The McGill Physiology Virtual Lab

Exercise Physiology Laboratory

 At the muscular level
 

Weight lifting: isometric contractions
  Cardiac output and blood pressure increase, and arterioles in the exercising muscles undergo vasodilation. However, once the contracting muscles exceed 10-15% of their maximal force, the blood flow to the muscle is greatly reduced because the muscles are physically compressing the blood vessels that run through them; the arteriolar vasodilation is completely overcome by the physical compression of the blood vessels.

Therefore, isometric contractions may be maintained only briefly before fatigue sets in. In addition, because of blood vessels compression, total peripheral resistance may go up considerably, contributing to a large increase in mean arterial blood pressure.

Maximal oxygen consumption (VO2max)

After VO2max is reached, work can be sustained only very briefly by anaerobic metabolism in the exercising muscle. Theoretically, VO2max can be limited by:

  1. the cardiac output.

  2. the respiratory system ability to deliver oxygen to the blood.

  3. the exercising muscle ability to use oxygen.

In normal people, except highly trained athletes, cardiac output is the factor that determines VO2max. With increasing work load, heart rate increases progressively until it reaches a maximum. Stroke volume increases less and tends to level off when 75% of VO2 max has been reached.

The major factors limiting the rise in stroke volume:

  1. the very rapid heart rate, which decreases diastolic filling time.

  2. inability of peripheral factors favoring venous return (respiratory pump, skeletal muscle pump, venous vasoconstriction, arteriolar vasodilatation) to increase ventricular filling further during the very short time available.

At rest, a trained individual has an increased stroke volume and decreased heart rate with no change in cardiac output. At VO2max, cardiac output increases mostly due to increase in stroke volume; maximal heart rate is not altered by exercise.

Increase in stroke volume is due to:

  1. effects of training on the heart: possibly greater ventricular contractility and thicker myocardium.

  2. peripheral effects: increased blood volume, increased number of blood vessels in skeletal muscles. Training also increases the concentrations of oxidative enzymes and mitochondria in the exercised muscle. These changes increase the speed and efficiency of metabolic reactions in the muscles and permit larger increases-200 to 300%- in exercise endurance, but they do not increase VO2max because they were not limiting it in the untrained individual.

Note

A sudden and exhausting exercise can sometimes trigger heart attack. In individuals who perform regular physical activity the risk is significantly reduced. In general, the more a person exercises, the better is the protective effect. The protective effect of exercise against heart attacks operates via a number of mechanisms:

  1. decreases heart rate and blood pressure, two major determinants of myocardial oxygen demand.

  2. increases diameter of coronary arteries.

  3. decreases hypertension and diabetes; two major risk factors for atherosclerosis.

  4. decreases total plasma cholesterol concentration with simultaneous increase in the plasma concentration of cholesterol-carrying lipoprotein (HDL-“good” cholesterol).

  5. decreases tendency of blood to clot and improves the ability of the body to dissolve blood clots.

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