Cardiac hypertrophy, characterized by an increase

in the size of cardiac myocytes, is an adaptive response to increased

workload on the cardiac tissue following physiological stimuli, such

as exercise, and pathological conditions, such as hypertension or

valvular heart disease. Typically, physiological hypertrophy induced

by various exercise modalities leads to beneficial adaptations, such

as improved contractile function and increased oxidative capacity.

Understanding the molecular mechanisms underlying physiological

cardiac hypertrophy is crucial for developing targeted therapeutic

strategies. This review provides a comprehensive overview of

current knowledge of physiological cardiac hypertrophy, with

a particular focus on adaptations induced by various exercise

modalities.We delved into the potential cellular and molecular

pathways involved in physiological hypertrophy including

IGF1/PI3K/AKT, angiotensin2, hepatocyte growth factor,

platelet-growth factor, MAPK/ERK cascade, calcineurin, Neurogelin2

and downstream transcriptional factors such as HAND2, GATA4, MEF2,

NKX2.5, TBX5, NFAT, c/EBPb, CITED4, PHLPP, as well as the role of

microRNAs (miRNAs) like miR-222 and miR-17 in mediating these

adaptations. Furthermore, we used comparative tables to illustrate

the differential effects of endurance, high-intensity interval

training (HIIT), and resistance training on structural, molecular,

and functional cardiac parameters, as markers of physiological

hypertrophy. We also presented pathway-specific percentage changes

observed across different exercise training modalities to highlight

key differences. The discussion integrated these findings to explore

translational perspectives and to offer the most beneficial exercise

training schedules that induce physiological hypertrophy.