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Russell, A.P., Somm, E., Praz, M., Crettenand, A., Hartley, O., Melotti, A., et al. (2003) UCP3 protein regulation in human skeletal muscle fibre types I, IIa and IIx is dependent on exercise intensity. Journal of Physiology, 550, 855-861. doi:10.1113/jphysiol.2003.040162

has been cited by the following article:

  • TITLE: Review of the adaptation of skeletal muscle in intermittent claudication

    AUTHORS: Risha Gohil, Tristan Robert Alexander Lane, Patrick Coughlin

    KEYWORDS: Muscle; Intermittent Claudication; Peripheral Arterial Disease

    JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.3 No.4, July 18, 2013

    ABSTRACT: Background: Despite awareness about the impact of intermittent claudication (IC) on mobility, balance and quality of life; the underlying pathophysiology and alterations in muscle architecture secondary to the disease are often overlooked. This review aimed to summarize the pathophysiological muscle changes present secondary to IC. Methods: The electronic databases, Medline, EMBASE, Cinahl and AMED, were searched for studies from 1967 to August 2011. Search terms included exercise, intermittent claudication and muscle. Studies about IC which were focused on muscle histology, muscle architecture, blood flow or changes with exercise were included. Results: Of 434 studies identified, 135 unique results were found. Only 78 of these were suitable from abstract review, of which 15 were unobtainable and a further nine were identified from hand-searching references. Studies in animal models demonstrated a predominance of type II muscle fibres and an improvement in animal exercise tolerance secondary to training. Exercise alone was never able to improve distances to that of healthy controls, however a lower limb fistula along with exercise did. Lower limb blood flow was demonstrated to be affected regionally, and most evident during exercise with a prolonged return to normal in patients with IC. At a cellular level, the myocytes metabolism increased in those with IC, but returned to normal post-revascularization. Conclusion: Treatment for claudicants includes either revascularization or exercise. Successful revascularization has demonstrated a return to normal muscle metabolism; the underlying physiological improvement secondary to exercise still requires clarification.