Muscle shortening increases fatigue of canine diaphragm.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
T L Clanton
Publications and source records attributed to T L Clanton.
Hyperoxia and moderate hypoxia fail to affect inspiratory muscle fatigue in humans.
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%.
Fatigue↗
Fatigue of the inspiratory muscle pump in humans: an isoflow approach.
A new method is described for measurement of inspiratory muscle endurance in humans that is based on isokinetic principles of muscle testing (i.e., measurement of maximum force during a constant velocity of shortening). Subjects inspired maximally while their lungs were inflated at a constant rate during each breath for 10 min. Inspiratory and expiratory time, flow rate, tidal volume, and end-tidal CO2 were maintained constant. In each subject, maximum inspiratory mouth pressure exponentially decayed over the first few minutes to an apparent sustainable value. Repeated tests in experienced subjects showed high reproducibility of sustainable pressure measurements. To determine the effects of flow, endurance tests were repeated in four subjects at flows of 0.75, 1.0, and 1.25 l/s, with a constant duty cycle. As flow increased, the maximum pressures that could be attained at rest and the maximum sustainable pressures decreased. At each flow, the sustainable pressure remained a constant fraction of the maximum pressure attainable at rest. We interpret the decay in mouth pressure during isoflow endurance tests to directly reflect the loss of net inspiratory muscle force available by maximum voluntary activation of the inspiratory pump.
Fatigue↗
Accelerated decay of inspiratory pressure during hypercapnic endurance trials in humans.
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.
Carbon Dioxide↗
Effects of swim training on lung volumes and inspiratory muscle conditioning.
Lung volumes and inspiratory muscle (IM) function tests were measured in 16 competitive female swimmers (age 19 +/- 1 yr) before and after 12 wk of swim training. Eight underwent additional IM training; the remaining eight were controls. Vital capacity (VC) increased 0.25 +/- 0.25 liters (P less than 0.01), functional residual capacity (FRC) increased 0.39 +/- 0.29 liters (P less than 0.001), and total lung capacity (TLC) increased 0.35 +/- 0.47 (P less than 0.025) in swimmers, irrespective of IM training. Residual volume (RV) did not change. Maximum inspiratory mouth pressure (PImax) measured at FRC changed -43 +/- 18 cmH2O (P less than 0.005) in swimmers undergoing IM conditioning and -29 +/- 25 (P less than 0.05) in controls. The time that 65% of prestudy PImax could be endured increased in IM trainers (P less than 0.001) and controls (P less than 0.05). All results were compared with similar IM training in normal females (age 21.1 +/- 0.8 yr) in which significant increases in PImax and endurance were observed in IM trainers only with no changes in VC, FRC, or TLC (Clanton et al., Chest 87: 62-66, 1985). We conclude that 1) swim training in mature females increases VC, TLC, and FRC with no effect on RV, and 2) swim training increases IM strength and endurance measured near FRC.
Adolescent↗
A simple dosimeter for bronchial provocation testing using a solid-state electronic timing module.
In conducting inhalational challenge tests of airway responsiveness to methacholine, we prefer to deliver the challenge aerosol intermittently, using a dosimeter that turns the nebulizer on for about 0.5 to 0.6 second to deliver each "puff." To avoid the considerable expense of commercially available dosimeters, we constructed our own electronically controlled device, which, in conjunction with a DeVilbiss Model 646 nebulizer, is easily calibrated and permits reproducible and precise timing of challenge puffs. The device was constructed of readily available components and cost us only $100. An experienced technician can use it to trigger on the nebulizer within 0.5 second of the start of inspiration, and in more than one year's experience we have found the system to be completely satisfactory and reliable.
Bronchial Provocation Tests↗
Effect of sinusoidal forcing of ventilatory volume on avian breathing frequency.
Awake chickens were unidirectionally ventilated at 3.6 l . min-1 with 3.2-4.8% CO2 in air. The air sacs on each side were made confluent and implanted with exit tubes connected to the following three devices: 1) a system of constant-flow generators which remove air at exactly the same rate that it entered the trachea, allowing no port for spontaneous volume changes; 2) a sinusoidal pump to force volume changes in the chicken; and 3) a pressure transducer to record air sac pressure, which reflected the sum of two pressure components, the passive pressure changes created by the pump and the active pressure changes due to breathing efforts. Over a range of pump frequencies, the amplitude of measured air sac pressure changes varied inversely with frequency. Above and below this range, pressure showed a beat pattern, indicating a difference in the frequencies of the two pressure components. Within the range lacking a beat pattern, breathing movements and the pump stroke had the same frequency. This range was greater at increased stroke volume. Breathing efforts worked with the pump at the high end of the range and against the pump at the low end. These findings show further evidence of the presence of a response to volume forcing and fit a previously described volume threshold model.
Animals↗
Effects of breathing pattern on inspiratory muscle endurance in humans.
Endurance of the inspiratory muscles was measured in normal volunteers using a threshold resistance that produced a relatively constant mouth-pressure load, independent of inspiratory flow rate (VTI). Breathing pattern was controlled by visual feedback from an oscilloscope. Endurance was measured as the length of time (Tlim) a target VTI could be maintained with maximum effort. Effects of changes in breathing pattern on Tlim were compared with control measurements made the same day. Increases in VTI or in duty cycle (inspiratory time/total period) shortened Tlim, whereas decreases lengthened Tlim. However, effects of changes in VTI were less than equivalent changes in tidal volume produced by alterations in duty cycle. Furthermore, when two breathing pattern changes were altered simultaneously to keep the rate of external inspiratory work (Winsp) constant, significant effects due to changes in duty cycle were still observed. In conclusion, 1) both VTI and duty cycle have significant effects on measurements of inspiratory muscle endurance and 2) the effects of VTI are less than the effects of duty cycle for the same Winsp.
