Chapter 01 - Safeguarding Exercise Capacity Throughout and After Cancer Treatment
Cardiorespiratory fitness is determined by the transport of oxygen from the environment to skeletal muscles via several components of the pulmonary and cardiovascular systems including blood and blood vessels and by the capacity of skeletal muscle to utilise this oxygen. Cancer and its treatment may affect cardiorespiratory fitness via several mechanisms. For example, pulmonary mechanics and gas exchange may be disrupted by a tumour in the lungs, and anaemia may reduce the oxygen-carrying capacity. Systemic therapy may result in cardiac limitations. For example, anthracyclines could lead to atrial and ventricular arrhythmias, pericarditis, myocarditis, a reduced ejection fraction, and cardiomyopathy. Alkylating agents such as cisplatin may result in myocardial ischaemia/ infarction, hypertension, heart failure, and arrhythmias. Chemotherapeutic agents may also reduce the muscle capacity for oxygen utilisation. Furthermore, radiotherapy in the chest area might cause cardiac or pulmonary limitations, such as angina, dyspnoea, heart failure, pericardial constriction, atherosclerosis, and mediastinal fibrosis, and may cause localised damage to muscle agents. In addition, androgen-suppression therapy results in considerable changes to the quantity and quality of skeletal muscle. Finally, low cardiorespiratory fitness levels may also result from reduced physical activity after cancer diagnosis, leading to a reduction in cardiac output, oxidative capacity, and muscle cross-sectional area.
The best direct measurement of cardiorespiratory fitness is the peak oxygen uptake (peakVO2). A review by Steins Bisschop and colleagues showed that most studies of cancer survivors reported reduced peakVO2 levels (between 16 and 25 mL/min/kg). Lower peakVO2 values in cancer survivors compared to the healthy population indicate decreased cardiorespiratory fitness levels and, consequently, are an indication for physical exercise training. Moreover, screening for cardiac, pulmonary, or musculoskeletal limitations before the start of an exercise programme is recommended. Low peakVO2 has also been shown to be related to an increased risk of premature death.
PeakVO2 can be measured during a cardiopulmonary exercise test (CPET) with continuous gas exchange analysis during incremental exercise, which is generally conducted on a cycle ergometer or treadmill and is considered feasible and safe. It can be used to monitor individual cardiorespiratory fitness and allows exercise programmes to be tailored to individual fitness levels by using either a percentage of peakVO2, a percentage of the peak heart rate, or the heart rate at the anaerobic threshold to guide exercise intensity.
Exercise during or after cytotoxic cancer treatment was found to be associated with significant improvements in peakVO2 compared to a nonexercise control group. Larger improvements were found in patients who participated in an exercise programme after completion of cancer treatment. This suggests that exercise during adjuvant therapy is of primary importance to maintain cardiorespiratory fitness.