Identification and characterisation of heel strike transient

Abstract

This study set out to ascertain the incidence of a heel strike transient (HST) and to verify whether modifications of muscle activation time could be correlated with the presence and the characteristic of a HST. Lower limb kinematics, kinetics and surface electromyography (SEMG) of normal subjects were examined during barefoot walking. A short-lived sharp HST was present in 76% of the trials while a smooth HST, of longer duration was seen in 13.3% of the trials. The transient phenomenon was absent in the remaining 10.7% of trials. The SEMG showed that alteration in the activation timing of muscles correlated with the presence of a HST.

Introduction

During normal walking the function of the foot at the onset of the support phase is to smooth impact with the ground thereby protecting the rear foot and shank from impulsive loads [1], [2]. The lower limb can be exposed to an impulsive load, the heel strike transient (HST), at heel strike (HS) [3], [4], [5]. In the literature the HST has been described as appearing in the vertical component of the ground reaction force (GRF) [6], [7] as an impulsive event located at 10% of the stance phase and characterised by a frequency range 10–75 Hz [3]. It has also been previously considered an artefact and the uncertain identification of a HST until 1985 was mainly due to the low cut-off of the filters used for force-plate data pre-processing [7], [8].

HST is correlated with the aetiology and progression of a variety of pathological conditions, such as osteoarthritis and low back pain [9], [10], [11]. It is considered potentially harmful for joints because of its intensity and its occurrence at each step. It has also been implicated in early prosthetic damage after total knee replacement [12], [13]. HST has also been observed in normal subjects [14].

The aetiology of HST has not yet been completely clarified. O’Connor and co-workers [15] hypothesised a relationship between the absence of quadriceps action and the presence of a HST. Their results were based on two subjects examined during free walking after an injection of xylocaine to the femoral nerve that produced a reversible paralysis of the quadriceps. This would have caused a deceleration of the lower limb before HS and a hard contact of the heel with the ground. Compensatory mechanisms induced by the temporary paralysis may also have been important and so the onset of HST may not have been due solely to the influence of quadriceps activation.

Both passive tissue properties and active movements of lower limbs contribute to cushioning of the foot at impact with the ground. The impact intensity on the floor can be reduced by shock-absorbing reactions at the ankle, knee and hip. Foot pronation is one of the mechanisms that reduce the impact and another is the control the acceleration of the leg landing on the ground just before foot contact [11], [15]. In both cases, muscle activation plays a key role [1], [2]. A HST is also seen in young healthy subjects [16], which warrants further investigation.

The purpose of our investigation was to characterise the HST further, to define it in terms of amplitude, time and frequency localisation and to investigate possible correlations between HST presence and alteration of muscular activation timing (AT).