Cardiorespiratory fitness-normalized peak exercise systolic blood pressure decreases after cardiac rehabilitation

Background Exercise-based cardiac rehabilitation (CR) lowers resting systolic blood pressure (SBP) and increases peak exercise SBP and peak oxygen uptake (VO₂peak), a surrogate of cardiac output and cardiorespiratory fitness. Because exercise SBP is strongly determined by exercise capacity, higher peak SBP and its increase after CR may reflect physiological training adaptations rather than an adverse haemodynamic response. Indexing SBP to VO₂peak accounts for fitness and may better distinguish benign increases related to improved cardiac output from pathological exercise blood pressure responses. The effect of CR on peak SBP/VO₂peak has not previously been investigated. Purpose To assess the impact of outpatient CR on changes in exercise blood pressure response, particularly peak SBP/VO₂peak. Methods This analysis included adults who underwent outpatient phase II exercise-based CR between September 2016 and December 2025 and agreed to be included in the registry. The 12-week programme comprised three supervised exercise sessions per week and structured education on the underlying disease, risk factor management, secondary prevention, medication adherence, psychosocial support, lifestyle modification, and nutrition. All patients underwent ergometer-based cardiopulmonary exercise testing (CPET) at CR admission and discharge. Results A total of 2,560 adults (median age 63 years; 23% women) were included. Most patients were referred to CR after acute coronary syndromes (39% STEMI, 36% NSTEMI) and heart failure (19%). From CR admission to discharge, peak workload (0.26 W/kg; 95% CI, 0.25 to 0.28), METs (0.65; 95% CI, 0.60 to 0.70), and VO₂peak (2.33 ml·kg⁻¹·min⁻¹; 95% CI, 2.16 to 2.5) improved (all p<0.001). Resting and peak SBP at admission were 125 mmHg (IQR 111-139) and 180 mmHg (IQR 158-201). From CR admission to discharge, resting SBP rose slightly by 1.0 mmHg (95% CI, 0.5 to 2; p<0.001) and peak SBP increased by 8.5 mmHg (95% CI: 7 to 9.5; p<0.001). In contrast, peak SBP/VO₂peak decreased by −0.65 mmHg per ml·kg⁻¹·min⁻¹ (95% CI, −0.74 to −0.56; p<0.001), and this remained significant after adjustment for number of antihypertensive medication and intake of a beta-blocker at admission and discharge (p<0.001). The reduction in peak SBP/VO₂peak did not differ in patients with and without heart failure with reduced ejection fraction (p for interaction=0.86) but greater in those with than without hypertension at admission (p for interaction=0.043). Conclusions In a large real-world cohort undergoing outpatient phase II CR, cardiorespiratory fitness and peak SBP increased, whereas peak SBP/VO₂peak decreased. Thus, higher peak SBP after CR likely primarily reflects physiological increases in cardiac output rather than an adverse haemodynamic response. Therefore, peak SBP/VO₂peak should be considered when interpreting exercise blood pressure, and its relationship with cardiovascular outcomes should be evaluated prospectively.