Effects of physical activity and experimental diabetes on carbonic anhydrase III and markers of collagen synthesis in skeletal muscle and serum

Abstract

The adaptations of skeletal muscle carbonic anhydrase III (CA III) and collagen and tendon collagen expression to immobilization and subsequent remobilization were studied. The adaptation of skeletal muscle collagen was also studied during denervation and subsequent reinnervation process. Collagen synthesis was evaluated by the activities of prolyl 4-hydroxylase (PH) and galactosyl-hydroxylysyl glucosyltransferase (GGT), and collagen content by the concentration of hydroxyproline (Hyp). The effects of streptozotocin-induced diabetes and endurance training were studied on CA III expression at mRNA and protein levels. In addition, the effects of concentric exercise were studied on the release of muscle proteins and markers of collagen synthesis. The specific PH and GGT activities decreased significantly after one week of immobilization in rat soleus muscle immobilized in shortened position, whereas in tibialis anterior muscle immobilized in stretched position, the activities increased. The degree of muscle stretch during immobilization seemed to be an important regulator of collagen expression in muscle. During the follow-up of remobilization, the activities of PH and GGT returned towards the control levels. In human vastus medialis muscle, total CA III decreased to the same extent as the muscle cross-sectional area during immobilization for six weeks. Denervation brought with it an increased level of collagen biosynthesis and Hyp concentration in rat skeletal muscle. During the follow-up of reinnervation, both the PH and GGT activities and the Hyp concentration decreased to the control level. Both streptozotocin-induced diabetes and endurance training increased CA III expression in rat skeletal muscle independently. The finding may represent an adaptation of skeletal muscle cells to increased oxidative stress, which is known to be caused by both treatments. A single bout of heavy concentric exercise caused protein leakage from human muscles and most probably the activation of type I collagen secretion from collagen synthetizing cells which seemed to depend on the strain and damage of the musculoskeletal system.