Pharmacological attenuation of group III/IV muscle afferents improves endurance performance when oxygen delivery to locomotor muscles is preserved

Abstract

We sought to investigate the role of group III/IV muscle afferents in limiting endurance exercise performance, independently of their role in optimizing locomotor muscle O₂ delivery. While breathing 100% O₂ to ensure a similar arterial O₂ content ([Formula: see text]) in both trials, eight male cyclists performed 5-km time trials under control conditions (H_CTRL) and with lumbar intrathecal fentanyl (H_FENT) impairing neural feedback from the lower limbs. After each time trial, common femoral artery blood flow (FBF) was quantified (Doppler ultrasound) during constant-load cycling performed at the average power of the preceding time trial. The assessment of end-tidal gases, hemoglobin content and saturation, and FBF facilitated the calculation of leg O₂ delivery. Locomotor muscle activation during cycling was estimated from vastus lateralis EMG. With electrical femoral nerve stimulation, peripheral and central fatigue were quantified by pre- to postexercise decreases in quadriceps twitch torque (ΔQ_tw) and voluntary activation (ΔVA), respectively. FBF (~16 mL·min^-1·W^-1; P = 0.6), [Formula: see text] (~24 mL O₂/dL; P = 0.9), and leg O₂ delivery (~0.38 mL O₂·min^-1·W^-1; P = 0.9) were not different during H_CTRL and H_FENT. Mean power output and time to completion were significantly improved by 9% (~310 W vs. ~288 W) and 3% (~479 s vs. ~463 s), respectively, during H_FENT compared with H_CTRL. Quadriceps muscle activation was 9 ± 7% higher during H_FENT compared with H_CTRL (P < 0.05). ΔQ_tw was significantly greater in H_FENT compared with H_CTRL (54 ± 8% vs. 39 ± 9%), whereas ΔVA was not different (~5%; P = 0.3) in both trials. These findings reveal that group III/IV muscle afferent feedback limits whole body endurance exercise performance and peripheral fatigue by restricting neural activation of locomotor muscle.NEW & NOTEWORTHY Group III/IV muscle afferent feedback facilitates endurance performance by optimizing locomotor muscle O₂ delivery but also limits performance by restricting neural drive to locomotor muscle. To isolate the performance-limiting effect of these sensory neurons, we pharmacologically attenuated their central projection during a cycling time trial while controlling for locomotor muscle O₂ delivery. With no difference in leg O₂ delivery, afferent blockade attenuated the centrally mediated restriction in motoneuronal output and improved cycling performance.

Keywords: blood flow; central fatigue; exercise limitation; metaboreflex; neural feedback.