ABSTRACT
AIM: Changes in muscle stiffness after exercise-induced muscle damage have been classically inferred from passive torque-angle curves. Elastographic techniques can be used to estimate the shear modulus of a localized muscular area. This study aimed to quantify the changes in shear elastic modulus in different regions of the elbow flexors after eccentric exercise and their relation to muscle length. METHODS: Shear elastic modulus and transverse relaxation time (T2 ) were measured in the biceps brachii and brachialis muscles of sixteen participants, before, 1 h, 48 h and 21 days after three sets of ten maximal isokinetic eccentric contractions performed at 120° s(-1) . RESULTS: The shear elastic modulus of the elbow flexors significantly increased 1 h (+46%; P = 0.005), with no significant change at 48 h and 21D, post-exercise. In contrast, T2 was not modified at 1 h but significantly increased at 48 h (+15%; P < 0.05). The increase in shear elastic modulus was more pronounced at long muscle lengths and reached a similar extent in the different regions of the elbow flexors. The normalized hysteresis area of shear elastic modulus-length relationship for the biceps brachii increased 1 h post-exercise (31%) in comparison with the pre-exercise value (18%), but was not significantly altered after five stretching cycles (P = 0.63). CONCLUSION: Our results show homogeneous changes in muscle shear elastic modulus within and between elbow flexors. The greater increase in shear elastic modulus observed at long muscle lengths suggests the putative involvement of both cross-bridges number and titin in the modifications of muscle shear elastic modulus after damaging exercise.
Subject(s)
Elastic Modulus/physiology , Muscle Contraction/physiology , Muscle, Skeletal/physiology , Adult , Elasticity Imaging Techniques , Female , Humans , Magnetic Resonance Imaging , Male , Young AdultABSTRACT
Sixteen portal cavernomas were examined with dynamic computed tomography (CT) and confirmed by sonography. Characteristic features included loss of the normal vascular structure and the presence of sinuous collateral pathways which were enhanced during the portal phase. Fifteen patients exhibited transient differences in hepatic attenuation and peripheral arterial concentration of contrast material. Increased arterial flow in the poorly perfused territories is suggested as a cause of these hemokinetic abnormalities.
