## 2 Materials and Methods
The change in circumference was recorded as voltage via a plethysmograph (EC6 Strain-Gauge Plethysmograph, Hokanson Inc., Bellevue, WA, USA). Following the calibration and attachment of the strain-gauge, two independently controlled rapid (\(<\)0.3 s) inflator and deflator cuffs (E20 Rapid Cuff Inflator, cuff: SC5 DTM 11 \(\times\) 85 cm, Hokanson, Bellevue, WA, USA) were attached to the upper arm and wrist and inflated using the Hokanson air source (AG101 Hokanson, Bellevue, WA, USA). To assess resting FBF, the upper arm cuff was inflated to 50 mmHg, ensuring sufficient pressure to occlude venous return in all participants, while the wrist cuff was inflated to a suprasystolic (\(\sim\)200 mmHg) value to occlude arterial and venous flow. The upper cuff was set to alternate between inflation and deflation at a duty cycle of 7 s inflated/8 s deflated. That is, one measure of FBF was recorded every 15 s [10]. This continued for four minutes. The last minute (i.e., last four resting FBF measures) were averaged and used to define a single resting FBF value. After the resting FBF phase, one minute of rest was provided without either cuff inflated. Subsequently, the upper cuff and wrist cuff were inflated to a suprasystolic (\(\sim\)200 mmHg) value for five minutes to induce transient ischemia. After precisely five minutes of ischemia, the upper arm cuff was deflated and immediately set to alternate between 4 s of inflation and 3 s of deflation, again at a pressure to only occlude venous return (50 mmHg). That is, eight FBF measures were collected during the first minute following ischemia. This period was defined as RH. Peak hyperemia was defined as the value that was recorded during the first inflation period (i.e., initial 7 s). After this first minute, the duty cycle was adjusted to the resting settings (7 s inflation, 8 s deflation) for an additional two minutes. Throughout the entire post-ischemia phase (three min), the wrist cuff remained inflated at \(\sim\)200 mmHg. As previously mentioned, the collected strain-gauge signals corresponded to changes in limb circumference (i.e., volume, due to venous pooling). Signals were transmitted to a personal computer (ThinkBook 15-IML, Lenovo, Beijing, China) with data acquisition hardware (PowerLab 8/35 SP, ADInstruments, Inc., Colorado Springs, CO, USA) and then processed as the rate of increase (i.e., slope) (LabChart Pro v8.1.16). The resulting slopes have been described to represent FBF (mL\({}^{-1}\cdot\)dl \(\mathrm{FAV^{-1}\cdot min^{-1}}\)) [9]. We have previously demonstrated suitable day-to-day reliability with this procedure [16], and this methodology has previously been supported [7]. To be clear, the NIRS device, as described above, was attached during the entirety of this VOP protocol adjacent and distal to the strain-gauge. Thus, simultaneous slopes were collected for FBF and all skeletal muscle oxygenation parameters. Additionally, throughout this procedure (four min rest, one min without occlusion, five min ischemia, and three min reperfusion phase), MAP and HR were recorded at set timepoints, the midpoint of rest and the initial point of RH. Statistical Analyses. Independent \(t\)-tests were used to examine potential mean sex differences among the participant characteristics (Table 1). The data used for analysis were normally distributed, as suggested by the Kolmogorov-Smirnov test. Two separate 2 (Sex: men and women) \(\times\) 2 (Time: rest and reactive hyperemia) mixed factorial ANOVAs were used to assess mean differences in MAP and HR. Partial eta squared (\(\eta_{p}^{2}\)) was reportedas a measure of effect for all ANOVA models (Table 2). Individual peak values of FBF, O2 Hb, HHB, tHb, and HbDiff were normalized to their respective resting value. [PERSON]'s correlation coefficients were used to evaluate the relationships between the normalized FBF and the NIRS-derived variables (Table 3). Additional Pearson's correlation coefficients were calculated for normalized FBF and NIRS-derived variables separated by sex.