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Biomedical subjects

N L Jones

Publications and source records attributed to N L Jones.

At least 163 records · Page 9Linked to original sources
PubMed1983

Pattern of breathing during exercise in patients with interstitial lung disease.

The responses to exercise were studied in 41 patients with pulmonary fibrosis, in whom vital capacity (VC) was reduced to 62% of predicted normal values. Maximum power output (POmax) was 53% predicted; there was a significant relationship between POmax and VC (r = 0.564). The maximum ventilation achieved during exercise was also related to VC (r = 0.614). Although arterial oxygen saturation (SaO2) fell by more than 5% in 13 of 31 patients, there was no relationship between either SaO2 at POmax or the exercise related fall in SaO2 and POmax. Heart rate responses were higher than normal predicted values in seven patients, all of whom showed a low POmax (36% predicted); this finding was due only in part to a fall in SaO2. The ventilatory response to exercise was within normal limits for the patients as a whole; those subjects with the lowest POmax showed relatively higher ventilatory responses to exercise but the difference was not significant. The pattern and timing of breathing was studied in 32 patients and compared with control subjects matched by sex, age, and size. Tidal volume (VT) was low in the patients; maximum VT was related to VC (r = 0.761), but at low values of VC VTmax was higher than in healthy subjects with comparable VC. The total breathing cycle time (Ttot) fell with progressive exercise in patients and controls; Ttot for a given ventilation was shorter in the patients. Inspiratory time (Ti) was shorter in patients than controls, as was Ti/Ttot. In most patients with diffuse pulmonary fibrosis exercise is limited by a reduced ventilatory capacity, despite the adoption of a short Ti and high inspiratory flow rate, both of which serve to optimise tidal volume and breathing frequency and presumably reduce both the force developed by inspiratory muscles and the sensation of breathlessness.

Adolescent↗
PubMed1983

Effect of glycogen depletion on the ventilatory response to exercise.

Five male subjects performed two graded exercise studies, one during control conditions and the other after reduction of muscle glycogen content by repeated maximum exercise and a high fat-protein diet. Reduction in preexercise muscle glycogen from 59.1 to 17.1 mumol X g-1 (n = 3) was associated with a 14% reduction in maximum power output but no change in maximum O2 intake; at any given power output O2 intake, heart rate, and ventilation (VE) were significantly higher, CO2 output (VCO2) was similar, and the respiratory exchange ratio was lower during glycogen depletion compared with control. The higher VE during glycogen depletion was associated with a higher VE/VCO2 ratio, lower end-tidal and mixed venous CO2 partial pressures, and higher blood pH than in the control studies. Changes in exercise VE accompanying glycogen depletion were not explained by changes in CO2 flux to the lungs suggesting that other factors served to modulate VE in these experimental conditions.

Adult↗
PubMed1983

A constant-velocity cycle ergometer for the study of dynamic muscle function.

A cycle ergometer has been designed to measure the force exerted on the pedal cranks during maximum effort at a variety of constant velocities. Preset crank velocities of 13-166 rpm are established by a controlled 3-hp motor and cannot be overcome by the subject. Torque is measured by strain gauges bonded to the crank shafts; peak torque, peak power, work, and average power are derived for each pedal cycle. Studies in 30 healthy male subjects established reproducibility and normal standards. During exercise for 45 s at a constant velocity of 60 rpm, there was a wide intersubject variation in both maximal torque (118-226 N . m) and the percentage decline in torque (27.2-52.0%). The decline in torque was inversely related to maximal O2 intake (r = 0.84). During short (10-s) periods of exercise at six crank velocities between 60-160 rpm, a linear inverse relationship between maximal peak torque and pedal crank velocity was observed. The peak torque-velocity relationship and the percentage decline in peak torque during 30 s exercise at 60, 100, and 140 rpm were reproducible within a given subject, the coefficient of variation was less than 10%.

Exercise Test↗
PubMed1983

Power output and fatigue of human muscle in maximal cycling exercise.

We studied maximal torque-velocity relationships and fatigue during short-term maximal exercise on a constant velocity cycle ergometer in 13 healthy male subjects. Maximum torque showed an inverse linear relationship to crank velocity between 60 and 160 rpm, and a direct relationship to thigh muscle volume measured by computerized tomography. Peak torque per liter thigh muscle volume (PT, N X ml-1) was related to crank velocity (CV, rpm) in the following equation: PT = 61.7 - 0.234 CV (r = 0.99). Peak power output was a parabolic function of crank velocity in individual subjects, but maximal power output was achieved at varying crank velocities in different subjects. Fiber type distribution was measured in the two subjects showing the greatest differences and demonstrated that a high proportion of type II fibers may be one factor associated with a high crank velocity for maximal power output. The decline in average power during 30 s of maximal effort was least at 60 rpm (23.7 +/- 4.6% of initial maximal power) and greatest at 140 rpm (58.7 +/- 6.5%). At 60 rpm the decline in power over 30 s was inversely related to maximal oxygen uptake (ml X min-1 X kg-1) (r = 0.69). Total work performed and plasma lactate concentration 3 min after completion of 30-s maximum effort were similar for each crank velocity.

