Blood flow restriction exercise stimulates mTORC1 signaling and muscle protein synthesis in older men.
The loss of skeletal muscle mass during aging, sarcopenia, increases the risk for falls and dependence. Resistance exercise (RE) is an effective rehabilitation technique that can improve muscle mass and strength; however, older individuals are resistant to the stimulation of muscle protein synthesis (MPS) with traditional high-intensity RE. Recently, a novel rehabilitation exercise method, low-intensity RE, combined with blood flow restriction (BFR), has been shown to stimulate mammalian target of rapamycin complex 1 (mTORC1) signaling and MPS in young men. We hypothesized that low-intensity RE with BFR would be able to activate mTORC1 signaling and stimulate MPS in older men. We measured MPS and mTORC1-associated signaling proteins in seven older men (age 70+/-2 yr) before and after exercise. Subjects were studied identically on two occasions: during BFR exercise [bilateral leg extension exercise at 20% of 1-repetition maximum (1-RM) with pressure cuff placed proximally on both thighs and inflated at 200 mmHg] and during exercise without the pressure cuff (Ctrl). MPS and phosphorylation of signaling proteins were determined on successive muscle biopsies by stable isotopic techniques and immunoblotting, respectively. MPS increased 56% from baseline after BFR exercise (P<0.05), while no change was observed in the Ctrl group (P>0.05). Downstream of mTORC1, ribosomal S6 kinase 1 (S6K1) phosphorylation and ribosomal protein S6 (rpS6) phosphorylation increased only in the BFR group after exercise (P<0.05). We conclude that low-intensity RE in combination with BFR enhances mTORC1 signaling and MPS in older men. BFR exercise is a novel intervention that may enhance muscle rehabilitation to counteract sarcopenia.
University of Texas Medical Branch, Sealy Center on Aging, Department of Physical Therapy, Division of Rehabilitation Sciences, 301 Univ. Blvd., Galveston, TX 77555-1144, USA.
Christopher S
CS
Fry
Erin L
EL
Glynn
Micah J
MJ
Drummond
Kyle L
KL
Timmerman
Satoshi
S
Fujita
Takashi
T
Abe
Shaheen
S
Dhanani
Elena
E
Volpi
Blake B
BB
Rasmussen
D000367:Age Factors; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001706:Biopsy; D015153:Blotting, Western; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006728:Hormones / Q000097:blood; D006801:Humans; D007328:Insulin / Q000378:metabolism; D008297:Male; D000076222:Mechanistic Target of Rapamycin Complex 1; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D046912:Multiprotein Complexes; D009119:Muscle Contraction; D009124:Muscle Proteins / Q000096:biosynthesis* / Q000235:genetics; D009929:Organ Size; D010100:Oxygen / Q000097:blood; D010766:Phosphorylation; D011506:Proteins; D052097:Quadriceps Muscle / Q000033:anatomy & histology / Q000098:blood supply* / Q000378:metabolism*; D020127:Recovery of Function; D012039:Regional Blood Flow; D055070:Resistance Training; D038601:Ribosomal Protein S6 / Q000378:metabolism; D038762:Ribosomal Protein S6 Kinases, 70-kDa / Q000378:metabolism; D012737:Sex Factors; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases; D013927:Thrombosis / Q000097:blood; D013997:Time Factors; D014157:Transcription Factors / Q000378:metabolism*
D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D006728:Hormones; D007328:Insulin; D046912:Multiprotein Complexes; D009124:Muscle Proteins; D011506:Proteins; D038601:Ribosomal Protein S6; D014157:Transcription Factors; C036309:fibrin fragment D; D000076222:Mechanistic Target of Rapamycin Complex 1; D038762:Ribosomal Protein S6 Kinases, 70-kDa; D058570:TOR Serine-Threonine Kinases; C448901:ribosomal protein S6 kinase, 70kD, polypeptide 1; D020928:Mitogen-Activated Protein Kinases; D010100:Oxygen