Exercise-induced decline in the density of LYVE-1-positive lymphatic vessels in human skeletal muscle.

BACKGROUND The investigation of lymphatic function and biology and its microvascular influence on tissue integrity, development and failure in various disease conditions constitutes an important field of medical research. To date several investigations were carried out investigating alterations of lymphatic vessel density under medical conditions e.g. in transplanted or failing heart. However, only few studies investigated aspects of exercise induced plasticity of lymphatic vessels. STUDY OBJECTIVE It was investigated, if alterations in lymphatic density can be observed in human skeletal muscle as a response to endurance exercise and if potential changes might be related to the distribution of myofibres. METHODS Muscle biopsies were taken from vastus lateralis muscle of male cyclists under resting conditions. Lymphatic capillary density and myofibre distribution were determined prior, as well as over the time course of a cycling training intervention. Lymphatic capillaries were stained by immunohistochemistry using LYVE-1 and Podoplanin antibodies. Myofibre distribution was classified by myofibrillar ATPase staining. RESULTS The density of LYVE-1/+ capillaries in skeletal muscle was observed to decrease significantly over the time course of the exercise intervention. It was further noticed that in consecutive cross sections a small part of vessels however showed either podoplanin or LYVE-1 staining. We did not recognize correlations of LYVE-1/+ vessel density to the distribution of the myofibre spectrum in trained skeletal muscle. CONCLUSION It was concluded that lymphatic vessels are rather normally distributed in skeletal muscle not dependent on a predominant myofibre type. The partial not observed co staining of LYVE-1 and podoplanin might be influenced by a shift in vessel phenotype. The finding of significantly decreased LYVE-1/+ capillary density over the time course of the applied exercise intervention gives rise to the assumption that exercise induced stimuli were able to induce alterations of lymphangiogenetic responses on a structural level.