Cutaneous Vascular Response to Local Warming: A Response to Letter from Cracowski and Roustit

As Cracowski and Roustit admirably review in their letter and papers, the cutaneous vascular response to local warming in healthy individuals is now well characterised and the mechanism contributing to both the early and later components of the local hyperaemic response extensively investigated [3,4]. It is for these reasons that we chose to use thermal provocation as our tool to investigate microvascular control in our study. We do agree with Cracowski and Roustit that our use of mean heated flux during the plateau phase of the response and area under the response curve (AUC) during 10 minutes of skin warming may disadvantage an interpretation of the physiological factors modulating the response. However our clearly stated aims were to explore associations between smoking habit, age and cutaneous blood flow and flow motion using the dynamic approach of power spectral density (PSD) analysis of the very low component frequencies of the laser Doppler flux trace to explore deficits in control rather than pharmacological intervention. PSD analysis was undertaken using the final 350 seconds of the 600 seconds recording acquired during the plateau phase of the response; i.e., commencing 150 seconds (2.5 minutes) after the start of warming and excluding the early phase of the thermally induced hyperaemia. In this way we were able to avoid biasing our spectral estimates though inclusion of the initial transient response—attributed to increased neurogenic axonreflex mediated activity—and to focus on the sustained largely endothelium-dependent response that we hypothesized would be influenced by age and smoking history. To maintain consistency in our analyses in the spectral and time domains, we used mean plateau flux (excluding the early response) as our flux measure. We also report the AUC of the total response above baseline as this has previously been shown to be a sensitive integrated indicator of the total response [6,7].