CAMK in Skeletal Muscle Stimulated by Caffeine to Promote Endurance Adaptation

Abstract

CAMKII is a kinase protein that forma an oligomer of 6 proteins that is highly seen in the muscle and brain. It can be activated by increasing the levels of Ca2+ within the skeletal muscle to promote the synthesis of PGC1-alpha mRNA to induce mitochondrial biogenesis. PURPOSE: To determine if caffeine can cause a shift in Ca2+ levels in skeletal muscle to stimulate CAMKII to promote mitochondrial biogenesis. METHODS: Mice were administered different amounts of caffeine, later tissue samples were collected to analyze and quantify levels of mitochondrial protein. Western Blots and qPCR analysis were used to determine changes in protein levels from control groups to the stimulated groups. Antibodies were used to determine the concentration of the proteins in question. These included p-CAMKII because CAMK activity is determined by measuring autophosphorylation, COX5 and 5.4, HAD, LCAD, MCAD, VLCAD, Cytochrome-C, CD36, CPT-1, GLUT4, Citrate Synthase, and PGC1-alpha. RESULTS: Our current findings suggest that as the caffeine dosage increases the levels of mitochondria biogenesis inducing proteins increases and so do mitochondrial proteins, suggesting that there are more mitochondria being made. At the moment we are unable to compare the findings to our control groups because we have yet to receive the key with respect to our control group’s protein levels from our sample provider. But with the preliminary data we have we suspect that higher dosages of caffeine induce mitochondrial biogenesis. CONCLUSION: At the moment we do not have sufficient data to make a conclusion but if the trend we are observing continues this may prove revolutionary to the way that endurance athletes train and what we will consider fast times in the future.