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Biomedical subjects

N L Jones

Publications and source records attributed to N L Jones.

At least 109 records · Page 6Linked to original sources
PubMed1990

A quantitative physicochemical approach to acid-base physiology.

An approach to acid-base physiology based on quantitative relationships between systems is presented. Key elements in the approach advocated by Stewart are, first, that changes in H+ or protons and bicarbonate are not considered "primary," or initiating disturbances, but rather as changes that are "dependent" on the interactions between several systems. Secondly, the Henderson-Hasselbalch equation is not used as a control equation; [H%] is not controlled by changes in PCO2 and/or [HCO3]. Thirdly, the "independent" variables within the systems may be used to describe their interaction in aqueous solutions, using a series of equations easily solved by computer. In plasma, the systems and variables are strong ions (strong ion difference, SID); weak acids, or buffers (ion equivalence of total protein concentration, AtOt); and carbon dioxide (PCO2, as influenced by alveolar ventilation). This system provides a quantitative description of the interplay between systems, and it makes it much simpler to understand the effects of ion movements between cells and plasma, renal control of acid-base, the influence of metabolism, and management of acid-base disorders.

Acid-Base Equilibrium↗
PubMed1990

Role of nonworking muscle on blood metabolites and ions with intense intermittent exercise.

The exchange of ions between blood and inactive muscle was studied in healthy males (n = 11) who performed four 30-s bouts of maximum isokinetic leg exercise, with 4 min of rest between bouts; recovery was followed for 90 min. Blood was sampled from the brachial artery and antecubital vein from inactive arm, and biopsies were taken from the nonworking deltoid muscles. During exercise, whole blood and plasma arteriovenous (a-v) differences across the arm showed increased net uptake of lactate (Lac-), K+, Na+, Cl-, glycerol, and O2. Arm glucose uptake also increased during exercise and the last 30 min of recovery, but there was no change in muscle glycogen content. Deltoid intracellular Lac- concentration [( Lac-]) increased 2.5-fold to 8.2 +/- 1.4 meq/l during exercise and 25 min of recovery. Despite evidence of uptake from blood and plasma a-v differences, deltoid intracellular K+, Na+, and Cl- concentrations did not change. During recovery, arm a-v differences showed no Lac- release, but Cl- and Na+ were released to venous blood for at least 90 min of recovery. During repeated exercise, the elevated Lac- uptake (a-v [Lac-] is 5-8 meq/l) and a HCO3- release (a-v HCO3- concentration is -8-11 meq/l) by the arm was suggestive of a possible anion exchange (Lac-/HCO3-). It is concluded that during heavy exercise non-working muscles take up and oxidize significant amounts of Lac-. Other inactive tissues also play a role in the regulation of ion and metabolite concentrations of blood.

Adult↗
PubMed1990

High-intensity endurance training in 20- to 30- and 60- to 70-yr-old healthy men.

Factors contributing to maximal incremental and short-term exercise capacity were measured before and after 12 wk of high-intensity endurance training in 12 old (60-70 yr) and 10 young (20-30 yr) sedentary healthy males. Peak O2 uptake in incremental cycle ergometer exercise increased from 1.60 +/- 0.073 to 2.21 +/- 0.073 (SE) l/min (38% increase) in the old subjects and from 2.54 +/- 0.141 to 3.26 +/- 0.181 l/min (29%) in the young subjects. Peak cardiac output, estimated by extrapolation from a series of submaximal measurements by the CO2 rebreathing method, increased by 30% (from 12.7 to 16.5 l/min) in the old subjects, associated with a 6% increase (from 126 to 135 ml/l) in arteriovenous O2 difference; in the young subjects there were equal 14% increases in both variables (18.0 to 20.5 l/min and 140 to 159 ml/l, respectively). Submaximal mean arterial pressure and cardiac output were lower posttraining in the old subjects; total vascular conductance and cardiac stroke volume increased. Although peak power at the start of a short-term maximal isokinetic test did not change, total work accomplished in 30 s at a pedaling frequency of 110 revolutions/min increased in both groups, from 11.2 to 12.6 kJ and from 15.7 to 16.9 kJ in the old and young, respectively; fatigue during the 30-s test was less, and postexercise plasma lactate concentrations were lower. In older subjects, increases in aerobic power after high-intensity endurance training are at least as large as in younger subjects and are associated with increases in vascular conductance, maximal cardiac output, and stroke volume.

