Unaffected arm muscle hypercatabolism in dysphagic subacute stroke patients: the effects of essential amino acid supplementation.

Roberto Aquilani,Maurizia Dossena,Federica Boschi,Andria Innocenza Bongiorno,Mirella Boselli,Paolo Iadarola,Paola Baiardi,Evasio Pasini,Simona Viglio,Manuela Verri,Annalisa Barbieri,Giuseppe D’Antona

doi:10.1155/2014/964365

Roberto Aquilani, Maurizia Dossena + Show 10 more

Open Access

https://doi.org/10.1155/2014/964365

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Abstract

Alterations in muscle protein turnover of the unaffected side of stroke patients could contribute to physical disability. We investigated whether hypercatabolic activity occurred in unaffected arm muscle and whether supplemented essential amino acids (EAAs) could limit muscle hypercatabolism (MH). Thirty-eight dysphagic subacute stroke subjects (<3 months after acute event) (29 males + 9 females; 69.7 ± 11.4 yrs) were enrolled and randomized to receive 8 g/day EAAs (n = 19; EAA group) or isocaloric placebo (maltodextrin; n = 19, Plac group). Before randomization, all patients had their arterial (A) and venous (V) amino acids measured and muscle (A − V) differences calculated in the unaffected arm. Eight matched and healthy subjects served as controls. When compared to healthy controls, the entire stroke population showed significant muscle release (= negative value A − V) of the amino acid phenylalanine (phenyl-) indicating a prevalence of MH. Moreover, randomized EAA and Plac groups had similar rates of MH. After 38 days from the start of the protocol, the EAA group but not the Plac group had MH converted to balanced protein turnover or anabolic activity. We concluded that muscle protein metabolism of the unaffected arm of dysphagic subacute stroke individuals could be characterized by MH which can be corrected by supplemented EAAs.

Highlights

Strokes are the world’s leading cause of disability
We investigated whether hypercatabolic activity occurred in unaffected arm muscle and whether supplemented essential amino acids (EAAs) could limit muscle hypercatabolism (MH)
We concluded that muscle protein metabolism of the unaffected arm of dysphagic subacute stroke individuals could be characterized by MH which can be corrected by supplemented EAAs

Summary

Introduction

Strokes are the world’s leading cause of disability. About onethird of stroke survivors are permanently disabled one year after the acute event [1, 2]. In addition to the loss of central trophic effects [7, 8] and transsynaptic degeneration of lower motor neurons [9,10,11], poststroke skeletal muscle changes can potentially contribute to disability. These changes include fibre-type shift in the paretic (= controlateral) side [12, 13], increased intramuscular fat (myosteatosis) substituting muscle tissue [14], spasticity [15], disuse [16, 17], malnutrition [18], and muscle unloading [19]

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