A recent study found the first evidence that sperm microRNAs act as carriers of epigenetic information, enabling the intergenerational transmission of paternal exercise capacity and metabolic health, thereby exerting profound effects on offspring development.

The bad news if you want an excuse for your poor fitness is this is epigenetics and only in mice, which means it is only EXPLORATORY. Mice are not little people and epigenetics lacks the same biological foundation as actual evolution and genetics.

Humans have always had write variation in physical performance. We are not all born equal to Usain Bolt and our ancestors also had large differences in sustained physical performance related ti hunting, migration, and predator evasion.

The new paper posits that our wealthier modern lifestyle makes exercise less essential for survival, which means sedentary behavior and physical inactivity have become the norm.


Credit: Cell Metabolism

Exercise is still a good thing but if kids don't play baseball or work on a farm as much, they are not getting as much exercise in second-order fashion. Instead, more people must proactively do it, which means more people can choose not to do so. The authors use that to argue paternal exercise influences offspring phenotypes for exercise capacity.

Enter the mice. The authors found that offspring sired by exercise-trained fathers exhibit intrinsic exercise adaptability and improved metabolic parameters compared to those from sedentary fathers.

Offspring of their transgenic mice with muscle-specific overexpression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) showed improved mitochondrial function, endurance and metabolic traits, even though they didn't inherited PGC-1α transgene.

The injection of sperm small RNAs from exercised fathers into normal zygotes reproduces exercise-trained phenotypes in the offspring at behavioral, metabolic, and molecular level, so both exercise training and muscular PGC-1α overexpression remodel the sperm microRNA profile, which directly suppress nuclear receptor corepressor 1 (NCoR1), a functional antagonist of PGC-1α, in early embryos, thereby reprogramming transcriptional networks to promote mitochondrial biogenesis and oxidative metabolism.

They conclude that their work establishes a causal role for paternal PGC-1α, sperm microRNAs, and embryonic NCoR1 in mediating the transmission of exercise-induced phenotypes and metabolic adaptations to offspring.

Citation: Yin et al. Paternal exercise confers endurance capacity to offspring through sperm microRNAs. Cell Metabolism. 6 October, 2025.