UBC Theses and Dissertations
Measuring cardiorespiratory and muscular deconditioning in fatigued and non-fatigued breast cancer survivors Neil, Sarah Elizabeth
Fatigue is one of the most commonly reported side effects during treatment for breast cancer, and for some individuals can continue for an extended period following treatment completion. Cancer-related fatigue is multi-factorial in nature, and one hypothesized mechanism of both development and persistence of cancer-related fatigue following treatment is cardiorespiratory and muscular deconditioning. The purpose of this study is to compare lactate threshold, VO₂ peak and central vs. peripheral causes of muscular fatigue in breast cancer survivors with persistent cancer-related fatigue (FG) and the control group (CG), breast cancer survivors without persistent cancer-related fatigue following treatment for breast cancer. METHODS: During first testing visit, power output at lactate threshold, lactate threshold as a percentage of peak power output, and absolute and relative VO₂ peak were determined using a graded incremental maximal exercise test on a cycle ergometer. During the second testing visit central and peripheral muscle fatigue following a sustained contraction of the right quadriceps were assessed using the twitch interpolation technique and measurement of voluntary activation, control twitch, maximum voluntary contraction and endurance time. RESULTS: There were no significant differences in age, body weight, or time since completion of treatment between groups. There were no significant differences between groups in power output at lactate threshold (FG 60.7±17.0 vs. CG 73.3±22.2 W, p=0.14), lactate threshold as a percentage of peak power output (FG 46.8±8.6 vs. CG 55.0±14.7%, p=0.11), peak power output (FG132.12±38.2 vs. CG 140.6±5.9 W, p=0.66), absolute VO2 peak (FG 1.51±0.39 vs. CG 1.74±0.38 L/min, p=0.19), or relative VO2 peak (FG 22.4±4.9 vs. CG 23.6±7.1 ml/kg/min, p=0.62). Results did approach significance for power output at lactate threshold (p=0.10) and absolute VO₂ peak (p=0.08) when adjusted for age. Central fatigue was responsible for muscular fatigue in the iv control group, while muscular fatigue in the cancer-related fatigue group was more due to peripheral mechanisms. CONCLUSION: While no statistically significant differences were found between groups, results suggest that deconditioning may play a role in cancer-related fatigue. Future research into the use of exercise training as a tool to improve deconditioning and thereby reduce this proposed aspect of cancer-related fatigue is warranted.
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