Question: 

Calcium (Ca²⁺) handling in skeletal muscle regulates to diverse pathologies and performance capacities as Ca²⁺ is involved in muscle contraction machinery. Ca²⁺ homeostasis is mainly regulated by transmembrane channel complexes of sarcoplasmic reticule, called ryanodine receptor-1 (RyR1). RyR1 associates to many regulatory proteins, of which calstabin-1 plays a key role. It was described that long-lasting exercise models hyperphosphorylate RyR1 at Ser2843 and thus induce a leaky channel leading to impaired muscle function by dissociating calstabin-1 from RyR1. However, time patterns of RyR1 hyperphosphorylation (pRyR1) is unknown wherefore short-term exercise stimuli and their effects on pRyR1 were investigated.

Methods: 

32 Sprague-Dawley rats were assigned to one of following groups: age-matched control (AC, sedentary), concentric (Conc, 0° decline) or eccentric (Ecc, -20° decline) exercise (each exercise lasted 15 min). pRyR1 was investigated by immunohistochemistry in both medial gastrocnemius and vastus lateralis.

Results: 

In lateralis muscle 15 min of either concentric or eccentric led to markedly increased levels of pRyR1 compared to AC. Furthermore, concentric led to significantly higher amounts of pRyR1 compared to eccentric exercise. In gastrocnemius muscle a similar pattern was observed. However, there was no difference between concentric and eccentric stimuli.

Discussion: 

The present results demonstrate that RyR1 is hyperphosporylated very fast, which is an additional finding compared to data from the literature. Importantly, different muscle types react in a comparable manner. Interestingly, concentric exercise seems to exert a more severe effect on RyR1 hyperphosphorylation, at least in lateralis. These findings give new insights into RyR1 regulation by exercise.