Cardiorespiratory and neuromuscular deconditioning in fatigued and non-fatigued breast cancer survivors

Fatigue is one of the most commonly reported side effects during treatment for breast cancer and can persist following treatment completion. Cancer-related fatigue after treatment is multifactorial in nature, and one hypothesized mechanism is cardiorespiratory and neuromuscular deconditioning. The purpose of this study was to compare cardiorespiratory and neuromuscular function in breast cancer survivors who had completed treatment and met the specified criteria for cancer-related fatigue and a control group of breast cancer survivors without fatigue. Participants in the fatigue (n = 16) and control group (n = 11) performed a maximal exercise test on a cycle ergometer for determination of peak power, power at lactate threshold, and VO2 peak. Neuromuscular fatigue was induced with a sustained submaximal contraction of the right quadriceps. Central fatigue (failure of voluntary activation) was evaluated using twitch interpolation, and peripheral fatigue was measured with an electrically evoked twitch. Power at lactate threshold was lower in the fatigue group (p = 0.05). There were no differences between groups for power at lactate threshold as percentage of peak power (p = 0.10) or absolute or relative VO2 peak (p = 0.08 and 0.33, respectively). When adjusted for age, the fatigue group had a lower power at lactate threshold (p = 0.02) and absolute VO2 peak (p = 0.03). There were no differences between groups in change in any neuromuscular parameters after the muscle-fatiguing protocol. Findings support the hypothesis that cardiorespiratory deconditioning may play a role in the development and persistence of cancer-related fatigue following treatment. Future research into the use of exercise training to reduce cardiorespiratory deconditioning as a treatment for cancer-related fatigue is warranted to confirm these preliminary findings.