There has been considerable prior work from this laboratory as well as others documenting that the time course of cardiac contraction in bulk muscle is prolonged with aging. Common measures of inotropy such as the maximal rate or amplitude of tension development appear unchanged with age. However, alterations in the cardiovascular response to stress occur with aging and have been attributed, in part, to a diminished effect of autonomic modulation of cardiovascular function. Whether these measurements represent fundamental characteristics or aging cells or are a reflection of an altered cellular composition of bulk muscle is unclear. Furthermore, what aging-associated alterations, if any, characterize the contractile properties of the fundamental contractile unit, the sarcomere, are unknown. We therefore measured the maximal velocity, amplitude, and time course of unloaded contractions of single isolated cardiac myocytes obtained from rates 2, 8, and 24 months old. We also combined these measurements with data on cell and sarcomere lengths which we have previously determined in similar cells. We find that the prolongation of the time course of contraction that occurs with aging is a fundamental property of the myocyte and must reflect changes in the basic processes governing excitation-contraction coupling. The maximal rate or extent of shortening of individual sarcomeres is unaltered with aging, and the series addition of sarcomeres (which we have previously shown to characterize the aging heart) appears to be an adaptation that may permit the aging heart to meet the challenge of the increased load against which it must function. A decreased contractile response to norepinephrine with adult aging can also be demonstrated directly in cardiac myocytes. This deficit may be specific to catecholamines since the response to a non-adrenergic calcium channel agonist, BayK, is not age-related.
| Lakatta, Edward G (2008) Arterial aging is risky. J Appl Physiol 105:1321-2 |
