• The large elastic arteries (aorta and its branches) show an increase in wall thickness and diameter with age.

• the formation of a thicker intima is believed by some to be a preclinical feature of atherosclerosis
  
  
• chemical analysis shows a relative decrease of elastin and an increase in collagen

• Large elastic arteries also become stiffer with age.

• this decrease in compliance results in an increase in pulse pressure as well as systolic pressure
  
  
• it also leads to an increase of the pulse wave velocity and as a result, a late augmentation of the systolic pressure (figure 46-1)

Therefore, within a healthy normotensives (as far as mean arterial blood pressure is concerned) the systolic pressure increases with age.

• There is mounting evidence that age-associated increases in arterial stiffness and pressure can be modified by lifestyle and diet

• reductions in salt intake may reduce vascular stiffening with age
  
  
• physical conditioning also appears to reduce vascular stiffening with age

• Heart mass increases with age, about 1 g/yr in men and 1.5 g/yr in women. This is due in large part to an increase in average myocyte size.
  
  
• Fat accumulation around the sinoatrial (SA) node sometimes produces a partial or complete separation of the node from the atrial musculature
  
  
• Beginning by age 60, there is a pronounced decrease in the number of pacemaker cells in the SA node

• Supine, basal heart rate does not change with age
  
  
• In the sitting position, heart rate decreases with age
  
  
• The intrinsic heart rate (after both sympathetic and parasympathetic blockade) decreases with age

• The duration of the isovolumetric relaxation phase increases with age.
  
  
• The peak rate at which the left ventricle fills during early diastole (just after the isovolumetric relaxation phase) is reduced with aging (by 50% between the ages of 20 and 80).
  
  
• With age, the atrial contribution to ventricular filling increases.

• This is due in part to left atrial enlargement
  
  
• This leads to an audible 4^th heart sound in healthy older individuals
  
  
• It makes older people more vulnerable to the adverse effects of atrial fibrillation

• As explained before, the decrease in arterial compliance and the increase in pulse wave velocity lead to an increase in systolic pressure, which is an increased load faced by the heart during each heart beat.

• The ratio of end-systolic arterial pressure to end-systolic volume, which is a crude index of contractility is not reduced at rest with age. (This index relates to fig. 10-8 in Rhoades and Tanner)

• Similarly, the ejection fraction, which is clinically used as an index of contractility, is not decreased with age.

• An important characteristic of older hearts is the prolonged Ca²⁺ transient. As a result, the older heart generates force for a longer time. This is a beneficial adaptation to the increased systolic pressure and especially the late systolic augmentation that the heart has to pump against.

• In older men, the upright seated cardiac index (cardiac output divided by body surface area) is unchanged. As mentioned earlier, the heart rate is decreased. This is compensated for by the increase in stroke volume index, due to an increase in end-diastolic volume index.
  
  
• In older women, the cardiac output index at rest in the sitting position may be slightly decreased.
  
  
  

• In healthy, active individuals, the arterial pressure is maintained with posture change; there is no dizziness and fainting.

• the acute heart rate increase to orthostatic stress is decreased with age and takes longer to achieve
  
  
• this is balanced by a lesser reduction in stroke volume index; this is probably due in part to a reduced venous compliance and therefore less of a fluid shift to the lower parts of the body

• Treadmill VO_2,max, adjusted for body weight, declines with age. This is due in part to:
  
  
  • a decline in maximum cardiac output with age
    
    
  • a reductuion in the number of muscle fibers and the muscle utilization of oxygen
    
    
• The decline in the maximum cardiac output is due mostly to a decrease in maximum cardiac contractility.
  
  
  • the index of myocardial contractility (ESVI/SBP), while not age associated at rest, decreases with age during vigorous exercise.
    
    
  • similarly, there is a smaller increase in ejection fraction with exercise in older versus younger individuals

• Both myocardial and vascular responses to b-adrenergic stimulation decline with age; as a result, the exercise hemodynamic profile of older subjects is very similar to that of younger subjects who exercise in the presence of b-adrenergic blockade
  
  
  • ß-adrenergic receptor stimulation elicits less of an increase in ejection fraction in older men
    
    
  • ß-adrenergic receptor stimulation elicits less of a relaxation of arterial smooth muscle, which in younger people decreases peripheral resistance and reduces afterload, facilitating blood ejection by the heart
    
    
• Possibly to compensate for this decreased sensitivity to b-adrenergic stimulation, the body produces more catecholamines.
  
  
  • in response to stress, the level of norepinephrine increases to greater extent in elderly than in younger individuals

• Physical conditioning can improve the aerobic capacity of older individuals; this improvement is due to increases in both cardiac output and oxygen utilization by the muscle
  
  
  • the cardiac output increases are derived only from increases in stroke volume, the reduction of maximum heart rate in older subjects persists even after conditioning
    
    
  • these increases in stroke volume are due to both an increase in contractility and a decrease in afterload, which is due in part to a decrease in arterial stiffness