Comprehensive Physiology Wiley Online Library

Inspiratory Muscle Fatigue

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Muscle Function and Fatigue
1.1 Force Generation
1.2 Central Fatigue
1.3 Peripheral Fatigue
1.4 Integrated View of Inspiratory Muscle Fatigue
2 Pathophysiology of Inspiratory Muscle Fatigue
2.1 Energy Balance—Theoretical Considerations
2.2 Respiratory Muscle Fatigue and Ventilatory Failure
2.3 Factors Predisposing to Inspiratory Muscle Fatigue
2.4 Improvement in Contractility and Endurance
3 Detection of Respiratory Muscle Fatigue
3.1 Measurement of Force
3.2 EMG Spectral Shift
3.3 Synergic Behavior of the Fatiguing Respiratory Muscles
Figure 1. Figure 1.

Force or pressure generated by supramaximal electrical nerve or muscle stimulation as percent maximum of force or transdiaphragmatic pressure (Pdi) at various stimulation frequencies. Force or pressure increases markedly in response to small changes in low‐frequency stimulation, whereas force or pressure is affected very little by large changes in high‐frequency stimulation.

From Roussos and Moxham 110
Figure 2. Figure 2.

Evolution of transdiaphragmatic pressure (Pdi), electromyogram, and electrical activity of phrenic nerve (Ephr) in one dog during hypotension and decreased cardiac output induced by pericardial tamponade. Top trace: Pdi; middle trace: integrated electrical activity of diaphragm (Edi); bottom trace: Ephr. Left panel: control; middle panel: 60 min after onset of shock; right panel: 140 min after onset of shock, 20 min prior to animal's death. Pdi decreases despite increased Ephr and Edi, and frequency of breathing increases, then decreases.

From Aubier, Trippenbach, and Roussos 6
Figure 3. Figure 3.

Maximum isometric voluntary contraction of adductor pollicis muscle in one male subject until exhaustion with unoccluded (A) and occluded (B) circulation. Top traces: force record; single twitches evoked by nerve shocks precede, follow, and are superimposed on voluntary contraction. Bottom traces: muscle action potentials after electrical stimulation. Bottom dots: time markers. Force is lost despite constancy of action potentials.

Adapted from Merton 71
Figure 4. Figure 4.

Progression of changes in pressure‐frequency curves of diaphragm of 4 subjects up to 30 min after fatigue. Solid lines, average of 3 curves before fatigue (control); dotted lines, average of 3 curves at different times during recovery from fatigue; bars, ± 1 SE. Transdiaphragmatic pressure (Pdi) is expressed as percent of Pdi generated with supramaximal phrenic nerve stimulation at frequency of 100 Hz (% Pdi,max); 30 min after fatigue, Pdi generated at high frequencies of stimulation (50 Hz) approaches control values, whereas low frequencies of stimulation cannot generate prefatigue Pdi values.

From Aubier et al. 4
Figure 5. Figure 5.

Interrelation of pressure (P), flow (VT/TI), and duty cycle (TI/TT) when mean muscle power and maximum energy uptake are equal to 8 kg/m.

From Roussos and Moxham 110
Figure 6. Figure 6.

Relationship between inspiratory duty cycle (TI/TT) and critical diaphragmatic pressure (Pdi/Pdi,max). Broken lines, 95% Pdi/Pdi,max confidence‐limit interval. Fatigue develops for all breathing patterns falling to the right of given interval but not for those to left. Pdi/Pdi,max decreases as TI/TT increases.

Adapted from Bellemare and Grassino 9
Figure 7. Figure 7.

Power of breathing traced as a function of endurance time for 2 subjects. Curve is asymptotic at a power that would permit ventilation (E) of ∼50% maximum breathing capacity (MBC).

Adapted from Tenney and Reese 102
Figure 8. Figure 8.

Top: closed triangles, effect of endurance training expressed as a change in sustained ventilatory capacity (ΔSVC) over a period of 5 wk; open triangles, control subjects. Small increase in SVC for control was probably due to learning by subjects; SVC in trained group declined after training ceased (5‐ to 20‐wk period). Bottom: changes in strength expressed as percent change in maximum pressure (Pmax) developed at 40% VC with time. Expiration and inspiration are denoted by solid and open circles, respectively; bars, ± SD. Strength declined after training ceased.

Adapted from Leith and Bradley 57
Figure 9. Figure 9.

Active length‐tension curves obtained from diaphragm strips of sedentary control (SC) and sedentary emphysematous (SE) animals. Left: tension expressed as kilograms per cross‐sectional area of muscle. Both groups achieve same Pmax. Right: fiber length expressed in absolute terms. Active length‐tension curve of SE group is significantly shifted to left; Pmax is generated at a shorter length in this group.

Adapted from Farkas and Roussos 31
Figure 10. Figure 10.

