Understanding the mechanisms of fatigue provides insight into the limits of human exercise performance and diseases in which fatigue is a symptom that limits activity. Both peripheral and central mechanisms contribute to muscle fatigue. Central fatigue is defined as a progressive exercise-induced reduction in the ability to voluntarily activate a muscle or muscle group to produce maximal force (Gandevia 2001).
One mechanism thought to contribute to central fatigue is feedback from small-diameter muscle afferents. They respond to the products of muscle work. One subset, termed nociceptors, provides feedback about muscle work associated with high-intensity, painful, and/or ischemic exercise (see for references Jankowski et al. 2013).
Recently, we have shown that nociceptive muscle afferents from fatigued elbow extensor muscles can act more widely to decrease voluntary activation and force production by unfatigued elbow flexor muscles (Kennedy et al. 2013). This suggests that the action of these muscle afferents to limit voluntary drive is not muscle specific but can act across agonist/antagonist pairs for large, proximal muscles. It is not known if these afferents from other muscles, particularly small, distal muscles, have a similar effect on other muscles of the same limb. Here we tested the hypothesis that maintained firing nociceptive muscle afferents in the hand after a fatiguing maximal contraction decreases voluntary drive not only to the fatigued distal muscle but also to proximal muscles in the same limb.
WHAT DID WE FIND?
The main finding is that maintained firing of nociceptive muscle afferents from adductor pollicis reduced voluntary activation and force of unfatigued elbow flexors. Our finding raises the possibility that nociceptive feedback from multiple muscles in the one limb may have additive effects on central drive, so that high-intensity multi-joint exercise may be particularly prone to central fatigue. In addition, it suggests between-muscle interactions, in which feedback from more fatigued muscles can alter performance of less fatigued muscles. Such an effect may be relevant when vascular pathology results in muscle pain with exercise. For example, foot or calf pain during walking may impair drive to the knee or hip muscles and thus, impair gait.
SIGNIFICANCE AND IMPLICATIONS:
Nociceptive muscle afferents from fatigued muscles can alter performance of unfatigued muscles in the same limb. This has implications for high intensity exercise and for painful exercise in patients with vaso-occlusive disorders.
Kennedy DS, McNeil CJ, Gandevia SC, Taylor JL (2014). Fatigue-related pain from distal muscles reduces central motor drive of proximal muscles of the same limb. J Appl Physiol 116, 385-94.
Gandevia SC (2001). Spinal and supraspinal factors in human muscle fatigue. Physiol Rev 81, 1725-1789.
Jankowski MP, Rau KK, Ekmann KM, Anderson CE, and Koerber HR (2013). Comprehensive phenotyping of group III and IV muscle afferents in mouse. J Neurophysiol 109, 2374-2381.
Kennedy DS, McNeil CJ, Gandevia SC, and Taylor JL (2013). Firing of antagonist small-diameter muscle afferents reduces voluntary activation and torque of elbow flexors. J Physiol 591, 3591-3604.