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Can microcurrent electrical neuromuscular stimulation decrease symptoms associated with delayed onset muscle soreness?
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|Title:||Can microcurrent electrical neuromuscular stimulation decrease symptoms associated with delayed onset muscle soreness?|
|Keywords:||Myalgia -- Prevention|
|Abstract:||Traumatic injury typically presents with the five cardinal signs of inflammation 'secondary to the release of histamine and norepinephrine. These chemical mediators increase capillary permeability, allowing exudate high in proteins and leukocytes, and phagocytic cells to destroy, and marginize damaged tissue. Injured tissues are electropositive but become electrical negative in the early stages of the healing process. These processes are dependent on membrane' permeability and active transport across the cell membrane (prentice, 1999; Starkey, 1999) Active transport theoretically increases with microcurrent electrical neuromuscular stimulation (MENS) thereby re-establishing the body's natural electrical balance resulting in adenosine triphosphate (ATP) replenishment and providing the metabolic energy necessary for healing to occur (Starkey). The biophysical efficacy of MENS (<500 µA) is based on the theory that currents less than 500 µA increase ATP levels while currents greater than µA decrease ATP levels. Currents less than 500 µA create a proton imbalance forcing them across the mitochondrial membrane, as they move from anode to cathode, causing an increase in the production of ATP (Baily, 2003; Starkey, 1999). Successful treatment of fracture and wounds using MENS is well documented (Assimacopoulos, 1968; Carley & Wainapel, 1985; Feedar et al., 1991; Gault & Gatens, 1976; Gentzkow et al., 1991; Mulder, 1991; Wolcott et al., 1969; Wood et al., 1993) These studies involved placing the cathode directly over the fracture site or ulcer in wound healing (Brighton et al., 1981; Connolly et al., 1997; DC Paterson et al., 1982). Conversely, MENS treatment of delayed onset muscle soreness (DOMS) is inconclusive, controversial, anecdotal and limited(Allen et al., 1999; Bonacci & Higbie, 1997; Lambert et al., 2001; Weber et al., 1994) Delayed onset muscle soreness is a soft tissue injury characterized by the disruption of the cell membrane and active transport system resulting in decreased ATP production and streaming of the Z-lines in type IIB muscle fibers (Friden, 1984; Newham et al., 1983), All but one (Lambert et al., 2001) of the aforementioned studies involved treatment with alternating polarity (Bonacci & Higbie, 1997; Denegar et al" 1992; Weber et al., 1994) or didn't specify (Allen et al., 1999) over the injury site during the treatment period, Conversely, Lambert was the only investigator who placed the cathode (negative) over the injury site, AdditionaI1y~ Lambert and Bonacci utilized extended treatment periods (96 continuous hours, 8 continuous hours, respectively), Therefore the purpose of this study was to examine the effect of MENS treatment protocols typically used in athletic training clinical practices with specific attention to polarity, The hypothesis for this study was that there will be no difference among MENS treatments relative to pain, edema, and range of motion and muscle strength associated with DOMS,|
|Description:||Thesis (M.S.)--University of Hawaii at Manoa, 2005.|
Includes bibliographical references (leaves 23-24).
vi, 89 leaves, bound 29 cm
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|Appears in Collections:||M.S. - Kinesiology and Leisure Science|
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