Long periods of skeletal muscle inactivity promote a loss of muscle protein resulting in fiber atrophy. This disuse-induced muscle atrophy results from decreased protein synthesis and increased protein degradation. Recent studies have increased our insight into this complicated process, and evidence indicates that disturbed redox signaling is an important regulator of cell signaling pathways that control both protein synthesis and proteolysis in skeletal muscle. The objective of this review is to outline the role that reactive oxygen species play in the regulation of inactivity-induced skeletal muscle atrophy. Specifically, this report will provide an overview of experimental models used to investigate disuse muscle atrophy and will also highlight the intracellular sources of reactive oxygen species and reactive nitrogen species in inactive skeletal muscle. We then will provide a detailed discussion of the evidence that links oxidants to the cell signaling pathways that control both protein synthesis and degradation. Finally, by presenting unresolved issues related to oxidative stress and muscle atrophy, we hope that this review will serve as a stimulus for new research in this exciting field.
Pain and difficulty in moving - Patients may also notice that they have frequent back pain or difficulty walking if they begin to develop muscle atrophy. These can be a result of either type of the disease. Other symptoms such as ham string contractures, limited range of neck motion or rigid spine may begin to form as your condition becomes worse. An overall stiffness or difficult, heavy feeling when you attempt to move has also been described by patients. Some of these side effects may be visible as you move, while others are internal so they cannot be witnessed. It is important to make note of whether or not you look differently and how you feel to determine if you may be developing muscle atrophy.