Some additional websearch on mitochondria

• the structure seems to be indeed tubular or maybe I should say anything but neatly folded. See e.g.
  • 3D images
  • Movies
• furthermore there is a difference in composition between inner and outer membrane:
  "inner membrane is highly impermeable; almost all ions and molecules require special membrane transporters to enter or exit the matrix." (ref)
• a highly interesting title in IUBMB Life. 2001 Sep-Nov;52(3-5):93-100.
  I've no access to the full text. Anybody else?

  Topology of the mitochondrial inner membrane: dynamics and bioenergetic implications.
  Mannella CA, Pfeiffer DR, Bradshaw PC, Moraru II, Slepchenko B, Loew LM, Hsieh CE, Buttle K, Marko M.
  Abstract Electron tomography indicates that the mitochondrial inner membrane is not normally comprised of baffle-like folds as depicted in textbooks. In actuality, this membrane is pleomorphic, with narrow tubular regions connecting the internal compartments (cristae) to each other and to the membrane periphery. The membrane topologies observed in condensed (matrix contracted) and orthodox (matrix expanded) mitochondria cannot be interconverted by passive folding and unfolding. Instead, transitions between these morphological states likely involve membrane fusion and fission. Formation of tubular junctions in the inner membrane appears to be energetically favored, because they form spontaneously in yeast mitochondria following large-amplitude swelling and recontraction. However, aberrant, unattached, vesicular cristae are also observed in these mitochondria, suggesting that formation of cristae junctions depends on factors (such as the distribution of key proteins and/or lipids) that are disrupted during extreme swelling. Computer modeling studies using the "Virtual Cell" program suggest that the shape of the inner membrane can influence mitochondrial function. Simulations indicate that narrow cristae junctions restrict diffusion between intracristal and external compartments, causing depletion of ADP and decreased ATP output inside the cristae.
  Publication Types:
  * Review
  * Review, Tutorial
  

  I looked in VCell and it is indeed mentioned as a "Virtual Cell Published Model" but I couldn't find it in the model database. Anybody else more experience with VCell? Would be very interesting to play with!
• paper in Am J Physiol Cell Physiol. 2005 Mar;288(3):C510-22 (see elib)

  Three-dimensional simulation of calcium waves and contraction in cardiomyocytes using the finite element method.
  Okada J, Sugiura S, Nishimura S, Hisada T.
  Abstract To investigate the characteristics and underlying mechanisms of Ca(2+) wave propagation, we developed a three-dimensional (3-D) simulator of cardiac myocytes, in which the sarcolemma, myofibril, and Z-line structure with Ca(2+) release sites were modeled as separate structures using the finite element method. Similarly to previous studies, we assumed that Ca(2+) diffusion from one release site to another and Ca(2+)-induced Ca(2+) release were the basic mechanisms, but use of the finite element method enabled us to simulate not only the wave propagation in 3-D space but also the active shortening of the myocytes. Therefore, in addition to the dependence of the Ca(2+) wave propagation velocity on the sarcoplasmic reticulum Ca(2+) content and affinity of troponin C for Ca(2+), we were able to evaluate the influence of active shortening on the propagation velocity. Furthermore, if the initial Ca(2+) release took place in the proximity of the nucleus, spiral Ca(2+) waves evolved and spread in a complex manner, suggesting that this phenomenon has the potential for arrhythmogenicity. The present 3-D simulator, with its ability to study the interaction between Ca(2+) waves and contraction, will serve as a useful tool for studying the mechanism of this complex phenomenon.

Added later on: interesting website from Wadsworth Center with

• Images
• Publication List