Effect of exercise training on ventilatory efficiency in patients with heart disease: a review

Abstract

The analysis of ventilatory efficiency in cardiopulmonary exercise testing has proven useful for assessing the presence and severity of cardiorespiratory diseases. During exercise, efficient pulmonary gas exchange is characterized by uniform matching of lung ventilation with perfusion. By contrast, mismatching is marked by inefficient pulmonary gas exchange, requiring increased ventilation for a given CO2 production. The etiology of increased and inefficient ventilatory response to exercise in heart disease is multifactorial, involving both peripheral and central mechanisms. Exercise training has been recommended as non-pharmacological treatment for patients with different chronic cardiopulmonary diseases. In this respect, previous studies have reported improvements in ventilatory efficiency after aerobic exercise training in patients with heart disease. Against this background, the primary objective of the present review was to discuss the pathophysiological mechanisms involved in abnormal ventilatory response to exercise, with an emphasis on both patients with heart failure syndrome and coronary artery disease. Secondly, special focus was dedicated to the role of aerobic exercise training in improving indices of ventilatory efficiency among these patients, as well as to the underlying mechanisms involved.

Figure 1.. End-tidal CO₂ pressure (P_ETCO₂) response during incremental exercise test in a healthy subject. VAT: ventilatory anaerobic threshold; RCP: respiratory compensation point.

Figure 2.. End-tidal CO₂ pressure (P_ETCO₂) response during incremental exercise test in 4 patients with chronic heart failure of progressive severity. Panel A, A 69-year-old male patient with dilated cardiomyopathy (left ejection fraction: 60%; peak oxygen consumption (VO₂): 23.7 mL·kg^-1·min^-1; VE/VCO₂ slope (rest-peak): 33.0). P_ETCO₂ at rest was 29.0 mmHg and change in P_ETCO₂ from rest to the highest value attained during exercise (ΔP_ETCO₂ rest-exercise) was 6.3 mmHg. Panel B, A 58-year-old male patient with ischemic heart failure (left ejection fraction: 42%; peak VO₂: 19.0 mL·kg^-1·min^-1; VE/VCO₂ slope (rest-peak): 40.5). P_ETCO₂ at rest was 25.1 mmHg and ΔP_ETCO₂ rest-exercise was 5.8 mmHg. Panel C, A 60-year-old female patient with ischemic heart failure (left ejection fraction: 38%; peak VO₂: 13.1 mL·kg^-1·min^-1; VE/VCO₂ slope (rest-peak): 47.1). P_ETCO₂ at rest was 23.0 mmHg and ΔP_ETCO₂ rest-exercise was 5.0 mmHg. Panel D, A 79-year-old female patient with Chagas cardiomyopathy (left ejection fraction: 29%; peak VO₂: 10.4 mL·kg^-1·min^-1; VE/VCO₂ slope (rest-peak): 63.8). P_ETCO₂ at rest was 24.9 mmHg and ΔP_ETCO₂ rest-exercise failed to increase.

Figure 3.. Four progressively worse ventilatory classes. P_ETCO₂: end-tidal CO₂ pressure; VE/VCO₂: ventilation to carbon dioxide production relationship. Adapted from reference (32).

Figure 4.. Potential mechanisms suggested for reduced ventilatory efficiency (increased ventilation to carbon dioxide production relationship (VE/VCO₂) in cardiac disease.

Figure 5.. Effects of continuous exercise (CET) and interval exercise training (IET) on indices of ventilatory efficiency in coronary artery disease patients. Panel A, Ventilation to carbon dioxide production relationship (VE/VCO₂) at ventilatory anaerobic threshold (VAT); Panel B, End-tidal CO₂ pressure (P_ETCO₂) at VAT. Pre: pre-intervention; Post: post-intervention. *P<0.05 vs pre-intervention. Adapted from reference (6).

Figure 6.. Absolute changes in ventilatory efficiency among coronary artery disease patients after aerobic exercise training program. Group 1 (n=34, peak VO₂ <17.5 mL·kg^-1·min^-1; lowest VE/VCO₂ ratio 33.5); group 2 (n=67, peak VO₂ >17.5 and <24.5 mL·kg^-1·min^-1; lowest VE/VCO₂ ratio 29.7) and group 3 (n=22, peak VO₂ >24.5 mL·kg^-1·min^-1; lowest VE/VCO₂ ratio 29.0). Note that group 1 showed a greater decrease in the lowest VE/VCO₂ ratio compared to the other two groups. VE/VCO₂: ventilation to carbon dioxide production relationship; VO₂: oxygen consumption. *P<0.05 vs group 1 (one-way ANOVA). Adapted from reference (7).

Figure 7.. Effect of a 12-week aerobic exercise training program in an 82-year-old female patient with coronary artery disease. Panel A, peak oxygen consumption (VO₂); panel B, VE/VO₂, ventilatory equivalent for oxygen; panel C, ventilation to carbon dioxide production relationship (VE-VCO₂) slope (rest-peak); panel D, dead space to tidal volume ratio (VD/VT). Note that after aerobic exercise training the patient showed improvement in both aerobic fitness and ventilatory efficiency (panels A and C, respectively). The patient demonstrated a marked shift to the right of the VAT suggesting improvement in aerobic efficiency (panel B). In addition, the patient demonstrated a sharper reduction in VD/VT showing improvement in gas exchange efficiency (panel D). pre: pre-intervention; post: post-intervention; VAT: ventilatory anaerobic threshold; VD/VT: estimate physiological dead space to tidal volume ratio.