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Whether running a marathon or toting a hefty biochemistry book up a staircase, exercising muscle places demand on the body through three mechanisms:
Increased oxygen and nutrient demand
Increased waste products of metabolism
Increased heat generation
The cardiovascular, respiratory, and temperature-regulating systems of the body must adapt to meet the demands of exercising muscles.
For a discussion of system structure, please refer to Chapter 9, Chapter 10, Chapter 11 (cardiovascular system) and Part V (respiratory system).
As previously mentioned, exercise adaptions fall into three main categories:
Cardiovascular adaptations
Respiratory adaptations
Temperature adaptations
There are two main types of muscle exercise ( Fig. 12.1 ):
Isotonic exercise occurs when contracting muscle shortens against a constant load.
Isometric exercise occurs when contracting muscle increases tension while maintaining its length.
Many common movements and exercises have both an isometric and an isotonic component. The mechanisms described later generally to dynamic exercise (e.g., marathon running) but not to isometric exercise (e.g., weight lifting) (see Fast Fact Box 12.1 ).
During sustained forceful isotonic muscle contraction, increased intramuscular pressure can exceed the systolic blood pressure, preventing adequate blood flow from reaching the exercising tissues. Despite the body’s other cardiovascular adaptations, this roadblock to oxygen and nutrient delivery to tissues during isometric exercise quickly leads to muscle fatigue.
The index of human fitness is maximal oxygen consumption or VO 2 max, expressed in L O 2 /min. Its three major determinants include:
Cardiac output.
Oxygen carrying capacity of the blood.
Amount of exercising muscle and ability to use oxygen (i.e., type I fibers) (see Fast Fact Box 12.2 ).
Note that only the first determinant, cardiac output, may be changed acutely.
At VO 2 max, there can be no further increase in oxygen uptake despite increases in workload ( Fig. 12.2 ).
Work can briefly be sustained by anaerobic metabolism.
This results in lactic acid build-up and prolonged increased oxygen consumption in recovery.
Trained athletes have a significantly higher VO 2 max compared with untrained athletes ( Table 12.1 ).
Women | Low | Fair | Avg | Good | High | Athletic | Olympic |
20–29 | <28 | 29–34 | 35–43 | 44–48 | 49–53 | 54–59 | 60+ |
30–29 | <27 | 28–33 | 34–41 | 42–47 | 48–52 | 53–58 | 59+ |
40–49 | <25 | 26–31 | 32–40 | 41–45 | 46–50 | 51–56 | 57+ |
50–65 | <21 | 22–28 | 29–36 | 37–41 | 42–45 | 46–49 | 50+ |
Men | |||||||
20–29 | <38 | 39–43 | 44–51 | 52–56 | 57–62 | 63–69 | 70+ |
30–39 | <34 | 35–39 | 40–47 | 48–51 | 52–57 | 58–64 | 65+ |
40–49 | <30 | 31–35 | 36–43 | 44–47 | 48–53 | 54–60 | 61+ |
50–59 | <25 | 26–31 | 32–39 | 40–43 | 44–48 | 49–55 | 56+ |
60–69 | <21 | 22–26 | 27–35 | 36–39 | 40–44 | 45–49 | 50+ |
During exercise, the cardiovascular system undergoes several adaptations to augment its usual function in delivery of oxygen and nutrients and removal of waste products of metabolism. These are summarized in Table 12.2 .
Acute | ↑ CO (↑ HR and SV) |
↓ total peripheral resistance | |
↑ MAP | |
↑ pulse pressure | |
↑ venous return | |
Chronic | Heart chamber enlargement |
Myocardial hypertrophy | |
↓ peripheral resistance at rest |
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