We also examined the relationships between V?Odos and the slopes of HR/V?O2, SpO2/V?O2, StO2/V?O2, and MOER/V?O2. The influence of V?O2 on the HR/V?O2 slope is partially expressed in the cardiac response, the SpO2/V?O2 slope in the respiratory response, and the StO2/V?O2 and MOER/V?O2 slopes in the muscle response. peak V?O2 did not correlate with any of the slopes (Fig. 3). In subject step step 1 the HR/V?O2, SpO2/V?O2, and StO2/V?O2 slopes were high and the MOER/V?O2 slope was low, compared with most of the other subjects. However, in subject 2 the HR/V?O2, SpO2/V?O2, 
and StO2/V?O2 slopes were low and the MOER/V?O2 slope was high. Figure 4 displays the relationships between V?O2 and HR, SpO2, StO2, and MOER for the different types of subjects (subjects 1 and 2). We determined that the severity of air-flow limitation was similar in both subjects, but peak V?O2 was greater in subject 1 than in subject 2 (see Table 1). The slopes of HR/V?O2 and SpO2/V?O2 were lower, but MOER/V?O2 was relatively higher in subject 1 than in subject 2.
Relationships between peak oxygen uptake (V?O2) and the slope of heart rate/V?O2, SpO2/V?O2, StO2/V?O2, and MOER/V?O2. The muscle oxygen extraction rate (MOER) was calculated as (SpO2 ? StO2)/SpO2 ? 100(%). StO2 = tissue oxygen saturation. 0 Subject 1. ? Subject 2. ? Subject 3. ? Subject 4. ? Subject 5. ¦ Subject 6. ? Subject 7. ? Subject 8.
O2) and heart rate (HR), SpO2, tissue oxygen saturation (StO2), and muscle oxygen extraction rate (MOER) for typical subjects. 0 Subject 1: age 71 y, % predicted FVC 69.3%, % predicted FEV1 36.1%, peak V?O2 17.0 mL/kg/min. ? Subject 2: age 74 y, % predicted FVC 65.5%, % predicted FEV1% 38.2%, peak V?O2 10.9 mL/kg/min. The MOER was calculated as (SpO2 ? StO2)/SpO2 ? 100 (%). The severity of air-flow limitation was similar in both subjects, but peak V?O2 was greater in Subject 1 than in Subject 2. The slopes of HR/V?O2, SpO2/V?O2 and StO2/V?O2 were lower, but MOER/V?O2 was relatively higher in Subject 1 than in Subject 2.
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The work rate of normal subjects is increased during exercise, and muscle oxygenation either remains constant near resting levels initially or decreases. 29 With an increasing work rate, tissue oxygenation decreases linearly or exponentially below the resting value, followed by a leveling off as the person reaches exhaustion. 30 These changes indicate there is a larger increase in oxygen extraction than in arterial blood flow during ramp load. In this study, most subjects with COPD exhibited similar changes (see Fig. 2). These results indicate that the balance between DO2 and O2 utilization in exercising muscle in subjects with COPD is similar to that in normal subjects. However, in 2 of the 8 subjects with COPD (subjects 2 and 6) there was little change in muscle oxygenation during exercise, and these subjects also had low MOERs (see Fig. 3).
Matchmaking anywhere between oxygen consumption (V?
Patients with COPD have been reported to have faster dynamics of muscle deoxygenation than their age-matched controls. 16,17 Chiappa et al 17 reported that the time constant ratio of O2 uptake to mean response time of deoxy-Hb concentration was significantly greater in patients with COPD after the performance of heavy-intensity exercise. It has been suggested that patients with COPD have slower kinetics of microvascular O2 delivery and impaired cardiovascular adjustments. Studies have also shown that muscle oxygenation in patients with COPD during exercise can be improved by bronchodilators, 18 heliox, 19 and proportional assist ventilation, 20 all of which reduced the rate of onset of dynamic hyperinflation and diminished respiratory muscle work. These findings suggest that a fraction of the available cardiac output can be redirected from respiratory muscles to the peripheral muscles, as a consequence of respiratory muscle unloading; and that decreased muscle oxygenation during exercise may be due to insufficient DO2 in patients with COPD.
