T. Wanke et al., INSPIRATORY MUSCLE PERFORMANCE RELATIVE TO THE ANAEROBIC THRESHOLD INPATIENTS WITH COPD, The European respiratory journal, 6(8), 1993, pp. 1186-1191
Rehabilitation programmes in chronic obstructive pulmonary disease (CO
PD) require exercise training above the anaerobic threshold. However,
not all COPD patients develop metabolic acidosis during exercise. The
hypothesis of this study was that non-exercise variables, characterizi
ng the mechanical load on the inspiratory muscles during breathing at
rest, can be used to reliably predict which patients with COPD are not
able to develop metabolic acidosis during exercise. Thirty participan
ts with COPD performed a symptom-limited cycle ergometer test. The oes
ophageal pressure/time index (PTIoes: the product of pressure magnitud
e and duration), the mean rate of pressure development during inspirat
ion (Poes/TI), and the mean airway resistance (Raw)/maximal oesophagea
l pressure (Poes(max)) served as indices for the mechanical load on th
e inspiratory muscles. The oxygen uptake (VO2) at which plasma standar
d bicarbonate was seen to decrease from its baseline value was taken a
s the anaerboic threshold (AT). Mean Raw was significantly higher in t
hose patients in whom the AT could not be detected. No other lung func
tion parameters measured at rest allowed the accurate selection of tho
se patients who did or did not develop exercise metabolic acidosis. On
the other hand, Raw/Poes(max), PTIoes and Poes/TI were significantly
different in the two patient groups. Additionally, whereas in the pati
ent group with identifiable AT exercise hyperpnoea produced a non-line
ar increase of Poes/TI with respect to PTIoes above the AT, in the pat
ient group without identifiable AT there was a linear relationship bet
ween Poes/TI and PTIoes throughout exercise. We conclude that the dete
rmination of inspiratory muscle load indices at rest may be useful in
pulmonary rehabilitation programmes, for identifying those patients wi
th COPD who do not develop exercise induced metabolic acidosis. Our re
sults indicate that exercise hyperpnoea produces a different pattern o
f inspiratory muscle output (when analysed in terms of the pressure de
veloped, as well as the duration of contraction and rate of pressure d
evelopment) in patients with and without identifiable AT.