Adult↗
PubMed1989

Stimuli of thirst in donkeys (Equus asinus).

A study of the stimuli of thirst was conducted on six feral donkeys. Donkeys were found to be stimulated to drink by overnight water deprivation, by the diuretic furosemide, and by hypertonic saline infusion, all in the absence of heat stress or work. Donkeys compensate accurately for the fluid deficit caused by overnight water deprivation. After 19 hr without water, they drank 8.8 +/- 2.4 (mean +/- SE) liters within 60 min. Their undeprived overnight intake was 8.4 +/- 1.5 liters. However, latency was longer and water intake was less than that of ponies with the same changes in blood parameters, suggesting that donkeys have a higher thirst threshold than ponies. Further, plasma volume fell less in donkeys, but osmotic changes were similar to those reported in ponies exposed to the same deprivation. Donkeys infused with 250 ml of 15% NaCl drank 0.7 +/- 0.6 liters of water within 45 min, and osmolality increased from 287 to 297 mosmol/kg water; they drank no water in the same time period when infused with 250 ml 0.9% NaCl (p less than 0.05). Donkeys injected IV with 2 mg/kg furosemide drank 3.8 +/- 1.1 liters within 3 hr. Plasma protein increased from 6.9 to 7.8 g/dl. When injected with 0.9% NaCl they drank 1.0 +/- 0.5 liters (p less than 0.05). In sum, the positive thirst responses of these donkeys to cellular and extracellular dehydration were similar to those earlier demonstrated in ponies, but the results suggest a less sensitive response, albeit combined with a better internal defense of blood volume.

Animals↗
PubMed1989

Renal responses to exercise-induced lactic acidosis.

Five healthy males performed four 30-s bouts of maximal exercise, separated by 4 min of rest, on an isokinetic cycle ergometer. Arterial blood and urine samples were taken from indwelling catheters at rest, immediately postexercise, and for 90 min of recovery. Inulin was continuously infused to measure glomerular filtration rate (GFR). Arterial plasma [Na+], [K+], and [Cl-] increased (P less than 0.05) with exercise; plasma lactate concentration ([Lac-]) increased from 1.3 +/- 0.2 to 21.0 +/- 1.0 (SE) meq/l (P less than 0.05). A significant decrease in the GFR occurred after exercise and during recovery associated with reductions in renal Na+ and K+ excretion (P less than 0.05). Renal excretion of Lac- reached a maximum of 293 +/- 79.4 mu eq.kg-1.h-1 (P less than 0.05), with Cl- excretion reaching a minimum of 4.8 +/- 0.95 mu eq.kg-1.h-1 (P less than 0.05). Urine [Lac-] was 189 +/- 25.6 meq/l, and urine [Cl-] was 6 +/- 1.7 meq/l at 30 min of recovery. There was a curvilinear relationship between urine [Cl-] and [Lac-] (r = -0.86; P less than 0.0001). Net Lac- production was estimated from arterial [Lac-] and after assuming a distribution volume. Less than 2% (13.1 meq) of the total estimated Lac- produced (678 meq) was excreted in the urine. Decreases in urine [Cl-] act to limit the fall in urine pH that accompanies increases in urine [Lac-].

Acidosis, Lactic↗
PubMed1989

Muscle glycogenolysis and H+ concentration during maximal intermittent cycling.

