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Biomedical subjects

P G Hanson

Publications and source records attributed to P G Hanson.

At least 19 recordsLinked to original sources

Cardiovascular response to static contraction in borderline hypertension.

Nine young males with borderline hypertension (BH) (mean age +/- SD, 25 +/- 5 yr) and 13 young male normotensive controls (NT) (24 +/- 3 yr) were studied to determine their cardiovascular responses to small and large muscle static contractions. The subjects performed one-arm handgrip and two-leg extension in a randomly assigned order for 3 min at 30% of maximal voluntary contraction. Mean intra-arterial blood pressure (MABP), heart rate (HR), and tension were measured throughout the contractions. Borderline hypertensive patients had a higher MABP at rest (p less than 0.005) and at the end of both types of static contractions (p less than 0.05). The average increases in MABP from rest to the end of exercise (delta MABP) were slightly greater for the BH patients (6 mmHg), but these differences were not significant (p greater than 0.1). However, a greater percentage of BH patients were hyperreactive to handgrip (delta BP greater than 35 mmHg) and leg extension (delta BP greater than 40 mmHg) when compared to controls. These data indicate that, in general, young men with borderline hypertension demonstrate normal cardiovascular regulation in response to static contraction, but that a portion of this population may be hyperreactive to this type of circulatory stress.

Adult

Exercise-induced arterial hypoxaemia in healthy human subjects at sea level.

We determined the incidence of exercise-induced arterial hypoxaemia and its determinants in sixteen highly trained, healthy runners who were capable of achieving and sustaining very high metabolic rates (maximal O2 uptake = 72 +/- 2 ml kg-1 min-1 or 4.81 +/- 0.13 l min-1). Arterial blood gases and acid-base status were determined at each load of a progressive short-term exercise test and repeatedly during constant-load treadmill running while breathing air and during inhalation of mildly hypoxic, hyperoxic, and helium-enriched gases. Three types of responses to heavy and maximum exercise were evident and highly reproducible within subjects. Four runners maintained arterial PO2 (Pa, O2) within 10 mmHg of resting values, another four showed 10-15 mmHg reductions in Pa, O2, and the remaining eight showed reductions of 21-35 mmHg, i.e. in all cases to a Pa, O2 of less than 75 mmHg and to less than 60 mmHg in two cases. During constant-load exercise, Pa, O2 was often maintained during the initial 30 s when hyperventilation was greatest; then hypoxaemia occurred and in most cases was either maintained or worsened over the ensuing 3-4 min. The most severe hypoxaemia during heavy exercise was associated with no or little alveolar hyperventilation (Pa, CO2 greater than 35 mmHg and PA, O2 less than 110 mmHg) and an alveolar to arterial PO2 difference [(A-a)DO2] in excess of 40 mmHg. During 3-4 min of heavy exercise alveolar PO2 (PA, O2) decreased by 20 mmHg in mild hypoxia (0.17 FI, O2; inspired % O2) and increased by 20 mmHg during mild hyperoxia (0.24 FI, O2) and 10 mmHg during the hyperventilation which accompanied normoxic helium breathing. In all cases Pa, O2 changed in proportion to PA, O2 with no consistent change in the alveolar to arterial PO2 difference [(A-a)DO2]. In view of the correction of hypoxaemia with mild hyperoxia and the very high ratios of alveolar ventilation to pulmonary blood flow (VA/QC = 4-6) achieved during heavy exercise, we think it unlikely that non-uniformity of the VA/QC distribution or veno-arterial shunt could explain the hypoxaemia observed in most of our subjects. By exclusion, we suggest that hypoxaemia may be attributed to a diffusion limitation secondary to very short red cell transit times in at least a portion of the pulmonary circulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult

Total cholesterol and HDL-cholesterol changes during acute, moderate-intensity exercise in men and women.

Chronic endurance exercise training has been associated with decreased levels of total cholesterol and increased HDL-cholesterol. To our knowledge rapid changes in cholesterol and HDL-cholesterol during acute exercise have not been described under controlled conditions. We studied 28 subjects (14 males and 14 females) during bicycle exercise for 40 min at a work intensity of 55% of their maximal oxygen consumption. Total and HDL-cholesterol levels were measured (and LDL-cholesterol calculated) at rest, 10, 20, 30, and 40 min of exercise, and 15 min postexercise. There was a significant (p less than 0.001) increase in HDL-cholesterol levels at 10 min of exercise (58.8 +/- 13.9 mg/dl, mean +/- SD) above rest (53.1 +/- 13.4 mg/dl) for all subjects. This increase persisted (p less than 0.001) at all time points throughout the exercise session, but declined by 15 min postexercise. There was a small, insignificant decline in LDL-cholesterol. It is concluded that apparent favorable changes in lipoprotein patterns occur acutely, and are sustained during short-term, moderate intensity exercise. Analyses of these changes appears necessary if the biochemical mechanisms which underlie these metabolic alterations are to be elucidated.

