Abstract
Skeletal muscle is responsible for altered acute and chronic workload as induced by exercise. Skeletal muscle adaptations range from immediate change of contractility to structural adaptation to adjust the demanded performance capacities. These processes are regulated by mechanically and metabolically induced signaling pathways, which are more or less involved in all of these regulations. Nitric oxide is one of the central signaling molecules involved in functional and structural adaption in different cell types. It is mainly produced by nitric oxide synthases (NOS) and by non-enzymatic pathways also in skeletal muscle. The relevance of a NOS-dependent NO signaling in skeletal muscle is underlined by the differential subcellular expression of NOS1, NOS2, and NOS3, and the alteration of NO production provoked by changes of workload. In skeletal muscle, a variety of highly relevant tasks to maintain skeletal muscle integrity and proper signaling mechanisms during adaptation processes towards mechanical and metabolic stimulations are taken over by NO signaling. The NO signaling can be mediated by cGMP-dependent and -independent signaling, such as S-nitrosylation-dependent modulation of effector molecules involved in contractile and metabolic adaptation to exercise. In this review, we describe the most recent findings of NO signaling in skeletal muscle with a special emphasis on exercise conditions. However, to gain a more detailed understanding of the complex role of NO signaling for functional adaptation of skeletal muscle (during exercise), additional sophisticated studies are needed to provide deeper insights into NO-mediated signaling and the role of non-enzymatic-derived NO in skeletal muscle physiology.
Highlights
Skeletal muscle tissue is highly plastic and shows a wide spectrum of adaptations towards mechanical and metabolic stress, as induced by physical exercise
The isoforms have been named after the tissues or cells from which they have been originally purified in order of their discovery, but they are expressed in other systems. nNOS activity was first shown in macrophages [73], but is present in human alveolar and bronchial epithelial cells [75], carcinoma cells, vascular smooth muscle cells or endothelial cells [76]. iNOS has been found in the nervous system, in skeletal muscles and the respiratory epithelium [75] and eNOS is present in the epithelium, and in the heart, skeletal muscle and in neurons [77,78]
These events are further supported by Ca2+-induced activations of nitric oxide synthases (NOS) proteins that in turn lead to cGMP production by which GSK-3β is inhibited and NFAT abundance is strengthened in the nucleus [195].This reveals in the long term the importance of nitric oxide (NO) for activity-dependent adaptations of skeletal muscle myofiber types on a structural level
Summary
Skeletal muscle tissue is highly plastic and shows a wide spectrum of adaptations towards mechanical and metabolic stress, as induced by physical exercise. An acute increase in substrate and oxygen uptake has to be initiated, in addition to the glycolytic and oxidative metabolic routes being turned on Both acute and chronic regulation of gene expression and protein levels, as well as posttranslational modifications of proteins, are required to achieve sustainable signaling and structural adaptations of skeletal muscle to maintain and to increase exercise performance capacities. NO was identified as the major vasodilator; NO production is not restricted to endothelial cells (ECs), but, interestingly, is produced in a variety of additional cell types, including skeletal muscles [1] These findings are of high relevance, as they attribute the important roles of NO in physiological signaling mechanisms to skeletal muscles. The importance of NO in skeletal muscle subsystems is highlighted with respect to exercise-induced adaptations to maintain the skeletal muscle function and structure and to improve physical performance capacities
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