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Biomedical subjects

B D Johnson

Publications and source records attributed to B D Johnson.

At least 109 records · Page 6Linked to original sources
PubMed1993

The multimeridional apparent frontoparallel plane: introduction of the induced effect.

The application of vertical rod stimuli to obtain apparent frontoparallel plane (AFPP) settings is well-known. A geometrical relation based on observation distance, interpupillary distance, and retinal disparity determines the deviation of the setting from the objective frontoparallel plane. Further developments of this procedure have established that a similar relation exists for oblique presentations of parallel rod stimuli, the orientation of the rods being an additional variable. This extension of the AFPP procedure is referred to as the multimeridional AFPP or MAFPP. It permits the determination of aniseikonia in oblique as well as horizontal meridians. Although oblique disparities contain a vertical component, an induced effect is absent as long as parallel rod stimuli are used alone. If an induced effect were present, the MAFPP geometrical relations would be expected to break down. To test this hypothesis, random dot arrays and a row of dots of the same frequency as a control stimulus of parallel lines were presented alone and in combination with the line stimuli. Binocular disparities were induced by a meridional afocal magnifier placed at various axes before one eye. It was found that the dot arrays caused a breakdown of the geometrical relation when presented alone or in combination with the parallel lines. The amount of deterioration varied only slightly with the number and arrangement of dot stimuli but increased as the vertical component of the oblique magnification increased. In addition to proving the main hypothesis, the data provide information pertaining to the MAFPP theory as well as offering some insight into the induced effect. The most important practical implication of the results is that the MAFPP theory can be used to measure unknown retinal disparities only if continuous parallel lines are presented in isolation.

Aniseikonia↗
PubMed1993

Exercise-induced diaphragmatic fatigue in healthy humans.

1. Twelve healthy subjects (33 +/- 3 years) with a variety of fitness levels (maximal oxygen uptake (VO2, max) = 61 +/- 4 ml kg-1 min-1, range 40-80), exercised at 95 and 85% VO2, max to exhaustion (mean time = 14 +/- 3 and 31 +/- 8 min, expired ventilation (VE) over final minute of exercise = 149 +/- 9 and 126 +/- 10 l min-1). 2. Bilateral transcutaneous supramaximal phrenic nerve stimulation (BPNS) was performed before and immediately after exercise at four lung volumes, and 400 ms tetanic stimulations were performed at 10 and 20 Hz. The coefficients of variation of repeated measurements for the twitch transdiaphragm pressures (Pdi) were +/- 7-10% and for compound muscle action potentials (M wave) +/- 10-15%. 3. Following exercise at 95% of VO2, max, group mean Pdi twitch values were reduced at all lung volumes (range -8 +/- 3 to -32 +/- 5%) and tetanically stimulated Pdi values were reduced at both 10 and 20 Hz (-21 +/- 3 and -13 +/- 2%, respectively) (P = 0.001-0.047). Following exercise at 85% VO2, max, stimulated Pdi values were reduced at all lung volumes and stimulating frequencies, but only significantly so with the twitch at functional residual capacity (-15 +/- 5%). Stimulated Pdi values recovered partially by 30 min post-exercise and almost completely by an average time of 70 min. 4. The fall in stimulated Pdi values post-exercise was significantly correlated with the percentage increase in diaphragmatic work (integral of Pdi min-1) from rest to end-exercise and the relative intensity of the exercise. 5. The integral of Pdi min-1 and the integral of Po min-1 (Po, esophageal pressure) rose together from rest through the fifth to tenth minute of exercise, after which integral of Pdi min-1 plateaued even though integral of Po min-1, VE and inspiratory flow rate all continued to rise substantially until exercise terminated. Thus, the relative contribution of the diaphragm to total respiratory motor output was progressively reduced with exercise duration. 6. We conclude that significant diaphragmatic fatigue is caused by the ventilatory requirements imposed by heavy endurance exercise in healthy persons with a variety of fitness levels. The magnitude of the fatigue and the likelihood of its occurrence increases as the relative intensity of the exercise exceeds 85% of VO2, max.

