Table 1.

Key features of pathological vs. physiological hypertrophy and their mitochondrial alterations

	Physiological hypertrophy	Pathological hypertrophy
Stimuli	Volume overload (isotonic exercise)	Volume overload (valvular disease, aortovenous fistula)
	Pressure overload (isometric exercise)	Pressure overload (arterial hypertension, aortic constriction)
	Pregnancy
Foetal gene expression	Normal	Up-regulated
Cardiac function	Normal/improved	Increasingly impaired during the time course
Decompensation	Not occuring	Occuring
Cardiac structure	Increased myocyte volume	Increased myocyte volume
	Formation of new sarcomers	Formation of new sarcomers
		Interstitial fibrosis
		Increased rates of apoptosis
Fatty acid oxidation	Unchanged or increased	Decreased
Glucose oxidation	Unchanged or increased	Unchanged
		Maybe reduced during heart failure
Mitochondrial biogenesis	In accordance to cellular hypertrophy	Unchanged during compensated hypertrophy
		Maybe diminished during heart failure
ATP production	Sufficient	Impaired