To assess speed- and gait-related changes in semitendinosus (ST) activ
ity, EMG was recorded from three cats during treadmill locomotion. Sel
ected step cycles were filmed, and hip and knee joint kinematics were
synchronized with EMG records. Swing-phase kinetics for trot and gallo
p steps at 2.25 m/s were compared for gait-related differences. Also,
swing kinetics for different gallop forms were compared. With few exce
ptions, ST-EMG was characterized by two bursts for each step cycle; th
e first preceded paw off (STpo), and the second preceded paw contact (
STpc). The two-burst pattern for the walk was defined by a high-amplit
ude STpo burst and a brief, low-amplitude STpc burst; at the slowest w
alk speeds, the STpc burst was occasionally absent. For the trot, the
STpo burst was biphasic, with a brief pause just after paw off. With i
ncreasing walk-trot speeds, the duration of both bursts (STpo, STpc) r
emained relatively constant, but recruitment increased. Also, the onse
t latency of the STpo burst shifted, and a greater proportion of the b
urst was coincident with knee flexion during early swing. At the trot-
gallop transition, there was an abrupt change in the two-burst pattern
, and galloping was characterized by a high-amplitude STpc burst and a
brief, low-amplitude STpo burst. At the fastest gallop speeds, the ST
po burst was often absent, and the reduction in or elimination of the
burst was associated with a unique pattern of swing phase kinetics at
the knee. Knee flexion during the gallop swing was sustained by two in
ertial torques related to hip linear acceleration (HLA) and leg angula
r acceleration (LAA); correspondingly, muscle contraction was unnecess
ary. Conversely, knee flexion at the onset of the trot swing relied on
a flexor muscle torque at the knee acting with an inertial flexor tor
que (LAA). Rotatory and transverse gallops at 4.0 m/s had similar swin
g phase kinetics and ST-EMG. Gait-related changes in ST-EMG, particula
rly at the trot-gallop transition, are not congruent with neural model
s assuming that details of the ST motor pattern are produced by a spin
al CPG. We suggest that motor patterns programed by the spinal CPG are
modulated by input from supraspinal centers and/or motion-related fee
dback from the hindlimbs to provide appropriate gait-specific activati
on of the ST.