Biomedical subjects
Publications and source records attributed to L H Hartley.
A demonstration cardiovascular evaluation and exercise testing program was assessed for feasibility, cost, and accuracy. More than 1,800 people were examined in three years. The conditions of as many as 55 people per day were examined at a cost of $60 to $70 each. Abnormalities uncovered were similar to those observed in other studies. The program was considered successful in rendering services conveniently at low cost and with accuracy.
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Oxygen consumption is usually considered to be predictable and unalterable at a fixed work intensity. The relaxation response is hypothesized to be an integrated hypothalamic response which results in generalized decreased sympathetic nervous system activity. One physiologic manifestation of the relaxation response is decreased oxygen consumption. The possibility that the elicitation of the relaxation response could decrease oxygen consumption at a fixed work intensity was investigated. Oxygen consumption was decreased 4 percent (p less than 0.05) in eight subjects working at a fixed intensity when the relaxation response was simultaneously elicited.
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Occasional complications and even death in subjects with sickle cell trait have been attributed to severe physical exertion. However, the extent to which sickling actually occurs during exercise has not been reported. This study examined the red blood cell morphological features immediately following near maximal upright graded bicycle exercise in five asymptomatic black subjects with hemoglobin AS. Exercise produced minimal sickling in vivo, which was not proportional to the intensity of exercise. The amount of sickling in vivo was small in comparison to that observed in the presence of severe hypoxia in vitro, never exceeding 0.75%. in seven normal subjects with hemoglobin AA, exercise did not cause changes in red blood cell morphological features. We conclude that exercise may initiate sickling in subjects with sickle cell trait.
To evaluate possible cardiovascular effects of emotional stress, a specially designed 12 minute tape-recorded stress quiz was administered to 43 subjects while blood pressure and the electrocardiogram were monitored. For the entire group, the heart rate and blood pressure rose from respective control levels of 76 beats/min and 136/87 mm Hg to a mean during the quiz of 87 beats/min and 158/94 mm Hg. This difference was highly significant. Of the 43 subjects, 33 were classified as executives and 10 as nonexecutives. There were three groups of executives: control and angina with and without a history of hypertension. Both groups of executives with angina responded with a significantly higher heart rate than that of the executive control group. Blood pressure response was significantly greater in executives with angina and hypertension than in the other groups. Heart rate and systolic blood pressure responses to the quiz were lower in nonexecutives with angina than in executives with angina. During the quiz, 10 of 14 executives with angina had S-T segment depression greater than 0.5 mm; of these, 7 evidenced greater than 1.0 mm depression, andin 3 of these the depression was greater than 1.5 mm and in 2 greater than or equal to 2.0 mm. None of the executive control subjects had S-T depression greater than 0.5 mm Among nonexecutives, 2 had S-T depression greater than 0.5 mm but none greater than 1.0 mm S-T depression. Seventeen of the patients also were given a bicycle exercise tolerance test. There was a significant correlation between S-T depression in response to exercise and to the quiz (r = 0.63; P less than 0.01). The quiz electrocardiogram is presented as a new research technique and diagnostic test for evaluating the relation of emotional stress to ischemic heart disease.
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Previous studies have shown that exposure to high altitude results in an initial increase in heart rate, followed by a return to sea-level values within several days; circulating catecholamines rise progressively during this time. Nine conscious dogs were studied in normoxia (N) and after 10 days' exposure to 445 torr (CH). The mean (plus or minus SE) hematocrit was higher in CH (50 plus or minus 2 vs. 42 plus or minus 1%) while Pa-o2 (53 plus or minus 1 vs. 97 plus or minus 2 torr) and PaCO2 (27 plus or minus 1 vs. 35 plus or minus 1 torr) were lower than in N. A 3.5-fold increase in plasma norepinephrine above the N value was found in CH. Arterial pH, heart rate (HR), and mean femoral arterial pressure (MAP) did not differ significantly in N and CH. Isoproterenol (ISO), 0.5 mug/kg iv, produced an average increase in HR of 92 plus or minus 9 beats/min in N, but only 66 plus or minus 8 beats/min in CH (P smaller than .02). Reduction in MAP after ISO were similar. Pretreatment with propranolol, 0.15 mg/kg iv, reduced HR equally in N and CH without affecting MAP, but diminished the HR response to ISO significantly more in CH than in N. The attenuated chronotropic response to beta-adrenoceptor stimulation following chronic hypobaric hypoxia suggests a relative cardiac refractoriness secondary to an increased level of sympathetic activity.
