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I have to Break this article into 2 Parts cause it won't fit.
Exploring the Mysteries of Exercise
Len Kravitz, Ph.D. Although the benefits of exercise are espoused daily in classes, newspapers, journals and on TV, less information has been dispersed regarding the underlying mechanisms causing these physiological changes. The responsibility of fitness instructors and personal trainers to their clients has grown vastly in the last few years. Being able to explain why and how certain physiological phenomena occur, from the regular participation in exercise, has become more of a daily necessity. This article will examine and explain some of the mechanisms how exercise may influence several bodily processes.
The Effect of Exercise on Resting Heart Rate
Regular participation in aerobic exercise often results in a decrease in resting heart rate by 5 to 25 beats per minute, although the explanation of this well-established phenomenon has not been conclusively elucidated. A complex network and interaction of nerves and chemicals regulate the speed of the heart as well as the openings in blood vessels to accommodate the distribution of blood throughout the body. The resting heart rate is under the influence of the autonomic nervous systems' sympathetic (accelerator) and parasympathetic (depressor) nerves. The lowered resting heart rate from exercise training is proposed to be due primarily to an increase in the parasympathetic activity with a minor decrease in sympathetic discharge (Katona, McLean, Dighton, & Guz, 1982; Smith, Hudson, Graitzer, & Raven, 1989).
An adaptation to the lowering of the resting heart rate, from aerobic training, is the heart's ventricles (specifically the left ventricle which pumps blood throughout the body) are able to accommodate a greater volume of blood. As the resting heart rate decreases there is then more time for filling the ventricles with blood, and more time for the delivery of oxygen and nutrients to the body and the heart muscle, making the heart more efficient in meeting circulatory challenges at rest.
The Effect of Exercise on Blood Pressure
High blood pressure is one of the most important risk factors for cerebrovascular diseases (NIH, 1993) . As many as 50 million Americans have elevated blood pressure [systolic blood pressure (SBP) of 140 mm Hg or greater and/or diastolic blood pressure of 90 mm Hg or greater] (NIH, 1993) . Regular moderate intensity physical activity (40% to 60% of maximum aerobic consumption) may be beneficial for both the prevention and treatment of hypertension, lowering SBP by approximately 10 mm Hg. The evidence is not as supportive on the effectiveness of resistance training in lowering blood pressure.
The mechanisms by which aerobic exercise may lower blood pressure partly involve the effects of two hormones, epinephrine and norepinephrine, on blood flow in the arteries. Both of these hormones are vasoconstrictors, which means that they decrease the diameter of the smallest arteries, referred to as arterioles. It has been shown that aerobic exercise can reduce the blood level of norepinephrine (Duncan et al., 1985), which limits the vasoconstriction of the arterioles, allowing for less peripheral resistance to blood pressure. In addition, there is a slight reduction in sympathetic neural activity that may help to mediate this decrease in blood pressure from aerobic exercise (Duncan et al., 1985).
The Effect of Exercise on Fat Utilization
It has been demonstrated that a result of regular endurance training is that the body uses fats more efficiently for the same submaximal task (Henriksson, 1977) . This increased ability of the aerobic energy system to produce energy using both carbohydrates and fats is probably related to an increased mitochondrial activity in the trained muscles. As more ATP is produced aerobically, there is a lesser need for involvement of the anaerobic pathways and thus less lactic acid will be produced. Lactic acid can have an inhibiting effect on the release of fatty acids from fat depots (because it blocks the action of epinephrine, a fat mobilizing hormone). Therefore, the result is more fatty acids are delivered to the muscle for energy utilization. In addition, evidence suggests that the hormone-sensitive lipase enzymes of the fat cells become more sensitive to epinephrine and norepinephrine after aerobic training (Lamb, 1984) . Thus a smaller production of these two hormones will still be able to positively stimulate the release of fatty acids for utilization.
