Jones Lee W, Eves Neil D, Haykowsky Mark, Freedland Stephen J, Mackey John R
Duke University Medical Center, Durham, North Carolina 27710, USA.
Lancet Oncol. 2009 Jun;10(6):598-605. doi: 10.1016/S1470-2045(09)70031-2.
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.
运动耐量反映了氧级联中各组分的综合能力，以供应足够的氧气用于三磷酸腺苷（ATP）再合成。传统的癌症治疗可同时影响该级联中的一个或多个组分，并降低身体输送或利用氧气及底物的能力，从而导致运动不耐受。我们提出，分子靶向治疗对调节运动受限的组分具有进一步的、更微妙的负面影响。我们概述了癌症患者运动不耐受的可能原因以及运动疗法在减轻或预防功能障碍方面的作用。我们还讨论了运动调节基因表达对癌症生物学和治疗效果的可能影响。更好地理解这些问题可能会导致更有效地整合运动疗法，以优化癌症患者的治疗和管理。