The relationships between muscle glycogenolysis, glycolysis, and H+ concentration were examined in eight subjects performing three 30-s bouts of maximal isokinetic cycling at 100 rpm. Bouts were separated by 4 min of rest, and muscle biopsies were obtained before and after bouts 2 and 3. Total work decreased from 20.5 +/- 0.7 kJ in bout 1 to 16.1 +/- 0.7 and 13.2 +/- 0.6 kJ in bouts 2 and 3. Glycogenolysis was 47.2 and 15.1 mmol glucosyl U/kg dry muscle during bouts 2 and 3, respectively. Lower accumulations of pathway intermediates in bout 3 confirmed a reduced glycolytic flux. In bout 3, the work done represented 82% of the work in bout 2, whereas glycogenolysis was only 32% of that in bout 2. Decreases in ATP and phosphocreatine contents were similar in the two bouts. Muscle [H+] increased from 195 +/- 12 to 274 +/- 19 nmol/l during bout 2, recovered to 226 +/- 8 nmol/l before bout 3, and increased to 315 +/- 24 nmol/l during bout 3. Muscle [H+] could not be predicted from lactate content, suggesting that ion fluxes are important in [H+] regulation in this exercise model. Low glycogenolysis in bout 3 may be due to an inhibitory effect of increased [H+] on glycogen phosphorylase activity. Alternately, reduced Ca2+ activation of fast-twitch fibers (including a possible H+ effect) may contribute to the low overall glycogenolysis. Total work in bout 3 is maintained by a greater reliance on slow-twitch fibers and oxidative metabolism.

Adenosine Triphosphate↗
PubMed1989

Influence of age and stature on exercise capacity during incremental cycle ergometry in men and women.

The present study re-evaluated the accuracy of standards for maximal exercise capacity (Wcap) recently reported from our laboratory by examining the interaction between height and age on Wcap achieved and predicted in 1,071 subjects (732 males and 339 females). They underwent an incremental exercise test on a cycle ergometer using the same incremental protocol and exercise mode as the previous study, and were retrospectively judged to be normal. Although Wcap predicted was either not significantly different (males) or underestimated Wcap by less than 5% (females, p less than 0.05), significant differences were found in subjects at the extremes of the population ranges for height and age. The influences of age 9yr) and height (m) were found to be nonlinear and interactive, as described by the equations: Males: Wcap = 1506*Ht2.70*Age-0.46(r = 0.78) (lower limit 81% pred) Females: Wcap = 969*Ht2.80*Age-0.43(r = 0.77) (lower limit 79% pred) Wcap (kpm/min) predicted by these equations was compared to Wcap achieved by the 100 subjects who took part in the original study; no significant differences were found (paired t test, p less than 0.05). The interactive influences of age and height expressed by the equations are more plausible from a biological point of view than the linear, additive relationships previously described. The equations should be more reliable than previous equations for patients referred for exercise testing.

Aging↗
PubMed1989

Measurement of cardiac output by carbon dioxide rebreathing methods.

Cardiac output may be measured noninvasively by applying the Fick principle to CO2; CO2 output is measured by expired gas analysis and the veno-arterial CO2 content difference is obtained from estimates of PVCO2 and PaCO2. PVCO2 is determined using the lung as a tonometer for the equilibration of CO2; two main methods are available. In the Defares or exponential method, a low concentration of CO2 is initially rebreathed. Complete equilibration is not reached between the lung and rebreathing bag and the PvCO2 is calculated as the asymptote of the exponential rise in PETCO2 during rebreathing and prior to recirculation. Even though several mathematical methods can be used to calculate PvCO2, the most precise is an iterative statistical analysis to obtain the best-fit curve for PETCO2 with time, from which PvCO2 is obtained from PETCO2 at 20 seconds after the start of rebreathing. In the Collier or equilibrium method, a bag having CO2 concentration higher than PvCO2 is rebreathed. If an appropriate initial bag volume CO2 has been selected, equilibration will occur in the lung-bag system, recognized as a plateau in the PCO2 rebreathing record. If a plateau is not obtained, PvCO2 can be estimated by extrapolating the line joining the points of expired PCO2 during the 8th and 12th seconds of rebreathing to that of the 20th second. With the equilibrium method, the plateau PCO2 is systematically higher than PvCO2 (downstream effect) and a correction is applied to obtain PvCO2. PaCO2 can be estimated from PETCO2 or from the mixed-expired PCO2 and an assumed physiologic dead space, except in patients with abnormal lung function, in whom PaCO2 must be measured directly. The content of CO2 in blood may be calculated from PCO2 by the equation: In(CCO2) = [0.396 X In(PCO2)] + 2.38 More complex algorithms are available to calculate CCO2 if the pH, hemoglobin, and arterial O2 saturation are widely divergent from resting values. The indirect Fick method applied to CO2 during exercise can be used to obtain a valid and reproducible measurement of Q comparable to that obtained by invasive methods.

