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Acute resistance exercise activates MAP kinase signaling in skeletal muscle of overweight women
Author(s) -
Crane Justin,
Douglass Matthew,
Trappe Todd,
Trappe Scott,
Harber Matthew
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb105-a
Subject(s) - kinase , medicine , endocrinology , p38 mitogen activated protein kinases , mitogen activated protein kinase , signal transduction , protein kinase a , biology , chemistry , microbiology and biotechnology
The mitogen‐activated protein (MAP) kinase pathways are responsive to exercise and function to regulate substrate selection and numerous other cellular processes. Recent evidence suggests that excessive rates of intramuscular lipid storage may alter basal MAP kinase signaling. However, it is unknown if high rates of lipid availability alter the MAP kinase signaling response to exercise. Therefore, the purpose of this study was examine the influence of acute resistance exercise (RE) on the activation of extracellular signal‐regulated kinase‐1/2 (ERK1/2), stress activated protein kinase/c‐Jun NH2‐terminal kinase (SAPK/JNK) and p38 in women with high body fatness. Six overweight women with a high percent body fat (age 29±3 yr, BMI 28±3 kg/m 2 , body fat 38±4%) performed 6 sets of 10 repetitions of knee extension exercise at 70% 1RM. Muscle biopsies were obtained from the vastus lateralis before, l min after (POST1), and 2 hrs after (POST2) exercise. Activation of ERK1/2, SAPK/JNK, and p38 were determined via western blotting. ERK1/2, SAPK/JNK, and p38 phosphorylation were increased (P<0.05) ~2–3‐fold at POST1 and ERK1/2 remained elevated and POST2 whereas SAPK/JNK and p38 returned to basal levels. These data suggest that high levels of body fatness do not impair the MAP kinase signaling response to exercise.