Adolescent

Similarity of cardiovascular response to upper and lower body static contraction in endurance-trained and untrained males.

The purpose of this study was to investigate the cardiovascular response to upper and lower body static contraction in endurance-trained (ET) and untrained (UT) males (both groups N = 6). The groups were similar in age, height, and weight. However, the ET group exhibited a markedly higher (P less than 0.01) VO2 max during treadmill running than the UT group (65.4 +/- 4.8 vs 49.9 +/- 2.8 ml X kg-1 X min-1, mean +/- SD). Both groups performed static handgrip and leg extension in a randomly assigned order at 30% of maximal voluntary contraction for 3 min. Heart rate and mean intra-arterial blood pressure (MABP) were measured at rest and throughout contraction. At rest, differences between the two groups were not significant for heart rate (54 +/- 10 vs 66 +/- 8 beats X min-1) or MABP (93 +/- 4 vs 91 +/- 5 mm Hg). During handgrip, the increases in heart rate (24 +/- 12 vs 15 +/- 6) and MABP (24 +/- 10 vs 27 +/- 12) were not significantly different between the two groups. During leg extension, the magnitude of the increases in heart rate (44 +/- 21 vs 46 +/- 27) and MABP (37 +/- 11 vs 41 +/- 10) were again not different for the two groups. These results suggest that cardiovascular regulation during static contraction is similar in endurance-trained and untrained individuals, even during contraction involving the trained musculature.

Adult

Increased cardiovascular response to static contraction of larger muscle groups.

The purpose of this study was to investigate the influence of the size of the active muscle mass on the cardiovascular response to static contraction. Twelve male subjects performed one-arm handgrip (HG), two-leg extension (LE), and a "dead-lift" maneuver (DL) in a randomly assigned order for 3 min at 30% of maximal voluntary contraction. O2 uptake (VO2), heart rate (HR), and mean intra-arterial blood pressure (MABP) were measured at rest and, in addition to absolute tension exerted, throughout contraction. There was a direct relationship between the size of the active muscle mass and the magnitude of the increases in VO2, HR, and MABP, even though all contractions were performed at the same relative intensity. Tension, VO2, HR, and MABP increased progressively from HG to LE to DL. It was concluded that at the same percentage of maximal voluntary contraction, the magnitude of the cardiovascular response to isometric exercise is directly influenced by the size of the contracting muscle mass.

Adult

Comparison of hemodynamic responses to static and dynamic exercise.

Eight healthy male adults (25-34 yr) were studied to compare hemodynamic responses to static exercise (30% MVC in leg extension), static-dynamic exercise (one-arm cranking, 66 and 79% VO2 max-arm), and dynamic exercise (two-leg cycling, 58 and 82% VOmax-legs). Leg extension (LE) strength was measured by a spring scale. Cranking and cycling were performed on a Quinton bicycle ergometer. VO2 was measured using an automated open-circuit system. Heart rate (HR) was monitored from a CM-5 ECG lead, and arterial pressure (Pa) was measured from an indwelling brachial artery catheter. Cardiac output (Q) was measured using a CO2-rebreathing procedure. Total peripheral resistance (TPR) was calculated using the mean arterial pressure (Pa) as the systemic pressure gradient. In 30% LE, a significant (P less than 0.05) Pa increase occurred (pressor response) mediated primarily by an increase in Q. One-arm cranking and two-leg cycling at similar relative VO2 demands resulted in nearly identical increases in Pa due to different contributions of Q and TPR. Q and the arteriovenous O2 difference varied as a function of VO2 regardless of the mode of exercise (static or dynamic). On the other hand, the HR response, which accounted for increased Q in the exercises containing a static component, and Pa varied with mode of exercise. Any generalized scheme of cardiovascular control during exercise must account for the potential influence of dynamic and static components of the exercise.

Adult

Immunological responses to training in conditioned runners.

1. We measured the concentrations of leucocyte subpopulations, immunoglobulins and complement in six well-conditioned runners before and after a typical 8-mile (12.8 km) training run at 70-75% of VO2 max. 2. Before running all components were within the normal range. Exercise failed to produce a significant rise in neutrophils. There was also no change in immunoglobulins or complement concentrations immediately or 24 h after exercise. Lymphocyte subpopulations were also unchanged except for a progressive rise in antibody-dependent cytotoxic effector cells (K-lymphocytes). 3. These results suggest chronic exercise training has no apparent adverse effect on circulating cellular or humoral immune components in healthy subjects. An increase in K-lymphocytes may provide added host defence capacity during periods of stress, although the mechanism of increase is unexplained.

