Contribution of diaphragmatic power output to exercise-induced diaphragm fatigue

Abstract

In nine normal humans we compared the effects on diaphragm fatigue of whole body exercise to exhaustion (86-93% of maximal O2 uptake for 13.2 +/- 2.0 min) to voluntary increases in the tidal integral of transdiaphragmatic pressure (integral of Pdi) while at rest at the same magnitude and frequency and for the same duration as those during exercise. After the endurance exercise, we found a consistent and significant fall (-26 +/- 2.9%, range -19.2 to -41.0%) in the Pdi response to supramaximal bilateral phrenic nerve stimulation at all stimulation frequencies (1, 10, and 20 Hz). Integral of Pdi.fB (where fB is breathing frequency) achieved during exercise averaged 509 +/- 81.0 cmH2O/min (range 304.0-957.0 cmH2O/min). At rest, voluntary production of integral of Pdi.fB, which was < 550-600 cmH2O/min (approximately 4 times the resting eupenic integral of Pdi.fB or 60-70% of Pdi capacity), did not result in significant diaphragmatic fatigue, whereas sustained voluntary production of integral of Pdi.fB in excess of these threshold values usually did result in significant fatigue. Thus, with few exceptions (5 of 23 tests) the ventilatory requirements of whole body endurance exercise demanded a level of integral of Pdi.fB that, by itself, was not fatiguing. The rested first dorsal interosseous muscle showed no fatigue in response to supramaximal ulnar nerve stimulation after whole body exercise. We postulate that the effects of locomotor muscle activity, such as competition for blood flow distribution and/or extracellular fluid acidosis, in conjunction with a contracting diaphragm account for most of the exercise-induced diaphragm fatigue.

Inspiratory muscle training abolishes the blood lactate increase associated with volitional hyperpnoea superimposed on exercise and accelerates lactate and oxygen uptake kinetics at the onset of exercise

“…Nevertheless, a limitation of the present study was that the work of breathing specifically associated with exercise hyperpnoea, i.e. the pressure-volume characteristics of each breath (Babcock et al 1995), was not mimicked. Therefore, since the work of breathing (particularly that associated with expiration) during volitional hyperpnoea exceeds that associated with an identical, spontaneous E V  during exercise (Klas and Dempsey 1989), the net increase in respiratory muscle lactate production in Our findings suggest that following IMT the relative work performed by the inspiratory muscles during volitional hyperpnoea was reduced (due to the 19% increase in inspiratory muscle strength) resulting in a reduction in net lactate production (Brown et al 2008;Johnson et al 2006).…”

Diaphragmatic function after intense exercise in congestive heart failure patients

“…Why might healthy young people develop diaphragmatic fatigue after exercise while older patients with CHF do not? It is felt that exercise-induced diaphragmatic fatigue requires a high level of sustained diaphragmatic work and an unspecified exercise-dependent factor [29]. The present subjects sustained exercise for a sufficient duration to result in fatigue.…”

Exercise-induced respiratory muscle fatigue: implications for performance

“…a mechanical ventilator (11). However, other factors besides respiratory muscle work must also be responsible for exerciseinduced respiratory muscle fatigue, because fatigue did not occur when the resting subject mimicked the magnitude and duration of diaphragmatic work incurred during exercise (13). Indeed, fatigue did not occur until the pressures developed by the diaphragm were voluntarily increased twofold greater than required during whole body exercise at intensities that caused exercise-induced diaphragmatic fatigue (13).…”

“…However, other factors besides respiratory muscle work must also be responsible for exerciseinduced respiratory muscle fatigue, because fatigue did not occur when the resting subject mimicked the magnitude and duration of diaphragmatic work incurred during exercise (13). Indeed, fatigue did not occur until the pressures developed by the diaphragm were voluntarily increased twofold greater than required during whole body exercise at intensities that caused exercise-induced diaphragmatic fatigue (13). The probable explanation for why the fatigue threshold of force production for the diaphragm was so much lower during whole body exercise than at rest is that, at rest, the volitional increases in diaphragmatic work mean that large shares of the total cardiac output are devoted to the diaphragm, whereas during exercise the diaphragm must compete with locomotor muscles for its share of the available cardiac output (39,40).…”

“…Exercise-induced diaphragmatic fatigue may affect performance by decreasing the relative contribution of the diaphragm to total ventilation over time with a requirement for accessory inspiratory and expiratory muscles to be recruited to deliver the progressive hyperventilatory response (6,12,13,52). The increasing use of accessory respiratory muscles as exercise continues may distort the chest wall (34,36), reduce the mechanical efficiency of breathing (23,42) and, hence, increase the metabolic and blood flow demands of these muscles (see EXERCISE DEMANDS ON THE RESPIRATORY MUSCLES).…”