Exploring the Mysteries of Exercise
Len Kravitz, Ph.D. Although the benefits of exercise are espoused daily in classes, newspapers, journals and on TV, less information has been dispersed regarding the underlying mechanisms causing these physiological changes. The responsibility of fitness instructors and personal trainers to their clients has grown vastly in the last few years. Being able to explain why and how certain physiological phenomena occur, from the regular participation in exercise, has become more of a daily necessity. This article will examine and explain some of the mechanisms how exercise may influence several bodily processes.
The Effect of Exercise on Resting Heart Rate
Regular participation in aerobic exercise often results in a decrease in resting heart rate by 5 to 25 beats per minute, although the explanation of this well-established phenomenon has not been conclusively elucidated. A complex network and interaction of nerves and chemicals regulate the speed of the heart as well as the openings in blood vessels to accommodate the distribution of blood throughout the body. The resting heart rate is under the influence of the autonomic nervous systems' sympathetic (accelerator) and parasympathetic (depressor) nerves. The lowered resting heart rate from exercise training is proposed to be due primarily to an increase in the parasympathetic activity with a minor decrease in sympathetic discharge (Katona, McLean, Dighton, & Guz, 1982; Smith, Hudson, Graitzer, & Raven, 1989).
An adaptation to the lowering of the resting heart rate, from aerobic training, is the heart's ventricles (specifically the left ventricle which pumps blood throughout the body) are able to accommodate a greater volume of blood. As the resting heart rate decreases there is then more time for filling the ventricles with blood, and more time for the delivery of oxygen and nutrients to the body and the heart muscle, making the heart more efficient in meeting circulatory challenges at rest.
The Effect of Exercise on Blood Pressure
High blood pressure is one of the most important risk factors for cerebrovascular diseases (NIH, 1993) . As many as 50 million Americans have elevated blood pressure [systolic blood pressure (SBP) of 140 mm Hg or greater and/or diastolic blood pressure of 90 mm Hg or greater] (NIH, 1993) . Regular moderate intensity physical activity (40% to 60% of maximum aerobic consumption) may be beneficial for both the prevention and treatment of hypertension, lowering SBP by approximately 10 mm Hg. The evidence is not as supportive on the effectiveness of resistance training in lowering blood pressure.
The mechanisms by which aerobic exercise may lower blood pressure partly involve the effects of two hormones, epinephrine and norepinephrine, on blood flow in the arteries. Both of these hormones are vasoconstrictors, which means that they decrease the diameter of the smallest arteries, referred to as arterioles. It has been shown that aerobic exercise can reduce the blood level of norepinephrine (Duncan et al., 1985), which limits the vasoconstriction of the arterioles, allowing for less peripheral resistance to blood pressure. In addition, there is a slight reduction in sympathetic neural activity that may help to mediate this decrease in blood pressure from aerobic exercise (Duncan et al., 1985).
The Effect of Exercise on Fat Utilization
It has been demonstrated that a result of regular endurance training is that the body uses fats more efficiently for the same submaximal task (Henriksson, 1977) . This increased ability of the aerobic energy system to produce energy using both carbohydrates and fats is probably related to an increased mitochondrial activity in the trained muscles. As more ATP is produced aerobically, there is a lesser need for involvement of the anaerobic pathways and thus less lactic acid will be produced. Lactic acid can have an inhibiting effect on the release of fatty acids from fat depots (because it blocks the action of epinephrine, a fat mobilizing hormone). Therefore, the result is more fatty acids are delivered to the muscle for energy utilization. In addition, evidence suggests that the hormone-sensitive lipase enzymes of the fat cells become more sensitive to epinephrine and norepinephrine after aerobic training (Lamb, 1984) . Thus a smaller production of these two hormones will still be able to positively stimulate the release of fatty acids for utilization.
. Morgan (1980) hypothesizes that physical exercise provides a distraction or diversion for anxiety provoking cognitions. A similar hypotheses is that exercise is a form of meditation which precipitates an altered state of consciousness that may relieve depression and anxiety (Van Andel, 1986) . Folkins and Sime (1981) hypothesize that fitness training enhances a person's ability to adapt and cope with the environment. Increases in fitness reduces the excitation of emotion-provoking stimuli by slowing autonomic responses (i.e. heart rate, blood pressure) thus decreasing somatic (pertaining to the body) "turmoil."
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