Effects of Agmatine Exposure on Skeletal Muscle of Aging Rats
Authors: Pascolla Jessica , Receno Candace N. , Liang Chen , Welch Mary C. , Barnes Jackson , DeRuisseau Keith C. 
Published: June 2021

Skeletal muscle from aging individuals is smaller and weaker than muscle from younger adults, which is a condition referred to as “sarcopenia”. The etiology of sarcopenia is complex as many factors and cellular responses are likely to contribute to the onset and progression of the condition. Thus, a strategy that might favorably affect multiple cellular responses may be more likely to impart beneficial effects on aging skeletal muscle. Agmatine is a compound that has potential to lessen age‐related muscle loss. The synthesis of agmatine occurs in the body via the decarboxylation of arginine, a conditionally essential amino acid. Although the formation of agmatine occurs principally in neurons it is detected in several tissues including skeletal muscle. While ample data support the role of agmatine as a neuromodulator and neurotransmitter, other physiological roles of agmatine have been revealed in the literature. Mounting evidence indicates a beneficial role of agmatine administration on various disease states and conditions. Notably, agmatine may produce beneficial effects through the activation or de‐activation of various cell signaling pathways. Collectively, alteration of cell signaling cascades by agmatine shown to occur in non‐muscle cells and tissues could induce responses that may benefit aging skeletal muscle. Thus, the purpose of this pilot experiment was to obtain evidence that agmatine supplementation may attenuate the development of sarcopenia in aging rats. Ten, thirty‐two‐month old male F344xBN F1 rats were singly housed and provided with either agmatine sulfate (0.2–0.25%) dissolved in drinking water, or plain water for a period of 4 weeks. Solutions were replaced with fresh mixtures every 3–4 days. Following the 4‐week supplementation period, plantaris force measures were tested in situ by stimulation of the sciatic nerve. Immediately afterwards the muscle was harvested for biochemical analyses. Body mass, muscle mass, muscle peak tetanic tension, and protein levels of inducible nitric oxide synthase (iNOS), manganese superoxide dismutase (MnSOD), and peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1a) were obtained. Due to low sample size only descriptive statistics are reported. All values are reported as mean ± SD for control and agmatine supplemented groups, respectively. Average body mass (g) (467.6 ± 44.4, n=4; 476.0 ± 19.5, n=3), plantaris mass (g) (0.36 ± 0.06, n=4; 0.30 ± 0.02, n=3) and muscle mass/body mass ratio (mg/g) (0.77 ± 0.13, n=4; 0.62 ± 0.01, n=3) values were similar or appeared lower in agmatine supplemented animals. Average maximal force production of the plantaris appeared to be similar (Po/muscle mass) (751.3 ± 198.1, n=4; 776.2 ± 260.8, n=3) between groups. Expression of iNOS (1.11 ± 0.96, n=5; 1.85 ± 1.53, n=4), PGC1a (0.16 ± 0.13, n=5; 0.22 ± 0.22, n=4) and MnSOD (4.82 ± 0.91, n=5; 5.05 ± 1.37, n=3) were either similar between the groups or slightly greater in agmatine supplemented rats, but low sample size likely affected variability of these measures. Our preliminary findings suggest that 4 weeks of agmatine administration does not favorably alter the functional or biochemical response of skeletal muscle in aging rats.

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This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.