Near-infrared spectroscopy can detect differences in vascular responsiveness to a hyperglycaemic challenge in individuals with obesity compared to normal-weight individuals

Abstract

Objective:

To examine whether the near-infrared spectroscopy combined with vascular occlusion test technique could detect differences in vascular responsiveness during hyperglycaemia between normal-weight individuals and individuals with obesity.

Methods:

A total of 16 normal-weight individuals (body mass index, 21.3 ± 1.7 kg/m²) and 13 individuals with obesity (body mass index, 34.4 ± 2.0 kg/m²) were submitted to five vascular occlusion tests (Pre, 30, 60, 90 and 120 min after glucose challenge). Vascular responsiveness was determined by the Slope 2 (Slope 2 StO₂) and the area under the curve (StO_2AUC) of oxygen saturation derived from near-infrared spectroscopy–vascular occlusion test.

Results:

The Slope 2 StO₂ increased from 1.07 ± 0.16%/s (Pre) to 1.53 ± 0.21%/s at 90 min (p < 0.05) in the control group, while in obese it increased from 0.71 ± 0.09%/s (Pre) to 0.92 ± 0.14%/s at 60 min (p < 0.05), and to 0.97 ± 0.10%/s (p < 0.01) at 120 min after glucose ingestion. The StO_2AUC decreased from 1729 ± 214% . sec (Pre) to 1259 ± 232% . sec at 60 min (p < 0.05) and to 1034 ± 172% . sec at 90 min (p < 0.05) in the normal-weight group, whereas it decreased at 90 min (637 ± 98% . sec; p < 0.05) and at 120 min (590 ± 93% . sec; p < 0.01) compared to 30 min (1232 ± 197% . sec) after glucose ingestion in individuals with obesity.

Conclusion:

Near-infrared spectroscopy–vascular occlusion test technique was capable of detecting differences in vascular responsiveness during hyperglycaemia between normal-weight individuals and individuals with obesity.

Keywords

Near-infrared spectroscopy hyperglycaemia obesity vascular responsiveness

Introduction

Among other conditions, obesity is associated with increased cardiovascular risk.¹ Individuals with obesity show lower arterial compliance than individuals with normal weight, with reportedly higher arterial stiffness.² Moreover, a number of studies have reported non-uniform development of endothelial dysfunction in various animal models of obesity.^3–5 As well, attenuated vascular responsiveness in individuals with obesity^6–8 is becoming more prominent in the post-prandial state or after ingesting high amounts of glucose.^9,10

Vascular responsiveness of conduit arteries has been widely assessed by a well-known technique called flow-mediated dilation (FMD). Using an ultrasound probe, the FMD measures the vasodilatory response of a vessel following a vascular occlusion test (VOT).¹¹ This technique has been combined with an oral glucose tolerance test (OGTT) to assess vascular responsiveness of larger vessels during hyperglycaemia in individuals who are healthy and those with obesity.^8–10 However, microvascular dysfunction has been identified as an early complication in obesity-related cardiovascular disease (CVD) that can lead to changes in the cardiovascular hemodynamic function.⁵ In this sense, previous studies have shown that microvascular dysfunction, assessed by analysing the reperfusion rate, may better predict general cardiovascular complications than FMD.^12,13 Thus, establishing changes in microvascular responses for early detection of complications that might detrimentally affect vascular function is important.¹⁴

In relation to this, recent studies have shown that vascular responsiveness can also be measured by near-infrared spectroscopy (NIRS) in combination with a VOT (NIRS-VOT) to reliably assess vascular reactivity within the microvasculature.^15,16 This vascular responsiveness test consists of evaluating the upslope of the NIRS-derived tissue oxygen saturation signal (Slope 2 StO₂ (%)) following reperfusion subsequent to a period of blood flow occlusion (i.e. cuff release). Additionally, estimations of blood flow have been proposed by examining the total area under the reperfusion curve above the StO₂ baseline (StO_2AUC).¹⁷ This NIRS-VOT assessment of microvascular reactivity has been shown to be able to detect cardiovascular fitness-related differences¹⁸ as well as differences in vascular responsiveness during hyperglycaemia in healthy lean individuals.¹⁷

Recently, the relevance of establishing changes in vascular function within the microcirculation for early detection of cardiovascular complications in individuals with obesity was investigated.¹⁹ Given the relevance of establishing changes in vascular function within the microcirculation for early detection of cardiovascular complications in individuals with obesity, the main goal of this study was to examine whether the NIRS-VOT technique could detect differences that were expected in the vascular responses within the microvasculature of otherwise healthy individuals with obesity versus healthy lean control individuals. We hypothesized that the detrimental effects of hyperglycaemia on vascular responsiveness would be more prominent in individuals with obesity compared to their lean counterparts and that these prolonged effects would be represented by a persistent increase in the Slope 2 of StO₂ and attenuation of StO_2AUC.

