The purpose of this study was to investigate changes in muscle hardness after eccentric exercise of the elbow flexors muscles that produce muscle shortening and swelling. To assess muscle hardness, a pressure method was used in which the force required to deform the tissue (skin, subcutaneous tissue, muscle) was recorded. Eleven healthy male students performed 24 maximal eccentric actions of the elbow flexor muscles with their non-dominant arms. Muscle hardness, maximal isometric force (MIF), muscle soreness, plasma creatine kinase (CK) activity, relaxed elbow joint angle (RANG), upper-arm circumference (CIR) and B-mode ultrasound transverse images were measured before, immediately after, and 1-5 days after exercise. A long-lasting decrease in MIF, muscle swelling shown by increases in CIR and muscle thickness, large increases in plasma CK activity, and development of muscle soreness indicated that damage occurred to the elbow flexor muscles. The RANG had decreased by approximately 20 degrees at 1-3 days after exercise and showed a gradual recovery thereafter. The CIR increased gradually after exercise and peaked on day 5 post-exercise, the mean amount of increase in CIR being 18 mm. Muscle hardness measured at the relaxed elbow position did not change until 3 days after exercise, but increased significantly (P < 0.01) on days 4 and 5 post-exercise. On the other hand, muscle hardness measured when forcibly extending the shortened elbow joint increased significantly (P < 0.01) with time and peaked at 3 days after exercise. Muscle hardness assessed by the pressure method seems to reflect changes in muscle stiffness and swelling.

This study aimed to investigate the relationship between muscle hardness and muscle tension in terms of length-tension relationship. A frog gastrocnemius muscle sample was horizontally mounted on the base plate inside a chamber and was stretched from 100 to 150% of the pre-length, in 5% increments. After each step of muscle lengthening, electrical field stimulation for induction of tetanus was applied using platinum-plate electrodes positioned on either side of the muscle submerged in Ringer's solution. The measurement of muscle hardness, i.e., applying perpendicular distortion, was performed whilst maintaining the plateau of passive and tetanic tension. The relationship between normalised tension and normalised muscle hardness was evaluated. The length-hardness diagram could be created from the modification with the length-tension diagram. It is noteworthy that muscle hardness was proportional to passive and total tension. Regression analysis revealed a significant correlation between muscle hardness and passive and total tension, with a significant positive slope (passive tension: r = 0.986, P < 0.001; total tension: r = 0.856, P < 0.001). In conclusion, our results suggest that muscle hardness depends on muscle tension in most ranges of muscle length in the length-tension diagram.

The purpose of the present study was to confirm the relationship between isolated frog muscle tension and muscle hardness by conducting physiological evaluation in vivo. Two different mounting forms of the muscle were adopted. One form placed the gastrocnemius muscle (GA) on a base plate; this dented the muscle as a "mass". The other form tightened the sartorius muscle (SA) between holders in Ringer's solution; this bent the muscle as a "string". The first experimental method allowed testing of muscle hardness during stretching up to 140% (experiment 1) and the other method allowed testing of hardness during tetanic muscle contraction (experiment 2). The response force to vertical distortion, measured as muscle hardness, increased linearly with resting tension increase and this relationship was not influenced by the hysteresis (experiment 1). The response force increments at each level of tetanic muscle tension were proportional to the contracting tension (experiment 2). Although the muscle mounting forms were different, the response force increment to muscle tension in GA and SA showed quite similar relationships in both tests. It seems likely that muscle hardness evaluated by the response force must depend on the amplitude of the tension at the instant of the hardness measurement, regardless of the mounting form or the stretching phase (ascending or descending). In conclusion, muscle hardness measured by perpendicular distortion has physiological significance related to the changes in passive and active muscle tension.

This study aimed to investigate the relationship between the muscle shear modulus of the biceps brachii, urinary titin N-terminal fragment (UTF), and other damage markers after eccentric exercise. Seventeen healthy males performed five sets of ten eccentric exercises with dumbbells weighing 50% of the maximum voluntary contraction (MVC) at the elbow joint. Muscle shear modulus with range of interest set to only biceps brachii muscle measured by ultrasound shear wave elastography, UTF, MVC, range of motion (ROM), and soreness (SOR) were recorded before, immediately after, and 1, 24, 48, 72, 96, and 168 h after eccentric exercise. Each marker changed in a time course pattern, as found in previous studies. The peak shear modulus showed a moderate negative correlation with peak MVC (r = –0.531, P < 0.05) and a strong positive correlation with peak UTF (r = 0.707, P < 0.01). Our study results revealed a significant relationship between muscle strength, shear modulus measured by ultrasound SWE, and titin measured by UTF, as a non-invasive damage marker after eccentric exercise to track changes in EIMD.