Pre-clinical models show that exercise training inhibits tumour growth, progression and metastasis. Epidemiological data suggests further links between physical activity volume (a product of intensity and duration) and reduced cancer incidence/improved survival. There are likely several mechanisms through which exercise reduces the risk of cancer development and progression. One potential mechanism that has been shown to reduce tumour growth in pre-clinical models involves an exercise-mediated immune cascade that influences the body’s innate natural killer (NK) cell response. A higher degree of NK cell infiltration of solid tumours is associated with increased survival rates in cancer patients, and reduced risk of disease progression. During acute exercise, catecholamines drive β-adrenergic mobilisation of NK cells from the marginal pools and myokine release from contracting skeletal muscle in turn redistributes NK cells to the periphery. NK cells with higher cytotoxic function are preferentially recruited via this mechanism, suppressing the growth of cancerous cells. Acute exercise is also postulated to promote normal angiogenesis; this mitigates the effects of tortuous, inefficient vasculature typical of solid tumours by reducing local hypoxia, and facilitating better tumour infiltration and local function of NK and other immune cells. However, the optimal dose (e.g. intensity) of exercise to maximise benefits via this particular biological mechanism is not clear; understanding the mechanisms, which can help to explain the relationships between physical activity and cancer prognosis, will help to inform specific prescription guidelines for exercise as adjunct therapy for cancer. This brief presentation provides evidence to support that exercise completed at higher intensities will elicit the strongest anti-cancer immune response.