WARREN, G. L., K. M. HERMANN, C. P. INGALLS, M. R. MASSELLI, and R. B. ARMSTRONG. Decreased EMG median frequency during a second bout of eccentric contractions. Med. Sci. Sports Exerc., Vol. 32, No. 4, pp. 820–829, 2000.
Purpose: Others have reported preferential recruitment of fast motor units in muscles during performance of eccentric contractions and there is evidence that fast muscle fibers are more susceptible to eccentric contraction-induced injury. We tested the hypothesis that during a second bout of maximal eccentric contractions 1 wk after the first, there would be a reduction in the electromyographic (EMG) median frequency (MF) with minimal change in the EMG root-mean-square (RMS), indicating greater reliance on slower motor units. This could provide an explanation for the enhanced resistance to eccentric contraction-induced injury after a single bout of eccentric exercise.
Methods: Human subjects performed 50 maximal voluntary eccentric (N = 10) or concentric (N = 10) contractions of the anterior crural muscles on two occasions separated by 1 wk. To determine whether MF changes during the second bout could be a consequence of injury to fibers in fast motor units, the anterior crural muscles of mice were electrically stimulated to perform 50 maximal eccentric (N = 10) or concentric (N = 9) contractions on two occasions separated by 1 wk. In both the humans and mice, torque production and tibialis anterior muscle RMS and MF were measured during the two exercise bouts.
Results: In human tibialis anterior muscle, MF was 30% lower (P < 0.01) during the second eccentric bout although RMS was the same. In the mice, RMS and MF were unchanged at any time after the first eccentric bout despite torque deficits similar to those observed in the humans.
Conclusions: The data indicate that with repetition of maximal voluntary eccentric contractions, there is an increased activation of slow motor units and a concomitant decrease in activation of fast units.
Asingle bout of exercise with eccentric contractions that induces injury is followed by a decreased susceptibility of the muscle to injury in subsequent bouts of eccentric exercise (6,28,29). The mechanism underlying this rapid adaptation has not been elucidated. Hypotheses proposed to explain the phenomenon include: 1) modification of susceptible structures within the muscles; and 2) alteration of patterns of fiber recruitment within or among muscles (6).
Motor unit recruitment with increasing force production normally progresses from slow (Type I fibers) to fast fatigue-resistant (Type IIa fibers) to fast fatiguable (Type IIb fibers) units (5). However, there is evidence that when muscles perform eccentric contractions, there is a greater reliance on fast motor units, both within muscles (16,26) and among synergistic muscles (27). In fact, Nardone and coworkers (26) have shown that some large, very high threshold (and presumably fast) motor units are recruited exclusively during eccentric contractions. In that study, ∼20% of the motor units studied in the gastrocnemius and soleus muscles discharged only during lengthening and not during maximal isometric or ballistic shortening contractions. In light of the evidence that fast muscle fibers are more susceptible to injury than slow fibers during performance of eccentric contractions (10,23,33), it is of interest that these motor units are preferentially recruited for these tasks.
It is not clear from the reported studies whether or not fast motor units continue to be preferentially recruited during eccentric contractions after the movement patterns are “learned.” In fact, there is evidence that in some stereotyped movements, slow fibers are primarily recruited during eccentric contractions. For example, during walking, cat soleus muscle (100% slow fibers) is active during the early stages of the stance phase when the muscle is stretched, with lesser activation of the faster gastrocnemius muscle (32). Also, during downhill walking in rats, most of the injury that occurs in the extensor muscles is in slow fibers (2). These various observations suggest one hypothesis that would explain the apparent anomaly: when confronted with unaccustomed eccentric contractions, the nervous system “naively” elicits an inappropriate recruitment pattern, but with continued performance of the movements, there is a shift to the more typical pattern of activation of motor unit types. Furthermore, a shift away from recruitment of faster motor units toward activation of slower motor units during eccentric contractions could provide a potential mechanism for the reported rapid adaptation that reduces susceptibility to injury in later bouts of eccentric exercise. Also, it may be the initial injury to fast fibers that necessitates greater activation of slower motor units.
The first objective of this study was to determine if electromyographic (EMG) median frequency (MF) was reduced during a second bout of eccentric contractions. Human subjects performed 50 maximal voluntary eccentric contractions of the anterior crural muscles on two occasions separated by one week. The initial EMG MF in tibialis anterior muscle was significantly decreased in the second bout, even though EMG root-mean-square (RMS) did not change. One interpretation of these results was that during the second bout, torque production was maintained through a greater contribution of slower motor units (11,12,22).
The second objective of this study was to determine whether the apparent change in motor unit recruitment in eccentric contractions between the two bouts was the result of injury to fast fibers. We sought to find out if mouse anterior crural muscles when electrically stimulated to perform 50 maximal eccentric contractions would result in injury to fast fibers and elicit a decreased EMG activity during subsequent contractions. The mouse data suggest that the reduction in MF observed in the human study was not a consequence of fibers in fast motor units becoming electrically unexcitable as a result of the injury.
Muscle Biology Laboratory, Department of Health and Kinesiology, Texas A&M University, College Station, TX 77843; and Muscle Biology Laboratory, Department of Physical Therapy, Georgia State University, Atlanta, GA 30303
Submitted for publication August 1998.
Accepted for publication January 1999.
Address for correspondence: Gordon L. Warren, Department of Physical Therapy, University Plaza, Georgia State University, Atlanta, GA 30303-3083; E-mail firstname.lastname@example.org.