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This Article Full Text Full Text (PDF) All Versions of this Article: 91/6/957    most recent expphysiol.2006.034249v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Russ, D. W. Articles by Lovering, R. M. Search for Related Content PubMed PubMed Citation Articles by Russ, D. W. Articles by Lovering, R. M. Related Collections Muscle

Departments of ¹ Physical Therapy & Rehabilitation Science² Physiology, University of Maryland-Baltimore School of Medicine, Baltimore, MD 21201, USA

Activation frequency as a regulator of physiological responses in skeletal muscle, independent of contractile force, has received little attention. Here, the length–tension and force–frequency relationships were employed to keep active contractile force equal, despite a twofold difference in stimulation frequency (15 versus 30 Hz). Rat tibialis anterior muscles were tested in situ using 15 Hz stimulation at optimal length (15 Hz) and 30 Hz stimulation at shortened and lengthened positions (30 Hz_sub and 30 Hz_supra). Muscles were subjected to 1, 15, 30 and 80 Hz stimulation trains before and after 2 min of fatiguing stimulation. The principal findings were that the two 30 Hz protocols produced greater 38 kDa MAPK (p38) phosphorylation than the 15 Hz protocol (1.4- to 1.5-fold versus 1.1-fold), as well as greater fatigue (65–78 versus 43% decline in contraction force). In contrast, c-jun amino terminal kinase (JNK) phosphorylation appeared most responsive to total (active plus passive) tension such that the changes followed the pattern: 30 Hz_supra > 15 Hz > 30 Hz_sub, while 44 and 42 kDa extracellular regulated kinase (ERK1/2) phosphorylation was not significantly increased in response to any of the protocols studied. Neither glycogen depletion nor myofibre damage accounted for any of the findings, but a decline in muscle excitation (m-wave) may have contributed to the greater fatigue seen at higher frequencies. These data suggest that neuromuscular activation frequency can influence certain signalling pathways in skeletal muscle, independent of force production.

(Received 24 April 2006; accepted after revision 17 July 2006; first published online 20 July 2006)
Corresponding author D. W. Russ: Department of Physical Therapy & Rehabilitation Science, University of Maryland-Baltimore, School of Medicine, 100 Penn Street, Baltimore, MD 21201, USA. Email: druss{at}som.umaryland.edu

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