Cold-induced vasodilation response in a Japanese cohort: insights from cold-water immersion and genome-wide association studies

Figures

• 

  Fig. 1. Representative blood flow and temperature in response to finger cooling for individuals with CIVD response at room temperature (25 °C). This figure is comparable to Fig. 1 in our previous study [9]. White and black dots indicate blood flow and temperature, respectively. The finger was exposed to cold water at 5 °C for 30 min following 10 min of rest (Baseline). The first minimum and maximum temperatures are indicated by black arrows and arrowheads, respectively, suggesting the presence of a CIVD event. The first maximum and minimum blood flows are indicated by white arrowheads and arrows, respectively. The onset time of CIVD (CIVD onset_sbf) is indicated by small arrows. Phase 1 (vasoconstriction; from the onset of cooling to minimum blood flow), phase 2 (prior to CIVD; from minimum blood flow to CIVD onset_sbf), and phase 3 (CIVD; from CIVD onset_sbf to maximum blood flow) are indicated in parentheses as 1–3, respectively. AU, arbitrary units

• 

  Fig. 2. Wavelet amplitudes of endothelial NO-independent, endothelial NO-dependent, and neurogenic activities in four phases, including the baseline phase, in the study subjects. These subjects showed the presence (a) or absence (b) of a CIVD response (a n = 84; b n = 10). All study subjects (n = 94) are shown in c. Phases 1, 2, and 3 represent “vasoconstriction,” “prior to CIVD,” and “CIVD,” respectively [9]. Data are means ± standard error of the mean. * p < 0.05 and ** p < 0.01 (compared with the baseline using Dunnett’s test). a.u., arbitrary units

• 

  Fig. 3. Representative blood flow and temperature in response to finger cooling for individuals without CIVD response at room temperature (25 °C). White and black dots indicate blood flow and temperature, respectively. The finger was exposed to cold water at 5 °C for 30 min following 10 min of rest (Baseline). The first maximum and minimum blood flows are indicated by white arrowheads and arrows, respectively. AU., arbitrary units

• 

  Fig. 4. Principal component analysis of genotype data from East Asian populations (a) and the JPQ cohort (b). Data were plotted according to the first (horizontal axis) and second (vertical axis) principal components. CDX: Chinese Dai in Xishuangbanna, China; CHB: Han Chinese in Beijing, China; CHS: Southern Han Chinese; JPQ: Japanese in Kyushu, Japan; JPT: Japanese in Tokyo, Japan; KHV: Kinh in Ho Chi Minh City, Vietnam

• 

  Fig. 5. Manhattan plots of p values [plotted as − log10(p)] in genome-wide association studies of CIVD responses with the additive model

• 

  Fig. 6. Wavelet amplitudes of neurogenic and endothelial NO-independent activities across four phases, including the baseline phase, in groups of subjects (n = 94). These subjects were differentiated by CIVD response and the genotypes of rs73619297 of COL4A2 (a) or rs931740 of PRLR (b). Phases 1, 2, and 3 represent “vasoconstriction,” “prior to CIVD,” and “CIVD,” respectively [9]. Data are means ± standard error of the mean. a.u., arbitrary units

• 

  Fig. 7. Network of CIVD-related factors (CIVD response, endothelial NO-independent activity, and neurogenic activity). “Presence” and “Absence” indicate the presence and absence of CIVD response, respectively. “Low” and “High” indicate lower-than-average and higher-than-average wavelet amplitudes, respectively, of endothelial NO-independent or neurogenic activities at phase 2. “Typical CIVD phenotype” group consisted of individuals with a CIVD response, lower-than-average neurogenic activity, and higher-than-average eNO-independent activity. “Typical NonCIVD phenotype” group consisted of individuals without a CIVD response, higher-than-average neurogenic activity, and lower-than-average eNO-independent activity