Final answer:
Cardiomyocytes can undergo both pathological and exercise-induced deviations, such as hypertrophic cardiomyopathy and physiological cardiac hypertrophy due to sustained exercise. Pathological changes can result in abnormal heart function, while exercise adaptations are generally beneficial unless they become excessive.
Step-by-step explanation:
Pathological and exercise-induced deviations affecting cardiomyocytes can significantly alter the function and structure of the heart. Two such deviations are:
- Hypertrophic cardiomyopathy (HCM), which is a form of pathological enlargement of the heart, generally occurring without a known cause. This enlargement can negatively impact the heart's ability to pump blood efficiently and is characterized by excessive thickening of the cardiac muscle.
- Exercise-induced cardiac hypertrophy, which is usually a physiological response wherein the heart muscle (myocardium) enlarges due to the increased demand placed on it by prolonged exercise. It's a normal adaptation that enhances the heart's ability to circulate blood during periods of sustained physical activity. However, if excessive or done without proper guidance, it can lead to pathological changes.
In both cases, alterations in the structure and function of intercalated discs and associated gap junctions play a fundamental role in cardiomyocyte communication and contractile mechanics. Pathological changes, such as those caused by the PTPN11 mutation linked to NSML, can lead to abnormal cell communication and contribute to cardiomyopathy. Exercise adaptions, on the other hand, enhance muscle performance by increasing mitochondrial density, myoglobin content, and capillary networks, primarily within SO (slow-oxidative) fibers of cardiomyocytes.