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Basic Science Review: The Myopathy of Peripheral Arterial Occlusive Disease: Part 2. Oxidative Stress, Neuropathy, and Shift in Muscle Fiber Type

Department of Surgery, University of Nebraska Medical Center and Nebraska-Western Iowa Veterans Affairs Medical Center, Omaha, Nebraska, ipipinos{at}unmc.edu

Andrew R. Judge

Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida

Joshua T. Selsby

Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida

Zhen Zhu, MD

Department of Surgery, University of Nebraska Medical Center and Nebraska-Western Iowa Veterans Affairs Medical Center, Omaha, Nebraska

Stanley A. Swanson

Department of Surgery, University of Nebraska Medical Center and Nebraska-Western Iowa Veterans Affairs Medical Center, Omaha, Nebraska

Aikaterini A. Nella, MD

Department of Surgery, University of Nebraska Medical Center and Nebraska-Western Iowa Veterans Affairs Medical Center, Omaha, Nebraska

Stephen L. Dodd

Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida

In recent years, an increasing number of studies have demonstrated that a myopathy is present, contributes, and, to a certain extent, determines the pathogenesis of peripheral arterial occlusive disease. These works provide evidence that a state of repetitive cycles of exercise-induced ischemia followed by reperfusion at rest operates in patients with peripheral arterial occlusive disease and mediates a large number of structural and metabolic changes in the muscle, resulting in reduced strength and function. The key players in this process appear to be defective mitochondria that, through multilevel failure in their roles as energy, oxygen radical species, and apoptosis regulators, produce and sustain a progressive decline in muscle performance. In this 2-part review, the currently available evidence that characterizes the nature and mechanisms responsible for this myopathy is highlighted. In part 1, the functional and histomorphological characteristics of the myopathy were reviewed, and the main focus was on the biochemistry and bioenergetics of its mitochondriopathy. In part 2, accumulating evidence that oxidative stress related to ischemia reperfusion is probably the major operating mechanism of peripheral arterial occlusive disease myopathy is reviewed. Important new findings of a possible neuropathy and a shift in muscle fiber type are also reviewed. Learning more about these mechanisms will enhance our understanding of the degree to which they are preventable and treatable.

Key Words: peripheral arterial occlusive disease • skeletal muscle • oxidative stress • bioenergetics • mitochondrial dysfunction

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