In pulmonary hypertension (PH), pulmonary vascular remodeling and excessive vasoconstriction leads to an increase in pulmonary vascular resistance, ultimately leading to a deleterious rise in pulmonary pressures. In heart failure (HF) patients with combined pre- and post-capillary PH, functional outcomes of gas exchange are correlated with this rise in pulmonary pressures. At rest, the transpulmonary gradient (i.e., pulmonary arterial-venous pressure gradient) is negatively correlated with pulmonary arterial (PaO2) and venous (PvO2) partial pressures of oxygen, as well as arterial (SaO2) and venous (SvO2) oxygen saturation [1]. This negative impact of increasing pulmonary pressures on gas exchange persists during submaximal exercise, where the diastolic pressure difference is positively correlated to dead space ventilation (VD/VT) and negatively correlated with end-tidal partial pressure of carbon dioxide (PETCO2) [2]. Older, otherwise healthy adults also experience remodeling of the pulmonary vasculature, leading to a subsequent increase in pulmonary pressures, particularly during exercise [3, 4]. Recent work suggests that an increase in basal pulmonary smooth muscle tone may also be present in the healthy older adult [5]. In concert, these age-dependent alterations reveal several similarities between the healthy older adult and the PH patient. Nevertheless, while individuals with diagnosed PH are negatively impacted by a rise in pulmonary pressures, this may not be the case in older individuals, for whom a modest increase in pulmonary pressures is often asymptomatic. Previous work aimed at understanding the role of pulmonary pressures during exercise in healthy older adults (>65 years) demonstrated that reducing the age-related increase in pulmonary pressures via a pharmacological intervention actually worsened lung diffusing capacity (DLCO), a critical functional gas exchange outcome [6]. In this study, 9 younger and 9 older healthy individuals completed an incremental cycling exercise protocol before and after 100 mg sildenafil. As expected, prior to sildenafil administration older individuals demonstrated greater pulmonary pressures and lower DLCO for a given cardiac output in comparison to their younger counterparts. Interestingly, however, the reduction in pulmonary pressures elicited by pharmacological vasodilation actually reduced DLCO during exercise, and this reduction became significantly greater as exercise intensity increased. Specifically, on average among all subjects (younger and older combined), pulmonary artery pressure was reduced by 5 mmHg, venous pressure by 2 mmHg, and thus the transpulmonary gradient fell by 3 mmHg following sildenafil administration (all p < 0.001). This reduction in the driving pressure through the pulmonary vasculature led to a fall in DLCO of 2 ml/min/mmHg at a cardiac output of 10 L/min and a fall of 4 ml/min/mmHg at a cardiac output of 15 L/min (p < 0.001). In other words, the loss in forward driving pressure elicited by the reduction in the transpulmonary gradient hindered effective ventilation and perfusion matching, causing a reduction in gas diffusion within the lungs. Therefore, these data may suggest that an increase in pulmonary pressure is necessary and advantageous in the older adult, particularly during exercise. Specifically, a rise in pulmonary pressures may occur to overcome the age-dependent increase in pulmonary vascular resistance, and thus act to maintain adequate perfusion of the pulmonary vasculature in the healthy older adult. In summary, pulmonary pressures are increased not only in the PH patient, but also in the healthy older adult during exercise. However, while the PH patient experiences detrimental impacts on various markers of cardiopulmonary function, there is evidence to suggest that the healthy older adult may require an increase in pulmonary pressures – albeit to a lesser extent – to maintain cardiopulmonary function during exercise. Thus, in terms of pulmonary gas exchange, pulmonary hypertension should be thought of as a continuum, where mild pulmonary hypertension can be functionally advantageous.