Supervisors info:
Αθανασόπουλος Σ., Επίκουρος Καθηγητής, ΤΕΦΑΑ, ΕΚΠΑ
Γελαδάς Ν.,Επίκουρος Καθηγητής, ΤΕΦΑΑ, ΕΚΠΑ
Δημόπουλος Κ., Καθηγητής, ΕΚΠΑ
Summary:
High intensity and/or unaccustomed exercise can cause damage to the muscle tissue, which is associated with structural and metabolic alterations of the muscle cells. Previous studies have reported a significant strength decline and a leak of muscle enzymes in the blood following muscle damage. However, little is known regarding the impairment of neuromuscular function and its relationship with the changes in biochemical markers of muscle damage. The present study examined the changes in neuromuscular function and inflammation indicators in the blood, following two different types of muscle damage- inducing exercise. Fourteen male volunteers, who had not been previously involved in a resistance training program, were divided into two groups and preformed either 50 maximal eccentric (eccentric exercise group; EE, n=7) or 50 maximal isometric contractions (isometric exercise group; IE, n=7), using the elbow flexors of the non-dominant arm. The isometric contractions were performed with the shoulder held at 45o extension from the neutral position, and the elbow at 140o. Neuromuscular function of the elbow flexors was assessed immediately before and after, and then daily for the 4 days following the muscle damage- inducing exercise. Measurements included maximal isometric force and time to peak force at 20o, 40o, 90o, 110o, and 130o of elbow flexion, perception of force production and joint position, flexed and relaxed elbow angle and muscle soreness. Blood samples were analyzed for creatine kinase (CK), CK-isoenzyme MB, lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT) and C-reactive protein (CRP). Data were analyzed using two-way analysis of variance, with repeated measures on one factor. Spearman and Pearson correlation coefficients were used where appropriate, to assess the relationships between variables.
Both types of muscle damage- inducing exercise (EE and IE) resulted in a more pronounced decrease of maximal isometric force at the more acute elbow angles (110o, and 130o), which was similar for the two groups. However, maximal isometric force with the elbow at the more extended position was reduced less following the IE, compared to the EE. Similarly, the ratio of the time to peak force: peak force, as well as the reported muscle soreness were higher at the EE, compared with the IE group (P<0.05). Changes in the relaxed and flexed elbow angles were similar between the two groups. The markers of muscle damage in the blood were increased in both groups, with a higher increase in the EE group. However, the inflammatory marker CRP remained unchanged. Significant correlations were obtained between the changes in maximal force production and the biochemical indicators of muscle damage, only in the EE group. Moreover, significant correlations were found between most of the measured parameters of muscle function.
The more pronounced decrease in maximal isometric force at the more acute elbow angles may be explained by the overextended sarcomeres theory, which relates the structural damage with the functional impairment of muscle tissue. Similarly, the changes in neuromuscular function found in this study may be related to structural disturbances of muscle spindles and Golgi tendon organs.
