## 3 Data Acquisition and Processing
### Statistics  
Assessment Duration  
Approximately one-third of the gait cycle has non-zero KIN knee moments yet absent or low-amplitude EMG. Forces and moments at adjacent joints can initiate motion at the knee [71; 72; 73]. At least four factors--not directly associated with muscle forces acting at the knee joint--contribute to the observed pre-swing and early swing knee flexion (Figure 3).  
Figure 3: Periods of the gait cycle where power is produced by factors other than knee muscle forces. These factors include (**A**) transverse plane rotation of the hip during pre-swing and early swing to advance the ipsilateral limb; (**B**) power is produced at the anterior hip by the hip joint capsule via elastic recoil; pre-swing plantar flexion (**C**) then passively flexes the knee prior to the onset of the swing phase. Concentric contraction by one of the quadriceps muscles (Rectus Femoris) actively flexes the hip (**D**), which leads to passive flexion of the ipsilateral knee. The percent gait cycle for each is shown on the abscissa for each curve.  
Coincident with contralateral initial foot contact, the transverse plane (horizontal) hip rotation changes direction (Figure 3A). This directional change in hip rotation begins in pre-swing as the ipsilateral hip rotates forward along the line of progression. Thus, the swing phase step length is enhanced. Non-contractile elements, such as the anterior aspect of the hip joint capsule, generate forces that generally restrain motion [40,74,75]. These forces (and resultant power) are substantial, particularly at the end range of motion. The net result at the hip is energy stored during pre-swing, then released as positive power to augment swing phase hip flexion (Figure 3).  
The vigorous plantar flexion observed in pre-swing (Figure 3C) leads to substantial knee flexion, as part of a closed kinetic chain [76]. Finally, early swing is notable for activation of ipsilateral hip flexors (Figure 3D) and associated knee flexion [39]. The combination of these four sequential events--hip transverse rotation, hip flexion due to passive soft tissue forces, ankle plantar flexion, and hip flexion due to concentric forces by hip muscles--leads to knee flexion in the absence of substantial force production by muscles crossing the knee.  
As the swing phase continues, hip flexion slows, and knee extension is generated due to the transfer of energy between linked leg segments [76]. Consequently, the EMG-to-force processing examination period began in early swing (68%GC) and concluded when all vastus or hamstring muscle activity ended (32% of the ensuing stride). Thus, each EMG-activity period was about 770 ms in duration, and two-thirds (about 64%GC) of the gait cycle had large power produced by only knee muscles.  
EMG activity was recorded from several muscles that cross both the knee and hip, affecting the net knee moment, yet their power production has been reported previously [39,40]. The rectus femoris (RF) power was out of phase with the other quadriceps muscles (VL, VI, VMO). RF is unique among the knee extensors as it is biaticular, and previous work has demonstrated its primary (perhaps only) role in gait is as a hip flexor [42]. Tensor Fascia Lata provides a modest amount of power and is included in this analysis to compare EFP and KIN methods only. TFL gait power has been reported elsewhere [42]. Finally, gastrocnemius pre-swing power (MGAST, LGAST) directly results in knee flexion [41]. Neither MGAST nor LGAST is active in swing and thus does not contribute to the knee flexion observed during that gait period. The power produced by these plantar flexor muscles has also been reported elsewhere [42].