Near-infrared spectroscopy assessment of post-occlusive reactive hyperemia and muscle metabolic responses to sustained isometric exercise across varying anchor scheme and occlusion conditions

This study examined post-occlusive reactive hyperemia (PORH) and muscle metabolic responses via near-infrared spectroscopy-vascular occlusion tests (NIRS-VOT) under four experimental conditions: (1) rating of perceived exertion (RPE)-Clamp, (2) blood flow restriction (BFR), (3) NON-BFR, each involving low-intensity, sustained isometric forearm flexion, and (4) PASSIVE BFR, a passive occlusion without exercise. Eighteen healthy young adults (11 males, 7 females) completed a sequence of pre-VOT, an experimental intervention, and post-VOT on separate days. During each intervention, time to task failure (TTF), percent changes in muscle oxygenation (SmO 2 ), and performance fatigability (PF) were also assessed. RPE-Clamp exhibited a significant, positive change in SmO 2 compared to negative changes in other conditions ( p < 0.003). PF did not differ between NON-BFR and BFR ( p = 1.000), but both were greater than RPE-Clamp and PASSIVE BFR, with RPE-Clamp greater than PASSIVE BFR ( p = 0.022). No differences were observed in TTF across conditions ( p = 0.455). Desaturation rate (oxygen extraction rate; slope 1) ( p < 0.001) and ischemic stimulus (MinSmO 2 ) ( p = 0.001) were greater pre- than post-VOT. Reperfusion slope (slope 2) showed no significant differences by time ( p = 0.119) or condition ( p = 0.448). Peak SmO 2 (MaxSmO 2 ) was higher pre- than post-VOT ( p = 0.017), with NON-BFR ( p < 0.001) and BFR ( p = 0.005) greater than PASSIVE BFR. Area under the curve (AUC) above baseline SmO 2 did not differ by time ( p = 0.695) but was greater in NON-BFR than PASSIVE BFR ( p = 0.010). Despite the distinct SmO 2 responses and fatigue profiles across conditions, immediate post-intervention occlusion following prolonged isometric exercise or occlusion may have reduced oxygen extraction capacity and facilitated metaboreflex-induced sympathetic overactivity, collectively attenuating PORH.