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

McKenzie, David K.; Allen, G M; Butler, Jane E.; Gandevia, Simon C.

doi:10.1152/jappl.1997.82.6.2011

Cited by 48 publications

(29 citation statements)

References 30 publications

(41 reference statements)

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“…4). Likewise, voluntary activation index has been reported to rise with carbon dioxide tension (PCO 2 ) during inspiratory resistive loading [28]. These observations suggest that chronic respiratory acidosis may enable hypercapnic patients with COPD to generate an increased voluntary activation of the diaphragm.…”

Section: Discussionmentioning

confidence: 94%

“…In patients with COPD, the highest diaphragmatic motor discharge frequencies during resting breathing appeared to occur in patients with the highest Pa,CO 2 levels, although the authors did not set out to determine if the discharge frequencies differed between hypercapnic and normocapnic patients [29]. In healthy subjects sustaining an inspiratory resistive load, MCKENZIE et al [28] noted that the development of hypercapnia was accompanied by an increase in the voluntary activation index of the diaphragm.…”

Section: Discussionmentioning

confidence: 99%

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The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

2001

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The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD. A. Topeli, F. Laghi, M.J. Tobin. #ERS Journals Ltd 2001. ABSTRACT: How do the respiratory centres of patients with chronic obstructive pulmonary disease (COPD) and hypercapnia respond to acute increases in inspiratory load? A depressed respiratory motor output has long been postulated, but studies on this issue have yielded inconsistent results, partly due to limitations of investigative techniques. Many of these limitations can be overcome by the twitch interpolation technique, which is capable of accurately quantifying the degree of diaphragmatic activation, termed the voluntary drive to breathe. The hypothesis that patients with COPD and hypercapnia compensate for an acute increase in mechanical load on the inspiratory muscles with a lower voluntary drive to breathe than is the case with normocapnic patients was tested.Measurements were obtained in 15 patients with COPD, six of whom displayed hypercapnia and nine normocapnia. The maximum degree of diaphragmatic activation, expressed as a voluntary activation index (mean¡SEM), was higher in hypercapnic than in normocapnic patients (98.7¡0.7 versus 94.5¡0.9% (p~0.006)), as was the mean value (94.5¡0.7 versus 88.5¡1.9% (p~0.01)). Within-patient values of the index were also less variable in the hypercapnic patients (coefficients of variation, 3.4¡0.3 versus 6.1¡0.9%, p~0.01). Multiple regression analysis revealed the ratio of dynamic elastance to maximum transdiaphragmatic pressure, an index of inspiratory muscle loading, and pH as the only variables that correlated with maximum voluntary activation index (r 2~0 .69, p~0.02 for each variable). Contrary to the hypothesis, it was concluded that voluntary activation of the diaphragm was greater and less variable in hypercapnic patients than normocapnic patients with severe chronic obstructive pulmonary disease during an acute increase in inspiratory mechanical load. Whether greater diaphragmatic recruitment during episodes of a severe exacerbation of chronic obstructive pulmonary disease provides a survival advantage for hypercapnic patients with chronic obstructive pulmonary disease remains to be determined.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

2001

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“…This is carried out either by progressively increasing the inspiratory load and measuring the highest load achieved (Eastwood et al 1994) or by holding an inspiratory load constant and measuring the time for which this load can be sustained (Zocchi et al 1993;Mador et al 1996;McKenzie et al 1997;Travaline et al 1997;Eastwood et al 1998;Laghi et al 1998). In recent years, however, several studies questioned the assumption that these methods do indeed indirectly measure inspiratory muscle -and in particular diaphragmatic-fatigability.…”

Section: Introductionmentioning

confidence: 99%

Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue?

et al. 2003

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The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO2 retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate (fR), paced at 18 min(-1), with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (P(es,tw)), gastric (P(ga,tw)), and transdiaphragmatic (P(di,tw)) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7) and 8.4 (3.5) min]. P(di,tw) significantly decreased from 33.1 to 25.9 cmH2O in the first run, partially recovered (27.6 cmH2O), and decreased further in the second run (23.4 cmH2O). P(es,tw) also decreased significantly (-5.1 and -2.4 cmH2O), while P(ga,tw) did not change significantly (-2.0 and -1.9 cmH2O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO2 ( PETCO2) rose from 37.2 to 44.0 and 45.3 mmHg, and arterial oxygen saturation (SaO2) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in PETCO2, and/or decreases in SaO2, probably contributed to task-failure.

