Effects of exercise training on inflammatory markers in patients with heart failure

Cardiologists now recognize that the cardio-centric model of heart failure does not sufficiently explain the entire traits particular to chronic heart failure. Evidence accumulates, that many features of the syndrome can be explained by the known biological effects of inflammatory mediators. Indeed, when expressed in experimental models at concentrations commonly observed in heart failure, inflammatory mediators such as tumor necrosis factor-alpha, interleukin-6, and nitric oxide can produce effects that mimic features of heart failure, including (but not limited to) progressive left-ventricular dysfunction, pulmonary edema, left-ventricular remodeling, and cardiomyopathy. As we witness anti-cytokine therapies and other strategies to avoid an increase in cytokines we have been shown that acute bouts of exercise are associated with an increase in pro-inflammatory cytokines and markers of oxidative stress. As a consequence we have been warned exercise may thus even further contribute to the deterioration of heart failure. However, there are several randomized trials which unanimously document that chronic--as opposed to acute bouts of--exercise does not only lead to a reduction of cytokines and oxidative stress, but that patients dramatically benefit by the increase in maximal oxygen consumption, exercise capacity, quality of life, reduction in hospitalization, morbidity, and mortality. Over the past two decades it has become evident that cytokine research has come to stay and that we will continue to see anti-cytokine treatment strategies for our patients. It is the aim of this review to shed some more light on the most commonly investigated and most relevant cytokines.