In the period 1971-76, much of Richard Edward's research was concerned with fatigue and, at the suggestion of David Hill, the first topic to be examined was slowing of relaxation from prolonged contractions (Edwards et al., 1972). Although initially studied with isometric contractions, it became evident that slow relaxation is symptomatic of a general reduction in the speed of shortening and is a major factor leading to loss of power. While maximum shortening velocity is reduced in these circumstances, we have shown that an increase in curvature of the force-velocity relationship is probably the more important factor causing the loss of power and argue that this is due to slower cross bridge attachment (Jones et al., 2006). Whilst these changes must, ultimately, have a metabolic origin, it proves difficult to identify the precise cause from measurements made with intact human muscle as there are poor correlations between the time courses of metabolite change and slowing of the muscle (Jones et al., 2009). It is notable, however, that during sustained contractions the slowing of contractile properties is most pronounced at a time when isometric force starts to decline rapidly, probably due to reduced calcium release. The rate of force redevelopment (ktr) is known to be sensitive to activating calcium and in low calcium solutions there is a reduction in the apparent rate constant for cross bridge attachment in skinned fibres. It is an interesting possibility, therefore, that during acute fatigue a failure of EC coupling affects not only the number of attached cross bridges but also their kinetic properties leading to the characteristic loss of power and performance. Edwards, R.H.T., Hill, D.K. & Jones, D.A. (1972) Journal of Physiology 227, 26-27P. Jones, D.A., de Ruiter, C.J. & de Haan, A. (2006) Journal of Physiology 576, 913-922. Jones, D.A., Turner, D.L., McIntyre, D.B. & Newham, D.J. (2009) Journal of Physiology 587, 4329-4338 begin_of_the_skype_highlightingend_of_the_skype_highlighting.