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R4580 --> 886.7 --> Unfamiliar exercises and/or muscle contractions during intense exercise, especially eccentric exercise, may cause muscle damage. Consequently, muscle protein creatine kinase (CK) and myoglobin (Mb) leaks into the bloodstream and titin N‐fragment is subsequently excreted through urine. Currently, blood (e.g., CK and Mb) and urine (e.g., titin N‐fragment) markers are generally used to monitor muscle damage in individuals who engage in intense training. However, these muscle damage markers in blood and urine have several limitations: 1) they cannot identify local damaged area, 2) several days are required to assess muscle damage thus immediate feedback is not possible, 3) assessment of blood markers requires invasive techniques, which may increase the risk of infection and/or can be painful to some individuals. Therefore, developing a new muscle damage marker without the above limitations is practically important. Interstitial fluid exists between cells. Previous studies reported that glucose concentrations of the interstitial fluid correlate well with those in the blood. Based on the information, minimally invasive wearable devices that can continuously predict blood glucose level by measuring skin interstitial glucose concentrations have been developed and now are available. However, it remains to be determined if muscle damage markers such as CK and titin N‐fragment can be detectable from skin interstitial fluid. Given that CK and titin N‐fragment leak into interstitial fluid before entering lymphatic vessels and blood, concentrations of CK and titin N‐fragment may appear earlier in the skin interstitial fluid relative to blood and/or urine. Furthermore, muscle damage marker concentrations in interstitial fluid appear to be specifically elevated in the muscle‐damaged area. However, these possibilities have never been assessed in human skin interstitial fluid. To assess these possibilities, muscle damage markers in blood, urine, and skin interstitial fluid were assessed in 12 healthy young adults (5 women, age: 26 ± 3 years; height: 168 ± 10 cm; body mass: 64 ± 10 kg) who performed 30 maximal isokinetic (60°/s) eccentric elbow flexor contractions using an isokinetic dynamometer (the non‐dominant arm). Intradermal microdialysis probes were implanted near the brachialis muscle in both the exercising and non‐exercising arms (i.e., 60‐70 % distal to the length between the acromial process and epicondylus lateralis humeri). Urinary and dialysate titin N fragment concentrations were assessed at baseline and 3 hours, 1, 4, and 7 days after the exercise. Serum and dialysate CK activity, serum and dialysate Mb concentrations, MVC torque, ROM, and muscle soreness were also assessed. After the eccentric exercise, titin N‐fragment in urine significantly increased at 4 and 7 days postexercise. Similarly, titin N‐fragment in dialysate significantly increased at 4 and 7 days postexercise. However, titin N‐fragment in dialysate did not increase in the non‐exercising arm at any postexercise periods. We conclude that the skin interstitial fluid can be used to assess a muscle damage marker, titin‐N fragment, and may reflect the site where muscle damage occurs. [ABSTRACT FROM AUTHOR]

R2647 --> Water immersion increases breathing effort against elevated hydrostatic pressure. Thus, aquatic exercise training may have a greater benefit for the respiratory function when compared to the same intensity of exercise performed on dryland. The purpose of this study was to investigate the effect of underwater cycling on the respiratory function and breathing pattern when compared to land‐based cycling performed at the matched exercise intensity. Ten healthy men performed maximal graded exercise test and 15 minutes of incremental water‐based cycling exercise (WE) and land‐based cycling exercise (LE) on separate days. In WE, cycling began at 30 rpm, and the cadence was increased by 15 rpm every 5 minutes. 