Biomedicines · Nov 2, 2026

The Effect of Physical Training on Myokines and Calcium Status in Spontaneously Hypertensive Rats and Healthy Rats

By Selvan D, Skrypnik K, Skrypnik D et al.

Background: Hypertension remains a major global health concern requiring multifactorial therapeutic approaches. Myokines mediate communication between skeletal muscle and the cardiovascular system, while calcium homeostasis plays a central role in vascular function and cardiac contractility. Aim: This study investigated the effects of long-term low-intensity exercise on blood pressure, myokines, and tissue calcium content in Wistar (healthy rats) and spontaneously hypertensive rats (SHRs). Methods: Thirty-two male rats were assigned to trained (n = 16) or sedentary (n = 16) groups and subjected to a 12-week treadmill protocol. Results: In SHRs, training was associated with increased cardiac FSTL-1, follistatin, and myostatin levels and decreased skeletal muscle apelin (all p ≤ 0.028). In Wistar rats, hepatic FSTL-1 increased (p = 0.015), hepatic musclin decreased (p = 0.001), and skeletal muscle calcium content was lower in trained rats. Calcium content remained largely unchanged in other tissues. SHR-T rats exhibited significantly lower systolic and diastolic blood pressure than SHR-NT rats at baseline and after training (all p ≤ 0.003). However, blood pressure changes from baseline to endpoint did not differ significantly between trained and non-trained rats in either strain (all p ≥ 0.234). Wistar-T rats had lower endpoint diastolic blood pressure than Wistar-NT rats (p = 0.028). Conclusions: Twelve weeks of low-intensity exercise were accompanied by tissue-specific alterations in myokine levels, whereas calcium concentrations in most tissues remained unchanged in both spontaneously hypertensive and Wistar rats. These findings indicate that exercise may influence myokine regulation without substantially altering tissue calcium status. While the effects of training on blood pressure were modest, the observed myokine alterations highlight potential mechanisms involved in exercise-related cardiovascular adaptation. Further research is needed to elucidate the mechanisms linking physical training, myokine responses, and calcium homeostasis in cardiovascular health.

doi.org/10.3390/biomedicines14112519Open accessInterventions

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