'Physiological hypertrophy of the heart' is a misnomer

*Corresponding Author:

Dr Karel Rakusan
Department of Cellular and Molecular Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario K1H 8M5.
E-mail: krakusan@uottawa.ca

This open-access article is distributed under the terms of the Creative Commons Attribution Non-Commercial License (CC BY-NC) (http://creativecommons.org/licenses/by-nc/4.0/), which permits reuse, distribution and reproduction of the article, provided that the original work is properly cited and the reuse is restricted to noncommercial purposes. For commercial reuse, contact support@pulsus.com

The term ‘hypertrophy’ means an abnormal growth (eg, cardiac hypertrophy is understood as an abnormal growth of cardiac mass due to an increase in the size of myocytes). A second meaning of the term ‘physiological’ is, according to the dictionary, normal. Taking the above interpretations into consideration, we arrive at an amusing semantic incompatibility: cardiac physiological hypertrophy would mean ‘normal abnormal growth of the heart’. Authors who coined this term most likely intended to refer to cardiac hypertrophy achieved by physiological stimuli.

The next logical question is whether there a specific subtype of cardiac hypertrophies mislabelled as ‘physiological’ hypertrophies. For example, in a recent authoritative review, Tomanek [1] divides hypertrophies into the following groups: hypertrophies due to: pressure overload; volume overload; hyperthyroidism; and cardiomyopathies. However, the term ‘physiological hypertrophy’ is avoided.

Most publications using the term ‘physiological hypertrophy’ concern changes in the heart after chronic physical exercise. Occasionally, it is also used to describe cardiac changes during pregnancy or in hyperthyroidism.

Several functional, morphological and/or biochemical differences between ‘physiological hypertrophy’ and the remaining types of ‘pathological’ cardiomegalies are reported. All of these changes are usually considered to be reversible. Generally, the distinctions are presented as differences between a ‘good’ hypertrophy and a ‘bad’ hypertrophy [2,3]. However, the line of distinction between these two types of hypertrophy is fuzzy. The so-called ‘bad pathological’ hypertrophy can be adaptive if the primary cause is reversed before the development of intrinsic myocardial disease, while ‘physiological’ hypertrophy can be maladaptive if it is quantitatively excessive and sustained [4]. For instance, Pelliccia et al [5] described a residual cardiac hypertrophy in >20% elite athletes after a long-term deconditioning period.

The degree to which an increase in cardiac mass induced by exercise is usually modest. An exception is the sizeable increase in cardiac mass due to an enhanced physical activity that is genetically coded in so-called ‘active’ animals. For example, a sizeable increase in cardiac mass was found in wild (ie, sewage) rats when compared with laboratory rats [6], as well as a significantly higher cardiac mass in hares compared with that in rabbits [7]. A clinical example of genetically coded cardiomegalies would be familiar hypertrophic cardiomyopathy mutations [8].

In conclusion, the term ‘physiological growth’ is acceptable in situations when there is a temporary increase in the mass of the uterus and breasts during pregnancy. On the other hand, the term ‘physiological hypertrophy’ to describe an increase in cardiac mass due to exercise is not accurate. In this case, the commonly used term ‘athlete’s heart’ would be more appropriate [9].

References

1. Tomanek RJ. In: Coronary Vasculature: Development, Structure- Function and Adaptations. New York: Springer Science, 2013.
2. McMullen JR, Jennings GL. Differences between pathological and physiological hypertrophy: Novel therapeutic strategies to treat heart failure. Clin Exp Pharmacol Physiol 2007;34:255-62.
3. Bernardo BC, Weeks KL, Pretorius L, McMullen JR. Molecular distinction between physiological and pathological cardiac hypertrophy. Experimental findings and therapeutic strategies. Pharmacol Ther 2010;128:191-227.
4. Dorn GW II. The fuzzy logic of physiological cardiac hypertrophy. Hypertension 2007;49:962-70.
5. Pelliccia A, Maron BJ, De Luca R, Di Paolo FM, Spatoro A, Culasso F. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation 2002;105:944-9.
6. Wachtlova M, Rakusan K, Poupa O. The terminal vascular bed of the myocardium in the wild rat (Rattus norvegicus) and the laboratory rat (Rattus norvegicus lab). Physiol Bohemoslov 1967;16:548-54.
7. Wachtlova M, Rakusan K, Poupa O. The coronary terminal vascular bed in the heart of the hare (Lepus europeus) and the rabbit (Oryctolagus domesticus). Physiol Bohemoslov 1965;14:328-31.
8. Seidman JG, Seidman G. The genetic basis for cardiomyopathy: From mutation identification to mechanistic paradigms. Cell 2001;104:557-67.
9. Baggish AL. The athlete’s heart. In: Ostadal B, Dhalla NS, eds. Cardiac Adaptations. New York, Heidelberg, Dordrecht, London: Springer, 2013:289-302.

