Effect of Central and Peripheral Fatigue on Maximal Voluntary Function

Abstract

Exhaustive high intensity endurance exercise causes fatigue comprised of a central and a peripheral component. Each component's relative contribution to this phenomenon is unknown and difficult to separate during voluntary whole-body exercise. PURPOSE: We used fatiguing single-leg cycling to induce peripheral muscle fatigue in the working leg and to simultaneously facilitate central fatigue by increasing the central projection of locomotor muscle afferents. Our purpose was to evaluate the influence of a) central fatigue on maximum single-leg cycling power (Pmax) of the rested contralateral leg and b) central and peripheral fatigue on Pmax of the fatigued ipsilateral leg. METHODS: On separate days, 5 male cyclists performed 10min cycling time trials (TT) with either their left or right leg. Ratings of perceived exertion of the body (RPEbody) and of the leg (RPEleg) were evaluated during the final minute of TT. Fatigue was estimated by comparing exercise-induced changes in Pmax as quantified via inertial-load cycling before and again 1 and 3 min following TT. RESULTS: RPEbody and RPEleg during the left and right leg TT did not differ (17.6±0.9 vs. 17.8±0.7 and 19.6±0.5 vs. 19.6±0.5 scale units, respectively). One min after TT, contralateral Pmax was reduced by 14±5% (596±25 vs. 511±39W, p=0.03) and returned to pre-fatigue levels within 3min. One min after TT, ipsilateral Pmax was significantly reduced by 33±2% (575±23 vs. 387±26W p<0.01) and remained reduced by 18±2% (590±20 vs. 483±29W, p<0.01) 3min following TT. CONCLUSION: Our data suggest that central fatigue mechanisms primarily accounted for the reduction in the contralateral Pmax, however, central fatigue was only short lasting as contralateral Pmax was restored within 3min following TT. Increased firing of muscle afferents innervating the peripherally fatigued ipsilateral leg may have exerted inhibitory influences on central motor drive with the subsequent consequence of limiting Pmax in the rested contralateral leg. Furthermore, our results indicate that a combination of central and peripheral mechanisms initially compromised ipsilateral Pmax. However, 3min after TT, ipsilateral Pmax recovered by 15% suggesting that central fatigue had been restored and that the remaining reductions in ipsalateral Pmax were primarily due to peripheral fatigue.