Carbon Dioxide↗
PubMed1989

Maximal isokinetic cycle ergometry in patients with coronary artery disease.

We assessed the utility of short-term (30 s) maximal isokinetic cycle ergometry as an additional method of investigating the limitations to exercise in 33 carefully selected patients with documented coronary artery disease. The technique proved safe and reproducible in these patients. In relation to normal standards, performance was better in the maximal isokinetic cycle ergometer test (peak power = 819 +/- 116 W; average power = 532 +/- 72 W; total work = 13.1 +/- 2.1 kJ; 95-101% of predicted) than in the progressive incremental exercise test (VO2 = 1.80 +/- 0.37 l.min-1; power output = 919 +/- 165 kpm.min-1; 70-80% of predicted). Beta blockade did not affect maximal performance during either isokinetic or progressive incremental cycling, although maximal heart rate was significantly lower during both tests in patients on beta blockade. Power output in the progressive exercise was not as strongly related to the indices measured during the 30 s isokinetic test (r = 0.59-0.63) as it was in previous studies of healthy individuals (r = 0.89). The ability to detect individual variations in short-term exercise capacity measured with maximal isokinetic cycle ergometry may have significant potential value 1) as an additional method of determining the limitations to exercise and 2) when executing an exercise prescription in patients with coronary artery disease.

Adrenergic beta-Antagonists↗
PubMed1989

Cardiopulmonary exercise testing.

Cardiopulmonary exercise testing is an objective method of assessing the functional capacity of a patient. In contrast to clinical assessment and resting investigations, exercise testing is useful in detecting early changes in patients with cardiac or respiratory disease. Although a number of different types of ergometers can be used for testing, the ones used commonly are the cycle and treadmill. Comparison of these two modes of exercise shows no significant clinical difference between them; therefore, either can be used for routine cardiopulmonary exercise testing. There are various types of exercise protocols, but generally the protocol should involve large muscle groups and should be tolerated by the population being tested. The main goal when selecting an exercise protocol is to strike a balance between workload increments that do not prematurely fatigue the subject and at the same time allow the subject to reach a maximum power output within 8 to 15 minutes. Whatever the exercise test protocol used, the intensity should be increased to a symptom-limited maximum. This procedure is safe as long as contraindications for starting a test and indications for terminating a test are adhered to strictly. The assessment of cardiorespiratory responses during exercise ranges from simple and noninvasive techniques to those that are invasive and complex. In the majority of cases all the information needed for proper assessment of the patient can be acquired with simple noninvasive techniques.

Electrocardiography↗
PubMed1989

Improvement in maximal isokinetic cycle ergometry with cardiac rehabilitation.

