MODULE SUPPLEMENT: CARDIOVASCULAR SYSTEM
Cellular Calcium

Another physiologic alteration relates to how the myocardial cells appear to handle calcium.

Calcium is of major importance to muscle contraction. This is true everywhere, but alterations in how myocardial cells handle calcium may be a factor in the changes seen in cardiac function with age.

During the action potential there's a rapid change in the membrane potential (reversed polarization) with sodium entering the cell. However, calcium is needed to activate the process by which this action potential triggers the events that allow the actin and myosin fibers of the cardiac muscle to interact.

Calcium is stored within the tubule system of the cell and in the sarcoplasmic reticulum. The calcium that enters the cell triggers the release of this intracellular calcium which binds with the troponin and uncovers the binding sites for the interaction of actin and myosin. This allows contraction to occur.

Calcium must then be re-sequestered within the sarcoplasmic reticulum for appropriate relaxation (and diastole) to occur. This is an ACTIVE, high energy consuming process, NOT a passive event.

The figure below is a schematic that shows several of the mechanisms by which calcium is removed from the cell and re-sequestered in the sarcoplasmic reticulum to allow relaxation to occur.

As you can see, this process uses a lot of ATP, so anything that depletes the cells supply of ATP, such as hypoxia, will make this process less efficient.

Data suggest that the process of getting calcium back into the sarcoplasmic reticulum is slower in older adults than in younger adults (Lakatta, 2002a). Although much of these data are from animal studies, this process also appears to be occurring in humans.

Slowing of the re-uptake of calcium prolongs (lengthens) the relaxation process, affects how fast the ventricles fill during diastole, and contributes to the "stiffness" of the myocardium. The potential clinical implications of this are discussed further during the discussion on congestive heart failure (Note: This link will open in a new browser window which you can close to return here).

Finally, the myocardial beta-adrenergic receptors becomes less responsive to norepinephrine. This is discussed briefly in the section on Other Consequences of Diminished B-adrenergic Receptor Responsiveness (Note: This link will open in a new browser window which you can close to return here), and has clinical implications. B-adrenergic receptors influence cardiac contractility and rate. They also promote vascular relaxation. Because they become less responsive to stimulation with age, older adults can not increase their heart rate in response to increased demands as much as younger adults. The vascular system may also shift toward more vasoconstrictive state, although some data suggest that alpha adrenergic responsiveness is also diminished with age (Jones, Shapiro, et al., 2001).

Consider the physiological processes involved and write down the clinical or functional implications that you feel these changes will have--compare your results with what's presented next.