Ryanodine Receptor Modifications Following Sprint Interval Exercise: Time Course and Fibre-Specific Responses in Human Skeletal Muscle
Date
2021-01-07
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Abstract
It was recently discovered that a single session of sprint interval training (SIT) resulted in fragmentation of the sarcoplasmic reticulum calcium (Ca2+)-release channel, ryanodine receptor 1 (RyR1), leading to an increase in intracellular [Ca2+], a known signal for mitochondrial biogenesis; however, it was unclear whether fragmentation could initiate mitochondrial biogenesis, as RyR1 fragmentation had only been observed 24 h post-exercise in humans, and most signalling events occur much earlier. The primary objective of this thesis was to characterize the time course of RyR1 modifications following SIT in whole muscle and pooled type I and type IIa muscle fibres in humans. The secondary objective was to assess if SIT affected the content of other Ca2+-handling proteins alongside RyR1. We collected muscle biopsy samples from recreationally-active males (n = 6) and females (n = 4) before and 3 h, 6 h, and ~24 h after they completed a single session of SIT (6 x 30-s ‘all-out’ with 4.5 min rest). Western blotting experiments showed that full-length RyR1 content was significantly lower at 6 h (-44 ± 31%; p = 0.01) and 24 h (-35 ± 42%; p = 0.02) compared to pre-exercise. RyR1 content was also lower than pre-exercise at 6 h in type IIa fibres (-21 ± 17%; p = 0.01) but not type I fibres (-2 ± 43%; p > 0.05). Aside from FKBP12, which was higher at 24 h compared to 3 h (26 ± 29%; p = 0.03) and 6 h (24 ± 23%; p = 0.03), Ca2+-handling protein content was stable in whole muscle (all p > 0.05). Our results indicate that RyR1 fragmentation is fibre type-dependent and occurs on a similar time course to other relevant signalling events reported elsewhere in the literature. RyR1 fragmentation, in conjunction with stable content of other Ca2+-handling proteins, supports previous work suggesting a post-SIT increase in intracellular [Ca2+] is primarily due to RyR1-related Ca2+ leak. Overall, this thesis supports a role of RyR1 modifications in triggering mitochondrial adaptations in response to sprint interval training.
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Keywords
Exercise physiology, mitochondria, calcium handling, skeletal muscle, ryanodine receptor, molecular exercise physiology, fibre type
Citation
Tripp, T. R. (2020). Ryanodine Receptor Modifications Following Sprint Interval Exercise: Time Course and Fibre-Specific Responses in Human Skeletal Muscle (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca.