Is the heart more relaxed when stretched or contracted, and how does it affect cross-bridge interactions?
The muscular portion of the heart is comprised of cardiac myocytes, elongated cells filled with bundles of actin and myosin called sarcomeres. These cells are similar in many respects to skeletal muscles, but are shorter, have only one nucleus, and slightly different isoforms (versions) of the proteins involved. The purpose of this cell, like the skeletal muscle cell, is contraction, or shortening on activation.

This image of cardiac muscle cells shows how full they are with long bands of proteins (proteins stain pink). 



Because the heart is a muscular chamber, instead of simply a band of muscle (like the bicep), the relevant dimension for the organ is volume instead of length. Where your bicep gets shorter when it contracts (and pulls your forearm toward your upper arm, bending at the elbow joint), when your heart muscle contracts, it twists and squeezes against the fibrous part of the organ, decreasing the volume of the chamber.  

Since there is no air in a healthy live heart, when the heart contracts, reducing the volume of the container, the blood is forced out of the heart (ejection) through whatever opening is available. This is called systole. When the heart relaxes, the volume of the container increases, and blood enters the container through whatever opening is available. this is called diastole.



Now, how is this related to cross-bridge interactions?

The mechanism for contraction itself, in both skeletal and cardiac muscle, is cross-bridge cycling. Those pink bundles of actin, myosin, and associated proteins in the picture above form bonds, change conformation, break bonds, change conformation, and form new bonds:


This cross-bridge cycling occurs during contraction when $Ca^{++}$ enters the cell as part of the cardiac action potential. Relaxation occurs when $Ca^{++}$ concentrations decrease, through the action of the $Ca^{++}$-ATPase, causing cross bridge interactions to decrease.