3 paddles were attached to the wheel of stationary bicycle to increase pedaling resistance. In LE, participants cycled continuously at 60 rpm for 15 minutes while wattage was adjusted to match oxygen uptake (VO2) to the WE condition. Using spirometry, respiratory function and respiratory muscle pressure were measured before and after cycling, and the magnitude of change between pre‐ and post‐ exercise was also measured. Breathing pattern was measured continuously during cycling. Water temperature and immersion level were kept at 31.5 ℃ and xiphoid appendix, respectively. VO2 duringcycling in water and on dryland was similar. Minute ventilation, inspiratory and expiratory volumes, and respiratory rate increased whereas, inspiratory and expiratory times decreased as the cycling intensity (VO2) increased (all P < 0.05). Respiratory rate was slightly higher at 60 rpm in WE than LE (27 ± 3 vs. 24 ± 3 bpm, P = 0.053). Inspiratory time was significantly higher at rest in WE than LE (1.4 ± 0.1 vs. 1.2 ± 0.0 sec, P < 0.05). After cycling exercise, change in the forced expiratory volume in one second and change in the peak expiratory flow were significantly lower in WE than LE (‐0.04 ± 0.15 vs. 0.06 ± 0.10 L, P < 0.05. ‐0.37 ± 0.87 vs. 0.04 ± 0.63 L, P < 0.05, respectively). These data suggest that the respiratory and breathing responses were mostly similar during underwater and land‐based cycling when VO2 is matched in both conditions. However, breathing may slightly be shallower during a higher‐intensity aquatic cycling which may have chronic effects on respiratory function after multiple bouts of aquatic cycling for a longer term. [ABSTRACT FROM AUTHOR]

R1627 --> Transient receptor potential (TRP) channels exist in various cells and tissues including nerves and vascular endothelium. TRP channels are implicated in the regulation of several sensory organs associated with pain, pressure, and temperature. While there exists a number of TRP channels, transient receptor potential vanilloid 1 (TRPV1) and 4 (TRPV4) channels in human skin have been shown to modulate cutaneous vasodilation (Fujii et al., 2019; Wong et. al., 2012). Transient receptor potential ankyrin 1 (TRPA1) subtype, which belongs to the TRP channel, is thought to be activated by cold and possibly warm/hot temperatures (Wang and Siemens, 2015). Recently, we showed that TRPA1 channel activation with cinnamaldehyde induced cutaneous vasodilation in humans (Fujii et al., 2020). However, the mechanisms underlying this response remains to be determined. A previous study using mouse ear showed that nitric oxide (NO) synthase (NOS), which is a meditator of endothelium‐dependent vasodilation, can modulate the TRPA1 channel induced cutaneous vasodilation (Aubdool et al., 2016). However, it is unclear if this relationship exists in humans. Moreover, whether cyclooxygenase (COX) and Ca2+ activated K+ (KCa) channels, which are also established modulators of endothelium‐dependent vasodilation, contribute to TRPA1 channel induced cutaneous vasodilation remains to be directly assessed in humans. Based on the above, we evaluated the hypothesis that NOS, COX, and KCa channels mediate the TRPA1 channel induced cutaneous vasodilation in humans. To assess our hypothesis, cutaneous vascular conductance (CVC) was assessed in 9 healthy young adults (29 ± 6 years, 4 women) at four dorsal forearm skin sites treated by intradermal microdialysis with either: 1) vehicle control (98 % propylene glycol + 0.015% lactated Ringer solution + 1.985 % dimethyl sulfoxide), 2)10 mM N(G)‐Nitro‐L‐arginine methylester, a non‐selective NOS inhibitor, 3)10 mM ketorolac, a non‐selective COX inhibitor, or 4) 50 mM tetraethylammonium, a non‐selective KCa channel blocker. Cinnamaldehyde, a TRPA1 channel activator, was administered to each skin site in a dose‐dependent manner (2.9, 8.8, 26 and 80% of cinnamaldehyde concentrations, each lasting at least 30min). Administration of ≥8.8 % cinnamaldehyde increased CVC from baseline at the vehicle control site (e.g., 27.4± 2.7 % increase in CVC, P<0.05). NOS inhibition attenuated the cinnamaldehyde induced‐cutaneous vasodilation at 2.9, 8.8, 26 and 80% concentrations relative to the vehicle control site (all P<0.05). COX inhibition and KCa channel blockade did not attenuate the cinnamaldehyde induced‐cutaneous vasodilation relative to the vehicle control site at all concentrations (all P>0.05). We conclude that in human skin in vivo, NOS plays a role in modulating the regulation of cutaneous vasodilation in response to TRPA1 channel activation with negligible contributions of COX and KCa channels. [ABSTRACT FROM AUTHOR]