Received April 24, 2006
Revised July 10, 2006
Accepted after revision July 17, 2006

¹ University of Maryland School of Medicine

^* To whom correspondence should be addressed. E-mail: druss{at}som.umaryland.edu.

	Abstract

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 2-fold difference in stimulation frequency (15 vs. 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, 30 Hz_supra). Muscles were subjected 1-, 15, 30- and 80-Hz stimulation trains prior to and following 2 min of fatiguing stimulation. The principle findings were that the two 30-Hz protocols produced greater p38 phosphorylation than the 15-Hz protocol (1.4-1.5 vs 1.1-fold), as well as greater fatigue (65-78% vs. 43% decline). In contrast, JNK phosphorylation appeared most responsive to total (active + passive) tension such that the changes followed the pattern: 30 Hz_supra > 15-Hz > 30 Hz_sub, while ERK 1/ 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 signaling pathways in skeletal muscle, independent of force production.

Key Words: Electrical stimulation, Muscle fatigue, Protein kinase

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