Acute hypoxia has previously been suggested to potentiate resistance traininginduced hypertrophy by activating satellite cell-dependent myogenesis rather than an improvement in protein balance in human. Here, we tested this hypothesis after a 4-week hypoxic vs normoxic resistance training protocol. For that purpose, 19 physically active male subjects were recruited to perform 6 sets of 10 repetitions of a one-leg knee extension exercise at 80% 1-RM 3 times/week for 4 weeks in normoxia (FiO 2 : 0.21; n = 9) or in hypoxia (FiO 2 : 0.135, n = 10). Blood and skeletal muscle samples were taken before and after the training period. Muscle fractional protein synthetic rate was measured over the whole period by deuterium incorporation into the protein pool and muscle thickness by ultrasound. At the end of the training protocol, the strength gain was higher in the hypoxic vs the normoxic group despite no changes in muscle thickness and in the fractional protein synthetic rate. Only early myogenesis, as assessed by higher MyoD and Myf5 mRNA levels, appeared to be enhanced by hypoxia compared to normoxia. No effects were found on myosin heavy chain expression, markers of oxidative metabolism and lactate transport in the skeletal muscle. Though the present study failed to unravel clearly the mechanisms by which hypoxic resistance training is particularly potent to increase muscle strength, 2 of 15 | van DOORSLaER DE tEn RYEn Et aL.

Mechanistic insights into the molecular events by which exercise enhances the skeletal muscle phenotype are lacking, particularly in the context of type 2 diabetes. Here, we unravel a fundamental role for exercise-responsive cytokines ( exerkines ) on skeletal muscle development and growth in individuals with normal glucose tolerance or type 2 diabetes. Acute exercise triggered an inflammatory response in skeletal muscle, concomitant with an infiltration of immune cells. These exercise effects were potentiated in type 2 diabetes. In response to contraction or hypoxia, cytokines were mainly produced by endothelial cells and macrophages. The chemokine CXCL12 was induced by hypoxia in endothelial cells, as well as by conditioned medium from contracted myotubes in macrophages. We found that CXCL12 was associated with skeletal muscle remodeling after exercise and differentiation of cultured muscle. Collectively, acute aerobic exercise mounts a noncanonical inflammatory response, with an atypical production of exerkines, which is potentiated in type 2 diabetes.

The purpose of this narrative review is to provide an overview of the currently available knowledge about the mechanisms by which physical activity may affect metastatic development. The search terms exercise [Title/Abstract] AND metastasis [Title/Abstract] returned 222 articles on PUBMED on the 10 February 2019. After careful analysis of the abstracts, a final selection of 24 articles was made. Physical activity regulates the levels of metastatic factors in each of the five steps of the process. Moderate intensity exercise appears to prevent tumor spread around the body, among others, by normalizing angiogenesis, destroying circulating tumor cells, and decreasing endothelial cells permeability. Contrarily, high-intensity exercise seems to favor cancer dissemination, likely through excessive stress, which can be somewhat counteracted by an appropriate warm-up. In conclusion, chronic adaptations to moderate-intensity endurance exercise seem the most effective way to achieve a preventive effect of exercise on metastases. Altogether, the data gathered here reinforce the importance of encouraging cancer patients to perform moderate physical activity several times a week. To limit the undesired events thereof, a good knowledge of the patient’s training level is important to establish an adapted exercise training program.

No abstract

Exercise modulates the circulating levels of the endocannabinoids ligands N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG) and possibly the levels of their receptors and downstream signaling in skeletal muscle. The aim of the present study was to investigate the regulation of the endocannabinoid system by several exercise paradigms in human skeletal muscle. A second aim was to compare endocannabinoid regulation in healthy and prediabetic people in response to an acute endurance exercise. Blood and muscle samples were taken before and after resistance and endurance exercise in normoxia and hypoxia to measure plasma endocannabinoid levels as well as muscle protein expression of CB1, CB2 and downstream signaling. We found that: 1) an acute resistance exercise session decreased plasma 2-AG and N-palmitoylethanolamine (PEA) levels in normoxia; 2) 4 weeks resistance training decreased plasma AEA, PEA and N-oleoylethanolamine (OEA) levels in both normoxia and hypoxia; 3) an acute moderate intensity endurance exercise increased plasma OEA levels in the healthy and prediabetic groups in normoxia and hypoxia while plasma 2-AG levels increased in the healthy group and AEA in the prediabetic group only in normoxia. The expression of the cannabinoid receptors was only marginally regulated by acute exercise, hypoxia and prediabetes and downstream signaling did not follow the changes detected in the endocannabinoid ligands. Altogether, our results suggest that resistance and endurance exercise regulate the levels of the endocannabinoid ligands and CB1 expression in opposite ways. The physiological impact of the changes observed in the endocannabinoid ligands in human skeletal muscle after exercise needs further investigation.