Adult↗
PubMed1983

Effects of pH on maximal power output and fatigue during short-term dynamic exercise.

Six healthy subjects performed four exercise studies in random order on separate days: a control study, metabolic acidosis induced by ammonium chloride, metabolic alkalosis induced by sodium bicarbonate, and respiratory acidosis induced by 5% CO2 inhalation. The subjects exerted maximal force on the pedals of a constant-velocity cycle ergometer at 100 rpm for 30 s; torque was measured and power calculated. Arterialized venous blood was sampled, and plasma lactate concentrations was measured immediately after and at 2-min intervals for 10 min following exercise. Although maximal peak power and total work, for the 30-s test, were lower in the two acidosis conditions, this effect was not statistically significant. Plasma lactate 30-s postexercise was lower in metabolic acidosis (2.8 +/- 1.6 mmol X 1(-1) (mean +/- SD) and respiratory acidosis (1.5 +/- 0.8 mmol X 1(-1) than in placebo conditions (5.9 +/- 3.3 mmol X 1(-1) and metabolic alkalosis 7.8 +/- 4.2 mmol X 1(-1). These differences were maintained but lessened during 10 min of recovery. In contrast to previous studies, which showed a marked reduction in endurance time during sustained heavy exercise, reductions in blood pH are associated with only small reductions in the total work performed in 30 s of maximal exercise. A delayed and smaller accumulation of lactate in plasma was observed following exercise during acidosis.

Acid-Base Equilibrium↗
PubMed1982

A pocket calculator program for noninvasive assessment of cardiorespiratory function.

A pocket calculator program is described which facilitates rapid evaluation of pulmonary function at rest and during exercise. It embodies the Fick Principle applied to carbon dioxide; mixed venous carbon dioxide tension is measured by rebreathing, obviating the need for central venous or pulmonary artery catheterisation. The program is in two parts, Gas Phase and Blood Phase, which may be used separately. The variables calculated include tidal volume, CO2 production, oxygen consumption, respiratory quotient, alveolar ventilation and dead space: tidal volume ratio (Gas Phase); bicarbonate concentration, base excess, veno-arterial CO2 content difference, cardiac output, mixed venous oxygen saturation and pulmonary venous admixture (Blood Phase). Use of the program enables these variables to be calculated rapidly and accurately. Accuracy is improved by the application of equations which correct for alveolar-to-blood tension differences, effects of differing hemoglobin concentrations, arterial oxygen saturations and acid-base abnormalities; these calculations are otherwise very lengthy, time consuming and prone to error. The program allows simple noninvasive measurements to be applied to patients with a wide variety of metabolic, cardiac and pulmonary abnormalities in rest and exercise.

Carbon Dioxide↗
PubMed1982

Legionella pneumophila in cooling water systems. Report of a survey of cooling towers in London and a pilot trial of selected biocides.

Fourteen recirculating cooling water systems were surveyed during the summer, 1981, to see what factors might influence the prevalence of Legionella pneumophila. The effect on the organism of three anti-microbials was studied, each in two systems, by intermittent treatment at two week intervals. L. pneumophila was isolated from six of the 14 cooling systems at the beginning of the trial but by the end was present in ten. An association was found between the presence of the organism and the concentration of dissolved solids, and chlorides and the pH. There also appeared to be associations with exclusion of light and higher water temperatures. Repeated tests on eight untreated systems showed that two were consistently infected, three became and remained infected, one was infected on a single occasion and two were never infected with L. pneumophila. Treatment of a contaminated system, either with a 10 p.p.m mixture of a quaternary ammonium compound and tributyltinoxide or slow release chlorine briquettes (maximum recorded free chlorine level 1.2 p.p.m.), did not eliminated legionellae. Treatment of two infected towers with a chlorinated phenol (100 p.p.m.) eliminated legionellae for at least three days, but after 14 days the organism was again found.

Air Conditioning↗
PubMed1982

Activation by exercise of human skeletal muscle pyruvate dehydrogenase in vivo.