Materials and methods

Participants

Participants were recruited by convenience sampling and were composed of 15 lean individuals (25.2 ± 1.2 years of age; 9 males and 6 females) and 13 individuals with obesity (23.4 ± 1.1 years of age; 10 males and 3 females) who had not been diagnosed with any disease. To minimize the burden of testing in the control participants, eight individuals were randomly selected from a larger sample from previously published data and the other seven were participants who had not been previously tested in our laboratory. Testing conditions were identical for all participants. Individuals with systolic blood pressure above 139 mmHg and/or diastolic blood pressure above 89 mmHg, or who were smokers or on long-term medications were excluded from study. Participants read and signed an informed consent form, before the start of the experimental procedure. The study adhered to the principles established in the Declaration of Helsinki and was approved by the Conjoint Health Research Ethics Board of the University of Calgary.

Experimental procedure

Upon arrival, after 12 h of overnight fasting, the participants’ baseline (Pre) blood pressure, blood glucose concentration and vascular responsiveness were measured. Following this, the participants ingested 75 g of glucose dissolved in 296 mL of water (Azer Scientific, Morgantown, PA, USA). Vascular responsiveness and blood glucose concentration were assessed at 30, 60, 90 and 120 min after ingestion (Figure 1). Capillary blood was collected by a finger prick using a lancet (Unistik 3, Owen Mumford, Maneta, GA, USA) and blood glucose concentration was measured with a glucometer (One Touch Ultra 2, Lifescan, ZUG, Switzerland) 1 min prior to each vascular responsiveness test. For all visits and thorough experimental protocol, the laboratory’s temperature was maintained at 21°C–22°C.

Figure 1.

Experimental protocol describing the tests performed at each time point before and following the glucose challenge. Pre, pre-glucose challenge; glucose challenge represents the time at which the subjects ingested 75 g of glucose; time 30–120 min represent the time points at which the vascular responsiveness was assessed subsequently of glucose challenge.

Vascular responsiveness assessment

Before the first occlusion occurred, participants lay supine quietly on an examination table for 10 min, with a small pillow placed underneath the ankle joint for comfort. Following this rest period, the NIRS probe was placed on the muscle belly of the tibialis anterior, secured via a tightened black elastic strap to mitigate movement (Figure 2), and covered with an optically dense, black vinyl sheet to minimize the intrusion of extraneous light. An elastic tensor bandage was loosely wrapped around the site so as to avoid blood flow constriction and to further minimize movement and light intrusion. The probe stayed attached to the participant for the duration of testing. A pneumatic cuff connected to an automatic rapid inflation system (Hokanson E20 AG101, Bellevue, WA, USA) was used for occlusion, and placed below the knee (approximately 5 cm distal to the popliteal fossa). Occlusion pressure was set to 250 mmHg for the occlusion time. NIRS measurements were collected continuously at an output frequency of 2 Hz for the entire duration of each test (5 min of baseline, 5 min of occlusion, and 8 min following cuff release, followed by a 12-min recovery period). Thus, each test was separated by 30 min when considering the interval of time between each cuff release, which comprised 25 min of rest between occlusions to allow blood flow to return to baseline resting levels (McLay et al., 2016).

Figure 2.

Cuff and NIRS probe placement during the experimental procedure. 1, cuff; 2, NIRS probe; 3, tibialis anterior muscle location. Note that in the picture the NIRS probe is displayed without the black vinyl sheet and the elastic tensor band that covers it for the purpose of identifying the probe location in the image.

Vascular responsiveness was evaluated as previously established.¹⁶ Briefly, baseline oxygen saturation (StO₂ (%)) was calculated as the average of the last 2 min StO₂ prior to ischaemia (Figure 3). The StO₂ reperfusion rate was quantified as the upslope of the StO₂ signal over a 10 s period immediately following cuff release (Slope 2 StO₂, %/s) (Figure 3). Over this period, the reperfusion rate represents a linear response which allows for a simple slope calculation. The StO₂ area under the curve (StO_2AUC) was calculated as the total area under the reperfusion curve, above the baseline value until the end of the 8 min post cuff release (Figure 3).

