“…Based on the above information, the combination of physical training with b-blocker therapy appears promising for HRR improvement following MI. However, three specific aspects regarding the interaction between physical training and bblocker therapy in terms of HRR improvement need to be further investigated: (i) although b-blockers may facilitate the execution of ET by lowering cardiac work and reducing myocardial O 2 consumption, the adaptations that derive from ET, such as improved total time, O 2 pulse, HR max and VO 2max , appear to become attenuated with the chronic use of this medication (Sable et al, 1982;Wolfel et al, 1986), (ii) The acute effect of b-blocker therapy, compared to chronic use, significantly alters the behaviour of several physiological variables, including resting HR, HR max , Blood pressure (BP), VO 2peak and plasma lactate and potassium levels (Gullestad et al, 1996;Peres et al, 2015). Thus, the presence of b-blockers during HRR evaluation may lead to a result that does not reflect the chronic aspects of the disease, exercise training or long-term b-blocker therapy itself, (iii) Patients initially presenting with an HRR above 12 bpm may show different adaptations compared to patients with a more compromised HRR, because a more normal HRR would reflect intact autonomic function, which consequently may be less affected by ET or b-blocker therapy (Malfatto et al, 2000;Peres et al, 2015).…”