In human locomotion the ability to generate and sustain mechanical power output is dependent on the organised variability in contractile and metabolic properties of the muscle fibres that comprise the active muscles.
In studies of maximum cycling exercise of short duration (10Ð25 s we used a microdissection technique to obtain fragments of single muscle fibres from needle biopsies before and after exercise. In this technique each fibre fragment was divided into two parts. One part was used to characterize the fibre type in respect of the heavy chain myosin isoform expressed. The other part of the fragment was used to determine high energy phosphate concentration (Sant’Ana Pereira et al. 1996; Karatzaferi et al. 2001). Fibres were classified on the basis of expressing either type I, type IIA, or type IIX myosin heavy chain isoforms. It should be noted, however, that in the type II population many fibres co-expressed both IIA and the IIX isoforms and we therefore characterized these fibres on the basis of the degree of co-expression. Moreover, while there were significant numbers of fibres expressing only the IIA isoform very few fibres were seen in our normal healthy subjects which only expressed IIX.
We were able to show that immediately following 25 s of maximal effort exercise, during which mechanical power output declined by ~50 %, phosphocreatine (PCr) was reduced to zero, or near zero levels in all fibres. ATP was also reduced from 53 to 34 % of resting levels in the type II fibre subgroups, and to ~75 % in type I fibres, with a concomitant increase in IMP (Sant’Ana Pereira et al. 1996).
Subsequently we sought to explore the time course of this dramatic depletion in high energy phosphate using shorter duration cycling exercise (~20 contractions in 10 s; Karatzaferi et al. 2001). In these experiments maximum power output decreased by ~23 %. Fibre fragments were classified as either type I, IIA, IIAx or IIXa (the latter two classifications of co-expressing fibres having respectively a predominance of type IIA or IIX isoform). Immediately post-exercise PCr content in the four fibre populations decreased to 54, 47, 38 and 41 % of resting values. ATP showed no change in type I fibres but decreased to 75, 33 and 30 % of resting values in type IIA, IIAx and IIXa fibre groups. There was no detectable IMP in the type I fibres but significant IMP production in type II fibre populations despite the presence of PCr. The results suggest that maximal all-out exercise presented a sequential metabolic challenge to first the type IIX-expressing fibres, then IIA fibres and finally the type I fibres. It seems entirely reasonable that during maximal activation those fibre populations with the fastest cross-bridge cycling rates, as determined by myosin heavy chain isoform expressed, will deplete high energy phosphates at the greatest rate, resulting in selective fatigue of that population. Thus although the whole muscle mechanical ouput may decrease by only 25 % in 20 contractions this may obscure the fact that some fibre populations may be generating very little mechanical ouput while others will be relatively unaffected. The progressive reduction of power during maximal sprint efforts may be interpreted as the cumulative effect of metabolic depletion in successive fibre type populations from IIX to IIXa to IIAx to IIA to I.
This interpretation would be consistent with a previous observation that prior exercise (6 min at 90 % VO2,max) resulted in a decrease in maximum leg extension power that was velocity dependent. As the contraction velocity at which maximum power was measured increased, so did the magnitude of the fatigue. It was suggested that this was due to the selective fatigue of the fastest fatigue-sensitive fibres, which in a mixed muscle will contribute an increasing proportion of the maximum power output as velocity increases (Beelen & Sargeant, 1991).
Nevertheless, the relative contribution of different muscle fibre populations to mechanical ouput during whole body human movement of different intensities, types, and velocity remains a matter of some conjecture. Although one important future application of our microdissection technique is that PCr content may be used as a very sensitive metabolic marker for fibre type recruitment during very short duration exercise involving only a few contractions. In a recent communication to the Society we have shown that after even four contractions of the knee extensor muscles there are detectable changes in PCr content (Beltman et al. 2001).
There are considerable difficulties in relating the contraction velocity of isolated muscle preparations to human whole body exercise and quantifying the contribution of different fibre type populations to mechanical output. Nevertheless the issue is of considerable interest, having as it does an impact on choice of movement cadence as it affects power output, mechanical efficiency, and strategies for improving muscle function including during, e.g. functional electrical stimulation and rehabilitation therapy. In a series of experiments since 1981 we have used cycling as an experimental model and believe that there is accumulating evidence to support the view that under normal conditions human type I fibres will be operating around their optimum for maximum power at a pedalling rate of about 60 rev min-1, with type IIA fibres, and those expressing increasing proportions of IIX myosin heavy chain isoform having optima at increasing pedalling speeds. Similarly we believe that the efficiency/velocity relationship can be placed in relation to whole body cycling exercise (Sargeant, 1999).
All procedures accord with current local guidelines and the Declaration of Helsinki.