Exercise therapy in the management of dyspnea in patients with cancer

Abstract

Purpose of review: Dyspnea is a frequent, debilitating, and understudied symptom in cancer associated with poor prognosis and reduced health-related quality of life. The purpose of this study is to review the incidence, pathophysiology, and mechanisms of dyspnea in patients diagnosed with cancer. We also discuss the existing evidence supporting the efficacy of exercise therapy to complement traditional approaches to reduce the impact of this devastating symptom in persons with cancer.

Recent findings: In other clinical populations presenting with dyspnea, such as chronic obstructive pulmonary disease, exercise therapy is demonstrated to be an efficacious strategy. In contrast, relatively few studies to date have investigated the efficacy of exercise training as a therapeutic strategy to mitigate dyspnea in patients with cancer.

Summary: Although much more work is required, exercise therapy is a promising adjunct strategy to systematically reduce dyspnea in the oncology setting that may also provide additive efficacy when prescribed in combination with other adjunct therapies including pharmacologic interventions.

FIGURE 1

Potential mechanisms of dyspnea in patients with cancer. The sensation of dyspnea involves a variety of sensations that include sensory and affective dimension that are generated by different brain areas (1). Disruptions in the function of the pulmonary system leads to increased afferent feedback from a variety of receptors that sense stretch, tension, irritation, and pressure. This is associated with a number of primary and secondary aspects of malignancy (2). There is increased efferent central motor drive in response to the afferent information being received from the respiratory, neuromuscular and cardiovascular systems (3). It is likely the mismatch between afferent feedback and the resulting response by the respiratory system that is a primary cause of dyspnea. Afferent feedback from the cardiovascular system may also occur when there is an increase in filling pressure (i.e., pulmonary artery hypertension, congestive heart failure) or the patient becomes anemic or hypoxemic that may occur due to cancer treatment or comorbidities (4). Muscle wasting and deconditioning can lead to acidosis/metabolic biproduct accumulation and increased muscular strain that increase afferent feedback from type III and IV afferents (5).