address the long-standing dichotomy of cycle ergometer tests in respirology [2] versus treadmill tests in cardiology [61]. This separation has negatively impacted the assessment of exercise normalcy and quantification of impairment in patients who frequently present with lung and heart diseases. Prospective multicentre studies should address the role of CPET as a screening test to identify the syndromes of exercise limitation in contemporary clinical populations with multiple coexisting diseases. Improving our understanding of the confounding effects of obesity on the patterns of exercise limitation is paramount: linear time trend forecasts suggest that by 2030, 51% of the North-American population will be obese [78]. With this in mind, large investigations are specifically warranted to test the incremental role (to standard metabolic gas exchange variables) of noninvasive measurements of lung mechanics and symptoms in the clarification of the causes of exertional dyspnoea. In view of the current limitations of CPET in unequivocally differentiating central cardiovascular from muscular-peripheral causes of exercise intolerance (further discussed by AGOSTONI and CATTADORI [49] elsewhere in this Monograph) and indicating poor ventilation/perfusion matching (further discussed by WEATHERALD and LAVENEZIANA [39] elsewhere in this Monograph), noninvasive estimates of stroke volume and PaCO2 (capillary or transcutaneous CO2 tension (PCO2)) might substantially improve “diagnostic” yield [109–111]. Mild, submaximal protocols might improve our ability to investigate the mechanisms of exercise intolerance in the growing population of severely disabled, elderly patients [112]. It is also crucial to address the large gaps in the knowledge relative to the independent contribution of common cardiovascular comorbidities to exertional dyspnoea in COPD and ILD. This might prove particularly helpful in conditions that are potentially associated with a high ventilatory drive secondary to increased pulmonary venous pressures such as (moderate-to-severe) diastolic dysfunction [81], left atrial enlargement [83, 84] and atrial fibrillation [82]. Last but not least, CPET-based criteria to differentiate chaotic/erratic breathing patterns from data noise would be of a great value in a specific scenario in which the test has a clear potential of impacting on clinical decision making [10] (abnormals patterns of response are discussed further later in this Monograph [14]. CPET for risk assessment: the key unmet clinical needs Table 1 presents a list of research areas that should be considered in the future investigation of risk assessment. Exercise responses may be more helpful in adding prognostic information to resting data in patients with more preserved lung function. There is therefore a need to prospectively test the prognostic value of CPET variables in patients with only mild or early chronic respiratory disease. Few data are currently available regarding the use of CPET for risk stratification in diseases other than COPD. Regardless of the specific disease, CPET variables are more likely to prove useful if added to multiparametric models of risk prediction, such as those developed for patients with heart failure with reduced ejection fraction [58, 59]. In the pre-operative assessment of lung resection surgery, more research is needed to clarify the precise role of CPET in relation to imaging (e.g. scintigraphy) and field or walking tests (SINGH and HARVEY-DUNSTAN [113] consider walking in the assessment of COPD patients later in this Monograph). Variables deemed to reflect exercise (in)tolerance, such as peak V′O2, are likely to be more informative if analysed in conjunction with potentially limiting https://doi.org/10.1183/2312508X.10015318 xix