1. The activity of pyruvate dehydrogenase in its active and inactive forms was measured in biopsy samples obtained from the vastus lateralis muscle of healthy subjects before and after exercise. 2. At rest, 40 +/- 4% (mean +/- SEM) of the enzyme was in the active form. 3. After progressive aerobic exercise to exhaustion (n = 5), 88 +/- 2.3% was in the active form. 4. After intermittent supramaximal short-term exercise (1 min exercise, 3 min rest) to exhaustion (n = 6), 60 +/- 2.2% was in the active form. 5. After isometric maximal exercise of 65 +/- 3.6 s duration (n = 3), only 39 +/- 1% of the enzyme was in the active form. 6. Muscle glycogen depletion was greatest with intermittent exercise and least with isometric maximal exercise; in contrast, the increase in muscle lactate was least with progressive exercise (1.3 to 9.4 mumol/g), intermediate in intermittent maximal exercise (1.2 to 13.1 mumol/g) and greatest after isometric exercise (1.8 to 17.6 mumol/g). There were no significant differences between the three studies in the changes in lactate/pyruvate ratios. 7. In three subjects who exercised with one leg, activation of the enzyme was twice as great in the exercise as in the inactive leg. 8. The ratio of active to total enzyme in biopsies of resting muscle was greater in four well-trained athletes than in four untrained control subjects (70% compared with 41% respectively). 9. The activation of pyruvate dehydrogenase appears to play an important part in regulating the use of glycogen and glucose during exercise in man.

Adult↗
PubMed1982

Impaired cardiac "acceleration" at the onset of exercise in patients with coronary disease.

The responses to two levels of exercise (400 and 800 kpm/min) were studied in nine untrained healthy subjects and seven patients with coronary artery disease. Measurements were made over 20-s time intervals to obtain the half times (t1/2) of the asymptotic rise in cardiac frequency (fc), O2 intake (VO2), CO2 output (VCO2), and ventilation (VE). Complete data were obtained in both groups at 400 kpm/min, but only in healthy subjects at 800 kpm/min, as patients were unable to exercise for longer than 2 min at this power. At the onset of 400 kpm/min, t1/2 for VO2 was similar, but t1/2 for fc, VCO2, and VE were all longer in the patients. At 800 kpm/min there was a delay in VO2 in the patients before stopping exercise. In patients and healthy subjects t1/2 for VCO2 and VE, but not VO2, were related to t1/2 for fc. The results emphasized the importance of tissue CO2 storage in attenuating the delivery of CO2 to the lungs and thus delayed the ventilatory response to a step increase in power output.

Adult↗
PubMed1982

Effect of respiratory acidosis on metabolism in exercise.

Five healthy males took part in two separate studies. In one study subjects breathed air (control, C) and in the other 5% CO2 in 21% O2 (respiratory acidosis, RA). Measurements were made at rest, during exercise at 30 and 60% maximal O2 uptake (VO2 max), (20 min each) and in recovery. RA was associated with higher arterial CO2 partial pressure (PCO2) and bicarbonate and lower pH than C. The increase with exercise in plasma lactate (mmol . l-1) was less in RA than C from 1.0 +/- 0.15 (SE) (C = 1.1 +/- 0.17) at rest to 5.3 +/- 1.25 (C = 6.8 +/- 0.98) at 60% VO2 max (P less than 0.10). Plasma pyruvate, alanine, and glycerol concentrations increased with exercise; free fatty acids did not change. There were no significant differences between RA and C in any of these metabolites. Norepinephrine concentrations were similar at rest but increased to a greater extent during exercise in RA than C (P less than 0.02). Epinephrine levels were also higher in RA than C at 60% VO2 max (NS); the two subjects in whom lactate was not lower with RA showed the greatest increase in epinephrine. Exercise in RA was associated with higher heart rates (P less than 0.05), blood pressures (NS), and ventilation (P less than 0.01). In hypercapnia the metabolic effects of acidosis are modified by increased levels of circulating catecholamines.

Acidosis, Respiratory↗
PubMed1982

Asthma induced by cold air and its relation to nonspecific bronchial responsiveness to methacholine.

We compared bronchial responsiveness to isocapnic hyperventilation of cold dry air at -18 degrees C and 0% humidity with bronchial responsiveness to inhaled methacholine in 24 subjects with current or previous asthma and 2 nonasthmatics. Two inhalation tests with each agent were carried out in random order on 4 consecutive days. The response to cold air was expressed as the respiratory heat exchange required to reduce the FEV1 by 10% (PD10 RHE) and the response to methacholine as the provocation concentration required to reduce the FEV1 by 20% (PC20 methacholine). There was a close positive linear correlation between PD10 RHE and PC20 (r = 0.86, p less than 0.001). The responsiveness to each agent was highly reproducible. The PD10 RHE could be measured in all 21 subjects with current symptoms of asthma and it could be obtained by extrapolation in 2 normal subjects, but it could not be measured in 3 subjects with a past history of asthma. The PC20 in the current asthmatics was 6.3 mg/ml or less, in the 2 nonasthmatic subjects, it was 14 and 16 mg/ml, and in the previous asthmatics it was between 26 and 54 mg/ml. The results indicate that nonspecific bronchial responsiveness is an important factor influencing the bronchial response to cold air, that either cold air or methacholine are suitable stimuli to measure nonspecific bronchial responsiveness, and that the differences in bronchial responsiveness observed between asthmatics and nonasthmatic subjects are in keeping with a quantitative rather than a qualitative difference in responsiveness.

Adult↗