Adult↗
PubMed1993

Photo-released intracellular Ca2+ rapidly blocks Ba2+ current in Lymnaea neurons.

1. The effect of intracellular Ca2+ on Ba2+ current flowing through voltage-dependent Ca2+ channels was studied using the whole-cell patch-clamp technique on isolated neurons from the snail Lymnaea stagnalis. Intracellular Ca2+ was increased by flash photolysis of the caged Ca2+ compound DM-nitrophen and measured with the optical indicator fluo-3. 2. After the highest intensity flashes, peak Ba2+ current was blocked by 42% with a time constant of 5 ms. The onset of the block followed a similar time course whether channels were activated or closed. The Ba2+ current surviving after the flash had the same voltage dependence of activation and rate of inactivation as did the total Ba2+ current before the flash. 3. Recovery of the Ba2+ current from block was nearly complete and occurred with a time constant of 16 s. Multiple episodes of photolysis-induced block could be studied in the same cell when 7-10 min were allowed between flashes. In some cells, recovery from block was accompanied by a transient enhancement of the current above the pre-block magnitude. 4. Neurons greatly reduced the ability of photolysis to increase Ca2+, both by unloading the DM-nitrophen before flashes were applied and by rapidly buffering the photolytically released Ca2+. Maximal flashes on extracellular droplets of the DM-Ca2+ solution created a Ca2+ jump from 110 nM to 40 microM. In contrast, the same flashes on DM-Ca(2+)-loaded neurons resulted in a Ca2+ transient starting from a baseline of 36 nM to a peak of 130 nM. This intracellular Ca2+ transient decayed with three time constants (120 ms, 2 s and 13 s). 5. Endogenous buffer(s) binds Ca2+ rapidly. When intracellular Ca2+ was monitored within 2 ms of the flash, no rapid Ca2+ spike due to binding of photo-released Ca2+ could be detected. Addition of dibromo-BAPTA to the intracellular solution reduced the block by one third, which is consistent with the measured reduction of intracellular Ca2+. This indicates that the endogenous buffer can bind Ca2+ as rapidly as dibromo-BAPTA and as fast as Ca2+ is released by photolysis. 6. The Ca2+ dependence of the block, obtained by varying flash intensity, indicates some saturation by 130 nM. A simple two-state model of the block consistent with both the time course of block and recovery and the concentration dependence gave a dissociation constant of approximately 50 nM and forward rate constant of 7 x 10(8) M-1 s-1.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetates↗
PubMed1993

Differential susceptibility of diaphragm muscle fibers to neuromuscular transmission failure.

The pattern of glycogen utilization was used to determine whether various muscle fiber types in the rat diaphragm are differentially susceptible to neuromuscular transmission failure. Muscle segments from the midcostal region were repetitively stimulated directly or via the phrenic nerve at 10 or 75 Hz. Muscle fiber types were classified histochemically as type I, IIa, or IIb. The amount of muscle fiber glycogen depletion with direct stimulation depended on stimulation rate (75 Hz > 10 Hz) and fiber type (IIb > IIa > I). However, with nerve stimulation, muscle fiber glycogen depletion did not display the same dependency on stimulation rate (10 Hz > 75 Hz), although with stimulation at 10 Hz, the same rank order of fiber depletion was observed (IIb > IIa > I). This rank order of depletion was reversed (I > IIa > IIb) during repetitive stimulation of the nerve at 75 Hz. By intermittently stimulating the muscle directly during continuous nerve stimulation, we determined that neuromuscular transmission failure contributed significantly to the force decline after 2 min of stimulation at 75 Hz but relatively little to the force decline after 2 min of stimulation at 10 Hz. A significantly greater fraction of the force decline could be attributed to neuromuscular transmission failure with repetitive bouts of stimulation at 10 Hz. We conclude that neuromuscular transmission failure causes a significant portion of the force decline after 8 min of stimulation at 10 and 75 Hz, that all diaphragm fiber types are susceptible to neuromuscular transmission failure, but that type IIb fibers are particularly susceptible at higher frequencies of stimulation.

