Human exercise capacity, as measured by cardiorespiratory fitness or maximal oxygen uptake, is a robust index of cardiovascular events and all-cause mortality in both healthy and diseased individuals. Exercise capacity is highly responsive to endurance training, but the magnitude of exercise capacity gains in response to a given dose of endurance training is highly heterogeneous. A potential decisive factor for the inter-individual differences in exercise capacity trainability is the insertion/deletion (I/D) polymorphism of the gene that encodes the angiotensin-converting enzyme (ACE). The notion that the ACE I/D polymorphism impacts the ability to adapt to exercise training by determining basal tissue and plasma ACE activity was first proposed more than 20 years ago. Surprisingly, no randomized controlled trials designed to determine the effect of manipulating ACE activity pharmacologically concurrent with systematic supervised exercise training in a healthy population have been conducted in the interim. The conduction of such a trial would elucidate the importance of ACE activity for exercise trainability and improve our basic understanding of the nature of the individual response to exercise training. In study 1 we conducted just such a randomised double-blinded placebo-controlled trial investigating the impact of pharmacological ACE inhibition on numerous training-sensitive physiological adaptations in response to 8 weeks of interval-based endurance exercise training in healthy individuals. Paper I revealed that the applied exercise training increased lean body mass and left atrial dimension, and that these effects were abolished by simultaneous ACE inhibitor treatment. In addition, total haemoglobin mass was decreased by ACE inhibition, but the improvement in exercise capacity was unaffected by ACE inhibitor treatment. In paper II, we observed that the training-induced changes in the obtained markers of skeletal muscle mitochondrial oxidative capacity, glycolytic profile and angiogenesis were largely independent of ACE inhibitor treatment. Finally, through determination of the participants’ ACE genotype we were able to assess the impact of the ACE genotype on the adaptation to exercise training. Nonetheless, we observed no effect of the ACE genotype per se on exercise trainability, and our findings displayed no confounding effect of the ACE genotype on the interaction between ACE inhibition and the ability to respond to exercise training. In study 2, we conducted a randomized controlled trial investigating the effect of 12 weeks of lowvolume high-intensity interval-based endurance training on exercise capacity in elderly patients with coronary artery disease, and whether the magnitude of exercise capacity improvements was affected by the ACE genotype. Paper III confirmed that the prescribed exercise training effectively improved exercise capacity, while paper IV revealed that the improvements in exercise capacity were not governed by the patients’ ACE genotype. In conclusion, the results from the present thesis demonstrate that pharmacological ACE inhibition may counteract augmented lean mass and left atrial enlargement following 8 weeks of exercise training in healthy individuals. In addition, ACE inhibitor treatment appears to compromise total haemoglobin mass, but despite the close link between the oxygen-carrying capacity of the blood and exercise capacity, the improvements in exercise capacity were independent of ACE inhibition. Thus, future studies should investigate whether periodization of ACE inhibitor treatment in combination with exercise training can enhance the health-beneficial outcome of exercise training in relevant patients. Finally, our results regarding the ACE genotype do not suggest a clinically relevant role for the ACE genotype in exercise capacity trainability in healthy individuals or patients with coronary artery disease.