[1] T-tubule structure and function are affected beat-by-beat by cardiomyocyte contraction,[2] as well as by diseases, potentially contributing to heart failure and arrhythmias.

T-tubules are tubules formed from the same phospholipid bilayer as the surface membrane or sarcolemma of skeletal or cardiac muscle cells.

[1] T-tubules are found in both atrial and ventricular cardiac muscle cells (cardiomyocytes), in which they develop in the first few weeks of life.

[1] T-tubules within the heart are closely associated with the intracellular calcium store known as the sarcoplasmic reticulum in specific regions referred to as terminal cisternae.

[9] Junctophilin-2 is encoded by the gene JPH2 and helps to form a junction between the T-tubule membrane and the sarcoplasmic reticulum, vital for excitation-contraction coupling.

[6] T-tubules are an important link in the chain from electrical excitation of a cell to its subsequent contraction (excitation-contraction coupling).

During an action potential, positively charged particles (predominantly sodium and calcium ions) flow across the membrane from the outside to the inside.

In cardiac muscle cells, as the action potential passes down the T-tubules it activates L-type calcium channels in the T-tubular membrane.

The rapid spread of the action potential along the T-tubule network activates all of the L-type calcium channels near-simultaneously.

Furthermore, beta adrenoceptors are also highly concentrated in the T-tubular membrane,[15] and their stimulation increases calcium release from the sarcoplasmic reticulum.

Chemicals such as glycerol[18] or formamide[14] (for skeletal and cardiac muscle respectively) can be added to the extracellular solution that surrounds the cells.

[19] Alternatively, the osmolarity of the extracellular solution can be decreased, using for example hypotonic saline, causing a transient cell swelling.

The very brief time lag between stimulating a striated muscle cell and its subsequent contraction was too short to have been caused by a signalling chemical travelling the distance between the sarcolemma and the sarcoplasmic reticulum.

It was therefore suggested that pouches of membrane reaching into the cell might explain the very rapid onset of contraction that had been observed.

This can increase the time taken for calcium levels within the cell to rise leading to weaker contractions and arrhythmias.