Hyperoxia and moderate hypoxia fail to affect inspiratory muscle fatigue in humans

1989 ◽  
Vol 66 (2) ◽  
pp. 894-900 ◽  
Author(s):  
B. T. Ameredes ◽  
T. L. Clanton
Keyword(s):  
Human Subjects ◽  
Initial Pressure ◽  
Inspiratory Muscles ◽  
Mouth Pressure ◽  
Rate Of Decay ◽  
Normal Humans ◽  
Normal Human ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Inspiratory Muscle Fatigue

Normal human subjects (n = 7) breathing 21% O2 (normoxia), 13% O2 (hypoxia), or 100% O2 (hyperoxia) performed repeated maximal inspiratory maneuvers (inspiratory duration = 1.5 s, total breath duration = 3.5 s) on an “isoflow” system, which delivered a constant mouth flow (1.25 or 1 l/s) while maintaining normocapnia (5.5% end-tidal CO2). Respective mean arterial O2 saturation values (ear lobe oximetry) were 98 +/- 1, 91 +/- 4 (P less than or equal to 0.01), and 99 +/- 1% (NS). Maximal mouth pressure (Pm) was measured during inspirations at rest and during a 10-min fatigue trial, and the Pm measurements obtained during the fatigue trials were fit to an exponential equation. The parameters of the equation included the time constant (tau), which describes the rate of decay of Pm from the initial pressure (Pi) to the asymptote, or “sustainable” pressure (Ps). The mean fraction of Pm remaining at the end of the fatigue trials (Ps/Pi) was 63 +/- 5%. No significant differences in Pi, Ps, or tau were observed between O2 treatments. This suggests that fatigue of the inspiratory muscles in normal humans occurs by a mechanism that is insensitive to changes in blood O2 content that occur during inspiration of O2 in the range of 13–100%.

Accelerated decay of inspiratory pressure during hypercapnic endurance trials in humans

1988 ◽  
Vol 65 (2) ◽  
pp. 728-735 ◽  
Author(s):  
B. T. Ameredes ◽  
T. L. Clanton
Keyword(s):  
Breathing Pattern ◽  
Human Subjects ◽  
Constant Flow ◽  
Force Output ◽  
Mouth Pressure ◽  
Residual Capacity ◽  
Flow Generator ◽  
Normal Human ◽  
End Tidal ◽  
End Tidal Co2

Seven normal human subjects inspired a CO2-O2 mixture from a constant-flow generator while performing maximal inspiratory maneuvers from functional residual capacity. End-tidal CO2 (ETCO2) was maintained at either 5.5 (normocapnia), 3.5 (hypocapnia), or 7% (hypercapnia) on separate testing days. Subjects attained maximal mouth pressure (Pm) while breathing at either 1.25 or 1 l/s, utilizing a fixed breathing pattern (duty cycle 0.43) with an inspiratory time of 1.5 s. Maximal Pm was measured at rest and then during a 10-min endurance trial in which subjects repeated maximal voluntary inspirations with constant flow and breathing pattern. The endurance Pm data were fit to nonlinear exponential regression. The results indicated that 1) maximal Pm at rest was unaffected by changing ETCO2; 2) the rate of Pm decay over time was accelerated by hypercapnia, whereas hypocapnia showed no consistent effects; and 3) "sustainable" Pm, attained toward the end of the endurance trial, was not decreased; therefore sustainable force output was preserved in response to changing ETCO2.

Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects

1997 ◽  
Vol 82 (6) ◽  
pp. 2011-2019 ◽  
Author(s):  
D. K. McKenzie ◽  
G. M. Allen ◽  
J. E. Butler ◽  
S. C. Gandevia
Keyword(s):  
Human Subjects ◽  
Voluntary Activation ◽  
Peripheral Fatigue ◽  
Task Failure ◽  
Peripheral Muscle ◽  
Inspiratory Muscles ◽  
Resistive Breathing ◽  
Resistive Loading ◽  
End Tidal ◽  
Diaphragm Fatigue

McKenzie, D. K., G. M. Allen, J. E. Butler, and S. C. Gandevia. Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects. J. Appl. Physiol. 82(6): 2011–2019, 1997.—Task failure during inspiratory resistive loading is thought to be accompanied by substantial peripheral fatigue of the inspiratory muscles. Six healthy subjects performed eight resistive breathing trials with loads of 35, 50, 75 and 90% of maximal inspiratory pressure (MIP) with and without supplemental oxygen. MIP measured before, after, and at every minute during the trial increased slightly during the trials, even when corrected for lung volume (e.g., for 24 trials breathing air, 12.5% increase, P < 0.05). In some trials, task failure occurred before 20 min (end point of trial), and in these trials there was an increase in end-tidal[Formula: see text]( P < 0.01), despite the absence of peripheral muscle fatigue. In four subjects (6 trials with task failure), there was no decline in twitch amplitude with bilateral phrenic stimulation or in voluntary activation of the diaphragm, even though end-tidal [Formula: see text] rose by 1.6 ± 0.9%. These results suggest that hypoventilation, CO2 retention, and ultimate task failure during resistive breathing are not simply dependent on impaired force-generating capacity of the diaphragm or impaired voluntary activation of the diaphragm.

Extrageniculate Contributions to Reflex Visual Orienting in Normal Humans: A Temporal Hemifield Advantage

1991 ◽  
Vol 3 (4) ◽  
pp. 322-328 ◽  
Author(s):  
Robert Rafal ◽  
Avishai Henik ◽  
Jean Smith
Keyword(s):  
Reaction Time ◽  
Visual Attention ◽  
Choice Reaction Time ◽  
Human Subjects ◽  
Visually Guided ◽  
Manual Responses ◽  
Visual Orienting ◽  
Normal Humans ◽  
Normal Human ◽  
Benefits And Costs

Evidence is presented that the phylogenetically older retin-otectal pathway contributes to reflex orienting of visual attention in normal human subjects. The study exploited a lateralized neuroanatomic arrangement of retinotectal pathways that distinguishes them from those of the geniculostriate system; namely, more direct projections to the colliculus from the temporal hemifield. Subjects were tested under monocular viewing conditions and responded to the detection of a peripheral signal by making either a saccade to it or a choice reaction time manual keypress. Attention was summoned by noninformative peripheral precues, and the benefits and costs of attention were calculated relative to a central precue condition. Both the benefits and costs of orienting attention were greater when attention was summoned by signals in the temporal hemifield. This temporal hemifield advantage was present for both saccade and manual responses. These findings converge with observations in patients with occipital and midbrain lesions to show that the phylogenetically older retinotectal pathway retains an important role in controlling visually guided behavior; and they demonstrate the usefulness of temporal-nasal hemifield asymmetries as a marker for investigating extrageniculate vision in humans.

Metabolic basis for inspiratory muscle fatigue in normal humans

1993 ◽  
Vol 75 (5) ◽  
pp. 2188-2194
Author(s):  
E. T. Mannix ◽  
T. Y. Sullivan ◽  
P. Palange ◽  
I. R. Dowdeswell ◽  
F. Manfredi ◽  
...  
Keyword(s):  
Muscle Fatigue ◽  
Respiratory Muscles ◽  
Inspiratory Muscle ◽  
Inspiratory Pressure ◽  
Inspiratory Muscles ◽  
Normal Humans ◽  
Controlled Breathing ◽  
Metabolic Basis ◽  
O2 Supply ◽  
Inspiratory Muscle Fatigue