Figure 3.

Oxygen saturation signal analysis, as previously established.¹⁷ Baseline, 2-min period previous to the blood flow occlusion; occlusion, 5-min period between cuff inflation and release; reperfusion, 8-min period after cuff release.

NIRS

StO₂ of the tibialis anterior muscle was monitored continuously throughout each VOT test with a frequency-domain multidistance NIRS system (Oxiplex TS, ISS, Champaign, IL, USA). Briefly, the system was composed of a single channel consisting of eight laser diodes operating at two wavelengths (λ = 690 and 828 nm, four at each wavelength), which were pulsed in rapid succession, and a photomultiplier tube. The lightweight plastic NIRS probe (connected to laser diodes and a photomultiplier tube by optical fibres) consisted of two parallel rows of light emitter fibres and one detector fibre bundle; the source-detector separations for this probe were 2.0, 2.5, 3.0 and 3.5 cm for both wavelengths. By measuring changes in light absorption at different wavelengths, changes in oxyhaemoglobin (HbO₂) and deoxyhaemoglobin (HHb) can be measured continuously, and StO₂ can be calculated (defined as [HbO₂]/[HbO₂ + HHb]). The NIRS device was calibrated at the beginning of the session following an instrument warm-up period of at least 30 min. The calibration was completed with the probe placed on a calibration block (phantom) with absorption (μ_a) and reduced scattering coefficients (μ_s′) previously measured; thus, correction factors were determined and were automatically implemented by the manufacturer’s software for the calculation of the μ_a and μ_s′ for each wavelength during the data collection. Calculation of [HbO₂] and [HHb] reflected continuous measurements of μ_s′ made throughout each testing session (i.e. constant scattering value not assumed).

Blood pressure

Blood pressure was assessed by an appropriately sized blood pressure cuff and sphygmomanometer according to the guidelines from the American Heart Association.²⁰

Statistical analysis

The sample size was calculated based on the results of a previous study examining the effects of hyperglycaemia on vascular responsiveness in lean individuals by NIRS-VOT technique.¹⁷ For a difference between means and standard deviation of the Slope 2 of StO₂ (%/s) baseline (1.01 ± 0.55%/s) and after 90 min (1.59 ± 0.50%/s) of glucose ingestion, and considering a type I error rate of 5% (2-tailed) and a power of 80%, the minimum sample size required was 13 participants per group. Data are presented as mean ± standard error. All data were tested for normality using D’Agostino and Pearson normality test. One-way repeated-measures analysis of variance (ANOVA) with between-subjects factor test was applied. When a significant interaction was found, a Bonferroni post hoc test was performed. A p value <0.05 was considered as the level of statistical significance. Data analysis was performed using the SPSS statistics version 23.

Results

Characteristics of study participants

Participants were young, normotensive adults who did not take any medication that would affect cardiovascular and/or hemodynamic responses (see Table 1).

Table 1.

General characteristics of the participants of the study.

	Control n = 15(Mean ± SE)	Obese n = 13(Mean ± SE)
Age (years)	25 ± 1	23 ± 1
BMI (kg/m²)	21.3 ± 1.7	34.4 ± 2.0*
Blood pressure
Systolic blood pressure	121 ± 3	119 ± 5
Diastolic blood pressure	72 ± 3	74 ± 3

SE: standard error; BMI: body mass index.

Different from control group (p < 0.05). A unpaired T test was performed to analyse differences between groups.

Glucose profile

Figure 4 shows the profiles of blood glucose concentration in the two participant groups (normal weight or obesity) throughout the testing protocol. Blood glucose concentration changed from 4.5 ± 0.1 mmol/L (Pre) to 7.2 ± 0.3 mmol/L at 30 min (p < 0.001), 7.2 ± 0.3 mmol/L at 60 min (p < 0.001), and 5.9 ± 0.3 mmol/L at 90 min (p < 0.01), and returned to near Pre values at 120 min (5.4 ± 0.1 mmol/L; p > 0.05) in the control group following glucose ingestion. Blood glucose concentration changed from 5.0 ± 0.3 (Pre) to 8.1 ± 0.4 mmol/L at 30 min (p < 0.001), 7.5 ± 0.3 mmol/L at 60 min (p < 0.001), 7.4 ± 0.3 mmol/L at 90 min (p < 0.01) and 6.8 ± 0.3 mmol/L at 120 min after the glucose challenge (Figure 4).

