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. 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. 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. 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. 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.

The diagnostics of anaerobic glycolytic metabolism which play a subordinate role in elite rowing and parameters such as maximum lactate accumulation rate (^ν_La.max) have thus far not been associated with ergometer rowing performance. The aim of the study was to quantify the glycolytic energy metabolism (W_Gly) during a 2000 m ergometer rowing time trial (RTT) and ^ν_La.max during a 10 s maximum ergometer rowing sprint test (RST) and to unravel associations between those variables and RTT performance. Combined post-exercise lactate measurements and oxygen uptake after RST and RTT were used to determine ^ν_La.max and glycolytic energy contribution (W_Gly) in seven male and three female German U 23 national rowers (N = 10, 19.8 ± 0.9 years, 183.2 ± 7.0 cm height, 79.9 ± 13.3 kg body mass, 16.4 ± 5.1 % body fat). W_Gly during RTT ranged from 7 to 15.5% and ^ν_La.max between 0.25 and 0.66 mmol∙L⁻¹∙s⁻¹. ^ν_La.max correlated with W_Gly (p < 0.05, r = 0.74) and the mechanical power output (W) for the first 300 m (300_first) during RTT (p < 0.05, r = 0.67). ^ν_La.max further correlated with ∆300_first−last (W) for the first and last 300 m (300_last) during RTT (p < 0.01, r = 0.87) and also within the subgroup of male rowers. ^ν_La.max displays a wide spectrum of individual differences in rowers. Due to this and its correlation to specific phases of RTT, it contributes to an individual energetic performance profile in rowing. Future studies must undermine the role of ^ν_La.max for exercise performance and whether it serves as a marker that can be specifically targeted for a training-induced increase or decrease.

Adenovirus (AdV) infections in the respiratory tract may cause asthma exacerbation and allergic predisposition, and the house dust mite (HDM) may aggravate virus-induced asthma exacerbations. However, the underlying mechanisms of whether and how AdV affects asthmatic patients remains unclear. To address this question, we investigated nasal epithelial cells (NAEPCs) derived from a pediatric exacerbation study cohort for experimental analyses. We analyzed twenty-one different green-fluorescent protein- and luciferase-tagged AdV types in submerged 2D and organotypic 3D cell culture models. Transduction experiments revealed robust transduction of AdV type 5 (AdV5) in NAEPCs, which was associated with an increased uptake of AdV5 in the presence of HDM. In healthy and asthmatic NAEPCs exposed to HDM before infection, we observed a time- and dose-dependent increase of AdV5 uptake associated with upregulation of entry receptors for AdV5. Furthermore, electron microscopic and histologic analyses of 3D cell cultures revealed an impairment of the respiratory cilia after HDM exposition. This ex vivo pilot study shows the impact of AdV infection and HDM exposition in a primary cell culture model for asthma.