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Abstract
Exercise tolerance reflects the integrative capacity of components in the oxygen cascade
to supply adequate oxygen for ATP resynthesis. Conventional cancer therapies can simultaneously
affect one or more components of this cascade and reduce the body's ability to deliver
or utilise oxygen and substrate, leading to exercise intolerance. We propose that
molecularly-targeted therapy is associated with a further, more subtle, negative effect
on the components that regulate exercise limitation. We outline possible causes of
exercise intolerance in patients with cancer and the role of exercise therapy to mitigate
or prevent dysfunction. We also discuss possible implications for exercise-regulated
gene expression for cancer biology and treatment efficacy. A better understanding
of these issues might lead to more effective integration of exercise therapy to optimise
the treatment and management of patients with cancer.