Animals↗
PubMed1993

Activation-induced reduction of SDH activity in diaphragm muscle fibers.

In this study, we examined whether exhaustive activation reduces succinate dehydrogenase (SDH) activity in diaphragm muscle fibers. In adult male rats (approximately 300 g), the costal diaphragm was excised and positioned in a chamber perfused with mammalian Ringer solution kept at 26 degrees C and oxygenated with 95% O2-5% CO2. The muscle was stimulated directly at 10 or 75 Hz in trains of 500 ms duration (1/s) for 8 min. An adjacent unstimulated segment of muscle served as control. The two muscle segments were frozen, and serial sections were stained for myofibrillar adenosinetriphosphatase activity after alkaline and acid preincubation to classify type I, IIa, and IIb fibers. The extent of glycogen utilization was also examined histochemically to confirm exhaustive activation of muscle fibers. SDH activity was quantified using a microdensitometric procedure implemented on an image-processing system. Exhaustive activation at both 10 and 75 Hz caused a significant decrease in SDH activity of all fiber types, with the decrease after 10-Hz stimulation being greater than that after 75-Hz stimulation. At both stimulation frequencies, type IIb fibers demonstrated the greatest decrease in SDH activity (36% after 10-Hz and 27% after 75-Hz stimulation), whereas type I and IIa fibers both displayed reductions of approximately 27 and approximately 19% after 10- and 75-Hz stimulation, respectively. The greater reduction of SDH activity in type IIb fibers indicates an inverse relationship between activation-induced reductions in SDH activity and fiber oxidative capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of treatment on antibody titer to Porphyromonas gingivalis in gingival crevicular fluid of patients with rapidly progressive periodontitis.

Twenty-eight patients diagnosed as having rapidly progressive periodontitis (RPP) were enrolled in a study in which samples of subgingival microflora were harvested from test teeth and assayed for the presence of Porphyromonas gingivalis, and GCF collected and analyzed by ELISA for specific antibody for P. gingivalis. Clinical conditions were measured and recorded, and treatment by scaling and root planing provided at baseline and at 3, 6, 9, and 12 months. Reduction in pocket depth, stabilization of attachment level, and resolution of inflammation were comparable to previously reported values. By 3 months, mean and median specific antibody concentration had decreased, and continued to decrease through 12 months. The proportion of samples in which specific antibody was not detectable increased from 27% at baseline to 73% at month 12. GCF samples from sites at which P. gingivalis was present had greater than 2-fold higher median specific antibody than samples from P. gingivalis-negative sites. At baseline, specific antibody titer of 30-second GCF samples positively correlated with pocket depth, and GCF volume significantly correlated with antibody titer and concentration, and with pocket depth. In addition, change in specific antibody titer of 30-second samples from baseline to both 6 and 12 months correlated positively with pocket depths. Thus sites infected by P. gingivalis manifested high levels of specific antibody, and levels were related to clinical status. Following treatment, antibody levels decreased significantly as pocket depths decreased, attachment levels stabilized, and inflammation resolved.

Adult↗
PubMed1993

Fluorescein angiography as a means of assessing retinal vascular pathology in oxygen-exposed newborn rats.

