**2. Exercise limitation and breathlessness in patients with Chronic Obstructive Pulmonary Disease (COPD)**

Dynamic hyperinflation (DH) is supposed to be the most important factor limiting exercise and contributing to dyspnea by restrictive constraints to volume expansion in patients with COPD [6]. Indirect evidence of the importance of DH has been provided by studies that have demonstrated that pharmacological treatment [7,8], and lung volume reduction sur‐ gery [9] explain in part the improvement in exercise performance and dyspnea by reducing DH in these patients. It has recently been found, however, that different patterns of chest wall kinematics may or may not be associated with different exercise performance in COPD patients [10,11]. There is little data available indicating that these patients may dynamically hyperinflate or deflate chest wall compartments during cycling while breathing air [10,12] or with oxygen supplementation [11]. As yet the contribution of reducing lung volume to dyspnea relief remains uncertain [11,13-15] in exercising COPD patients. It also remains to be determined whether changes in operational chest wall volumes substantially affect the response to endurance exercise rehabilitation programs. It should be remembered that (i) an increase in end-expiratory-volume of the chest wall constrains the potential for the tidal vol‐ ume to increase; thus exacerbating the sensation of dyspnea; (ii) on the other hand, shifting abdominal volumes towards a lower operational point might not be able to reduce restric‐ tive constraints on volume displacement if the rib cage dynamically hyperinflates. Argua‐ bly, rib cage hyperinflation would result in a higher volumetric load to the intercostal inspiratory muscles [16] and a higher sensory perception of dyspnea [17]; (iii) the possibility that abdominal deflation contributes *per se* to dyspnea should not be disregarded [16]. Evi‐ dence has indeed been provided that a decrease in abdominal volume resulting from in‐ creased abdominal muscle activity as soon as exercise starts even at minimal work rate [4] may contribute *per se* to increasing the work of breathing [10] and breathlessness [16], to re‐ ducing venous return and cardiac output [18], and to decreasing exercise capacity [4] in pa‐ tients with COPD.

face [2]. The number and the position of used markers depends on the thoraco-abdominal model chosen. As proposed by Ward & Macklem [5] we use a three compartment chest wall model: the upper rib cage, lower rib cage and abdomen. Due to the fact that the upper por‐ tion of the rib cage is exposed to pleural pressure whereas the lower portion is affected by abdominal pressure, a model able to dynamically return changes in volume of each com‐ partment and, as a sum, of the entire chest wall has been developed [2]. The number of used

To measure the volume of chest wall compartments from surface markers we define: 1) the boundaries of the upper rib cage as extending from the clavicles to a line extending trans‐ versely around the thorax at the level of the xiphoid process (corresponding to the top of the area of the apposition of the diaphragm to the rib cage at end expiratory lung volume in sit‐ ting posture, confirmed by percussion); 2) the boundaries of lower rib cage as extending from this line to the costal margin anteriorly down from the xiphosternum, and to the level of the lowest point of the lower costal margin posteriorly; and 3) the boundaries of abdomen as extending caudally from the lower rib cage to the level of the anterior superior iliac crest. The markers are placed circumferentially in seven horizontal rows between the clavicles and the anterior superior iliac spine. Along the horizontal rows the markers are arranged anteri‐ orly and posteriorly in five vertical rows, and there is an additional bilateral row in the mid‐ axillary line. The anatomical landmarks for the horizontal rows are: 1) the clavicular line; 2) the manubrio-sternal joint; 3) the nipples (~ 5 ribs); 4) the xiphoid process; 5) the lower costal margin (10th rib in the midaxillary line); 6) umbilicus; 7) anterior superior iliac spine. The landmarks for the vertical rows are: 1) the midlines; 2) both anterior and posterior axillary lines; 3) the midpoint of the interval between the midline and the anterior axillary line, and the midpoint of the interval between the midline and the posterior axillary line; 4) the mid‐ axillary lines. An extra marker is added bilaterally at the midpoint between the xiphoid and the most lateral portion of the 10th rib to provide better detail of the costal margin; two markers are added in the region overlying the lung-apposed rib cage and in the correspond‐ ing posterior position. This marker configuration has previously been validated in normal subjects, along with a sensitivity analysis which assesses accuracy in estimating change in lung volume as a function of marker number and position [2]. When compared with the gold standard (water sealed spirometer) the accuracy in the volume change measurements of the 89 markers model is very high, showing volume differences smaller than 5% [2].

**2. Exercise limitation and breathlessness in patients with Chronic**

Dynamic hyperinflation (DH) is supposed to be the most important factor limiting exercise and contributing to dyspnea by restrictive constraints to volume expansion in patients with COPD [6]. Indirect evidence of the importance of DH has been provided by studies that have demonstrated that pharmacological treatment [7,8], and lung volume reduction sur‐

**Obstructive Pulmonary Disease (COPD)**

markers is 89, 42 placed on the front and 47 on the back of the subject.

472 Optoelectronics - Advanced Materials and Devices

Dyspneic patients with COPD who are markedly hyperinflated are considered especially likely to display abnormalities in rib cage motion such as a paradoxical (inward) inspiratory movement of their lower rib cage [19-22]. Studies in healthy humans have led to the hypoth‐ esis that the primary mechanism of abnormal chest wall motion in patients with COPD is probably an abnormal alteration of forces applied to chest wall compartments [3,23] and an increase in airway resistance [24]. Chihara *et al*. [23] have speculated that when rib cage dis‐ tortion is present, greater degree of recruitment of inspiratory rib cage muscles and greater predisposition to dyspnea for a given load and strength do occur. On the other hand, the role of hyperinflation on abnormal chest movement is questionable in healthy subjects [24]. Accordingly, it has recently been shown that paradoxical movement of the lower rib cage cannot be fully explained by static lung hyperinflation [19] or dynamic rib cage hyperinfla‐ tion [25] in patients with COPD. By contrast, Aliverti *et al*. [26] have shown that lower rib cage paradox results in an early onset of dynamic hyperinflation as a likely explanation for the increased exertional breathlessness in these patients. Nonetheless, the link between changes in operational lung volumes and exertional breathlessness has not been definitely established in normoxic COPD patients [13,14,27].

Now the questions arise: does exercise reconditioning reduce rib cage distortion, and, if any, does rib cage distortion contribute to restoring exercise capacity and to relieving breathless‐ ness Does exercise reconditioning relieve dyspnea regardless of whether compartmental chest wall volumes are shifted toward upper or lower operational points?
