To examine the extent of regional variations in cutaneous vasodilatation during rapid and gradual local thermal hyperaemia (LTH) in young adults. In thirty young adults (21 ± 3 years, 15 females), cutaneous vascular conductance, normalized to maximum local skin heating at 44 °C (%CVCmax), was assessed at the upper chest, abdomen, dorsal arm, dorsal forearm, thigh, and medial calf during rapid (33-42 °C at 1 °C·20 s-1) and gradual (33-42 °C at 1 °C·5 min-1) LTH on separate days. For both protocols, local temperatures were held at 42 °C for up to 35 min, followed by 20-30 min at 44 °C. During rapid LTH, between-region responses were evaluated at baseline, the initial vasodilator peak, and 42 °C plateau. During gradual LTH, responses were assessed at baseline and the 42 °C plateau. There were significant main effects of body region on %CVCmax for the initial peak and plateau during rapid LTH and for the plateau during gradual LTH (all P < 0.001) Conversely, main effects of sex and the sex by region interaction were not significant (all P > 0.05). The magnitudes of between-region differences varied across the body (~1-17% range). The greatest effects were observed for the abdomen, wherein responses were consistently lower compared to other regions. Further, responses were consistent between males and females across all body regions and heating phases. Regional variations in the cutaneous vasodilator response to local heating are evident for rapid and gradual LTH in young adults, with the largest effects observed for the abdomen, albeit regional differences were similar between sexes.

Hyper-beta-alaninemia is a rare metabolic condition that results in elevated plasma and urinary β-alanine levels and is characterized by neurotoxicity, hypotonia, and respiratory distress. It has been proposed that at least some of the symptoms are caused by oxidative stress; however, only limited information is available on the mechanism of reactive oxygen species generation. The present study examines the hypothesis that β-alanine reduces cellular levels of taurine, which are required for normal respiratory chain function; cellular taurine depletion is known to reduce respiratory function and elevate mitochondrial superoxide generation. To test the taurine hypothesis, isolated neonatal rat cardiomyocytes and mouse embryonic fibroblasts were incubated with medium lacking or containing β-alanine. β-alanine treatment led to mitochondrial superoxide accumulation in conjunction with a decrease in oxygen consumption. The defect in β-alanine-mediated respiratory function was detected in permeabilized cells exposed to glutamate/malate but not in cells utilizing succinate, suggesting that β-alanine leads to impaired complex I activity. Taurine treatment limited mitochondrial superoxide generation, supporting a role for taurine in maintaining complex I activity. Also affected by taurine is mitochondrial morphology, as β-alanine-treated fibroblasts undergo fragmentation, a sign of unhealthy mitochondria that is reversed by taurine treatment. If left unaltered, β-alanine-treated fibroblasts also undergo mitochondrial apoptosis, as evidenced by activation of caspases 3 and 9 and the initiation of the mitochondrial permeability transition. Together, these data show that β-alanine mediates changes that reduce ATP generation and enhance oxidative stress, factors that contribute to heart failure.