Effects of Exercise on the Cardiovascular System

AGHE Annual Meeting  
San Jose, California  
February 22-25, 2001  

Ken Kaloustian, Ph.D.  
Professor Of Biology  
Quinnipiac University  

Hamden, Ct  06518  
Tel. (203) 582-8676  
Fax (203) 582-8706  

Page topics

General Cardiovascular Changes With Aging
Cardiovascular Response to Exercise
Risk of Exercise in the Elderly
Effects of Estrogen on Cardiovascular System


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Elderly (65 and over) constitute a growing proportion of the population.  Cardiovascular disease (CVD) is a common denominator for this age group, negatively affecting quality of life and life expectancy. 

The effects of CVD in women is even more striking.  Approximately 500, 000 women (primarily postmenopausal) die each year from CVD.  Statistically, slightly more than one out of every two women in U.S. will die of CVD.  Since 1984, the number of female deaths due to CVD has inched above the number of male deaths (American Heart Association).  Although CVD develops 10-15 years later in women, the risk, however, rises exponentially after menopause.

A major mechanism to counteract CVD is physical exercise.  Benefits of physical activity have been documented in healthy and chronically ill elderly while the risks have been found to be modest.  Unfortunately, epidemiological studies indicate that only 30% of the elderly regularly participate in some type of physical activity.  Furthermore, only 2 to 5% of the elderly report that they participate in vigorous physical activity. 

American College of Sports Medicine and Centers for Disease Control and Prevention recommend every adult should participate in at least 30 minutes of moderate intensity physical activity in most, but preferably all, days of the week.  In addition, they also recommend additional hours of physical activities such as gardening, home cleaning and repairing. 


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1.  Reduction in total heart cell mass, including muscle tissue.
2.  Number of muscle fibers decrease.  However, unlike the skeletal muscle fibers, cardiac muscles compensate by increasing in size and hence, maintaining cardiac ventricular fiber mass.  In the very old individuals, myocardial atrophy occurs.  Consequently, in the very old it is difficult to distinguish between disease versus effects of aging.
3.  Increase in organ fat
4.  Modest decrease in metabolic rate and O2 consumption per unit of body weight.
5.  Connective tissue, although small percentage of heart mass, increases with aging.
6.  Mild ventricular hypertrophy with increase in end – diastolic left ventricular volume of 5 to 10%.
7.  Increase in volume of left atrium.  More pronounced in males than females.
8.  Pacemaker, Sino-Atrial Node (SA), undergoes marked age-related change.  SA node cell numbers decline by as much as 90%.  Connective tissue spreads around SA node influencing spread of impulses.  At this time we are not sure what is the minimum number of SA node cells that are needed for survival.  The changes in SA node increases chances of supraventricular arrhythmias and first degree AV blocks.
9.  Unlike SA node, AV node cell numbers are maintained.  However there is increase in the age-related  delay through the AV node.
10.     Decrease of 50% in cell fiber numbers in the left branch of the Bundle of His.
11.  Changes in responsiveness to neurohormonal stimuli.  This may be the reason why spontaneous variations of heart rate over 24 hours period in men decrease with age.
12.   Intrinsic  sinus rate (measured in the presence of both sympathetic and parasympathetic blockade) is significantly diminished with age.
13.   Maximum cardiac output (not resting) tends to decrease in a linear fashion after the age of 30 in both males and females.  This is primarily due to decrease in heart rate with age.
14.  Arterial walls stiffen with age and the aorta becomes dilated and elongated.
15.  Age-related reduction in compliance of arterial walls resulting in higher end-systolic afterload.  Consequently, the aging ventricles must work against a higher end-diastolic afterload.
16.  Decrease in H2O content, more at the extracellular level.  This has important effects on blood flow and volume of distribution of H2O – soluble molecules and drugs.  This phenomenon is also referred to as age-related “drying”.

Heart Rate (Maximum) = 220 – age (years)


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1.  At beginning of exercise there is a rapid increase in heart rate (HR), stroke volume (S.V.), and cardiac output (C.O.).  H.R. and C.O. increase within one second after muscular exercise.  If work rate is constant and below lactate threshold, a steady-state plateau in H.R., S.V. and C.O. is reached within two to three minutes. Recovery from short-term, low-intensity exercise is generally rapid, while the slope of the recovery phase is the same for both trained and untrained subjects, trained subjects however recover faster since they do not achieve as high a H.R. as untrained subjects.
 2.  Maximum aerobic capacity (VO2 max) decreases by approximately 1% each year after age 20.  This decline can be interrupted with exercise.  For example, the expected decline in VO2 max , in middle age and elderly individuals, over a twenty year period show half the expected decrease.  This is particularly true in males. The decline in VO2 max in the elderly is probably due to among many factors to the following:
     a.   Decrease in physical activity
     b.  Increase in body fat and decrease in body muscles (i.e. decrease in lean body mass)
     c.   Since VO2 max declines normally  with aging, the ability of the elderly to engage comfortably in normal physical activities is reduced.

      The above factors initiate a vicious cycle that leads to lower levels of cardiorespiratory fitness.
                 Total Body O2 consumption = C.O.  (Arteriovenous O2 difference)
                     (VO2 max )                                                   (A- VO2 )

 Possible limiting factors:  




Declining blood volume

Altered pulmonary function

Altered circulation time

Altered hemoglobin concentration

Altered contractile state

Declining muscle mass

Altered afterload

Altered percent extraction




  3.    Decrease in plasma fibrinogen (blood clotting factor) (particularly in postmenopausal women) leading to lower risks of CVD
 4.  Lower H.R., higher S.V. (due to increase in end-diastolic volume, EDV) and reduced vascular stiffness.
  5.   Improved diastolic filling, particularly in males.
  6.   Increased ejection fraction due to increase in S.V.
  7.    Increase in HDL, decrease in LDL and triglycerides.

  1. Increase activity of lipoprotein lipase on VLDL ® increase in HDL.
  2. Increase activity of lecithin-cholesterol acetyltransferase ®  leads to increase in the inverse transport of cholesterol.
  3. Reduction in hepatic clearance of HDL by inhibiting activity of hepatic triglyceride-lipase.
  4. Conflicting reports on lipoprotein (a), a risk factor in CVD.  Some reports indicate decrease, others no change in lip(a) with physical activity.
  5. Decrease in central adiposity (abdominal fat).
  6. Decrease arterial hypertension (probably due to weight loss, alteration in the reactivity of the sympathetic nervous system, change in catecholamine concentration, and decrease in insulin resistance).


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1.  Exercise-induced ventricular arrhythmias
2.  Contraindicated for the following conditions:
    a.   Dementia
    b.  Chronic cerebrovascular disease
    c.   Pressure ulcers
    d.  Gait disturbances and falls
    e.   Urinary incontinence


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1.   Orally administered estrogen alone or with progesterone increase levels of HDL in postmenopausal women.  In women with low HDL risk of heart disease is 7X.
2.   Decreases fibrinogen (blood-clotting factor) in plasma.
3.  Decreases levels of plasminogen activator inhibitor (enzyme which blocks the actions of natural clot dissolver, tissue plasminogen activator).
4.  Stimulates relaxation of blood vessels.
5.  Promotes angiogenesis (new blood vessel development) decreasing vascular resistance leading to decrease in blood pressure.
6.  Inhibits production of endothelin, a potent vasoconstrictor produced by endothelial cells of vessels, leading to high blood pressure.

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Copyright 2000 Ken Kaloustian, Ph.D.  Professor Of Biology  Quinnipiac University  Hamden, Ct  06518