Adult↗
Inspiratory muscle conditioning using a threshold loading device.
We demonstrate the effectiveness of a new conditioning technique for increasing the strength and endurance of the inspiratory muscles. The technique employs a threshold loading device which allows for maximization of exercise intensity with a minimum of exercise duration. After ten weeks, with approximately 25 minutes of exercise time per week, four test subjects showed an average increase in maximum inspiratory pressure (PImax) of 50 (+/- 9 SD) cm H2O (p less than 0.02), whereas four control subjects undergoing submaximal inspiratory muscle exercise showed no significant change. The time the test subjects could endure 65 percent of their prestudy PImax increased from an average of 3.58 +/- 1.65 SD min to over 10 min in all four subjects. No significant change was seen in control subjects. Further testing showed the test subjects could endure 100 percent of their prestudy PImax after conditioning for an average duration 5.15 +/- 1.65 min. This technique should be useful for conditioning the inspiratory muscles in subjects with pulmonary disease.
Adolescent↗
Ventilatory pressure loading at constant pulmonary FCO2 in Gallus domesticus.
Seven White Leghorn roosters were unidirectionally ventilated at constant flows and CO2 concentrations. The birds were awake and stood or crouched in a plethysmograph. A servo system clamped the pressure in the air sacs at constant values from -10 to +10 cm H2O in 2 cm H2O increments. Therefore, the animals could inflate or deflate the air sacs with breathing movements without affecting intrapulmonary pressures. Decreasing air sac pressure less than atmospheric caused inspiratory duration (TI), expiratory duration (TE), total period (TTOT) and tidal volume (VR) to decrease, and the ratio, TI/TE to increase. Increasing air sac pressures to 6 cm H2O above atmospheric caused, TE to increase, TI and TI/TE to decrease and VT and TTOT to change very little. After bilateral vagotomy air sac pressure changes caused little or no changes in TI, TE, TTOT or TI/TE, but produced percentage changes in VT similar to before vagotomy. Comparison of end expiratory volumes with apneic volumes (produced by lowering CO2 in the insulfating gas) over the range of air sac pressures clamped shows: (1) chickens actively exhale at pressures as low as -10 cm H2O, and (2) the change of mean air sac volume due to imposed pressure is less during breathing than during apnea. These findings, we believe, are due to a reflex initiated by mechanoreceptors with projections in the vagus nerves.
Air Sacs↗
Effects of hypercapnia on Breuer-Hering threshold for inspiratory termination.
The effects of CO2 concentration on the timing of inspiratory duration (TI) and expiratory duration (TE) and the responses to lung inflation were studied in decerebrate paralyzed cats. With lung volume held at functional residual capacity during the breath cycle, hypercapnia (fractional concentration of inspired CO2 = 0.04) caused variable changes in TI and significant increases in TE. To obtain the Breuer-Hering threshold relationship [tidal volume (VT) vs. TI] and the timing relationship between TE and the preceding TI (TE vs. TI), ramp inflations of various sizes were used to terminate inspiration at different times in the breath cycle. Hypercapnia caused the VT vs. TI curves to shift in an upward direction so that at higher lung volumes TI was lengthened. Also, the slope of the TE vs. TI relationship was increased. The results suggest that hypercapnia diminished the sensitivity of the Breuer-Hering reflex to the lung volume, thus allowing volume to increase with little effect on TI. In addition, TE appears to become more sensitive to changes in the preceding TI. A model is presented which provides a possible neural mechanism for these responses.
Animals↗
Rapid ventilatory responses to changes in insufflated CO2 in awake roosters.
The ventilatory responses to pulses or steps in the fraction of CO2 in the insufflated gas stream (FICO2) in awake, unidirectionally ventilated White Leghorn roosters (Gallus domesticus) were studied. Within 0.2-0.5 s of the change in FICO2 at the syrinx, a change in inspiratory or expiratory flow occurred. Increases in FICO2 increased flow and tidal volume (VT), whereas decreases in FICO2 decreased flow and VT. Expiratory duration (TE) was markedly prolonged by decreases in FICO2 and shortened by increases. Inspiratory duration was affected little by FICO2 changes. The TE response to pulses of FICO2 (0.2-0.4 s duration) revealed a time dependency such that a maximum effect occurred when the pulses arrived at the syrinx at approximately midexpiration. The magnitudes of the responses were approximately proportional to the amplitude and duration of the FICO2 changes, but decreases in FICO2 had greater effects than increases. A likely receptor site for these responses is the intrapulmonary chemoreceptors, which appear to function in a reflex controlling airflow and timing of the ongoing breath.
Animals↗
Ventilatory phase duration in the chicken: role of mechanical and CO2 feedback.
Awake upright White Leghorn roosters (Gallus domesticus) were unidirectionally ventilated. Electromyographic activity from inspiratory and expiratory muscles was recorded to demarcate inspiration and expiration. During inspiration, the rate of inflation of the air sac system was varied while the CO2 concentration of the gas passing through the lungs was maintained constant. Inspiratory duration was inversely related to the rate of inflation, producing an inspiratory volume-time threshold (VT) curve with a negative slope. When the CO2 concentration was increased in the lungs, the inspiratory VT curve shifted to the right with a concurrent increase in slope. If the rate of deflation was varied during expiration, it was found that expiratory duration was inversely related to the rate of deflation, producing an expiratory VT curve with a positive slope. Increasing the CO2 concentration shifted the curve to the left with an increased slope. These results indicate that inspiratory and expiratory phase durations are a function of both mechanical and chemical feedback.
Animals↗