Cardiac muscle
Cardiac muscle is a specialised striated muscle producing long-lasting effort and more than 2 billion contractions in a life time. The main myosin HC gene expressed in the heart is the same as that found in slow, Type I muscles. The elongated cardiac cells, or cardiomyocytes, are much smaller than skeletal muscle cells, and do not attach to tendons. myocytes attach to their neighbours to form what is known as a functional syncytium. Cells are connected to each other via specialised connections, the intercalated disks, which allow the propagation of electrical depolarisation and the structural and mechanical integrity of the heart. Unsurprisingly, cardiomyocytes are rich in mitochondria and the tissue is well vascularised to allow long term maintenance of function.
Pictures on the left: Cardiomyocytes in which the ATP binding site of myosin is labelled with the fluorescent ATP analogue DEAC-ATP. Pictures on the right show the same cells in the bright-field microscope. The sarcomeres are less distinct than in skeletal muscle because they are less regular, and because they are obscured by additional material such as mitochondria and sarcoplasmic reticulum. Picture taken by Delisa Ibanez-Garcia.
The organisation of the mammalian heart is complex, with four contractile chambers, powered valves and a complex flow of depolarisation to achieve optimal function, namely the pumping of blood through the pulmonary and systemic circulation. In addition, cardiac activity quickly responds to the body's demands by speeding-up or slowing-down the heart rate. Rapid feed-back mechanisms adjust cardiac output to changes in blood pressure, and to the oxygen and carbon dioxide content of the blood. The heart responds to naturally occurring hormones and to drugs to strengthen the heart beat. Neurotransmitters and drugs also affect the heart rate. Exercise, diet and genes affect cardiac development and life-time remodelling. A particular feature of the mammalian heart is the strengthening of the contraction (a phase in the cardiac cycle known as systole) which occurs when the heart is stretched by blood filling during the dilation or diastole phase of the cycle. This process is known as the Franck-Starling Law of the Heart. The molecular basis of this process is still ill-understood and is the subject of research in our laboratory.
However failing cardiac performance is a major cause of chronic disease and death. Damage to the cardiac vasculature impairs oxygen supply and leads to damage. Genetic defects lead to cardiac hypertrophy or dilation and potential cardiac failure. Infections can also damage the heart. Much clinical, pharmacological and lab-based research aims to repair or alleviate cardiac damage and insufficiencies. Surgery can repair developmental defects, damaged vasculature and can replace valves or even whole hearts. Artificial pumps can temporarily replace the heart and may allow time for the heart to repair itself. Heart transplant is often successful but limited by the lack of suitable hearts. The use of stem cells to repair damaged regions of the heart by recreating new myocytes is an exciting and rapidly developing area of research.