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“…All have been implicated in respiratory pump failure, but there is no consensus about either their relative contributions or the sequence in which they occur. Even with similar protocols in healthy human subjects (27,33) or animal models (1, 39), different groups report conflicting data about the role of diaphragmatic fatigue in the development of respiratory pump failure. This lack of consensus reflects, in part, a lack of understanding of the variables involved in the development of respiratory pump failure.…”

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confidence: 99%

Cardiorespiratory failure in rat induced by severe inspiratory resistive loading

Simpson¹,

Iscoe²

2007

Journal of Applied Physiology

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Simpson JA, Iscoe S. Cardiorespiratory failure in rat induced by severe inspiratory resistive loading. J Appl Physiol 102: [1556][1557][1558][1559][1560][1561][1562][1563][1564] 2007. First published December 7, 2006; doi:10.1152/japplphysiol.00785.2006.-The mechanisms underlying acute respiratory failure induced by respiratory loads are unclear. We hypothesized that, in contrast to a moderate inspiratory resistive load, a severe one would elicit central respiratory failure (decreased respiratory drive) before diaphragmatic injury and fatigue. We also wished to elucidate the factors that predict endurance time and peak tracheal pressure generation. Anesthetized rats breathed air against a severe load (ϳ75% of the peak tracheal pressure generated during a 30-s occlusion) until pump failure (fall in tracheal pressure to half; mean 38 min). Hypercapnia and hypoxemia developed rapidly (ϳ4 min), coincident with diaphragmatic fatigue (decreased ratio of transdiaphragmatic pressure to peak integrated phrenic activity) and the detection in blood of the fast isoform of skeletal troponin I (muscle injury). At ϳ23 min, respiratory frequency and then blood pressure fell, followed immediately by secondary diaphragmatic fatigue. Blood taken after termination of loading contained cardiac troponin T (myocardial injury). Contrary to our hypothesis, diaphragmatic fatigue and injury occurred early in loading before central failure, evident only as a change in the timing but not the drive component of the central respiratory pattern generator.Stepwise multiple regression analysis selected changes in mean arterial pressure and arterial PCO 2 during loading as the principal contributing factors in load endurance time, and changes in mean arterial pressure as the principal contributing factor in peak tracheal pressure generation. In conclusion, the temporal development of respiratory failure is not stereotyped but depends on load magnitude; moreover respiratory loads induce cardiorespiratory, not just respiratory, failure. diaphragm; fatigue; heart; injury; troponin WHEN THE RESPIRATORY MUSCLES are subjected to contractile demands that exceed their energy supply, respiratory pump failure (inadequate pressure generation) eventually occurs (e.g., 35). Pump failure can result from central failure (inadequate output from the respiratory central pattern generator; sometimes referred to as central fatigue) (50), peripheral fatigue (35) (neurotransmission failure, decreased contractile function; 9), or some combination. Central failure is denoted by a decrease in central neural output despite adequate chemical drive, peripheral fatigue by a reduction in force-generating capacity that is reversible by rest (35), and neurotransmission failure by impaired transmission of the action potential across the neuromuscular junction. All have been implicated in respiratory pump failure, but there is no consensus about either their relative contributions or the sequence in which they occur. Even with similar protocols in healthy human subjects (27,33) o...

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

Cited by 48 publications

References 30 publications

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

The voluntary drive to breathe is not decreased in hypercapnic patients with severe COPD

Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue?

Cardiorespiratory failure in rat induced by severe inspiratory resistive loading

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