Recently a new technique was reported in which examination of the retina of oxygen reared newborn rats was made using indirect fluorescence microscopy (Invest. Ophthal. Vis. Sci. 31:810). We have now improved this technique and systematically employed it as a means of studying oxygen-induced retinopathy in the newborn rat as an animal model for retinopathy of prematurity (ROP). Immediately after birth, litters of pigmented rats were exposed to an elevated oxygen atmosphere that varied in a cyclic fashion between 40% and 80% every 12 hours for 14 days. Rats raised simultaneously in room air served as controls. At the end of the treatment period, rats were deeply anesthetized, their pupils dilated, and 100 microliters of 3% sodium fluorescein was administered via tail venipuncture. After angiography, rats were awakened and returned to their mothers in room air for future assessment. Angiography was performed again at 4, 7, 38 or 56 days after oxygen treatment. Our results suggest that retinal pathology in the rat model parallels that of the human infant with ROP with respect to loss of patent retinal blood vessels in oxygen and subsequent abnormal vasoproliferation upon return to room air. Angiograms performed on room air-raised control rats at 14 days of age demonstrated our ability to resolve the smallest retinal capillaries. Angiograms conducted at the same age in oxygen-exposed rats revealed extensive areas of retinal non-perfusion and substantial arterio-venous shunting between adjacent primary vessels. If rats were maintained in room air for 4 or 7 days following oxygen exposure, a variety of pathologic signs became obvious including: 1) tortuosity of primary vessels mimicking human "plus disease", 2) frequent abnormal budding of tertiary vessels and capillaries, 3) retinal fluorescein leaks indicative of hemorrhages and 4) abnormal capillary tufts not evident at the time of removal from oxygen. By 38 and 56 days post-exposure, all four of these phenomena were still observed. Many of these pathologic phenomena could not have been observed with conventional methods currently used for retinal vascular assessment in small animals.

Animals↗
PubMed1993

Delayed infusion of normal donor cells after MHC-matched bone marrow transplantation provides an antileukemia reaction without graft-versus-host disease.

When allogeneic BMT is used for the treatment of leukemia, depletion of T cells from the donor BM to avoid GVHD may be accompanied by persistence of host cells and post-transplant relapse. In this report, a murine model of MHC-compatible BMT was used to show that delayed infusion of immunocompetent donor cells early after T cell-deficient BMT eliminated residual host cells and provided an antileukemic effect without causing lethal GVHD. AKR (H-2k) recipient mice were pre-conditioned with 9 Gy total body irradiation (LD50) and transplanted with 10(7) BM cells from MHC-matched B10.BR donors. These mice did not develop GVHD and became stable, long-term mixed (donor-host) T cell chimeras. In this model, mixed or incomplete donor T cell chimerism was associated with decreased GVL reactivity. AKR hosts that were transplanted with B10.BR bone marrow admixed with 3 x 10(7) B10.BR spleen cells (as a source of T cells) became complete donor T cell chimeras, but they developed severe and lethal GVHD. However, when the infusion of donor spleen cells was delayed until 21 days after BMT, few mice exhibited any clinical signs of GVHD, and > 95% of the mice became long-term survivors. The infused spleen cells eliminated residual host T cells by 21 days after infusion, and most chimeras were able to resist a supralethal challenge with AKR leukemia/lymphoma cells. Thus, post-transplant adoptive immunotherapy with normal mononuclear cells from the marrow donor may be an effective way to eliminate residual disease or treat leukemia relapse after BMT without causing significant GVHD.

AKR murine leukemia virus↗
PubMed1992

Analogues of platelet activating factor. 7. Bis-aryl amide and bis-aryl urea receptor antagonists of PAF.

A series of bis-aryl amide (13-57 and 66-81) and bis-aryl urea (58 and 85) antagonists of platelet-activating factor (PAF) was prepared that contain, separating the two aromatic rings, linear amide linkages of the form -(CH2)nCONH- (n = 0-2), -OCH2CONH-, and -(CH2)nNHCO- (n = 0-1), branched amide linkages of the form -(CH2)nN(COR)- (n = 1-3, R = CH3 or n-C3H7), and -N(COCH3)CH2-, and urea linkages of the form -NHCONH- and -CH2N(CONHCH3)-. These compounds were examined for their ability to inhibit PAF-induced platelet aggregation of rabbit platelets. These in vitro data were compared to similar data obtained for a number of known PAF antagonists. The compounds were evaluated in vivo, in the mouse, for their ability to prevent death induced by a lethal challenge of PAF. The relationships between the biological activity and the nature, lipophilicity, and position of substituents of the aromatic rings were studied. Best activity was observed for compounds having linkages of the type -CH2CONH-, -CH2N(COR)-, and -CH2NHCO-. Many of these compounds inhibit PAF-induced platelet aggregation with IC50's under 1 microM.

