TY - JOUR
T1 - Skeletal muscle glucose uptake during short-term contractile activity in vivo
T2 - Effect of prior contractions
AU - Mossberg, K. A.
AU - Mommessin, J. I.
AU - Taegtmeyer, H.
N1 - Funding Information:
From the Division qf Cardiology, Deputttnent of Medicine. Uiniver-sity of Texas Health Scietw Center, ffouwn, T,Y. Submitted November 13. 1992: accepted Fcbtzam I?+ 199.3. Supported in puti bv a granl-in-aid frotn the American ffeurt Association-Te.uas Affiiaze and US Public Health Scnkc Grant No. ROI-HL43133. Address reprint requests to K4. Mossberg, PhD. Llepartmem of Physical Therapy, School of Allied Health Scimces. Unil,ersity of Texas Medical Branch, Galveston, TX 77555-102X. Copytight g: 1993 hy W.B. Saunders Cotnpatrv 00260-1951931~212-0017$03.00/,)
PY - 1993/12
Y1 - 1993/12
N2 - The goal of the present study was to examine the time course of skeletal muscle glucose uptake and changes in intracellular metabolites occurring with the onset of in situ stimulation, and to assess the effect of a prior period of contractions on subsequent contraction-induced increases in glucose uptake. Hindlimb muscle in anesthetized rabbits was studied noninvasively using the positron-emitting glucose analog 18F-2-fluoro-deoxy-d-glucose (FDG). Fractional rates of FDG phosphorylation were measured on a minute-to-minute basis during rest, 3.5 minutes of priming exercise (PE), 15 or 30 minutes of PE recovery, and a subsequent 15-minute period of contractions. Muscles were electrically stimulated at 2 Hz, and force production was held constant during the contraction period(s). FDG uptake did not differ from control values either during PE or during 60 minutes of recovery from PE. In response to 15 minutes of contractions, muscle stimulated without PE demonstrated increased FDG uptake, but only after a delay of 5.0 ± 0.7 minutes. Muscle with PE but rested 15 minutes had increased FDG uptake with a delay of 0.5 ± 0.2 minutes, and muscle with PE but rested 30 minutes had increased FDG uptake after a delay of 8.0 ± 0.9 minutes (P < .01 all groups). All groups reached similar levels of FDG uptake by the end of 15 minutes of contractions. Both groups with PE had control levels of adenosine triphosphate (ATP), phosphocreatine (PCr), and glucose-6-phosphate (G6P) after PE recovery, but glycogen level was lower than the control value (P < .05). During the subsequent 15-minute contractile period, metabolites and glycogen demonstrated similar changes despite differences in rates of FDG uptake. In summary, we have demonstrated that (1) the kinetics of glucose uptake in contracting skeletal muscle can be quantified on a minute-to-minute basis using a positron-emitting 2-deoxyglucose tracer, (2) the early time course of glucose uptake in contracting muscle can be modified by prior contractions, and (3) uptake in the first minutes of contractile activity is determined by factors other than glycogen, G6P, PCr, and ATP.
AB - The goal of the present study was to examine the time course of skeletal muscle glucose uptake and changes in intracellular metabolites occurring with the onset of in situ stimulation, and to assess the effect of a prior period of contractions on subsequent contraction-induced increases in glucose uptake. Hindlimb muscle in anesthetized rabbits was studied noninvasively using the positron-emitting glucose analog 18F-2-fluoro-deoxy-d-glucose (FDG). Fractional rates of FDG phosphorylation were measured on a minute-to-minute basis during rest, 3.5 minutes of priming exercise (PE), 15 or 30 minutes of PE recovery, and a subsequent 15-minute period of contractions. Muscles were electrically stimulated at 2 Hz, and force production was held constant during the contraction period(s). FDG uptake did not differ from control values either during PE or during 60 minutes of recovery from PE. In response to 15 minutes of contractions, muscle stimulated without PE demonstrated increased FDG uptake, but only after a delay of 5.0 ± 0.7 minutes. Muscle with PE but rested 15 minutes had increased FDG uptake with a delay of 0.5 ± 0.2 minutes, and muscle with PE but rested 30 minutes had increased FDG uptake after a delay of 8.0 ± 0.9 minutes (P < .01 all groups). All groups reached similar levels of FDG uptake by the end of 15 minutes of contractions. Both groups with PE had control levels of adenosine triphosphate (ATP), phosphocreatine (PCr), and glucose-6-phosphate (G6P) after PE recovery, but glycogen level was lower than the control value (P < .05). During the subsequent 15-minute contractile period, metabolites and glycogen demonstrated similar changes despite differences in rates of FDG uptake. In summary, we have demonstrated that (1) the kinetics of glucose uptake in contracting skeletal muscle can be quantified on a minute-to-minute basis using a positron-emitting 2-deoxyglucose tracer, (2) the early time course of glucose uptake in contracting muscle can be modified by prior contractions, and (3) uptake in the first minutes of contractile activity is determined by factors other than glycogen, G6P, PCr, and ATP.
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U2 - 10.1016/0026-0495(93)90158-K
DO - 10.1016/0026-0495(93)90158-K
M3 - Article
C2 - 8246777
AN - SCOPUS:0027137213
SN - 0026-0495
VL - 42
SP - 1609
EP - 1616
JO - Metabolism
JF - Metabolism
IS - 12
ER -