Journal of Energy Bioscience 2025, Vol.16, No.1, 42-52 http://bioscipublisher.com/index.php/jeb 46 and Adriano (2019) found that creatine supplementation can increase muscle strength and improve overall health. If the body lacks creatine transporters, creatine cannot enter muscle cells, causing muscles to become weaker, lose strength, and even atrophy (Stockebrand et al., 2018; Duran-Trio et al., 2021) (Figure 3). Figure 2 The primary metabolic changes and the secondary celluar injuries during myocardial ischemia/reperfusion (Adopted from Hao et al., 2021) Image caption: The ischemic myocardium primarily utilizes creatine phosphate (CrP) as an energy source, followed by ATP, ADP, and AMP. The breakdown of AMP into adenosine and hypoxanthine reduces the adenine nucleotide pool, while glycolysis-induced lactate accumulation causes intracellular acidosis. Loss of high-energy phosphates (HEPs) disrupts calcium homeostasis, leading to intracellular Ca2+ overload. This overload impairs mitochondrial oxidative phosphorylation due to excessive Ca2+ sequestration. The activation of xanthine oxidase generates oxygen free radicals, oxidizing membrane phospholipids and producing malondialdehyde (MDA), contributing to membrane instability. Additionally, the accumulation of metabolic intermediates such as AMP, lactic acid, Ca2+, and H+ activates phospholipases, degrading membrane lipids into lysophospholipids (LPLs), further destabilizing the membrane. Increased ADP levels also promote platelet aggregation. ADP, adenosine diphosphate; AMP, adenosine monophosphate; ATP, adenosine triphosphate; CrP, creatine phosphate; HEPs, high-energy phosphates; LPLs, lysophospholipids; MDA, malondialdehyde (Adapted from Hao et al., 2021) 5.2 Creatine phosphate deficiency syndromes and their impact on energy homeostasis Some people suffer from creatine phosphodeficiency syndrome due to mutations in the creatine transporter (CT1). This disease causes the body's energy regulation system to be out of balance. In the muscles of these patients, PCr and ATP levels are significantly reduced, resulting in muscle weakness and even atrophy (Stockebrand et al., 2018; Duran-Trio et al., 2021). The body will try to compensate, such as increasing the expression of enzymes related to creatine synthesis. But these compensation methods are usually not enough to restore energy levels to normal. And the problem is not just in the muscles. The metabolism of the entire body is also affected, such as changes in glucose metabolism and activation of AMPK (an energy-sensing enzyme) (Stockebrand et al., 2018).
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