Phosphorylated beta-guanidinopropionate as a substitute for phosphocreatine in rat muscle

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Abstract
To evaluate phosphorylated beta-guanidinopropionate (beta-GPAP) as a substitute for phosphocreatine (PC), hypoxic tibialis anterior muscles were stimulated to contract isometrically in situ until twitch tension fell to 25 percent of the peak value. Muscles from rats fed beta-guanidinopropionic acid (beta-GPA) failed to exhibit the staircase phenomenon, and they developed 28 percent less tension than control muscles. In control muscles lactate increased from 0.75 to 20.99, ADP increased from 0.89 to 1.20, ATP decreased from 5.09 to 2.73, and PC decreased from 15.78 to 1.52 mumol/g. In muscles from rats fed beta-GPA, lactate increased from 0.85 to 14.31, ADP increased from 0.86 to 1.05, ATP decreased from 2.69 to 1.71, PC decreased from 0.73 to 0.30, and beta-GPAP decreased from 30.34 to 19.45 mumol/g. From these measurements, the use of high-energy phosphate was calculated to be reduced 32 percent in muscles from rats fed beta-GPA. The relationships between the use of high-energy phosphate was calculated to be reduced 32 percent in muscles from rats fed beta-GPA. The relationships between the use of high-energy phosphate and tension development confirm experimentally the ability of beta-GPAP to substitute for PC as a source of energy to sustain muscle contraction.

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