Neuromuscular electrical stimulation increases muscle protein synthesis in elderly type 2 diabetic men.
Physical activity is required to attenuate the loss of skeletal muscle mass with aging. Short periods of muscle disuse, due to sickness or hospitalization, reduce muscle protein synthesis rates, resulting in rapid muscle loss. The present study investigates the capacity of neuromuscular electrical stimulation (NMES) to increase in vivo skeletal muscle protein synthesis rates in older type 2 diabetes patients. Six elderly type 2 diabetic men (70 ± 2 yr) were subjected to 60 min of one-legged NMES. Continuous infusions with L-[ring-¹³C₆]phenylalanine were applied, with blood and muscle samples being collected regularly to assess muscle protein synthesis rates in both the stimulated (STIM) and nonstimulated control (CON) leg during 4 h of recovery after NMES. Furthermore, mRNA expression of key genes implicated in the regulation of muscle mass were measured over time in the STIM and CON leg. Muscle protein synthesis rates were greater in the STIM compared with the CON leg during recovery from NMES (0.057 ± 0.008 vs. 0.045 ± 0.008%/h, respectively, P < 0.01). Skeletal muscle myostatin mRNA expression in the STIM leg tended to increase immediately following NMES compared with the CON leg (1.63- vs. 1.00-fold, respectively, P = 0.07) but strongly declined after 2 and 4 h of recovery in the STIM leg only. In conclusion, this is the first study to show that NMES directly stimulates skeletal muscle protein synthesis rates in vivo in humans. NMES likely represents an effective interventional strategy to attenuate muscle loss in elderly individuals during bed rest and/or in other disuse states.
Department of Human Movement Sciences, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, The Netherlands.
Benjamin T
BT
Wall
Marlou L
ML
Dirks
Lex B
LB
Verdijk
Tim
T
Snijders
Dominique
D
Hansen
Pascal
P
Vranckx
Nicholas A
NA
Burd
Paul
P
Dendale
Luc J C
LJ
van Loon
D000368:Aged; D001284:Atrophy / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D001510:Bed Rest / Q000009:adverse effects; D001707:Biopsy, Needle; D002247:Carbon Isotopes; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D004599:Electric Stimulation Therapy / Q000379:methods; D005786:Gene Expression Regulation; D006801:Humans; D007103:Immobilization / Q000009:adverse effects; D007700:Kinetics; D008297:Male; D009124:Muscle Proteins / Q000096:biosynthesis* / Q000235:genetics; D055435:Myostatin / Q000096:biosynthesis / Q000235:genetics; D009469:Neuromuscular Junction / Q000503:physiopathology*; D010649:Phenylalanine / Q000097:blood / Q000378:metabolism; D052097:Quadriceps Muscle / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D055948:Sarcopenia / Q000150:complications / Q000209:etiology / Q000517:prevention & control*
D002247:Carbon Isotopes; C525911:MSTN protein, human; D009124:Muscle Proteins; D055435:Myostatin; D012333:RNA, Messenger; D010649:Phenylalanine