Amides↗
PubMed1992

A decrease in graft-vs.-host disease without loss of graft-vs.-leukemia reactivity after MHC-matched bone marrow transplantation by selective depletion of donor NK cells in vivo.

It is thought that natural killer cells may play a role in graft-vs.-host reactions after allogeneic bone marrow transplantation, but the use of NK cell-specific reagents has been limited. In this report, an NK allele-specific monoclonal antibody, anti-NK 1.1, was used to study the impact of in vivo donor NK cell depletion on GVH disease, graft-vs.-leukemia (GVL) reactivity and donor T cell chimerism after allogeneic murine BMT. AKR/J (H-2k) recipient mice were preconditioned with suboptimal irradiation (9 Gy = LD50) and transplanted with major histocompatibility complex-matched B10.BR (H-2k) BM cells with or without added spleen cells as a source of T cells. The addition of increasing numbers of spleen cells to the BM inoculum produced GVHD of varying intensities. The beneficial effect of NK depletion on GVHD was dependent on the intensity of the GVH reaction. Donor NK cell depletion had no effect on the survival of mice with severe GVHD after MHC-matched BMT (B10.BR into AKR) or after MHC-mismatched BMT (B10.BR into DBA/2; H-2k into H-2d). However, donor NK depletion increased survival of AKR hosts given sufficient B10.BR splenic T cells to induce mild-to-moderate GVHD. Ex vivo depletion of donor CD8+ T cells also reduced GVH-associated mortality, but the use of both CD8 and NK depletion offered no improvement over either alone, suggesting an interaction between CD8+ and NK 1.1+ cells. In contrast to CD8 depletion, donor NK depletion did not compromise the rapid and complete establishment of donor T cell chimerism nor the ability of chimeras to mount an effective GVL reaction. Thus, elimination of donor NK cells provides an alternate strategy for reducing GVHD without loss of GVL reactivity following MHC-matched allogeneic BMT.

Animals↗
PubMed1992

Vagal contributions to respiratory muscle activity during eupnea in the awake dog.

We examined the effects of reversible vagal cooling on respiratory muscle activities in awake chronically instrumented tracheotomized dogs. We specifically analyzed electromyographic (EMG) activity and its ventilatory correlates, end-expiratory lung volume (EELV) and diaphragmatic resting length via sonomicrometry. Elimination of phasic and tonic mechanoreceptor activity by vagal cooling doubled the EMG activity of the costal, crural, and parasternal muscles, with activation occurring sooner relative to the onset of inspiratory flow. Diaphragmatic postinspiration inspiratory activity in the intact dog coincided with a brief mechanical shortening of the diaphragm during early expiration; vagal blockade removed both the electrical activity and the mechanical shortening. Vagal blockade also doubled the EMG activity of a rib cage expiratory muscle, the triangularis sterni, but reduced that of an abdominal expiratory muscle, the transversus abdominis. Within-breath electrical activity of both muscles occurred sooner relative to the onset of expiratory flow during vagal blockade. Vagal cooling was also associated with a 12% increase in EELV and a 5% decrease in end-expiratory resting length of the diaphragm. We conclude that vagal input significantly modulates inspiratory and expiratory muscle activities, which help regulate EELV efficiently and optimize diaphragmatic length during eupneic breathing in the awake dog.

Afferent Pathways↗
PubMed1992

Vagal modulation of respiratory muscle activity in awake dogs during exercise and hypercapnia.