Hormonal responses to graded exercise of eight low altitude residents were examined at sea level (SL) and after 1 (acute) and 11 (chronic) days at 4,300 m (HA). Caloric, water, and electrolyte intakes were controlled, as were temperature and humidity. Blood was sampled at rest and during light and moderate upright bicycle exercise (20 min at 40% and 75% of maximal O2 uptake, respectively). Mean VO2 max at HA was 27% lower than at SL. Resting plasma levels of aldosterone (Aldo), renin, and angiotensin II (A II) were significantly lower (P smaller than 0.05) on day 1 at HA compared to SL, but returned to SL values by day 11. Plasma cortisol values at rest were similar at SL and HA and were not significantly altered by light or moderate exercise. Renin, A II, and Aldo rose progressively with increasing workload in each environment. With acute HA, renin and Aldo were lower than at either SL or chronic HA. The chronic HA levels tended to approximate SL findings, implying adaptation. The data suggest that aldosterone is predominantly under the control of the renin-angiotensin system during graded exercise at sea level and that the response of this system is altered on acute high-altitude exposure.
The supine pulmonary venous admixture (shunt) has been measured at Cerro de Pasco, 4,350 m altitude in eight subjects native to high altitude (HAN) under resting condition. Alveolar-arterial O2 tension difference (AaDO2) was also determined at rest and during exercise. The same subjects were studied again after 10 days' sojourn at sea level in Lima at 150 m altitude. They were compared with four subjects from sea level (SLN) who were studied first at Lima and after 2 and 10 days at Cerro de Pasco. At altitude, AaDO2 was smaller in HAN than SLN both at rest and during exercise. Shunt was the same in both groups. It is concluded that HAN show more even ventilation/perfusion relationship (VA/Q) at altitude, probably due to their high pulmonary artery pressure. On the contrary, SLN show less even VA/Q on altitude exposure, since their shunt decreased 37%. At sea level, HAN increased their AaDO2 due partially to an increase of 110% in their shunt, and in part due to less even VA/Q as shown by augmented VD/VT ratios. Each group tended to have a more effective gas exchange in its own environment.
Serial changes in serum magnesium (Mg2+) were assessed in unacclimatized males during treadmill exercise in a hot (49 degrees/27 degrees C, dry/wet bulb) environment. Eight subjects walked at 5.6 km/h on a 0% grade, and at 90 min of exercise had a mean heart rate of increase of 70 plus or minus 5 (S.E.) beats/min, rise in rectal temperature of 2.1 degrees plus or minus 0.1 degrees C, and a weight loss of 2.07 plus or minus 0.10 kg. There was a significant (p less than 0.01) decrease in mean serum Mg2+ concentration (control: 1.87 plus or minus 0.06 mEq/I; 45 min: 1.81 plus or minus 0.07; 90 min: 1.72 plus or minus 0.08). The Mg2+ concentration in sweat samples collected over 90 min of work in the heat averaged 0.28 mEq/I (range 0.13 to 0.45). Thus, in normal man, exercise in an hot, dry environment resulted in a fall in serum magnesium which was not wholly explicable on the basis of sweat loss of this ion.
Exercise of moderate intensity results in an increase in growth hormone concentrations. During prolonged moderate work, growth hormone levels fall toward resting values, but training causes these levels to be maintained. Circulating norepinephrine increases with work, and the increment is less following physical training. The adjustments to endurance training may be mediated through the sympathetic nervous system.