It is unclear whether improvements in short-term (30 s) exercise capacity are associated with the increased aerobic exercise tolerance frequently observed in cardiac patients following training. Carefully selected patients with documented coronary artery disease were randomly allocated either to a control group (N = 10) or to 12 wk of endurance exercise training (N = 12); both progressive incremental cycle ergometer testing (maximal power output and peak VO2) and 30 s maximal isokinetic cycle ergometry (peak power, total work, and fatigue index) were measured on entry into the study and 12 wk later. Initial maximum performance measures in progressive incremental exercise and in maximal short-term isokinetic cycling were similar in both groups. Following the training program, maximum power output measured during progressive incremental exercise increased by 21% (P less than 0.005) and peak VO2 increased by 18% (P less than 0.005) in the exercise group, but they were unchanged in the control group. Isokinetic peak power and total work improved by 14% (P less than 0.001) and 11%, respectively, in the exercise group, whereas there were corresponding reductions of 6 and 8% in the control subjects, with little change in fatigue index in either group. The similar relative increases in isokinetic peak power and peak VO2 suggest that improvement in short-term exercise capacity may be an important contributor to the improvement in aerobic exercise tolerance frequently observed in cardiac patients undergoing an endurance exercise program.

Coronary Disease↗
PubMed1988

Inspiratory muscles during exercise: a problem of supply and demand.

The capacity of inspiratory muscles to generate esophageal pressure at several lung volumes from functional residual capacity (FRC) to total lung capacity (TLC) and several flow rates from zero to maximal flow was measured in five normal subjects. Static capacity was 126 +/- 14.6 cmH2O at FRC, remained unchanged between 30 and 55% TLC, and decreased to 40 +/- 6.8 cmH2O at TLC. Dynamic capacity declined by a further 5.0 +/- 0.35% from the static pressure at any given lung volume for every liter per second increase in inspiratory flow. The subjects underwent progressive incremental exercise to maximum power and achieved 1,800 +/- 45 kpm/min and maximum O2 uptake of 3,518 +/- 222 ml/min. During exercise peak esophageal pressure increased from 9.4 +/- 1.81 to 38.2 +/- 5.70 cmH2O and end-inspiratory esophageal pressure increased from 7.8 +/- 0.52 to 22.5 +/- 2.03 cmH2O from rest to maximum exercise. Because the estimated capacity available to meet these demands is critically dependent on end-inspiratory lung volume, the changes in lung volume during exercise were measured in three of the subjects using He dilution. End-expiratory volume was 52.3 +/- 2.42% TLC at rest and 38.5 +/- 0.79% TLC at maximum exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Calculation of whole blood CO2 content.

Currently used methods for calculating whole blood CO2 content from calculated plasma content, measured blood pH, hemoglobin concentration ([Hb]), and O2 saturation yield materially different results. In this study the constants of the fundamental equations relating blood CO2 content to plasma content have been reevaluated. An iterative computer technique was used to empirically derive appropriate constants from data obtained from nine healthy male subjects at rest and at several exercise work loads. A calculation was derived that fitted the data well [difference 0.02 +/- 1.19 ml/100 (SD) ml, r = 0.98] blood CCO2 = plasma CCO2 (Formula: see text) where plasma CCO2 = 2.226.s.plasma PCO2.(1 + 10pH-pK'), CCO2 is CO2 content, SO2 is O2 saturation, s is the plasma CO2 solubility coefficient, and pK' is the apparent pK [s and pK' are from the equations of Kelman (Respir. Physiol. 3: 111-115, 1967)].

Adult↗
PubMed1988

Factors influencing hydrogen ion concentration in muscle after intense exercise.

To assess the importance of factors influencing the resolution of exercise-associated acidosis, measurements of acid-base variables were made in nine healthy subjects after 30 s of maximal exercise on an isokinetic cycle ergometer. Quadriceps muscle biopsies (n = 6) were taken at rest, immediately after exercise, and at 3.5 and 9.5 min of recovery; arterial and femoral venous blood were sampled (n = 3) over the same time. Intracellular and plasma inorganic strong ions were measured by neutron activation and ion-selective electrodes, respectively; lactate concentration ([La-]) was measured enzymatically, and plasma PCO2 and pH were measured by electrodes. Immediately after exercise, intracellular [La-] increased to 47 meq/l, almost fully accounting for a reduction in intracellular strong ion difference ([SID]) from 154 to 106 meq/l. At the same time, femoral venous PCO2 increased to 100 Torr and plasma [La-] to 9.7 meq/l; however, plasma [SID] did not change because of a concomitant increase in inorganic [SID] secondary to increases in [K+], [Na+], and [Ca2+]. During recovery, muscle [La-] fell to 26 meq/l by 9.5 min; [SID] remained low (101 and 114 meq/l at 3.5 and 9.5 min, respectively) due almost equally to the elevated [La-] (30 and 26 meq/l) and reductions in [K+] (from 142 meq/l at rest to 123 and 128 meq/l). Femoral venous PCO2 rose to 106 Torr at 0.5 min postexercise and fell to resting values at 9.5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

