Abstract

Aging and frailty are associated with a decline in muscle force generation, which is a direct consequence of reduced muscle quantity and quality. Among the leading contributors to aging is the generation of reactive oxygen species, the byproducts of terminal oxidation. Their negative effects can be moderated via antioxidant supplementation. Krill oil and astaxanthin (AX) are nutraceuticals with a variety of health promoting, geroprotective, anti-inflammatory, anti-diabetic and anti-fatigue effects. In this work, we examined the functional effects of these two nutraceutical agents supplemented via pelleted chow in aging mice by examining in vivo and in vitro skeletal muscle function, along with aspects of intracellular and mitochondrial calcium homeostasis, as well as cognition and spatial memory. AX diet regimen limited weight gain compared to the control group; however, this phenomenon was not accompanied by muscle tissue mass decline. On the other hand, both AX and krill oil supplementation increased force production without altering calcium homeostasis during excitation-contraction coupling mechanism or mitochondrial calcium uptake processes. We also provide evidence of improved spatial memory and learning ability in aging mice because of krill oil supplementation. Taken together, our data favors the application of antioxidant nutraceuticals as geroprotectors to improve cognition and healthy aging by virtue of improved skeletal muscle force production.

Highlights

  • Aging is a physiological process causing a general receding of physical and mental capacities

  • Following AX but not krill oil supplementation our qPCR measurements revealed significantly increased dynamin-related protein 1 (Drp1) transcript levels, whereas on protein level a significant decrease was detected compared to the untreated group (Supplementary Figure S2)

  • In our recent work [39] we propose a possible mode of action of AX in skeletal muscle: AX acts on the insulin receptor substrate (IRS) activating the PI3K/Akt pathway which induces

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Summary

Introduction

Aging is a physiological process causing a general receding of physical and mental capacities. Skeletal muscle is highly affected as there is a gradual loss of muscle mass and function (sarcopenia), fatigue/exhaustion, weakness and mobility deterioration (frailty) which impairs the quality of life in elderly people [1]. Several theories were proposed to explain it such as genetic predisposition, programmed senescence, DNA deterioration, endocrine malfunction, the free radical rationale and mitochondrial dysfunction [3,4,5]. Understanding the cellular mechanism of aging and its pathogenesis are essential tasks for the development of prophylactic and therapeutic strategies to ensure healthy aging and improve the life quality of those affected

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