Figure 4.

Blood glucose concentration: Pre, 30, 60, 90 and 120 min after glucose ingestion.

To compare the differences of blood glucose concentrations within and between groups, an one-way repeated-measures ANOVA with between-subjects factors was performed.

A significant interaction between time and group was found for blood glucose concentration (p = 0.02), such that the blood glucose concentration of individuals with obesity was significantly greater than that of the control group at 90 min (7.5 ± 0.4 vs 5.9 ± 0.2 mmol/L; p < 0.001) and at 120 min (6.8 ± 0.3 vs 5.4 ± 0.2 mmol/L; p < 0.01) (Figure 4).

Vascular responsiveness assessments

Table 2 shows no differences in baseline, undershoot and overshoot values for oxygen saturation at each time point. Figure 5 depicts the changes in the Slope 2 StO₂ throughout the testing protocol in the participants. The Slope 2 StO₂ increased from 1.07 ± 0.16%/s (Pre) to 1.53 ± 0.21%/s at 90 min (p < 0.05) in the control group following glucose ingestion (Figure 5). In individuals with obesity, the Slope 2 StO₂ increased from 0.71 ± 0.09%/s (Pre) to 0.92 ± 0.14%/s at 60 min (p < 0.05), 0.88 ± 0.09%/s at 90 min (p < 0.05) and 0.97 ± 0.10%/s at 120 min (p < 0.01) after glucose ingestion. The Slope 2 StO₂ was statistically greater in the group with normal weight compared to obesity at 90 min (1.53 ± 0.21 vs 0.88 ± 0.09%/s) (p < 0.05) after the glucose challenge. A significant interaction between time and group was found for Slope 2 StO₂ (p < 0.05).

Table 2.

Baseline, undershoot and overshoot mean ± SE values of oxygen saturation (StO₂ (%)) for each time point.

	Time points
	Pre(Mean ± SE)	30 min(Mean ± SE)	60 min(Mean ± SE)	90 min(Mean ± SE)	120 min(Mean ± SE)
Baseline StO₂
Control	77.1 ± 2.1	76.4 ± 2.4	77.0 ± 2.4	77.7 ± 3.2	77.8 ± 0.9
Obese	75.4 ± 1.3	74.6 ± 1.0	74.9 ± 1.7	75.6 ± 1.4	75.9 ± 1.10
Undershoot StO₂
Control	53.0 ± 6.4	54.8 ± 5.2	53.9 ± 5.4	53.4 ± 3.0	55.5 ± 3.7
Obese	59.0 ± 0.3	57.5 ± 3.2	57.0 ± 1.6	58.6 ± 6.0	58.2 ± 1.3
Overshoot StO₂
Control	86.6 ± 2.3	87.0 ± 2.3	87.1 ± 2.7	87.7 ± 2.6	88.6 ± 2.8
Obese	82.2 ± 2.0	83.1 ± 2.8	83.0 ± 1.8	82.8 ± 1.8	83.3 ± 2.2

SE: standard error.

Baseline represents the average of the 2 min previous to the blood flow occlusion; undershoot represents the lowest value of oxygen saturation reached at the end of the occlusion period; overshoot represents the highest value of oxygen saturation reached after cuff release. To compare the oxygen saturation averages with and between groups, a one-way repeated-measures ANOVA with between-subjects factor was performed.

Figure 5.

Mean ± SE of the Slope 2 of StO2 at Pre, 30, 60, 90 and 120 min after glucose ingestion.

Figure 6 displays the profiles of the StO_2AUC in the groups over time. The control group decreased significantly from 1729 ± 214% . sec (Pre) to 1259 ± % . sec at 60 min (p < 0.05) and to 1034 ± 172% . sec at 90 min (p < 0.05) after glucose ingestion. The StO_2AUC at 120 min (1546 ± 194% . sec) was significantly higher than the StO_2AUC at 60 min 1259 ± 232% . sec; p < 0.05) and at 90 min (1034 ± 172% . sec; p < 0.01) after the glucose load and not different from the Pre values (p > 0.05) (Figure 6). In individuals with obesity, the StO_2AUC decreased significantly at 90 min (637 ± 98% . sec; p < 0.05) and at 120 min (590 ± 93% . sec; p < 0.01) after the glucose challenge when compared to 30 min (1232 ± 197% . sec). The StO_2AUC of the group with obesity was smaller than the control group at Pre (1729 ± 214 vs 818 ± 178% . sec; p < 0.01) and at 120 min (1546 ± 194 vs 590 ± 93% . sec; p < 0.001). There was a significant interaction between time and group for StO_2AUC (p < 0.01).