Adult

Exertional heatstroke in novice runners.

Heatstroke occurred in four apparently normal but inexperienced runners who were involved in road races of 10, 16, 32, and 42 km. Each of the runners attempted to increase his running pace by approximately 1 min/km during the last 5 km of the race. Symptoms of heatstroke occurred within five to ten minutes of the onset of increased effort. In three cases, environmental conditions (temperatures, 24 to 26 degrees C) were contributory. Specific guidelines and instructions are needed for inexperienced runners who enter distance road races.

Adult

Role of cerebrospinal fluid [H+] in ventilatory deacclimatization from chronic hypoxia.

Once ventilatory acclimatization begins in sea level residents sojourning at high altitude, abrupt restoration of normal oxygen tensions will not restore ventilation to normal. We have investigated the role of cerebrospinal fluid (CSF) [H(+)] in this sustained hyperventilation by measuring CSF acid-base status in seven men (lumbar) and five ponies (cisternal) in normoxia, first at sea level and then periodically over 13-24 h of "deacclimatization" after 3-5 d in hypoxia (P(B) = 440 mm Hg). After 1 h deacclimatization, hyperventilation continued at a level only slightly less than that obtained in chronic hypoxia (+1-2 mm Hg Pa(CO2)), whereas CSF pH was either equal (in man) or alkaline (in pony, +0.02, P < 0.01) to sea level values. Between 1 and 12-13 h deacclimatization in all humans and ponies Va fell progressively (Pa(CO2) increased 4-7 mm Hg) and CSF pH became increasingly more acid (-0.02 to -0.05, P < 0.01). Between 12 and 24 h of normoxic deacclimatization in ponies, Pa(CO2) rose further toward normal, coincident with an increasing acidity in CSF (-0.02 pH). Similar negative correlations were found between changes in arterial pH and Va throughout normoxic deacclimatization. We conclude that [H(+)] in the lumbar or cisternal CSF is not the mediator of the continued hyperventilation and its gradual dissipation with time during normoxic deacclimatization from chronic hypoxia. These negative relationships of Va to CSF [H(+)] in normoxia are analogous to those previously shown during acclimatization to hypoxia.

Acclimatization

Locus of control and behavior in treatment groups.

Studied the Rotter Locus of Control scale for effective prediction of behavior in small groups. Subjects were 205 male VA Hospital patients participating in self-directed groups who completed the AGCT, Psychological and Somatic Symptom Scales, and Rotter's I-E measure of locus of control. Group behavior was measured through sociometry and a Group Member Evaluation form. Three hypotheses were not supported: (a) Persons scoring high in the direction of internal control (internals) will be more likely to act to influence their social environment; (b) internals will be more active than externals in gathering and processing information in group discussions, and (c) internals will be more self-directed and less susceptible to being influenced by others. Two hypotheses were supported: (a) externals will express more somatic and psychological complaints than internals, and (b) externals will be perceived as behaving more defensively than internals. In contrast, intelligence was correlated with a large number of group process measures. Locus of control and intelligence measures predict different kinds of behavior in groups.

Adjustment Disorders

Influence of breathing pattern on oxygen exchange during hypoxia and exercise.

During hypoxia, arterial oxygen saturation (SaO2) measured by ear oximeter shows cyclic fluctuations which are related to the pattern and rate of breathing. Continuous recordings of SaO2 may be corrected for distortion, due to circulatory transport, to yield approximate values for pulmonary end-capillary saturation (Sc'O2). This permits calculation of the corresponding end-capillary PO2 (Pc'O2). We have used this technique to study the effect of spontaneous and imposed breathing patterns on mean Pc'O2, amplitude of Pc'O2 (delta Pc'O2) and minute ventilation (VE). The studies were conducted during mild hypoxia, at rest and exercise. The amplitude of delta Pc'O2 is inversely related to breathing frequency. When frequency is constant, patterns with with prolonged expiration or end-expiratory pauses produce large delta Pc'O2 and greater VE. This effect is reversed with prolonged inspiration or end-inspiratory pauses. Spontaneous breathing patterns produced smaller delta Pc'O2, with lower VE than imposed patterns. These findings are compatible with animal studies which suggest the magnitude of PaO2 fluctuations produced by the breathing pattern may act as a feedback stimulus to ventilation. The breathing patterns, which are spontaneously chosen, produce the minimum delta Pc'O2 and VE.

Adult