Resistance but not endurance training suppresses glucocorticoid-induced leucine zipper (GILZ) expression in human skeletal muscle.

Abstract

Within human skeletal muscle, statin treatment leads to elevated levels of the glucocorticoid-induced leucine zipper (GILZ). Further, GILZ mediates the muscle-related side effects of statins. Physical exercise leads to GILZ suppression, in a mechanosensitive manner. Given that statin treatment is rarely tolerated by habitually exercising individuals due to statin-associated muscle symptoms (SAMS), it appears that the opposing regulation of GILZ facilitates this detrimental interaction of two key measures of cardiovascular prevention, specifically for exercise modalities with high muscle strain. Similarly, opposing regulation of atrophy associated genes (atrogenes) may be a further mechanism. If confirmed, these results might have implications for the exercise prescription of statin-users. A systematic search of the Gene Expression Omnibus (GEO) repository for studies reporting the acute effects of either endurance (END), conventional resistance (RT), or eccentric resistance training (ECC) was conducted. GILZ, as well as the expression of pivotal atrogenes (e.g., muscle atrophy F-box, cathepsin L, etc.) were quantified. 15 studies with 204 participants (22 females; 182 males) were included. RT resulted in the highest GILZ suppression, significantly differing from the expressional change after END ( - 0.46 ± 1.11 vs. - 0.07 ± 1.08), but not from ECC ( - 0.46 ± 1.11 vs. - 0.46 ± 0.95). Similar results were seen for various atrogenes. Our results strengthen the assumption that mechanical loading can be considered a key mediator of exercise-induced changes in GILZ and atrogene expression.