The Spinal Contribution To Central Fatigue

Abstract

Caffeine increases endurance time in sustained and intermittent isometric fatigue protocols. The drug also increases post-activation potentiation of the motor-evoked potential (MEP) in first dorsal interosseous and quadriceps femoris with single-pulse transcranial magnetic stimulation (TMS). If caffeine offsets central failure by enhancing central excitability, the effect may be spinal or supraspinal. PURPOSE To determine the spinal contribution to central fatigue using Hoffman reflex (H-reflex) recruitment curves to assess spinal excitability, and caffeine as a perturbation. METHODS We used a double-blind, repeated measures experimental design, with ten male subjects who attended two separate laboratory sessions one week apart. Only drug administration [caffeine (6mg/kg body weight) vs. placebo (all-purpose flour)] differed in the two sessions. Maximal contractile force (MVC), percent activation, and H-reflex recruitment curves were produced before, and one hour after drug administration, as well as immediately after completion of the fatigue protocol, and during recovery. The maximum instantaneous rate of rise (dH/dI:dM/dI) of the developmental slope of H-reflex recruitment curves was used to assess spinal excitability. RESULTS MVC declined from pre-fatigue to immediately post-fatigue in both placebo (26.9±4.0%) and caffeine (30.6±2.6%) trials, and did not recover within 15 minutes post-exercise. A decline in percent activation was observed from pre-fatigue to immediately post-fatigue in both placebo (4.8±1.0%) and caffeine (4.5±1.6%) trials, and a further decline in percent activation was observed at 5 minutes of recovery [placebo (8.2±1.8%), caffeine (8.5±4.5%)]. A decline in spinal excitability from pre-fatigue to immediately post-fatigue was observed in the placebo trial (33.1±11.1%), and recovered within 10 minutes post-fatigue. Caffeine attenuated the fatigue-induced decline in excitability, and potentiated spinal excitability during the recovery period. CONCLUSIONS These data suggest that the progressive decline in the ability to generate maximal force during a fatigue protocol is partially due to the loss of excitability at the level of the spinal cord. However, these data do not allow us to determine the relative contribution of the change in spinal excitability to the total loss of force. Supported by NSERC (EC) and an ACSM Foundation Grant (JMK).