Novel methods for cold exposure of skeletal muscle in vivo and in vitro show temperature-dependent myokine production

Krapf, Solveig A; Schjølberg, Tiril; Asoawe, Lucia; Honkanen, Susanna Kyllikki; Kase, Eili Tranheim; Thoresen, G. Hege; Haugen, Fred

doi:10.1016/j.jtherbio.2021.102930

Cited by 13 publications

(10 citation statements)

References 66 publications

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“…While for diabetic patients, 6 months of resistance training had no effect on serum IL-6 concentration under the same weight loss condition (Miller et al, 2017). Besides, IL-6 mRNA expression in the muscle of one hind limb of rat at 18 °C was significantly lower than that of the opposite limb at 37 °C, Frontiers in Physiology frontiersin.org while CXCL1 mRNA expression was higher at 18 °C than that at 37 °C (Krapf et al, 2021). When human skeletal muscle cells were heated from 18 to 37 °C, IL-6 and CXCL1 mRNA expression increased significantly.…”

Section: The Mechanism Underlying Exerciseinduced Expression Of Myokinesmentioning

confidence: 87%

The role of exercise-induced myokines in promoting angiogenesis

Song

Wang

et al. 2022

Front. Physiol.

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Ischemic diseases are a major cause of mortality or disability in the clinic. Surgical or medical treatment often has poor effect on patients with tissue and organ ischemia caused by diffuse stenoses. Promoting angiogenesis is undoubtedly an effective method to improve perfusion in ischemic tissues and organs. Although many animal or clinical studies tried to use stem cell transplantation, gene therapy, or cytokines to promote angiogenesis, these methods could not be widely applied in the clinic due to their inconsistent experimental results. However, exercise rehabilitation has been written into many authoritative guidelines in the treatment of ischemic diseases. The function of exercise in promoting angiogenesis relies on the regulation of blood glucose and lipids, as well as cytokines that secreted by skeletal muscle, which are termed as myokines, during exercise. Myokines, such as interleukin-6 (IL-6), chemokine ligand (CXCL) family proteins, irisin, follistatin-like protein 1 (FSTL1), and insulin-like growth factor-1 (IGF-1), have been found to be closely related to the expression and function of angiogenesis-related factors and angiogenesis in both animal and clinical experiments, suggesting that myokines may become a new molecular target to promote angiogenesis and treat ischemic diseases. The aim of this review is to show current research progress regarding the mechanism how exercise and exercise-induced myokines promote angiogenesis. In addition, the limitation and prospect of researches on the roles of exercise-induced myokines in angiogenesis are also discussed. We hope this review could provide theoretical basis for the future mechanism studies and the development of new strategies for treating ischemic diseases.

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Section: The Mechanism Underlying Exerciseinduced Expression Of Myokinesmentioning

confidence: 87%

The role of exercise-induced myokines in promoting angiogenesis

Song

Wang

et al. 2022

Front. Physiol.

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“…This hypothesis is supported by some of our results and by the work of other groups. Krapf et al (2021) have analyzed secreted VEGF-A protein expression in human myotubes immediately after 18 h of cold exposure as well as after 3 h and 24 h of post-cooling rewarming. Secreted VEGF-A levels were initially decreased by cold exposure, similar to our findings.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have investigated the angioadaptive impact of cold stress exposure on skeletal or cardiac muscle capillarization ( Heroux and St. Pierre, 1956 ; Sillau et al, 1980 ; Wickler, 1981 ; Banchero et al, 1985 ; Duchamp et al, 1992 ; Snyder et al, 1992 ; Suzuki et al, 1997a ; Suzuki et al, 1997b ; Mathieu-Costello et al, 1998 ; Egginton et al, 2001 ; Deveci and Egginton, 2002 ; Egginton, 2002 ; Bae et al, 2003 ; Deveci and Egginton, 2003 ; Wagatsuma et al, 2006 ; Ihsan et al, 2014 ; Joo et al, 2016 ; Sugasawa et al, 2016 ; D’Souza et al, 2018 ; Al-horani et al, 2019 ; Opichka et al, 2019 ; Magalhães et al, 2020 ; Shute et al, 2020 ; Krapf et al, 2021 ). Comparing these studies can be challenging.…”

Section: Introductionmentioning

confidence: 99%

“…Skeletal muscle angioadaptation requires communication between endothelial cells, as main capillary constituents, and myofibers as an important source of local angiokines ( Birot et al, 2003 ; Olfert and Birot, 2011 ; Hellsten and Hoier, 2014 ). While cold has been reported to alter the expression of myokines ( Nascimento et al, 2020 ; Krapf et al, 2021 ), it remains largely unknown whether cold could regulate angioadaptation through the regulation of myocytes-specific angiokines. To date, a few studies have combined cold and exercise and measured expression levels of the pro-angiogenic VEGF-A.…”

