On the Influence of Group III/IV Muscle Afferent Feedback on Endurance Exercise Performance

Abstract

This review discusses evidence suggesting that group III/IV muscle afferents affect locomotor performance by influencing neuromuscular fatigue. These neurons regulate the hemodynamic and ventilatory response to exercise and, thus, assure appropriate locomotor muscle O2 delivery, which optimizes peripheral fatigue development and facilitates endurance performance. In terms of central fatigue, group III/IV muscle afferents inhibit motoneuronal output and thereby limit exercise performance.

Figure 1:

Consequences of group III/IV muscle afferent feedback for the development of neuromuscular fatigue and whole body exercise performance. Muscle contraction-induced increases in group III/IV afferent feedback raise circulation and pulmonary ventilation during exercise and thereby assure adequate oxygen delivery to the working locomotor muscle. This attenuates the development of peripheral fatigue and facilitates exercise performance (left side). On the other side (right side), group III/IV muscle afferent feedback restricts spinal motoneuron output and voluntary muscle activation, i.e. promotes central fatigue and impairs exercise performance. Black dashed arrow represents the central projection of group III/IV muscle afferents during exercise. The red and blue arrows represent locomotor muscle oxygen delivery and descending neural input to the locomotor muscle, respectively.

Figure 2:

Blood pressure, ventilatory, and neuromuscular responses to exhaustive whole body exercise with intact (Placebo or CTRL) and blocked (Fentanyl or FENT) group III/IV muscle afferent feedback. Panel A, peripheral locomotor muscle fatigue following constant-load cycling (80% of peak power) to exhaustion (Placebo ~9 min; Fentanyl ~7 min); exercise-induced quadriceps fatigue is illustrated as the pre- to post-exercise decrease in potentiated twitch torque of the quadriceps (Q_tw,pot). †P < 0.05 vs Placebo. Panel B, mean arterial pressure (MAP) at rest, 3 minutes into strenuous constant-load cycling (80% of peak power), and at exhaustion (Placebo ~9 min; Fentanyl ~7 min). * P < 0.05 vs. Placebo. Panel C, pulmonary ventilation (V̇_E) during constant-load cycling exercise to exhaustion. Panel D, exercise-induced central fatigue, illustrated as the percent change in voluntary quadriceps activation (VA) from before to after constant-load cycling exercise to exhaustion (80% of peak power; ~8.5 min in both conditions) (post-1, post-2, and post-3 measure were taken ~1 min, ~2.5 min, and ~4 min, respectively, after exercise). #P < 0.05 vs. Control. Panel E, changes in motor cortical excitability during strenuous cycling exercise to task failure (80% of peak power; ~8.5 min in both conditions); increases in the ratio of motor-evoked potential (MEP) and cervicomedullary motor-evoked potential (CMEP) reflect an increase in motor cortical excitability; the illustrated ratios were obtained at the start of exercise and again at task failure (i.e. exhaustion). ‡P < 0.05 vs. Start. (Panels A–C. Reprinted from (30). Copyright © 2011 John Wiley and Sons. Used with permission.) (Panels D-E. Reprinted from (28). Copyright © 2017 Elsevier. Used with permission.)

Figure 3:

Time to completion, muscle activation, and power output during the 5 km cycling time trials performed under normoxic conditions (NORM) and with a hyperoxic inspirate (H). This strategy compensated for the impact of afferent blockade on convective O₂ transport and permitted adequate locomotor muscle O₂ delivery during the time trial performed with intact (H_CTRL) and blocked (H_FENT) group III/IV muscle afferents. Panel A, time to complete the 5 km time trials. Panel B, vastus lateralis EMG normalized to the EMG response recorded during pre-exercise maximal voluntary contraction. Panel C, power output during the time trials. * P < 0.05 vs NORM, † P < 0.05 vs H_CTRL. (Reprinted from (57). Copyright © 2019 The American Physiological Society. Used with permission.)