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Effects of Reactive Oxygen Species on Aspects of Excitation‐Contraction Coupling in Chemically Skinned Rabbit Diaphragm Muscle Fibres
Author(s) -
Darnley G. M.,
Duke A. M.,
Steele D. S.,
MacFarlane N. G.
Publication year - 2001
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/eph8602109
Subject(s) - excitation–contraction coupling , contraction (grammar) , rabbit (cipher) , biophysics , diaphragm muscle , diaphragm (acoustics) , muscle contraction , chemistry , oxygen , coupling (piping) , anatomy , materials science , medicine , biology , skeletal muscle , physics , respiratory system , mathematics , acoustics , statistics , organic chemistry , metallurgy , loudspeaker
Oxidants have been suggested to enhance contractile function in unfatigued muscle. In this study we aimed to determine the effect of oxidants on ‘chemically skinned’ diaphragm muscle fibre bundles. The sarcoplasmic reticulum and contractile proteins were exposed to superoxide anions (O 2 − ) and hydrogen peroxide (H 2 O 2 ) under controlled conditions. Application of O 2 − initially increased maximum Ca 2+ ‐activated force but subsequently reduced maximum Ca 2+ ‐activated force without altering myofilament Ca 2+ sensitivity. Unlike myocardium, caffeine‐induced Ca 2+ release from the sarcoplasmic reticulum was also inhibited by O 2 − exposure in diaphragm fibre bundles. Application of H 2 O 2 also increased maximum Ca 2+ ‐activated force but had additional effects on resting tension (which increased to 25% of the control maximum Ca 2+ ‐activated force). H 2 O 2 was without effect on myofilament Ca 2+ sensitivity or caffeine‐induced Ca 2+ release from the sarcoplasmic reticulum. These data demonstrate that oxidants can potentiate contractile force in the diaphragm through a direct action on the contractile proteins. The potentiation of force is not sustained, however, and under these conditions the detrimental effects of O 2 − on Ca 2+ release from the sarcoplasmic reticulum combined with the effects of oxidants on the contractile proteins will ultimately compromise excitation‐contraction coupling in the diaphragm.