Figure 6.

Mean ± SE of area under the curve of oxygen saturation (StO2) of control and obese group at Pre, 30, 60, 90 and 120 min after glucose ingestion.

To compare the differences of area under the curve of (StO₂) within and between groups, a one-way repeated-measures ANOVA with between-subjects factors was performed.

Discussion

To the best of our knowledge, this is the first study to assess vascular responsiveness during hyperglycaemia by NIRS-VOT technique in individuals with obesity. The two main findings were as follows: (1) while the Slope 2 of StO₂ returned to baseline values at 120 min after glucose ingestion in the control group, the Slope 2 of StO₂ remained steeper in participants with obesity at the same time point compared to the baseline response; (2) the area under the curve of StO₂ decreased at 90 min after glucose ingestion in the control group and returned to baseline values by 120 min; which differed from the group with obesity that showed decreased area under the curve of StO₂ at 90 and at 120 min after the glucose challenge when compared to the baseline value. Overall, the findings from this study showed that, in addition to being able to examine vascular responsiveness in healthy lean individuals, this new methodological approach using NIRS-VOT technique can detect differences in hemodynamic responses within the microvasculature between participants with normal weight and participants with obesity.

A recent study demonstrated that the NIRS-VOT approach was capable of detecting differences in vascular responsiveness following a hyperglycaemia challenge compared to baseline values in lean individuals.¹⁷ This study expands those findings by showing that the NIRS-VOT technique can detect differences in hemodynamic responses within the microvasculature before and after a hyperglycaemia challenge in participants with obesity. Previous studies have shown that NIRS-VOT assessments on the microvasculature are correlated with the FMD responses,¹⁵ more repeatable than FMD,¹⁶ strongly associated with cardiovascular risk,¹² and can differentiate fitness status.¹⁸ Importantly, some studies have indicated that vascular impairments may start within the microcirculation and that early detection of vascular dysfunction has significant clinical relevance.^13,19 Thus, being able to assess vascular function in individuals with obesity using a technique that provides information of microvascular responses is an advancement that could lead to potential early diagnosis of CVD.

This study showed that the Slope 2 StO₂ was significantly steeper only at 90 min after glucose challenge in lean individuals. However, in individuals with obesity, the steepness of Slope 2 StO₂ was greater 60 min after glucose ingestion and, contrary to the lean group, showed a persistent increase up to 120 min after the hyperglycaemic challenge. As discussed elsewhere,¹⁷ it is known that the high levels of circulating insulin induced by hyperglycaemia are associated with increases in vessel diameter, as well as faster blood flow velocity and reduced vascular resistance^21–25 with the peak in blood insulin concentration occurring at approximately 30 min after the peak in blood glucose.²⁶ The earlier and prolonged effects of hyperglycaemia in the Slope 2 StO₂ in the individuals with obesity might be related to the dynamics of the glucose concentration and, likely insulin levels, after glucose ingestion. Although this study has not measured insulin concentrations, individuals with obesity have been reported to show a threefold greater insulin response to an OGTT than lean individuals, higher levels of blood glucose concentration and longer time of exposure to hyperglycaemia and insulin after glucose challenge^27,28 which are associated with increased blood flow and microvascular perfusion.^22,29 Given that the increase in the steepness of Slope 2 StO₂ induced by hyperglycaemia observed in our results may reflect a faster reperfusion rate induced by insulin and not FMD per se, the finding of an earlier and more sustained increase in Slope 2 steepness in the individuals with obesity is not surprising and is in agreement with previous studies describing the hemodynamic effects of hyperglycaemia on the micro- and macro-vasculature.^3,22,30,31

