The mechanisms responsible for exercise intolerance in early-stage breast cancer: What role does chemotherapy play?

In this narrative review of the literature, we discuss the influence of chemotherapy treatment on peak aerobic power (VO2peak) for women with breast cancer and the mechanisms for exercise intolerance. In specific, we examine the central, peripheral, and oxygen transport mechanisms responsible for exercise intolerance in women living with breast cancer. Our findings indicate that reduced ventricular contractility, reduced left ventricular (LV) compliance, and increased afterload are (in part) responsible for exercise intolerance secondary to chemotherapy treatment. It appears that changes in central haemodynamics and morphology often occur preceding clinical diagnosis of cardiotoxicity (LV ejection fraction <55%), which explain the attenuated exercise tolerance for this population. Patients with breast cancer are unable to make use of the Frank–Starling mechanism to increase stroke volume in response to an increase in end-diastolic volume. They may be able to increase preload during exercise conditions; however, reduced LV filling mechanics (in part due to an increase in pericardial restraint) and decreased contractile reserve may ultimately contribute to a reduced exercise tolerance for women with breast cancer. Recent evidence indicates that peripheral maladaptations and alterations in haemoglobin concentration are additional mechanisms that may limit VO2peak and exercise tolerance in patients with breast cancer.