Using chronically instrumented awake tracheotomized dogs, we examined the contributions of vagal feedback to respiratory muscle activities, both electrical and mechanical, during normoxic hypercapnia (inspired CO2 fraction = 0.03, 0.04, 0.05, and 0.06) and during mild treadmill exercise (3, 4.3, and 6.4 km/h). Cooling exteriorized vagal loops eliminated both phasic and tonic mechanoreceptor input during either of these hyperpneas. At a given chemical or locomotor stimulus, vagal cooling caused a further increase in costal, crural, parasternal, and rib cage expiratory (triangularis sterni) muscles. No further change in abdominal expiratory muscle activity occurred secondary to vagal cooling during these hyperpneas. However, removal of mechanoreceptor input during hypercapnia was not associated with consistent changes in end-expiratory lung volume, as measured by the He-N2 rebreathe technique. We conclude that during these hyperpneas 1) vagal input is not essential for augmentation of expiratory muscle activity and 2) decrements in abdominal expiratory muscle activity may be offset by increments in rib cage expiratory muscle activity and contribute to the regulation of end-expiratory lung volume.

Afferent Pathways↗
PubMed1992

Oxygen cost of exercise hyperpnea: measurement.

To quantitate the O2 cost of maximal exercise hyperpnea, we required eight healthy adult subjects to mimic, at rest, the important mechanical components of submaximal and maximal exercise hyperpnea. Expired minute ventilation (VE), transpulmonary and transdiaphragmatic (Pdi) pressures, and end-expiratory lung volume (EELV) were measured during exercise at 70 and 100% of maximal O2 uptake. At rest, subjects were given visual feedback of their exercise transpulmonary pressure-tidal volume loop (WV), breathing frequency, and EELV, which they mimicked repeatedly for 5 min per trial over several trials, while hypocapnia was prevented. The change in total body O2 uptake (VO2) was measured and presumed to represent the O2 cost of the hyperpnea. In 61 mimicking trials with VE of 115-167 l/min and WV of 124-544 J/min, VE, WV, duty cycle of the breath, and expiratory gastric pressure (Pga) integrated with respect to time (integral of Pga.dt/min) were not different from those observed during maximum exercise. integral of Pdi.dt/min was 14% less and EELV was 6% greater during maximum exercise than during mimicking. The O2 cost measurements within a subject were reproducible over 3-12 trials (coefficient of variation +/- 10% range 5-16%). The O2 costs of hyperpnea correlated highly and positively with VE and WV and less, but significantly, with integral of Pdi.dt and integral of Pga.dt. The O2 cost of VE rose out of proportion to the increasing hyperpnea, so that between 70 and 100% of maximal VO2 delta VO2/delta VE increased 40-60% (1.8 +/- 0.2 to 2.9 +/- 0.1 ml O2/l VE) as VE doubled.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Oxygen cost of exercise hyperpnea: implications for performance.

We addressed two questions concerned with the metabolic cost and performance of respiratory muscles in healthy young subjects during exercise: 1) does exercise hyperpnea ever attain a "critical useful level"? and 2) is the work of breathing (WV) at maximum O2 uptake (VO2max) fatiguing to the respiratory muscles? During progressive exercise to maximum, we measured tidal expiratory flow-volume and transpulmonary pressure- (Ptp) volume loops. At rest, subjects mimicked their maximum and moderate exercise Ptp-volume loops, and we measured the O2 cost of the hyperpnea (VO2RM) and the length of time subjects could maintain reproduction of their maximum exercise loop. At maximum exercise, the O2 cost of ventilation (VE) averaged 10 +/- 0.7% of the VO2max. In subjects who used most of their maximum reserve for expiratory flow and for inspiratory muscle pressure development during maximum exercise, the VO2RM required 13-15% of VO2max. The O2 cost of increasing VE from one work rate to the next rose from 8% of the increase in total body VO2 (VO2T) during moderate exercise to 39 +/- 10% in the transition from heavy to maximum exercise; but in only one case of extreme hyperventilation, combined with a plateauing of the VO2T, did the increase in VO2RM equal the increase in VO2T. All subjects were able to voluntarily mimic maximum exercise WV for 3-10 times longer than the duration of the maximum exercise. We conclude that the O2 cost of exercise hyperpnea is a significant fraction of the total VO2max but is not sufficient to cause a critical level of "useful" hyperpnea to be achieved in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise↗
PubMed1992

Mechanical constraints on exercise hyperpnea in endurance athletes.

