Pathological vs. physiological cardiac hypertrophy.

Abstract

‘Pathological’ cardiac hypertrophy is a condition that is characterized by the thickening of the heart muscle, a decrease in the size of the chambers of the heart, and a reduced capacity of the heart to pump blood to the tissues and organs around the body. Two common causes of pathological cardiac hypertrophy are high blood pressure (hypertension) and heart valve stenosis, and this type of hypertrophy is considered to be a major independent risk factor for morbidity and mortality (Meijs et al. 2010). On the other hand, ‘physiological’ cardiac hypertrophy can be provoked by exercise training and can lead to increase cardiac size that is characterized by normal cardiac morphology with a normal and/or enhanced cardiac function (Ooi et al. 2014). In addition, exercise training has been shown to be the only practical and sustainable countermeasure capable of providing cardioprotection by improving myocardial tolerance to ischaemia–reperfusion injury (e.g. heart attack) (Powers et al. 2014). Although both types of cardiac hypertrophy are initiated by an overload to the heart, the distinct differences between the two can be attributed to the type of overloading stimuli. However, data also implicate duration and intensity of the cardiac overload in determining whether the cardiac hypertrophy that develops is ‘pathological’ or ‘physiological’. Indeed, even the benefits of exercise can be dose dependent. For example, very high intensity/duration exercise can result in unfavourable cardiac structural and electrical cardiac remodelling. In this issue of The Journal of Physiology, a group of researchers form Portugal performed a study to address the question of whether submitting the heart to intermittent and tolerable amounts of stress, independent of its nature, could induce a cardiac phenotype that would fit within the ‘physiological’ spectrum (Moreira-Goncalves et al. 2015). To answer their question the authors compared three groups of animals: (1) Sedentary+Placebo, (2) Exercise, and (3) Sedentary+Dobutamine (simulated exercise: similar haemodynamic demand to the exercise group). Following an 8 week protocol, the authors collected data at rest and during cardiac overload induced by banding of the aorta. The exercise and simulated exercise groups had lower body weight, faster cardiac relaxation, cardiomyocyte hypertrophy, and improved mitochondrial complex IV and V activity. The latter finding is of particular importance because it can indicate an enhanced capacity to support cardiomyocyte energetic cost without compromising the ATP that is needed to maintain intracellular homeostasis. In summary, the authors’ results show that regardless of the nature of the controlled intermittent cardiac overload the heart responds favourably and undergoes adaptive hypertrophy. Importantly, the adaptive and ‘physiological’ hypertrophy in both the exercise and simulated exercise groups protected against an acute pressure overload insult. In conclusion, I am in full agreement with the authors’ statement that we need further research to fully elucidate why some cardiac overloading stimuli are beneficial while others are deleterious. None declared.