Muscle metaboreflex activation via post-exercise ischemia increases intercostal muscle blood flow index without evidence of local vasoconstriction in humans.

Abstract

Muscle metaboreflex is activated in limb skeletal muscles during high-intensity exercise that increases respiratory demand, but its effects on respiratory muscle blood flow remain unknown. Therefore, we investigated whether metaboreflex activation in the forearm alters blood flow in the intercostal muscles. Sixteen healthy young male subjects performed isometric handgrip at 30% of maximal voluntary contraction for 2 minutes, followed by either post-exercise muscle ischemia (PEMI; metaboreflex activation condition) or a control recovery. Respiratory variables were controlled post-exercise to match baseline levels. Microvascular blood flow index (BFI) in the left intercostal muscles was monitored using diffuse correlation spectroscopy (DCS), and cardiovascular variables were recorded. To reduce respiratory motion artifacts, BFI and vascular resistance index (VRI) were analyzed during breath-holding periods. During PEMI, both mean arterial pressure (MAP) and BFI were significantly elevated compared to rest [medians (IQRs), MAP: 92.1 (84.4-94.4) vs. 110.2 (102.4-116.4) mmHg, p < 0.001; BFI: 3.5 (2.8-4.9) vs. 4.2 (3.8-6.4) ×10⁻⁹ cm²·s⁻¹, p = 0.002] and higher than in the control condition [MAP: 91.0 (89.4- 101.7) vs. 110.2 (102.4-116.4) mmHg, p < 0.001; BFI: 3.3 (2.5-4.5) vs. 4.2 (3.8-6.4) ×10⁻⁹ cm²·s⁻¹, p < 0.001], whereas VRI remained unchanged [23.4 (19.0-29.9) vs. 23.2 (17.4-30.4) mmHg·(×10⁻⁹ cm²·s⁻¹)⁻¹, p = 0.375]. These findings suggest that muscle metaboreflex activation enhances intercostal muscle BFI via a pressor response without evidence of significant local vasoconstriction. This study demonstrates reflex-mediated increases in intercostal muscle BFI and highlights the role of the metaboreflex in supporting ventilation.