Exercise training as therapy for heart failure: current status and future directions

Jerome L Fleg, Lawton S Cooper, Barry A Borlaug, Mark J Haykowsky, William E Kraus, Benjamin D Levine, Marc A Pfeffer, Ileana L Piña, David C Poole, Gordon R Reeves, David J Whellan, Dalane W Kitzman, National Heart, Lung, and Blood Institute Working Group, Jerome L Fleg, Lawton S Cooper, Barry A Borlaug, Mark J Haykowsky, William E Kraus, Benjamin D Levine, Marc A Pfeffer, Ileana L Piña, David C Poole, Gordon R Reeves, David J Whellan, Dalane W Kitzman, National Heart, Lung, and Blood Institute Working Group

No abstract available

Keywords: heart failure; therapy.

Figures

Figure 1

The figure presents a model of how left ventricular systolic dysfunction, induced by a myocardial insult with decreased CO, can lead to impaired exercise tolerance and how exercise training may reverse such changes. Pathophysiologic responses at each step are represented in large type and the corresponding mechanisms are represented in small type in brackets. Potential points at which exercise training has been shown to induce a physiologic response that might block progression to symptomatic exercise intolerance are shown with flat headed arrows. Adapted from reference 27.

Figure 2

Schematic illustrating how the muscle perfusive (curved lines, Fick principle, VO2 = Qm x (arterial-venous O2 content) and diffusive O2 (straight lines from origin, Fick’s law, VO2 = DO2m x (PmicrovascularO2 – PintracellularO2) conductances conflate to yield VO2 during exercise (e.g., cycling). In chronic HF (dashed lines) VO2 is reduced by both impaired perfusive and diffusive O2 conductances and microvascular O2 partial pressures may either be the same or lower than found in health notwithstanding the presence of marked diffusional derangements (i.e., lower DO2m). Note that correction of DO2m deficits by improving capillary hemodynamics has the potential to increase VO2 even in the absence of improved muscle perfusion. From reference 37.

Figure 3

Possible mechanisms of exercise intolerance in HF as related to gender. Areas that have been associated with women are in bold. The modifiers of the responses are in red in italics. Thus, age may have a more profound effect on the exercise intolerance of women with HF as well as the level of fitness prior to disease onset. Estrogen as a modifier has been poorly studied in HF.

Figure 4

The figure presents a theoretical hierarchy of possible RCT outcomes and their relationship to the sample size required.