Though exercise training is part of most pulmonary rehabilitation programs, whether there is a physiologic basis for increased exercise tolerance is unclear. We sought to determine whether patients with chronic obstructive pulmonary disease (COPD) are capable of obtaining a physiologic training effect, as manifested by a reduction in blood lactate and ventilation (VE) at a given level of exercise. We also sought to determine whether training work rate determines the size of the training effect. Nineteen participants with COPD of predominantly moderate severity in an inpatient rehabilitation program performed two cycle ergometer exercise tests at a low and a high work rate for 15 min or to tolerance and also an incremental exercise test to tolerance. Arterial blood was sampled for blood gas and lactate analyses. Identical tests were performed before and after 5-day-per-week cycle ergometer training for 8 wk either for 45 min/day at a high work rate (average, 71 W) or for a proportionally longer time at a low work rate (average, 30 W). Average FEV1 was 56 +/- 12% predicted and did not change with training. Peak exercise lactate (average, 6.5 mEq/L) was not correlated with FEV1. For the high work rate training group, identical work rates engendered less lactate (4.5 versus 7.2 mEq/L) and less VE (48 versus 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p less than 0.01). Further, endurance time for the high constant work rate increased 73% in the high work rate training group but only 9% in the low work rate training group. At identical work rates, VE decrease average 2.5 L/min per mEq/L decrease in lactate (r = 0.75). We conclude that most COPD subjects studied increased blood lactate at low work rates. Many of these patients were able to achieve a physiologic training effect. Though total work was the same, training at a high work rate was more effective than was training at a low work rate. The lower VE requirement to perform exercise was in proportion to the lower lactate level, but the VE decrease for a given decrease in lactate was smaller than that seen in normal subjects (7.2 L/min/mEq/L), apparently because patients with COPD fall to hyperventilate in response to lactic acidosis (PaCO2 does not drop). These findings provide a physiologic rationale for exercise training of patients with COPD.

To assess physiologic effects of continuous positive airway pressure (CPAP) and positive end-expiratory pressure (PEEP) during noninvasive pressure support ventilation (PSV) in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD), we measured in seven patients the breathing pattern, lung mechanics, diaphragmatic effort (PTPdi), and arterial blood gases under four conditions: (1) spontaneous breathing (SB); (2) CPAP; (3) PSV of 10 cm H2O; and (4) PSV plus PEEP (PEEP + PSV). CPAP and PEEP were set between 80 and 90% of dynamic intrinsic PEEP (PEEPidyn) measured during SB and PSV, respectively. PEEPidyn was obtained (1) from the decrease in pleural pressure (delta Ppl) preceding inspiration, and (2) subtracting the fall in gastric pressure (delta Pga) caused by relaxation of the abdominal muscles from the delta Ppl decrease. Abdominal muscle activity made PEEPidyn overestimated in almost all instances (p < 0.0001). PSV increased minute ventilation, improved gas exchange, and decreased PTPdi. PEEP added to PSV, likewise CPAP compared with SB, further significantly decreased the diaphragmatic effort (PTPdi went from 322 +/- 111 to 203 +/- 63 cm H2O.s) by counterbalancing PEEPidyn, which went from 5.4 +/- 4.0 to 3.1 +/- 2.3 cm H2O. These data support the use of low levels of PEEP (80 to 90% of PEEPidyn) to treat acute exacerbation of COPD by means of mask PSV.

To investigate the mechanisms underlying ventilator-dependence in patients with chronic obstructive pulmonary disease (COPD), and to assess the effects of the combination of positive end-expiratory pressure (PEEP) and pressure-support ventilation (PSV) on inspiratory muscle effort, we investigated respiratory mechanics in eight ventilator-dependent COPD patients. The patients' breathing pattern, lung mechanics, diaphragmatic effort (PTPdi), diaphragmatic tension-time index (TTdi), and arterial blood gases were measured during both spontaneous breathing (SB) and ventilatory assistance consisting of PSV alone (15, 20, and 25 cm H2O) and PSV combined with a PEEP of 5 cm H2O (reducing PSV to 10, 15, and 20 cm H2O, respectively, to maintain equivalent inspiratory pressure). The different levels of ventilatory support were delivered in a randomized sequence. Maximal inspiratory (MIP), esophageal (PpImax) and transdiaphragmatic (Pdi(max)) pressures and respiratory drive (P(0.1)) were measured at the beginning of the procedure during SB. We found a high P(0.1) (6.1 +/- 1.7 cm H2O), which seemed to rule out an impairment of respiratory-center output. Apparently, inspiratory muscle strength was compatible with successful weaning (38.5 +/- 8.8, 50.9 +/- 9.7, and 51.8 +/- 9.5 cm H2O for MIP, PPImax and Pdi(max), respectively). However, abnormal respiratory mechanics (particularly an intrinsic positive end-expiratory pressure (PEEPi) of 8.3 +/- 1.9 cm H2O and pulmonary resistance 24.7 +/- 9.5 cm H2O/L/s imposed an excessive load on the inspiratory muscles, as indicated by a high PTPdi (499 +/- 122 cm H2O x s). Increasing levels of PSV progressively and significantly unloaded the patients' inspiratory muscles, although at pressures above 20 cm H2O uncoupling occurred between patient and ventilator respiratory frequency. Application of PEEP during PSV improved ventilatory assistance by further reducing the inspiratory effort (by 17% on average) and by ameliorating patient-ventilator interaction. We conclude that the excessive mechanical load, and in particular the high PEEPi, is the major determinant of ventilator-dependence in COPD patients. Application of PEEP improves the efficiency of PSV in unloading these patients' inspiratory muscles, and can sometimes improve patient-ventilator interaction.

This study, featuring the largest cohort so far reported in the literature, shows that PR is equally effective in the more severe COPD patients, i.e. those with CRF, and supports the prescription of PR also in these patients.