Section: Introductionmentioning

confidence: 99%

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Angiostatic freeze or angiogenic move? Acute cold stress prevents angiokine secretion from murine myotubes but primes primary endothelial cells for greater migratory capacity

2022

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The skeletal muscle tissue can adapt to exercise and environmental stressors with a remarkable plasticity. Prolonged cold stress exposure has been associated to increased skeletal muscle capillarization. Angioadaptation refers to the coordinated molecular and cellular processes that influence the remodeling of skeletal muscle microvasculature. Two cell types are central to angioadaptation: the myocytes, representing an important source of angiokines; and the skeletal muscle endothelial cell (SMECs), targets of these angiokines and main constituents of muscle capillaries. The influence of cold stress on skeletal muscle angioadaptation remains largely unknown, particularly with respect to myocyte-specific angiokines secretion or endothelial cell angioadaptive responses. Here, we use an in vitro model to investigate the impact of cold stress (28°C versus 37°C) on C2C12 myotubes and SMECs. Our main objectives were to evaluate: 1) the direct impact of cold stress on C2C12 cellular expression of angiokines and their release in the extracellular environment; 2) the indirect impact of cold stress on SMECs migration via these C2C12-derived angiokines; and 3) the direct effect of cold stress on SMECs angioadaptive responses, including migration, proliferation, and the activation of the vascular endothelial growth factor receptor-2 (VEGFR2). Cold stress reduced the secretion of angiokines in C2C12 myotubes culture media irrespective their pro-angiogenic or angiostatic nature. In SMECs, cold stress abrogated cell proliferation and reduced the activation of VEGFR2 despite a greater expression of this receptor. Finally, SMECs pre-conditioned to cold stress displayed an enhanced migratory response when migration was stimulated in rewarming conditions. Altogether our results suggest that cold stress may be overall angiostatic. However, cold stress accompanied by rewarming may be seen as a pro-angiogenic stressor for SMECs. This observation questions the potential for using pre-cooling in sport-performance or therapeutic exercise prescription to enhance skeletal muscle angioadaptive responses to exercise.

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“…Interestingly, cold exposure has also been reported to facilitate modulating the expression and release of myokines, thus increasing adipose tissue metabolism [ 12 ]. In this context, it was hypothesized that exercise combined with cold exposure might be the optimal regimen to regulate the myokine profile and a couple of studies have been conducted.…”

Section: Introductionmentioning

confidence: 99%

The Potential Roles of Myokines in Adipose Tissue Metabolism with Exercise and Cold Exposure

Jiang

Bae

Wang

et al. 2022

IJMS

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Exercise and cold exposure are two stimuli that have been suggested as solely effective to modulate adipose tissue metabolism and improve metabolic health in obese populations. The two primary organs involved in energy metabolism during exercise and/or cold exposure are skeletal muscle and adipose tissue. Adipose tissue can be divided mainly into two types: white adipose tissue (WAT), which primarily stores energy, and brown adipose tissue (BAT), known as the primary source of thermogenesis. The exercise-stimulated release of myokines allows for crosstalk between skeletal muscle and adipose tissue, partially mediating the beneficial effects of exercise. Cold exposure is another trigger for the regulation of myokine secretions, thus increasing adipose tissue metabolism, especially via activation of BAT. Therefore, this has generated the hypothesis that exercise in conjunction with cold exposure might be the optimal regimen to regulate myokine profiles and gain more beneficial health effects. However, to date, human experimental data regarding different exercise (frequency, type, time and intensity) and cold exposure (temperature, time and frequency) patterns are scarce. In this review, we will summarize the current human clinical trials investigating the regulation of myokines induced by exercise combined with cold exposure, to elaborate on the roles of myokines in mediating adipose tissue metabolism.

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Novel methods for cold exposure of skeletal muscle in vivo and in vitro show temperature-dependent myokine production

Cited by 13 publications

References 66 publications

The role of exercise-induced myokines in promoting angiogenesis

The role of exercise-induced myokines in promoting angiogenesis

Angiostatic freeze or angiogenic move? Acute cold stress prevents angiokine secretion from murine myotubes but primes primary endothelial cells for greater migratory capacity

The Potential Roles of Myokines in Adipose Tissue Metabolism with Exercise and Cold Exposure

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