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Contractile activation and force generation in skinned rabbit muscle fibres: effects of hydrostatic pressure.
Author(s) -
Fortune N S,
Geeves M A,
Ranatunga K W
Publication year - 1994
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1994.sp020021
Subject(s) - crossbridge , hydrostatic pressure , chemistry , isometric exercise , calcium , biophysics , muscle contraction , tension (geology) , contraction (grammar) , myosin , anatomy , biochemistry , medicine , endocrinology , compression (physics) , materials science , thermodynamics , biology , physics , organic chemistry , composite material
1. Effects of hydrostatic pressure (range 0.1‐10 MPa) on the isometric tension of skinned (rabbit psoas) muscle fibres were examined at 12 degrees C and at different levels of Ca2+ activation (pCa range 4‐7); the effects on both the steady tension and the tension transients induced by rapid pressure release (< 1 ms) are described. 2. The steady tension was depressed by increased pressure (approximately 1% MPa‐1) at a high level of Ca2+ activation (pCa approximately 4) whereas it was potentiated at lower Ca2+ levels (pCa > 6); the effects were reversible. 3. At maximal Ca2+ activation, the tension recovery following pressure release (10 MPa to atmospheric) consisted of a fast (approximately 30 s‐1) and a slow (2‐3 s‐1) phase; the rate and the normalized amplitude (normalized to the steady tension at atmospheric pressure for a particular pCa) of the fast phase were invariant with changes in Ca2+ level. 4. The effects of changing Ca2+ level on the slow phase were complex; its positive amplitude at high Ca2+ levels changed to negative and the rate decreased to approximately 1 s‐1 at low Ca2+ levels (pCa > 6.0). 5. Results are discussed in relation to previous studies on the effect of pressure on intact muscle fibres and the actin‐myosin interaction. This work supports calcium regulation of cross‐bridge recruitment rather than calcium regulation of the rate of a specific step in the cross‐bridge cycle.