Biophysical Journal
Volume 77, Issue 3, September 1999, Pages 1666-1682
Analysis of the Mechanisms of Mitochondrial NADH Regulation in Cardiac Trabeculae
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Definitions and abbreviations
SL
Sarcomere length
SR
Sarcoplasmic reticulum
[Ca2+]c
Cytosolic [Ca2+]
[Ca2+]o
Extracellular [Ca2+]
[Ca2+]m
Mitochondrial [Ca2+]. Depends on Av[Ca2+]c.
Av[Ca2+]c
Time-averaged [Ca2+]c. Depends on pacing frequency and Ca2+-transient amplitude (and relaxation rate).
FAv
Time-averaged developed force. Depends on Av[Ca2+]c and SL.
FAv0
Time-averaged developed force for reference protocol (see Table 1, Protocol P0).
W
Total (rate of) work performed (= WForce + WTrsp + Wother).
WForce
Work performed by the myofilaments resulting in ATP hydrolysis. Depends on FAv.
WTrsp
Work performed by Ca2+-transport resulting in ATP hydrolysis. Depends on Av[Ca2+]c.
Wother
Work performed by other processes.
NADH
Semicalibrated [NADH]m from Nratio (see Eq. 2) or nicotineamid adenine dinucleotide (reduced form).
[NADH]m
Mitochondrial [NADH]
NADH MIN
Minimum level of NADH following increased work. Depends independently on increased WForce and WTrsp.
NADH REC
Amount of NADH recovery following prolonged work. Depends on [Ca2+]m (which depends on Av[Ca2+]c).
NADH MAX
Maximum level of NADH following reduced work. Depends on [Ca2+]m (which depends on Av[Ca2+]c) before reducing work.
P0–n
Going from Protocol Pn (n = 1–6) to Protocol P0 (Reference protocol) causes changes in the variables controlling NADH and, consequently, in NADH MIN, NADH REC, and NADH MAX
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