Epidemiology, risk factors, and pathophysiology of ischemic heart disease.

Epidemiological studies have identified several risk factors that increase the likelihood of developing ischemic heart disease (IHD). Many of these factors, including hypertension, smoking, elevated blood fats, sedentary life style, and Type A personality, are related to life-style habits and, therefore, are modifiable. Studies indicate that the major risk factors directly influence the basic mechanisms of atherogenesis. Evidence from the primary and secondary prevention trials shows that reducing the risk factors decreases the likelihood of coronary disease progression and coronary morbidity and mortality. Therapeutic exercise programs for primary or secondary prevention clients can lead to significant risk-factor reduction. For therapists to design such programs safely and effectively, they must 1) be knowledgeable in the epidemiology, risk factors, and pathophysiology of IHD and 2) be able to relate this knowledge to a given client.

Vitamin E supplementation and respiratory effects of ozone in humans.

To determine whether vitamin E (di-alpha-tocopherol) supplementation could protect against short-term respiratory responses to O3 exposure its effects were investigated in young healthy adult volunteers. Experimental groups received 800 or 1600 IU vitamin E per day for 9 or more wk, while control groups received placebo. Subjects were then exposed for 2-h periods to 0.5 ppm O3, with secondary stresses of heat and intermittent light exercise. Responses to O3 exposure, evaluated in terms of symptoms, forced expiratory performance, and single-breath nitrogen washout, were not significantly different between vitamin E and placebo groups.

Long-term effects of physical training on coronary patients with impaired ventricular function.

Eighteen patients with coronary heart disease and an ejection fraction of 0.40 or less were entered into an individualized exercise training program. Maximal symptom-limited exercise stress test and cardiac catheterization studies were performed initially and 12--42 months (average 18.5 months) after exercise training. At the time of the follow-up study, the mean functional aerobic impairment (FAI) improved from 32.1 to 23.4% (p less than or equal to 0.01); resting and submaximal heart rates were significantly lower (p less than 0.01 and 0.05, respectively). There was no significant change in the pulmonary artery or left ventricular end-diastolic pressure, cardiac index, stroke index, left ventricular end-diastolic volume or ejection fraction. Exercise training, therefore, can be beneficial even for patients with impaired ventricular function. Increase in physical work capacity was not correlated with improvement of ventricular function; on the other hand, exercise training did not cause deterioration of ventricular function.

Health effects of ozone exposure in asthmatics.

To investigate whether ambient air quality standards for ozone adequately protect high-risk populations, we assessed pulmonary and biochemical responses of 22 asthmatic volunteers to 2-hour controlled exposures to ozone at concentrations approximating 0.2 ppm, with secondary stresses of heat and intermittent exercise. All subjects had physician-diagnosed asthma; clinically, they covered a range from minimal wheezing to persistent marked abnormality in forced expiratory performance. Control experiments included repeated sham exposures (to purified air with no ozone added) as well as brief exposures to the odor of ozone followed by purified air. No meaningful changes in forced expiratory measures, lung volumes, or single-breath N2 indices were found after ozone exposure relative to control. Symptoms, scored semiquantitatively, increased slightly but not significantly with exposure to ozone. Small but significant (P is less than 0.05) group mean blood biochemical changes occurred with exposure to ozone; these included increased glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities, increased erythrocyte fragility, and decreased concentration of reduced glutathione. Hemoglobin concentration and acetylcholinesterase activity decreased with ozone and decreased to a lesser extent in control studies. Concentrations of ozone readily attainable in smog episodes thus appear to be capable of affecting blood biochemistry in at least some asthmatic persons, in the absence of obvious adverse pulmonary responses. Whether the biochemical effects represent harm to health or a normal response to stress remains to be determined.

Metabolic energy cost of unrestrained walking.

Physiologic factors of metabolic energy cost as well as selected mechanical characteristics of gait are described in a group of 40 presumably normal men and women between the ages of 20 and 60 years. Special emphasis was placed on unrestrained (free cadence) walking to provide a reliable baseline for comparison to persons with physical gait impairments. Velocity of walking was the most important factor in determining oxygen uptake and was independent of age or sex. An empirical equation was established relating oxygen uptake to the speed of walking. The average velocity for men in unrestrained walking trials was 89 meters per minute; for women 74 meters per minute. These differences were related to the greater stride length in men. The average cadence selected by both sexes was 116 steps per minute. None of these factors was age dependent. Of the physiologic measures only systolic blood pressure was age dependent predictably rising with age. The mean heart rate was 103 beats per minute and did not vary significantly between men and women. The mean respiratory rate was 19 per minute; the mean respiratory quotient, 0.85, neither being age or sex dependent. Oxygen uptake values averaged 12.95 ml/kg-min for the population studied and again were neither age nor sex dependent.