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K ATP channel deficiency impairs Ca 2+ release, Ca 2+ regulation and causes fiber damage during fatigue in single FDB muscle fibers.
Author(s) -
Bourassa François,
Cifelli Carlo,
Renaud JeanMarc
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a809-b
Subject(s) - calcium , contraction (grammar) , chemistry , muscle fatigue , medicine , muscle contraction , biophysics , endocrinology , calcium channel blocker , voltage dependent calcium channel , calcium channel , kir6.2 , biology , biochemistry , neuroscience , protein subunit , electromyography , gene
K ATP channel deficiency causes fiber damage in mouse type IIB fibers during treadmill running, large increase in resting tension during fatigue and reduction in the capacity to recover force following fatigue. The objective of this study was to determine how a K ATP channel deficiency affects intracellular calcium levels between and during contractions in single FDB muscle fibers fatigued at 37°C with one tetanic contraction every sec for 3 min. For all wild type fibers (control), peak calcium level during contraction increased forthe first 10–15 sec before it decreased. The decreases in peak calcium were divided into two patterns. For the first pattern, the decrease was slow and after 3 min peak calcium was still above the pre‐fatigue level (fatigue resistant fibers). For the second pattern, the decrease was much faster and peak calcium was significant less than pre‐fatigue level after 3 min (non‐fatigue resistant fibers). K ATP channel deficient muscle fibers were obtained i) by exposing wild type fibers to glibenclamide, a channel blocker, or ii) by using fibers from the null mice for the Kir6.2 gene. The lack of K ATP channel activity did not affect the initial increase in peak calcium. However, the subsequent decrease in peak calcium was much faster and greater than in control fibers. Furthermore, many fibers completely stop releasing calcium upon stimulation. Finally, several fibers were damaged in the absence of K ATP channel activity. The calcium levels between contraction increased during fatigue and to a greater extent in K ATP channel deficient fibers; the largest increases being in damaged fibers. It is suggested that in the absence of K ATP channel activity the greater resting tension is linked to greater resting calcium level while the decreased capacity to recover force is linked to loss of damaged fibers.