We determined how close highly trained athletes [n = 8; maximal oxygen consumption (VO2max) = 73 +/- 1 ml.kg-1.min-1] came to their mechanical limits for generating expiratory airflow and inspiratory pleural pressure during maximal short-term exercise. Mechanical limits to expiratory flow were assessed at rest by measuring, over a range of lung volumes, the pleural pressures beyond which no further increases in flow rate are observed (Pmaxe). The capacity to generate inspiratory pressure (Pcapi) was also measured at rest over a range of lung volumes and flow rates. During progressive exercise, tidal pleural pressure-volume loops were measured and plotted relative to Pmaxe and Pcapi at the measured end-expiratory lung volume. During maximal exercise, expiratory flow limitation was reached over 27-76% of tidal volume, peak tidal inspiratory pressure reached an average of 89% of Pcapi, and end-inspiratory lung volume averaged 86% of total lung capacity. Mechanical limits to ventilation (VE) were generally reached coincident with the achievement of VO2max; the greater the ventilatory response, the greater was the degree of mechanical limitation. Mean arterial blood gases measured during maximal exercise showed a moderate hyperventilation (arterial PCO2 = 35.8 Torr, alveolar PO2 = 110 Torr), a widened alveolar-to-arterial gas pressure difference (32 Torr), and variable degrees of hypoxemia (arterial PO2 = 78 Torr, range 65-83 Torr). Increasing the stimulus to breathe during maximal exercise by inducing either hypercapnia (end-tidal PCO2 = 65 Torr) or hypoxemia (saturation = 75%) failed to increase VE, inspiratory pressure, or expiratory pressure. We conclude that during maximal exercise, highly trained individuals often reach the mechanical limits of the lung and respiratory muscle for producing alveolar ventilation. This level of ventilation is achieved at a considerable metabolic cost but with a mechanically optimal pattern of breathing and respiratory muscle recruitment and without sacrifice of a significant alveolar hyperventilation.

Adult↗
PubMed1992

Demand vs. capacity in the healthy pulmonary system.

This review examines the lung and chest wall adaptation to exercise in health in persons of widely varying degrees of fitness. First we examine the regulation of breathing and gas exchange in the sedentary young adult who shows a near perfect regulation of alveolar gases, ventilation to perfusion distribution, diffusion equilibrium in the lung during all levels of exercise. This individual's respiratory muscles are also ideally recruited both tonically and phasically so as to meet multi-faceted postural, locomotory and respiratory demands. The topic of plasticity in the pulmonary system is discussed with specific reference to the effects of physical training and athleticism. The key point made here is that both homeostasis of gas transport and mechanical efficiency, with which the pulmonary system meets the demands of muscular exercise will depend upon the ability to maintain a significant margin between demand vs. structural capacity. Pulmonary diffusion capacity and at least some aspects of respiratory muscle function seem to be "overbuilt" in the young untrained adult. This margin of safety no longer prevails as the athlete becomes fitter. The cause is to be found in the relative lack of adaptability of the lung and chest wall to the training stimulus. Examples of demand coming very close or exceeding the capacity of the pulmonary system include the highly trained young endurance athlete and the aged athlete. Examples of "failure" or near failure in the pulmonary system's response to exercise include: a) exercise induced arterial hypoxemia via diffusion limitation; b) diaphragmatic fatigue in endurance exercise; c) expiratory flow limitation at VO2max.; d) achieving the capacity of inspiratory muscles for pressure generation at VO2max. and e) oxygen cost of breathing which is in excess of 15% of VO2max. in those athletes who experience the most mechanical limitation.

Adaptation, Physiological↗