Inspiratory muscle fatigue, a common event in patients in the intensive care unit, is under multifactorial control. To test the hypothesis that systemic oxygenation is a factor in this event, we subjected five healthy males (age 42 +/- 3 yr) to continuous inspiratory pressure (75% of maximal inspiratory pressure, -95 +/- 5 cmH2O) with the use of a controlled breathing pattern while they breathed normoxic (21% O2), hyperoxic (30% O2), and hypoxic (13% O2) mixtures. Inspiratory muscle endurance (IME; time that pressure could be maintained) and other cardiorespiratory parameters were monitored. Room air IME (3.3 +/- 0.4 min) was shortened (P < 0.05) during 13% O2 breathing (1.6 +/- 0.4 min) but was unaffected during 30% O2 breathing (4.0 +/- 0.6 min). Inspiratory loading lowered the respiratory exchange ratio (RER) during the 21 and 30% O2 trials (1.02 +/- 0.01 to 0.80 +/- 0.03% and 1.05 +/- 0.05 to 0.69 +/- 0.01%, respectively) but not during the 13% O2 trials (1.03 +/- 0.03 to 1.06 +/- 0.07%). At the point of fatigue during the 13% O2 trials, RER was lower compared with the same time point during the 21 and 30% O2 trials. A significant relationship was observed between IME and RER (r = -0.73, P = 0.002) but not between IME and any of the other measured variables. We conclude that 1) hypoxemia impairs the ability of the inspiratory muscles to sustain a mechanical challenge and 2) substrate utilization of the respiratory muscles shifts toward a greater reliance on lipid metabolism when O2 is readily available; this shift was not observed when the O2 supply was reduced.

Acute effects of thixotropy conditioning of inspiratory muscles on end-expiratory chest wall and lung volumes in normal humans

2006 ◽  
Vol 101 (1) ◽  
pp. 298-306 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Michiko Iwase ◽  
Yasuyoshi Ohshima ◽  
Ikuo Homma
Keyword(s):  
Chest Wall ◽  
Lung Volume ◽  
Human Subjects ◽  
Esophageal Pressure ◽  
Acute Effects ◽  
Lung Volumes ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Normal Human ◽  
Inflated Lung

Thixotropy conditioning of inspiratory muscles consisting of maximal inspiratory effort performed at an inflated lung volume is followed by an increase in end-expiratory position of the rib cage in normal human subjects. When performed at a deflated lung volume, conditioning is followed by a reduction in end-expiratory position. The present study was performed to determine whether changes in end-expiratory chest wall and lung volumes occur after thixotropy conditioning. We first examined the acute effects of conditioning on chest wall volume during subsequent five-breath cycles using respiratory inductive plethysmography ( n = 8). End-expiratory chest wall volume increased after conditioning at an inflated lung volume ( P < 0.05), which was attained mainly by rib cage movements. Conditioning at a deflated lung volume was followed by reductions in end-expiratory chest wall volume, which was explained by rib cage and abdominal volume changes ( P < 0.05). End-expiratory esophageal pressure decreased and increased after conditioning at inflated and deflated lung volumes, respectively ( n = 3). These changes in end-expiratory volumes and esophageal pressure were greatest for the first breath after conditioning. We also found that an increase in spirometrically determined inspiratory capacity ( n = 13) was maintained for 3 min after conditioning at a deflated lung volume, and a decrease for 1 min after conditioning at an inflated lung volume. Helium-dilution end-expiratory lung volume increased and decreased after conditioning at inflated and deflated lung volumes, respectively (both P < 0.05; n = 11). These results suggest that thixotropy conditioning changes end-expiratory volume of the chest wall and lung in normal human subjects.

Changes in total pulmonary resistance and PCO2 between wakefulness and sleep in normal human subjects

1995 ◽  
Vol 78 (4) ◽  
pp. 1339-1349 ◽  
Author(s):  
M. J. Morrell ◽  
H. R. Harty ◽  
L. Adams ◽  
A. Guz
Keyword(s):  
Continuous Positive Airway Pressure ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Human Subjects ◽  
Stage Iv ◽  
Pulmonary Resistance ◽  
Inspiratory Resistance ◽  
Normal Human ◽  
End Tidal