*Corresponding Author:

Dr Karel Rakusan
Department of Cellular and Molecular Medicine, University of Ottawa, 451 Smyth Road, Ottawa, Ontario K1H 8M5.
E-mail: krakusan@uottawa.ca

This open-access article is distributed under the terms of the Creative Commons Attribution Non-Commercial License (CC BY-NC) (http://creativecommons.org/licenses/by-nc/4.0/), which permits reuse, distribution and reproduction of the article, provided that the original work is properly cited and the reuse is restricted to noncommercial purposes. For commercial reuse, contact support@pulsus.com

Abstract

The term ‘hypertrophy’ means an abnormal growth (eg, cardiac hypertrophy is understood as an abnormal growth of cardiac mass due to an increase in the size of myocytes). A second meaning of the term ‘physiological’ is, according to the dictionary, normal. Taking the above interpretations into consideration, we arrive at an amusing semantic incompatibility: cardiac physiological hypertrophy would mean ‘normal abnormal growth of the heart’. Authors who coined this term most likely intended to refer to cardiac hypertrophy achieved by physiological stimuli.

The term ‘hypertrophy’ means an abnormal growth (eg, cardiac hypertrophy is understood as an abnormal growth of cardiac mass due to an increase in the size of myocytes). A second meaning of the term ‘physiological’ is, according to the dictionary, normal. Taking the above interpretations into consideration, we arrive at an amusing semantic incompatibility: cardiac physiological hypertrophy would mean ‘normal abnormal growth of the heart’. Authors who coined this term most likely intended to refer to cardiac hypertrophy achieved by physiological stimuli.

The next logical question is whether there a specific subtype of cardiac hypertrophies mislabelled as ‘physiological’ hypertrophies. For example, in a recent authoritative review, Tomanek [1] divides hypertrophies into the following groups: hypertrophies due to: pressure overload; volume overload; hyperthyroidism; and cardiomyopathies. However, the term ‘physiological hypertrophy’ is avoided.

Most publications using the term ‘physiological hypertrophy’ concern changes in the heart after chronic physical exercise. Occasionally, it is also used to describe cardiac changes during pregnancy or in hyperthyroidism.

Several functional, morphological and/or biochemical differences between ‘physiological hypertrophy’ and the remaining types of ‘pathological’ cardiomegalies are reported. All of these changes are usually considered to be reversible. Generally, the distinctions are presented as differences between a ‘good’ hypertrophy and a ‘bad’ hypertrophy [2,3]. However, the line of distinction between these two types of hypertrophy is fuzzy. The so-called ‘bad pathological’ hypertrophy can be adaptive if the primary cause is reversed before the development of intrinsic myocardial disease, while ‘physiological’ hypertrophy can be maladaptive if it is quantitatively excessive and sustained [4]. For instance, Pelliccia et al [5] described a residual cardiac hypertrophy in >20% elite athletes after a long-term deconditioning period.

The degree to which an increase in cardiac mass induced by exercise is usually modest. An exception is the sizeable increase in cardiac mass due to an enhanced physical activity that is genetically coded in so-called ‘active’ animals. For example, a sizeable increase in cardiac mass was found in wild (ie, sewage) rats when compared with laboratory rats [6], as well as a significantly higher cardiac mass in hares compared with that in rabbits [7]. A clinical example of genetically coded cardiomegalies would be familiar hypertrophic cardiomyopathy mutations [8].

In conclusion, the term ‘physiological growth’ is acceptable in situations when there is a temporary increase in the mass of the uterus and breasts during pregnancy. On the other hand, the term ‘physiological hypertrophy’ to describe an increase in cardiac mass due to exercise is not accurate. In this case, the commonly used term ‘athlete’s heart’ would be more appropriate [9].

References

1. Tomanek RJ. In: Coronary Vasculature: Development, Structure- Function and Adaptations. New York: Springer Science, 2013.
2. McMullen JR, Jennings GL. Differences between pathological and physiological hypertrophy: Novel therapeutic strategies to treat heart failure. Clin Exp Pharmacol Physiol 2007;34:255-62.
3. Bernardo BC, Weeks KL, Pretorius L, McMullen JR. Molecular distinction between physiological and pathological cardiac hypertrophy. Experimental findings and therapeutic strategies. Pharmacol Ther 2010;128:191-227.
4. Dorn GW II. The fuzzy logic of physiological cardiac hypertrophy. Hypertension 2007;49:962-70.
5. Pelliccia A, Maron BJ, De Luca R, Di Paolo FM, Spatoro A, Culasso F. Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning. Circulation 2002;105:944-9.
6. Wachtlova M, Rakusan K, Poupa O. The terminal vascular bed of the myocardium in the wild rat (Rattus norvegicus) and the laboratory rat (Rattus norvegicus lab). Physiol Bohemoslov 1967;16:548-54.
7. Wachtlova M, Rakusan K, Poupa O. The coronary terminal vascular bed in the heart of the hare (Lepus europeus) and the rabbit (Oryctolagus domesticus). Physiol Bohemoslov 1965;14:328-31.
8. Seidman JG, Seidman G. The genetic basis for cardiomyopathy: From mutation identification to mechanistic paradigms. Cell 2001;104:557-67.
9. Baggish AL. The athlete’s heart. In: Ostadal B, Dhalla NS, eds. Cardiac Adaptations. New York, Heidelberg, Dordrecht, London: Springer, 2013:289-302.