Shock absorption during forefoot running and its relationship to medial longitudinal arch height.

BACKGROUND: Overuse injuries to the lower extremity have often been connected with the repetitive loading of the foot and in particular its ability to absorb shock. The shock absorbing ability of the foot is thought to relate to its structure, particularly the height of the medial longitudinal arch. The purpose of this study was to investigate the shock absorption characteristics of the foot in forefoot running as measured by the dynamic load rate of the vertical ground reaction forces during the early stages of ground contact and to relate these characteristics to the height of the medial longitudinal arch. METHODS: Eighteen normal athletic adult volunteers were used as subjects and all had clinically normal feet. An Arch Index was computed from lateral radiographs taken with the foot in a full weightbearing position. Dynamic load rate was computed as the first differential of the vertical force as measured by a Kistler force platform. Each subject performed ten trials of running at a speed of 3 m.s-1 using forefoot running style. RESULTS: The dynamic load rate showed three definite peaks (mean 93, 18, and 16 kNs-1 respectively), and two intervening troughs (mean 18 and 3 kNs-1 respectively), showing that the process of shock absorption was one that was progressive over the foot loading phase. The time at which these features occurred indicated a consistency in process of shock absorption. However, none of the force peaks or load rate peaks correlated with the Arch Index. CONCLUSION: It was concluded that the structure of the foot as characterized by the Arch Index, was not the major factor in determining the way in which force is transmitted to the musculoskeletal system in forefoot running. These findings support the concept that the height of the arch, although a commonly used clinical descriptor of foot type does not appear to be important in defining the functional capacity of the foot in action.

Ischaemic preconditioning of skeletal muscle. 1. Protection against the structural changes induced by ischaemia/reperfusion injury.

Ischaemic preconditioning is a process by which exposure of a tissue to a short period of non-damaging ischaemic stress leads to resistance to the deleterious effects of a subsequent prolonged ischaemic stress. It has been extensively described in the heart, but few studies have examined the possibility that it can occur in skeletal muscle. We have used a rat model of ischaemia of one limb to examine this possibility. Exposure of the hind limb to a period of ischaemia of five minutes and reperfusion for five minutes significantly protected the tibialis anterior muscle against the structural damage induced by a subsequent period of limb ischaemia for four hours and reperfusion for one hour. This protection was evident on examination of the muscle by both light and electron microscopy. Longer or shorter times of prior ischaemia had no effect.

Ischaemic preconditioning of skeletal muscle 2. Investigation of the potential mechanisms involved.

We have previously shown that prior exposure of rat hind limbs to ischaemia for five minutes and reperfusion for five minutes reduced the structural damage to skeletal muscle which followed a subsequent period of ischaemia for four hours and reperfusion for one hour. We have now examined the potential mechanisms by which this ischaemic preconditioning protocol may be effective in reducing damage to skeletal muscle induced by prolonged ischaemia and reperfusion. Prior exposure of the hindlimb to ischaemia for five minutes and reperfusion for five minutes did not prevent the fall in the ATP content of tibialis anterior which occurred after a subsequent period of ischaemia for four hours and reperfusion for one hour. Similarly, no effect of the preconditioning protocol was seen on the elevated muscle myeloperoxidase, indicative of an elevated neutrophil content, or abnormal muscle cation content. Reperfused ischaemic muscle was also found to have an increased content of heat-shock protein (HSP) 72, but the preconditioning protocol did not further increase the content of this or other HSPs indicating that it was not acting by increasing the expression of these cytoprotective proteins. The protective effects of preconditioning appeared to be mimicked by the infusion of adenosine to animals immediately before exposure to the four-hour period, indicating a potential mechanism by which skeletal muscle may be preconditioned to maintain structural viability.