We investigated the possible role of an increase in total pulmonary resistance in the sleep-related hypoventilation that occurs in healthy subjects. Eight nonsnoring volunteers were studied during quiet wakefulness and stage IV sleep. Airflow was measured via a nasal mask with a low dead space, and breathing pattern, end-tidal PCO2 (PETCO2), and a continuous estimate of total pulmonary resistance were estimated. From wakefulness to sleep, mean inspiratory resistance increased from 5.5 +/- 2.4 (SD) to 8.1 +/- 4.3 cmH2O.l–1.s, PETCO2 increase from 38.7 +/- 3.0 to 40.7 +/- 3.5 Torr, and ventilation decreased from 7.12 +/- 1.15 to 6.47 +/- 1.68 l/min. In five of the eight subjects, low levels of continuous positive airway pressure were applied during stage IV sleep to reverse any increase in resistance. In these subjects, continuous positive airway pressure reduced mean inspiratory resistance from 9.3 +/- 4.3 +/- 3.0 cmH2O.l–1.s but had little effect on mean PETCO2 (from 39.8 +/- 4.0 to 39.6 +/- 4.0 Torr) and mean ventilation (from 6.79 +/- 1.93 to 6.91 +/- 1.80 l/min). These findings suggest that in nonsnoring subjects reductions in alveolar ventilation cannot be accounted for by an increase in airway resistance.

Fatigue of inspiratory muscles and their synergic behavior

1979 ◽  
Vol 46 (5) ◽  
pp. 897-904 ◽  
Author(s):  
C. Roussos ◽  
M. Fixley ◽  
D. Gross ◽  
P. T. Macklem
Keyword(s):  
Transpulmonary Pressure ◽  
Normal Subjects ◽  
Abdominal Pressure ◽  
Inspiratory Capacity ◽  
Inspiratory Muscles ◽  
Mouth Pressure ◽  
Residual Capacity ◽  
Resistive Loads ◽  
Accessory Muscles ◽  
Inspiratory Muscle Fatigue

The time (tlim) required to produce inspiratory muscle fatigue was measured in five normal subjects breathing at functional residual capacity (FRC) against a variety of high inspiratory resistive loads. In every breathing test the subjects generated with each inspiration a mouth pressure (Pm) that was a predetermined fraction of maximum Pm (Pmmax). They continued breathing until they were unable to generate this Pm. The Pm/Pmmax that could be generated indefinitely (Pmcrit) was around 60%. The inspiratory power output at that level of breathing was 6.6 kg.m/min (Wcrit). In three of those subjects the same experiment was conducted at an end-expiratory volume of FRC + one-half inspiratory capacity (1/2IC). The higher lung volume was actively maintained by the subjects watching end-expiratory transpulmonary pressure on an oscilloscope. For any fraction of the maximum mouth pressure at FRC + 1/2IC (Pm'max), tlim was shorter than FRC. Pmcrit decreased to 30% Pm'max and Wcrit to 2.6 kg.m/min. Monitoring the abdominal pressure revealed that the contribution of the diaphragm and intercostal accessory muscles alternated in time, possibly postponing the onset of fatigue.

Ventilatory responses to inspiratory threshold loading and role of muscle fatigue in task failure

1994 ◽  
Vol 76 (1) ◽  
pp. 185-195 ◽  
Author(s):  
P. R. Eastwood ◽  
D. R. Hillman ◽  
K. E. Finucane
Keyword(s):  
Breathing Pattern ◽  
Normal Subjects ◽  
Compensatory Mechanisms ◽  
Recruitment Pattern ◽  
Transdiaphragmatic Pressure ◽  
Task Failure ◽  
Inspiratory Muscles ◽  
End Tidal ◽  
Arterial O2 Saturation