With the exception of the baseline measurement in the participants with obesity, the StO_2AUC showed the opposite profile in lean and obese group when compared to the Slope 2 StO₂ signal. The smaller StO_2AUC at 90 min and its return to baseline values at 120 min after glucose ingestion in the control group coincided with the steepest slope and return to baseline for the Slope 2 StO₂. Similarly, the Slope 2 StO₂ in the participants with obesity showed changes that were opposite to those observed in the StO_2AUC during the testing protocol. Importantly, the increased steepness of the Slope 2 StO₂ and the decrease in the StO_2AUC lasted longer in the group with obesity, showing a persistent response even 120 min after glucose ingestion. In agreement with our findings, previous studies evaluating the effects of hyperglycaemia on vascular responsiveness demonstrated that lean individuals recovered from the vascular effects of hyperglycaemia 120 min after glucose ingestion, while the %FMD response remained suppressed in individuals with obesity at the same time point.^10,32–35

Similar to a previous report,¹⁷ this study indicated that the Slope 2 StO₂ and the StO_2AUC displayed opposite responses. Importantly, the present data support this differential response given that the profiles observed in the individuals with obesity represent a mirror image between the Slope 2 StO₂ and the StO_2AUC signals, despite the fact that they are not similar to those observed in lean participants. Even though this is an important observation from this study, the mechanisms that control these opposite profiles remain to be elucidated. As previously suggested,¹⁷ the hyperglycaemia induced by the glucose ingestion would increase the production of reactive oxygen species (ROS) and have a detrimental role in the endothelial function.^34,36,37 Furthermore, hyperglycaemia has been shown to result in an approximately 50% reduction in the volume of endothelial glycoproteins (glycocalyx) that are associated with the vasodilatory response induced by changes in blood flow, thereby impairing endothelial function.^38–41 Obesity is a state associated with higher exposure to ROS and glycocalyx loss.^4,8,42 Thus, a combination of these and/or other mechanisms involved in impaired hemodynamic responses in obesity might play a role and exacerbate the opposite responses observed in the Slope 2 StO₂ compared to the StO_2AUC.

Albeit not significant, an interesting observation of this study was that the StO_2AUC at baseline was reduced compared to the 30-min measure after glucose ingestion in the group with obesity. In this regard, a previous study investigating the effects of an OGTT on markers of inflammation and oxidative stress in individuals with obesity showed that the systemic oxidative stress, as indicated by plasma peroxide concentrations, decreased significantly at 30 min after glucose challenge.⁴³ Even though the magnitude of this decrease might be small, it is likely that the fasting period of 12 h in participants with obesity was associated with elevated levels of oxidative stress, which might result in reduced vascular responsiveness.^8,43,44

Limitations of the study

Although this study established that the NIRS-VOT measure of microvascular responsiveness was able to detect the expected differences in vascular responsiveness between lean individuals and individuals with obesity before and after exposure to hyperglycaemia, this study did not investigate the mechanisms responsible for the observed responses. Thus, although the observed responses are important from a functional perspective, the mechanisms that control those responses are speculated based on previous reports showing similar responses in lean individuals compared to those with obesity when exposed to the same glucose load. Further studies investigating the mechanisms responsible for such differences in vascular responsiveness profiles during hyperglycaemia between lean individuals and the individuals with obesity are warranted.

Another limitation to consider is that although this technique has been previously used in other studies and contrasted against FMD,^15,16 no specific validation has been performed in obese populations. However, it should be noted that (1) given that the area of NIRS interrogation used in this study (i.e. the tibialis anterior muscle) is not largely affected by the subcutaneous adipose tissue in individuals with obesity compared to their lean counterparts, it seems unlikely that the validity of the measure would be affected; (2) the time between tests was enough to return the measures to baseline values. Finally, the fact that insulin concentration, lipid profiles and other blood markers that could be linked to vascular function were not measured in this study can be considered a limitation.

In conclusion, this study demonstrated that the NIRS-VOT technique is capable of detecting differences in hemodynamic responses to an acute hyperglycaemic challenge between lean individuals and individuals with obesity. Although the mechanisms that control the observed responses warrant further investigation, the prolonged increase in the steepness of the Slope 2 StO₂ and the decrease in the area under the curve of StO₂ during hyperglycaemia observed in the participants with obesity is in agreement with previous work assessing vascular responsiveness in individuals with normal weight and obesity during hyperglycaemia using FMD.^6,8 Thus, the NIRS-VOT is a tool that can help with the evaluation of vascular responsiveness within the microcirculation in participants with normal weight or obesity and that can assist with early detection of vascular complications.

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.

Funding

The authors acknowledge the Coordenadoria de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Brazil for the support.

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