Tracings of experimental run in a man breathing against an inspiratory resistive load. With each breath, subject generated 75% of maximum mouth pressure. All pressures, except transdiaphragmatic pressure, were measured relative to atmospheric pressure. Only gastric and transdiaphragmatic pressures varied; mouth and esophageal pressures remained constant throughout the run. Gastric pressure increased during periods A and C and declined during periods B and D, indicating alternation of inspiratory muscle recruitment.

From Roussos et al. 94


Figure 1.

Force or pressure generated by supramaximal electrical nerve or muscle stimulation as percent maximum of force or transdiaphragmatic pressure (Pdi) at various stimulation frequencies. Force or pressure increases markedly in response to small changes in low‐frequency stimulation, whereas force or pressure is affected very little by large changes in high‐frequency stimulation.

From Roussos and Moxham 110


Figure 2.

Evolution of transdiaphragmatic pressure (Pdi), electromyogram, and electrical activity of phrenic nerve (Ephr) in one dog during hypotension and decreased cardiac output induced by pericardial tamponade. Top trace: Pdi; middle trace: integrated electrical activity of diaphragm (Edi); bottom trace: Ephr. Left panel: control; middle panel: 60 min after onset of shock; right panel: 140 min after onset of shock, 20 min prior to animal's death. Pdi decreases despite increased Ephr and Edi, and frequency of breathing increases, then decreases.

From Aubier, Trippenbach, and Roussos 6


Figure 3.

Maximum isometric voluntary contraction of adductor pollicis muscle in one male subject until exhaustion with unoccluded (A) and occluded (B) circulation. Top traces: force record; single twitches evoked by nerve shocks precede, follow, and are superimposed on voluntary contraction. Bottom traces: muscle action potentials after electrical stimulation. Bottom dots: time markers. Force is lost despite constancy of action potentials.

Adapted from Merton 71


Figure 4.

Progression of changes in pressure‐frequency curves of diaphragm of 4 subjects up to 30 min after fatigue. Solid lines, average of 3 curves before fatigue (control); dotted lines, average of 3 curves at different times during recovery from fatigue; bars, ± 1 SE. Transdiaphragmatic pressure (Pdi) is expressed as percent of Pdi generated with supramaximal phrenic nerve stimulation at frequency of 100 Hz (% Pdi,max); 30 min after fatigue, Pdi generated at high frequencies of stimulation (50 Hz) approaches control values, whereas low frequencies of stimulation cannot generate prefatigue Pdi values.

From Aubier et al. 4


Figure 5.

Interrelation of pressure (P), flow (VT/TI), and duty cycle (TI/TT) when mean muscle power and maximum energy uptake are equal to 8 kg/m.

From Roussos and Moxham 110


Figure 6.

Relationship between inspiratory duty cycle (TI/TT) and critical diaphragmatic pressure (Pdi/Pdi,max). Broken lines, 95% Pdi/Pdi,max confidence‐limit interval. Fatigue develops for all breathing patterns falling to the right of given interval but not for those to left. Pdi/Pdi,max decreases as TI/TT increases.

Adapted from Bellemare and Grassino 9


Figure 7.

Power of breathing traced as a function of endurance time for 2 subjects. Curve is asymptotic at a power that would permit ventilation (E) of ∼50% maximum breathing capacity (MBC).

Adapted from Tenney and Reese 102


Figure 8.

Top: closed triangles, effect of endurance training expressed as a change in sustained ventilatory capacity (ΔSVC) over a period of 5 wk; open triangles, control subjects. Small increase in SVC for control was probably due to learning by subjects; SVC in trained group declined after training ceased (5‐ to 20‐wk period). Bottom: changes in strength expressed as percent change in maximum pressure (Pmax) developed at 40% VC with time. Expiration and inspiration are denoted by solid and open circles, respectively; bars, ± SD. Strength declined after training ceased.

Adapted from Leith and Bradley 57


Figure 9.

Active length‐tension curves obtained from diaphragm strips of sedentary control (SC) and sedentary emphysematous (SE) animals. Left: tension expressed as kilograms per cross‐sectional area of muscle. Both groups achieve same Pmax. Right: fiber length expressed in absolute terms. Active length‐tension curve of SE group is significantly shifted to left; Pmax is generated at a shorter length in this group.

Adapted from Farkas and Roussos 31


Figure 10.

Tracings of experimental run in a man breathing against an inspiratory resistive load. With each breath, subject generated 75% of maximum mouth pressure. All pressures, except transdiaphragmatic pressure, were measured relative to atmospheric pressure. Only gastric and transdiaphragmatic pressures varied; mouth and esophageal pressures remained constant throughout the run. Gastric pressure increased during periods A and C and declined during periods B and D, indicating alternation of inspiratory muscle recruitment.

From Roussos et al. 94
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How to Cite

Charis Roussos, Peter T. MacKlem. Inspiratory Muscle Fatigue. Compr Physiol 2011, Supplement 12: Handbook of Physiology, The Respiratory System, Mechanics of Breathing: 511-527. First published in print 1986. doi: 10.1002/cphy.cp030329