Experiments were carried out to test the effect of prolonged and repeated passive stretching (RPS) of the triceps surae muscle on reflex sensitivity. The results demonstrated a clear deterioration of muscle function immediately after RPS. Maximal voluntary contraction, average electromyographic activity of the gastrocnemius and soleus muscles, and zero crossing rate of the soleus muscle (recorded from 50% maximal voluntary contraction) decreased on average by 23.2, 19.9, 16.5, and 12.2%, respectively. These changes were associated with a clear immediate reduction in the reflex sensitivity; stretch reflex peak-to-peak amplitude decreased by 84. 8%, and the ratio of the electrically induced maximal Hoffmann reflex to the maximal mass compound action potential decreased by 43. 8%. Interestingly, a significant (P < 0.01) reduction in the stretch-resisting force of the measured muscles was observed. Serum creatine kinase activity stayed unaltered. This study presents evidence that the mechanism that decreases the sensitivity of short-latency reflexes can be activated because of RPS. The origin of this system seems to be a reduction in the activity of the large-diameter afferents, resulting from the reduced sensitivity of the muscle spindles to repeated stretch.

The spring-mass model, representing a runner as a point mass supported by a single linear leg spring, has been a widely used concept in studies on running and bouncing mechanics. However, the measurement of leg and vertical stiffness has previously required force platforms and high-speed kinematic measurement systems that are costly and difficult to handle in field conditions. We propose a new “sine-wave” method for measuring stiffness during running. Based on the modeling of the force-time curve by a sine function, this method allows leg and vertical stiffness to be estimated from just a few simple mechanical parameters: body mass, forward velocity, leg length, flight time, and contact time. We compared this method to force-platform-derived stiffness measurements for treadmill dynamometer and overground running conditions, at velocities ranging from 3.33 m·s–1to maximal running velocity in both recreational and highly trained runners. Stiffness values calculated with the proposed method ranged from 0.67% to 6.93% less than the force platform method, and thus were judged to be acceptable. Furthermore, significant linear regressions (p< 0.01) close to the identity line were obtained between force platform and sine-wave model values of stiffness. Given the limits inherent in the use of the spring-mass model, it was concluded that this sine-wave method allows leg and stiffness estimates in running on the basis of a few mechanical parameters, and could be useful in further field measurements.

The observed constant ankle joint stiffness may depend on (constant) tendon stiffness because of its dominating role in triceps surae muscle-tendon unit. Thus, we conclude that in sprint running the spring-like behavior of the leg might be adjusted by changing the stiffness of the knee joint. However, in complicated motor task, such as sprint running, ankle and knee joint stiffness might be controlled by the individual mechanical and neural properties.

Almost 10% of young men had poor fitness and apparently low physical activity, but they reported very high physical activity by IPAQ. An evident need therefore exists to develop IPAQ further to solve the apparent overreporting by a considerable proportion of sedentary individuals.

The increased EMG of working muscles and the associated increase in power output may partly explain the increased energy expenditure with increasing running speed. Lower performances in running economy by some of the athletes may also be explained by poor running technique, such as unusually high braking and mediolateral forces, which may be caused by limited action of the hamstring muscles. However, no exclusive biomechanical parameters could be identified to explain the running economy.

Electromyographic (EMG) activity of the leg muscles and the ground reaction forces were recorded in 17 elite male middle-distance runners, who performed isometric maximal voluntary contractions (MVC) as well as running at different speeds. Electromyograms were recorded from the gluteus maximus, vastus lateralis, biceps femoris, gastrocnemius and tibialis anterior. The results indicated that the averaged EMG (aEMG) activities of all the muscles studied increased (P < 0.05) with increasing running speed, especially in the pre-contact and braking phases. At higher speeds, the aEMG activities of the gastrocnemius, vastus lateralis, biceps femoris and gluteus maximus exceeded 100% MVC in these same phases. These results suggest that maximal voluntary contractions cannot be used as an indicator of the full activation potential of human skeletal muscle. Furthermore, the present results suggest that increased pre-contact EMG potentiates the functional role of stretch reflexes, which subsequently increases tendomuscular stiffness and enhances force production in the braking and/or propulsive phases in running. Furthermore, a more powerful force production in the optimal direction for increasing running speed effectively requires increased EMG activity of the two-joint muscles (biceps femoris, rectus femoris and gastrocnemius) during the entire running cycle.

The mechanisms related to the acute and delayed secondary impairment of the stretch reflex function were investigated after long-lasting stretch-shortening cycle exercise. The results demonstrated a clear deterioration in muscle function immediately after fatigue, which was accompanied by a clear reduction in active and passive reflex sensitivity. For active and passive stretch reflexes, this reduction was biphasic (P < 0.05 to P < 0.001). However, for the ratio of the electrically induced maximal Hoffmann reflex to the maximal mass compound action potential, only one significant reduction was seen immediately after fatigue (71.2%, P < 0.01). A similar significant (P < 0.01) decrease in the stretch-resisting force of the muscle was also detected. Clear increases were found in the indirect markers of muscle damage (serum creatine kinese activity and skeletal troponin I), which could imply the occurrence of ultrastructural muscle damage. It is suggested that the acute reduction in reflex sensitivity is of reflex origin and due to two active mechanisms, disfacilitation and presynaptic inhibition. However, the delayed second decline in the sensitivity of some reflex parameters may be attributable to the secondary injury, because of some inflammatory response to the muscle damage. This might emphasize the role of presynaptic inhibition via group III and IV muscle afferents.

The present study was designed to investigate interactions between running economy and mechanics before, during, and after an individually run marathon. Seven experienced triathletes performed a 5-min submaximal running test on a treadmill at an individual constant marathon speed. Heart rate was monitored and the expired respiratory gas was analyzed. Blood samples were drawn to analyze serum creatine kinase activity (S-CK), skeletal troponin I (sTnI), and blood lactate (B-La). A video analysis was performed (200 frames x s(-1)) to investigate running mechanics. A kinematic arm was used to determine the external work of each subject. The results of the present study demonstrate that after the marathon, a standardized 5-min submaximal running test resulted in an increase in oxygen consumption, ventilation, and heart rate (P < 0.05), with a simultaneous decrease in the oxygen difference (%) between inspired and expired air, and respiratory exchange ratio (P < 0.05). B-La did not change during the marathon, while sTnI and S-CK values increased (P < 0.05), peaking 2 h and 2 days after the marathon, respectively. With regard to the running kinematics, a minor increase in stride frequency and a similar decrease in stride length were observed (P < 0.01). These results demonstrate clearly that weakened running economy cannot be explained by changes in running mechanics. Therefore, it is suggested that the increased physiological loading is due to several mechanisms: increased utilization of fat as an energy substrate, increased demands of body temperature regulation, and possible muscle damage.