scholarly journals Fatigue-related group III/IV muscle afferent feedback facilitates intracortical inhibition during locomotor exercise

2018 ◽  
Vol 596 (19) ◽  
pp. 4789-4801 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Dorothea Rosenberger ◽  
Jacob E. Jessop ◽  
...  
2020 ◽  
Vol 128 (1) ◽  
pp. 149-158 ◽  
Author(s):  
Christopher Latella ◽  
Onno van der Groen ◽  
Cassio V. Ruas ◽  
Janet L. Taylor

Fatiguing exercise causes a reduction in motor drive to the muscle. Group III/IV muscle afferent firing is thought to contribute to this process; however, the effect on corticospinal and intracortical networks is poorly understood. In two experiments, participants performed sustained maximal isometric finger abductions of the first dorsal interosseous (FDI) muscle, with postexercise blood flow occlusion (OCC) to maintain the firing of group III/IV afferents or without occlusion (control; CON). Before and after exercise, single- and paired-pulse transcranial magnetic stimulation (TMS) tested motor evoked potentials (MEPs), intracortical facilitation [ICF (12 ms)], and short-interval intracortical inhibition [SICI2 (2 ms), SICI3 (3 ms)]. Ulnar nerve stimulation elicited maximal M waves (MMAX). For experiment 1 ( n = 16 participants), TMS intensities were 70% and 120% of resting motor threshold (RMT) for the conditioning and MEP stimuli, respectively. For experiment 2 ( n = 16 participants), the MEP was maintained at 1 mV before and after exercise and the conditioning stimulus individualized. In experiment 1, MEP/MMAX was reduced after exercise (~48%, P = 0.007) but was not different between conditions. No changes occurred in ICF or SICI. In experiment 2, MEP/MMAX increased (~27%, P = 0.027) and less inhibition (SICI2: ~21%, P = 0.021) occurred after exercise for both conditions, whereas ICF decreased for CON only (~28%, P = 0.006). MEPs and SICI2 were modulated by fatiguing contractions but not by group III/IV afferent firing, whereas sustained afferent firing appeared to counteract postexercise reductions in ICF in FDI. The findings do not support the idea that actions of group III/IV afferents on motor cortical networks contribute to the reduction in voluntary activation observed in other studies. NEW & NOTEWORTHY This is the first study to investigate, in human hand muscles, the action of fatigue-related group III/IV muscle afferent firing on intracortical facilitation and inhibition. In fatigued and nonexercised hand muscles, intracortical inhibition is reduced after exercise but is not modulated differently by the firing of group III/IV afferents. However, facilitation is maintained for the fatigued muscle when group III/IV afferents fire, but these results are unlikely to explain the reduction in voluntary activation observed in other studies.


2020 ◽  
Vol 48 (4) ◽  
pp. 209-216
Author(s):  
Markus Amann ◽  
Hsuan-Yu Wan ◽  
Taylor S. Thurston ◽  
Vincent P. Georgescu ◽  
Joshua C. Weavil

2019 ◽  
Vol 127 (5) ◽  
pp. 1257-1266 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Hsuan-Yu Wan ◽  
Jayson R. Gifford ◽  
...  

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 (HCTRL) and with lumbar intrathecal fentanyl (HFENT) 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 (ΔQtw) 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 HCTRL and HFENT. 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 HFENT compared with HCTRL. Quadriceps muscle activation was 9 ± 7% higher during HFENT compared with HCTRL ( P < 0.05). ΔQtw was significantly greater in HFENT compared with HCTRL (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.


2019 ◽  
Vol 117 (1) ◽  
pp. 698-707 ◽  
Author(s):  
Luis F. Queme ◽  
Alex A. Weyler ◽  
Elysia R. Cohen ◽  
Renita C. Hudgins ◽  
Michael P. Jankowski

Group III/IV muscle afferents transduce nociceptive signals and modulate exercise pressor reflexes (EPRs). However, the mechanisms governing afferent responsiveness to dually modulate these processes are not well characterized. We and others have shown that ischemic injury can induce both nociception-related behaviors and exacerbated EPRs in the same mice. This correlated with primary muscle afferent sensitization and increased expression of glial cell line-derived neurotrophic factor (GDNF) in injured muscle and increased expression of GDNF family receptor α1 (GFRα1) in dorsal root ganglia (DRG). Here, we report that increased GDNF/GFRα1 signaling to sensory neurons from ischemia/reperfusion-affected muscle directly modulated nociceptive-like behaviors and increased exercise-mediated reflexes and group III/IV muscle afferent sensitization. This appeared to have taken effect through increased cyclic adenosine monophosphate (cAMP) response element binding (CREB)/CREB binding protein-mediated expression of the purinergic receptor P2X5 in the DRGs. Muscle GDNF signaling to neurons may, therefore, play an important dual role in nociception and sympathetic reflexes and could provide a therapeutic target for treating complications from ischemic injuries.


2007 ◽  
Vol 4 (5) ◽  
pp. 1694-1697 ◽  
Author(s):  
Y. J. Zhou ◽  
Z. Q. Li ◽  
A. EL Boukili ◽  
Z. M. Simon Li

2009 ◽  
Vol 40 (5) ◽  
pp. 827-837 ◽  
Author(s):  
Vincent Martin ◽  
Erick Dousset ◽  
J��r��me Laurin ◽  
Julien Gondin ◽  
Maxime Gautier ◽  
...  

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