Presented at NACOB 98: North American Congress on Biomechanics Canadian Society for Biomechanics - American Society of Biomechanics University of Waterloo Waterloo, Ontario, Canada August 14-18, 1998

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FORCE DEPRESSION FOLLOWING SHORTENING IN MAMMALIAN SKELETAL MUSCLE:
ENERGY CONSIDERATIONS

W. Herzog ¹ , J.Z. Wu ¹ , T.R. Leonard ^1
1 Faculty of Kinesiology, The University of Calgary
Calgary, AB, Canada T2N 1N4

INTRODUCTION

The fact that isometric forces in skeletal muscles following shortening are lower compared to the corresponding isometric forces of a purely isometric contraction has been known for almost half a century (Abbott and Aubert, 1952). However, a convincing explanation for these force depressions following shortening has not been found, and neither is there an accepted mathematical model for this observation. Qualitatively, many factors have been implicated with the force depressions following shortening; primarily the speed of shortening and the magnitude of shortening. The latter of these two factors (the magnitude of shortening) has been well accepted, whereas the former (the speed of shortening) has been criticized most recently by Herzog and Leonard (1997). The criticism on the speed of shortening as a factor related to force depression was based on the fact that muscle shortening at high speeds causes low forces during shortening while the opposite is correct for low speeds of shortening. Therefore, it was not obvious whether the speed or the force during the shortening phase was the factor responsible for the observed force depressions following muscle shortening.

Hypothesis: Based on our previous research, we hypothesize that the distance of shortening and the force during shortening are the primary factors associated with force depressions in mammalian skeletal muscle. If so, the integral of force over the distance shortened (i.e. the work performed by the muscle during shortening) might explain much of the steady-state force depression following shortening contractions.

Purpose: The purpose of this study was to test the hypothesis that steady-state force depression following shortening in mammalian skeletal muscle is explained to a large degree by the work performed by the muscle during shortening, independent of the contractile conditions.

METHODS

Experimental preparation: Experiments were performed on cat soleus muscles (n=8). Experiments in which soleus force dropped below 90% of the initial reference contraction during the experimental period (about 14 hours) were disregarded, leaving six muscles for analysis. Animal preparation, muscle preparation and experimental set up have been described in detail elsewhere (Herzog and Leonard, 1997) and will not be repeated here.

Protocol: Six tests were performed with each of the muscles. The tests were aimed at providing a variety of different contractile conditions and to change one contractile parameter while leaving others constant. In test 1, the activation and speed of shortening of the muscle were kept constant while the shortening distance was varied systematically from 0 to 8 mm in steps of 2 mm (Fig. 1). In test 2, the activation and shortening distance were kept constant while systematically varying the speed (and therefore, the force) of shortening. In test 3, the shortening distance and speed were kept constant while varying the activation of the muscle (Fig. 2). Activation was altered by changing the current for tibial nerve stimulation, thereby changing the number of activated motor units. Test 4 was identical to test 3 except that there was no muscle shortening while the activation of the muscle was changed from a standard activation to a lower than standard activation and back to the standard activation. Finally, in tests 5 and 6, muscle shortening was performed with changing (i.e. non-constant) speeds and activations, respectively.

RESULTS

The two basic predictions in this study were that force depressions increase with increasing shortening distance and increasing force during shortening. Both of these predictions were supported (Figs. 1,2).

Fig. 1: Force-time histories for contractions of varying shortening distances

Fig. 2: Force-time histories for contractions at varying forces

The hypothesis to be tested was that the work performed during the shortening phase (i.e. o dr) was directly related to the steady-state force depression, that is the larger the work the more pronounced the force depression. This hypothesis was also supported in the current study (Fig. 3).

Fig. 3: Force depression as a function of muscular work

DISCUSSION AND CONCLUSION

For the past 50 years, force depressions in skeletal muscles following shortening were associated with the speed of shortening and were typically assumed to be multi-factorial (e.g. Abbott and Aubert, 1952). Here, we provide first evidence that force depressions may not be related to the speed of shortening, but rather to the force of shortening which varies as a function of the speed according to the force-velocity relationship (Hill, 1938). Furthermore, we suggest that the steady-state force depressions following muscle shortening may depend on a single scalar variable, the work performed by the muscle during the shortening phase. To date, the work performed by the muscle has never been associated with force depression but it fits nicely into our proposed mechanism of force depression; a stress-dependent inhibition of cross-bridge attachments in the zone of newly formed myofilament overlap during shortening (Herzog and Leonard, 1997).

Force depressions were related to muscular work independent of the contractile conditions and the level of activation. Therefore, the results obtained here appear to be general and may apply to any contractile conditions during the shortening phase.

The result that muscular work during the shortening phase explains most (if not all) of the experimentally observed force depression is appealing as it is easy to implement into existing cross-bridge models of muscular contraction (Huxley, 1957). Furthermore, and in contrast to previous attempts of accounting for force depressions in cross-bridge models, the present model is based on a biological mechanism rather than a mathematically convenient but biologically untenable (memory) function.

REFERENCES

1. Abbott, B.C. and Aubert, X.M. J. Physiol (London), 117:77-86, 1952

2. Herzog, W. and Leonard, T.R. J. Biomech. 30(9):865-872, 1997

3. Hill, A.V. p. 136-195, In: Proc. Royal Soc. London, 1938

4. Huxley, A.F. Prog. Biophys. Biophys. Chem. 7:255-318, 1957

ACKNOWLEDGMENTS

NSERC of Canada