Role of lungs and inactive muscle in acid-base control after maximal exercise.

The pulmonary responses and changes in plasma acid-base status occurring across the inactive forearm muscle were examined after 30 s of intense exercise in six male subjects exercising on an isokinetic cycle ergometer. Arterial and deep forearm venous blood were sampled at rest and during 10 min after exercise; ventilation and pulmonary gas exchange variables were measured breath by breath during exercise and recovery. Immediately after exercise, ventilation and CO2 output increased to 124 +/- 17 1/min and 3.24 +/- 0.195 l/min, respectively. The subsequent decrease in CO2 output was slower than the decrease in O2 intake (half time of 105 +/- 15 and 47 +/- 4 s, respectively); the respiratory exchange ratio was greater than 1.0 throughout the 10 min of recovery. Arterial plasma concentrations of Na+, K+, and Ca2+ increased transiently after exercise. Arterial lactate ion concentration ([La-]) increased to 14-15 meq/l within 1.5 min and remained at this level for the rest of the study. Throughout recovery there was a positive arteriovenous [La-] difference of 4-5 meq/l, associated with an increase in the arteriovenous strong ion difference ([SID]) and by a large increase in the venous Pco2 and [HCO3-]. These findings were interpreted as indicating uptake of La- by the inactive muscle, leading to a fall in the muscle [SID] and increase in plasma [SID], associated with an increase in muscle PCO2. The venoarterial CO2 content difference was 38% greater than could be accounted for by metabolism of La- alone, suggesting liberation of CO2 stored in muscle, possibly as carbamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

The effects of human cytomegalovirus infection on cytoskeleton-associated polysomes.

Human cytomegalovirus (HCMV) infection induces disruption of the host cell's cytoskeleton (CSK). This disruption is accompanied by three transient phases of actin depolymerization that occur at 20 min, 5 to 10 h and 48 to 72 h post infection (pi). During the 20 min peak of actin depolymerization, the level of cellular polysomes associated with the CSK was reduced, due to release of ribosomes from CSK-associated polysomes. Cellular mRNAs previously existing in these polysomes, however, remained associated with the CSK. Also during this period, nuclear to cytoplasmic transport of host cellular mRNA as well as the association of newly synthesized mRNA with the CSK was temporarily delayed. By 60 min pi, ribosomes, preexisting host cellular mRNA, and newly synthesized mRNAs (host and viral) had reestablished a distribution in the infected cell comparable to that of uninfected cells. Sedimentation profiles of soluble and CSK fractions at various times throughout the viral infection indicated that, although the amount of polysomes associated with the CSK at 20 min pi was reduced, essentially all HCMV and all host cell polysomes present were associated with the CSK. The majority of HCMV DNA hybridizable poly(A)+ RNAs were associated with the CSK throughout the viral infection. These early events appear to correlate with a transient interruption of host cellular mRNA translation early in infection and may represent a process whereby HCMV gene expression becomes competitive with that of the host cell.

Cell Fractionation↗
PubMed1988

Respiratory muscles and dyspnea.

This article reviews the classical basis on which dyspnea is identified and quantified. The sensation or sensations of discomfort experienced during breathing are then viewed using a background of sensory physiology. Exploiting psychophysical techniques, the origin of the sensation of discomfort is viewed within the constraints of the presently-known sensory structures. The contribution of these sensory structures to the quality and quantity of discomfort is suggested, indicating the central role played by the respiratory muscles.

Dyspnea↗