To examine respiratory muscle recruitment pattern during inspiratory loading and role of fatigue in limiting endurance, we studied seven normal subjects on 17 +/- 6 days during breathing against progressive inspiratory threshold load. Threshold pressure (Pth) was progressively increased 14 +/- 5 cmH2O every 2 min until voluntary cessation (task failure). Subjects could adopt any breathing pattern. Tidal volume (VT), chest wall motion, end-tidal PCO2, and arterial O2 saturation were measured. At moderate loads [50–75% of maximum Pth (Pthmax)], inspiratory time (TI) decreased and VT/TI and expiratory time increased, increasing time for recovery of muscles between inspirations. At high loads (> 75% Pthmax), VT/TI decreased, which, with progressive decrease in end-expiratory lung volume (EELV) throughout, increased potential for inspiratory force development. Progressive hypoxia and hypercapnia occurred at higher work loads. Immediately after task failure all subjects could recover at high loads and still reachieve initial Pthmax on reimposition of progressive loading. Respiratory pressures were measured in subgroup of three subjects: transdiaphragmatic pressure response to 0.1-ms bilateral supramaximal phrenic nerve stimulation at end expiration initially increased with increasing load/decreasing EELV, consistent with increasing mechanical advantage of diaphragm, but decreased at highest loads, suggesting diaphragm fatigue. Full recovery had not occurred at 30 min after task failure. We demonstrated that progressive threshold loading is associated with systematic changes in breathing pattern that act to optimize muscle strength and increase endurance. Task failure occurred when these compensatory mechanisms were maximal. Inspiratory muscles appeared relatively resistant to fatigue, which was late but persistent.

Observations on a Relationship between Steroid Metabolism and the Concentration of Plasma Fibrinogen

1963 ◽  
Vol 10 (02) ◽  
pp. 400-405 ◽  
Author(s):  
B. A Amundson ◽  
L. O Pilgeram
Keyword(s):  
Blood Coagulation ◽  
Methyl Ether ◽  
Broad Spectrum ◽  
Human Subjects ◽  
Plasma Fibrinogen ◽  
Steroid Metabolism ◽  
Specific Site ◽  
Chain Reaction ◽  
Normal Human ◽  
A Chain

SummaryEnovid (5 mg norethynodrel and 0.075 mg ethynylestradiol-3-methyl ether) therapy in young normal human subjects causes an increase in plasma fibrinogen of 32.4% (P >C 0.001). Consideration of this effect together with other effects of Enovid on the activity of specific blood coagulatory factors suggests that the steroids are exerting their effect at a specific site of the blood coagulation and/or fibrinolytic system. The broad spectrum of changes which are induced by the steroids may be attributed to a combination of a chain reaction and feed-back control.

Relationship Between Mepacrine-Labelled Dense Body Number, Platelet Capacity to Accumulate 14C-5-HT and Platelet Density in the Bernard-Soulier and Hermansky-Pudlak Syndromes

1979 ◽  
Vol 42 (02) ◽  
pp. 694-704 ◽  
Author(s):  
F Rendu ◽  
A T Nurden ◽  
M Lebret ◽  
J P Caen
Keyword(s):  
Dense Body ◽  
Human Subjects ◽  
Human Platelets ◽  
Dense Bodies ◽  
Storage Organelle ◽  
Hereditary Disorders ◽  
Labelling Procedure ◽  
Normal Human ◽  
Hermansky Pudlak Syndrome ◽  
Bernard Soulier Syndrome

SummaryWe have used the mepacrine-labelling procedure to measure the dense body (serotonin storage organelle) content of the platelets of 2 hereditary disorders where abnormalities in dense body number were suspected. The platelets were incubated with mepacrine and examined by fluorescence microscopy. A mean number of 5.4 ± 0.8 (SD) dense bodies per platelet was calculated from the data obtained using platelets isolated from 40 normal human subjects. In contrast the platelets of 2 patients with the Bernard-Soulier syndrome contained an average of 14 and 17 labelled granules. This increase was associated with a much greater capacity of the platelets to accumulate 14C-5-HT. The opposite result was obtained using the platelets from 2 patients with the Hermansky-Pudlak syndrome which contained few granules labelled by mepacrine and took up less 14C-5-HT than normal human platelets. Centrifugation of the patients’ platelets on discontinuous sucrose gradients showed that the platelets of the 2 Bemard-Soulier patients were much denser than normal whereas a high proportion of low density platelets was observed in the Hermansky-Pudlak syndrome. These results further define the platelet abnormalities in the two syndromes and suggest that dense body number may be one of the factors governing platelet density.

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