Training Intensity, Not Duration, May Be Key to Upregulating Presynaptic Proteins of Calcium Dynamics and Calcium-Dependent Exocytosis in Fast- and Slow-Twitch Skeletal Muscles, in Addition to Maintaining Performance After Detraining.

Abstract

Neuromuscular adaptations are essential for improving athletic performance. However, little is known about the effect of different endurance training protocols and their subsequent detraining on the gene expression of critical factors for neuromuscular synaptic transmission. Therefore, this study investigated the effects of endurance training (high-intensity interval training [HIIT], continuous [cEND], mixed interval [Mix], and all protocols combined [Comb]) and detraining on performance and gene expression (GE) of the alpha-1a, synaptotagmin II (Syt-II), synaptobrevin II (Vamp2), and acetylcholinesterase (AChE) in the gastrocnemius and soleus of Wistar rats. Eighty rodents were randomly divided into control, HIIT, cEND, Mix, Comb, and detraining groups. The rodents trained for 6weeks (5 × /week), followed by 2weeks of detraining. Performance improved in all training groups and decreased following detraining (p < 0.05), except HIIT. In the gastrocnemius, alpha-1a GE was upregulated in the Mix. Syt-II and AChE GE were upregulated in HIIT, Mix, and Comb. Vamp2 GE was upregulated in all groups. In the soleus, alpha-1a GE was upregulated in HIIT, Mix, and Comb. Syt-II and Vamp2 GE were upregulated in all groups. AChE GE was upregulated in cEND, Mix, and Comb. Detraining downregulated mostly the gene expression in the skeletal muscles. We conclude that training intensity appears to be a key factor for the upregulation of molecules involved in neuromuscular synaptic transmission. Such changes occur to be involved in improving running performance. On the other hand, detraining negatively affects synaptic transmission and performance.