Simulating vortex generation to investigate the propulsive and braking mechanisms of breaststroke kick using computational fluid dynamics on a breaststroke swimmer.

Swimmers primarily increase their forward velocity through lower limb motion in breaststroke, making the breaststroke kick crucial for optimizing race times. Recent studies have highlighted the generation of vortices around the swimmer's entire body to propel forward during swimming. However, the investigation of vortex generation during breaststroke kicks remains unexplored. This study aimed to reveal the propulsive and braking mechanisms of breaststroke kicks by simulating vortex generation using computational fluid dynamics (CFD). Kinematic data during the breaststroke kick and a three-dimensional digital model were collected to conduct CFD for a male breaststroke swimmer. Vortex generation was determined during one breaststroke kick from the CFD results. Vortices, which potentially induce a decrease in forward velocity, were generated by the swimmer's lower legs and feet during the recovery phase. The swimmer generated vortices on the dorsal side of the feet and the posterior and lateral sides of the lower legs to increase the forward velocity during the out-sweep phase. The swimmer generated vortices on the lateral sides of the thighs and lower legs and the dorsal and lateral sides of the feet during the in-sweep phase to maintain forward velocity. Moreover, vortices generated from the out-sweep to the in-sweep merged and were shed backward relative to the swimming direction after the in-sweep phase. This study is the first to reveal the propulsive and braking mechanisms of breaststroke kicks by analyzing the vortex generation.

Immunohistochemical characterization of transient receptor potential vanilloid types 2 and 1 in a trinitrobenzene sulfonic acid-induced rat colitis model with visceral hypersensitivity.

Transient receptor potential vanilloid type 2 (TRPV2) and type 1 (TRPV1) are originally identified as heat-sensitive TRP channels. We compared the expression patterns of TRPV2 and TRPV1 in the rat distal colon and extrinsic primary afferent neurons, and investigated their roles in visceral hypersensitivity in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis rats. Both TRPV2 and TRPV1 expressions in the colon, dorsal root ganglion (DRG), and nodose ganglion (NG) were significantly upregulated in the TNBS-induced colitis model. TRPV2 cell bodies co-localized with the intrinsic primary afferent marker NeuN and the inhibitory motor neuronal marker nNOS in the myenteric plexus. TRPV2 expressions were further detected in the resident macrophage marker ED2 in the mucosa. In contrast, no TRPV1-expressing cell bodies were detected in the myenteric plexus. Both TRPV2- and TRPV1-positive cell bodies in the DRG and NG were double-labeled with the neuronal retrograde tracer fluorescent fluorogold. Large- and medium-sized TRPV2-positive neurons were labeled with the A-fiber marker NF200, calcitonin gene-related peptide (CGRP), and substance P (SP) in the DRG while small-sized TRPV1-positive neurons were labeled with the C-fiber markers IB4, CGRP, and SP. TRPV2- and TRPV1-positive NG neurons were labeled with NF200 and IB4. TNBS treatment increased p-ERK1/2-positive cells in TRPV2 and TRPV1 neurons but did not affect the TRPV2 and TRPV1 subpopulations in the DRG and NG. Both TRPV2 and TRPV1 antagonists significantly alleviated visceral hypersensitivity in TNBS-induced colitis model rats. These findings suggest that intrinsic/extrinsic TRPV2- and extrinsic TRPV1-neurons contribute to visceral hypersensitivity in an experimental colitis model.