and discuss their possible biological implications.
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            Irisin is expressed and produced by human muscle and adipose tissue in association with obesity and insulin resistance.

            Recently irisin (encoded by Fndc5 gene) has been reported to stimulate browning and uncoupling protein 1 expression in sc adipose tissue of mice. The objective of the study was to investigate FNDC5 gene expression in human muscle and adipose tissue and circulating irisin according to obesity, insulin sensitivity, and type 2 diabetes. Adipose tissue FNDC5 gene expression and circulating irisin (ELISA) were analyzed in 2 different cohorts (n = 125 and n = 76); muscle FNDC5 expression was also evaluated in a subcohort of 34 subjects. In vitro studies in human preadipocytes and adipocytes and in induced browning of 3T3-L1 cells (by means of retinoblastoma 1 silencing) were also performed. In both sc and visceral adipose tissue, FNDC5 gene expression decreased significantly in association with obesity and was positively associated with brown adipose tissue markers, lipogenic, insulin pathway-related, mitochondrial, and alternative macrophage gene markers and negatively associated with LEP, TNFα, and FSP27 (a known repressor of brown genes). Circulating irisin and irisin levels in adipose tissue were significantly associated with FNDC5 gene expression in adipose tissue. In muscle, the FNDC5 gene was 200-fold more expressed than in adipose tissue, and its expression was associated with body mass index, PGC1α, and other mitochondrial genes. In obese participants, FNDC5 gene expression in muscle was significantly decreased in association with type 2 diabetes. Interestingly, muscle FNDC5 gene expression was significantly associated with FNDC5 and UCP1 gene expression in visceral adipose tissue. In men, circulating irisin levels were negatively associated with obesity and insulin resistance. Irisin was secreted from human adipocytes into the media, and the induction of browning in 3T3-L1 cells led to increased secreted irisin levels. Decreased circulating irisin concentration and FNDC5 gene expression in adipose tissue and muscle from obese and type 2 diabetic subjects suggests a loss of brown-like characteristics and a potential target for therapy.
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              Muscles and their myokines.

              In the past, the role of physical activity as a life-style modulating factor has been considered as that of a tool to balance energy intake. Although it is important to avoid obesity, physical inactivity should be discussed in a much broader context. There is accumulating epidemiological evidence that a physically active life plays an independent role in the protection against type 2 diabetes, cardiovascular diseases, cancer, dementia and even depression. For most of the last century, researchers sought a link between muscle contraction and humoral changes in the form of an 'exercise factor', which could be released from skeletal muscle during contraction and mediate some of the exercise-induced metabolic changes in other organs such as the liver and the adipose tissue. We have suggested that cytokines or other peptides that are produced, expressed and released by muscle fibres and exert autocrine, paracrine or endocrine effects should be classified as 'myokines'. Given that skeletal muscle is the largest organ in the human body, our discovery that contracting skeletal muscle secretes proteins sets a novel paradigm: skeletal muscle is an endocrine organ producing and releasing myokines, which work in a hormone-like fashion, exerting specific endocrine effects on other organs. Other myokines work via paracrine mechanisms, exerting local effects on signalling pathways involved in muscle metabolism. It has been suggested that myokines may contribute to exercise-induced protection against several chronic diseases.
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                Author and article information

                Contributors
                sliwicka@awf.poznan.pl
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                10 April 2020
                10 April 2020
                2020
                : 10
                Affiliations
                [1 ]Poznan University of Physical Education, Department of Physiology and Biochemistry, Poznań, Poland
                [2 ]State University of Applied Science in Nowy Sącz, Department of Physiotherapy, Nowy Sącz, Poland
                [3 ]Poznan University of Physical Education, Department of Physical Therapy and Sports Recovery, Poznań, Poland
                [4 ]State University of Applied Sciences in Kalisz, Faculty of Rehabilitation and Sport, Kalisz, Poland
                Article
                63002
                10.1038/s41598-020-63002-x
                7148349
                32277130
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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                biochemistry, physiology

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