Myocardial Relaxation

Mechanical Control of Relaxation

Our primary research focus is to better understand how muscle relax- and make them relax faster.

There are three well known molecular components to muscle relaxation- essentially the reverse of contraction.  To relax a muscle, first calcium must be removed from the cytosol (or at least decreased).  Second, binding sites controlled by a regulatory protein complex called troponin must deactivate.  Thirdly, myosin must detach from actin to reduce force (e.g. relax the muscle).  Interestingly, researchers are finding it difficult to accelerate relaxation by making these processes faster- but it is easy to slow relaxation by making these three processes slower.

A commonly held theory was that reducing afterload would accelerate the relaxation of muscle.  Our studies confirmed the correct theory that stretching a muscle accelerates detachment of myosin from actin (detaches crossbridges) which will make a muscle relax faster.  This work is detailed in a publication (pubmed link), and its implications are discussed in a recent review (pubmed link).  Recently, we wrote an editorial thinking more deeply on what myosin might be doing when it is stretched (pubmed link).

The relationship between relaxation rate and end systolic strain rate can be modulated. We found that reducing preload can increase the sensitivity of relaxation rate to strain rate (pubmed link).