Increased spinal excitability does not offset central activation failure.

We hypothesized that if reduced spinal excitability contributes to central activation failure, then a caffeine-induced increase in spinal excitability would enhance postfatigue maximal voluntary activation and maximal voluntary contraction (MVC). Ten male volunteer subjects attended two laboratory sessions separated by at least 1 week. Contractile and electrical properties were assessed before, and 1 h after oral administration of caffeine (6 mg/kg) or placebo (all-purpose flour), and again following a fatigue protocol. The slope of the H reflex recruitment curve, normalized to that of the M wave (H(slp)/M(slp)), was used to estimate spinal excitability. Maximal voluntary activation was assessed using maximal EMG (EMG(max)) and twitch interpolation. Postfatigue, MVC torque declined (P<0.05) to 75.2+/-12.7 and 70.2+/-9.3% of the prefatigue values in the placebo (PL) and caffeine (CF) trials, respectively, and remained depressed throughout the recovery period. This was accompanied by a decline in % activation (P<0.05) from 99.6+/-0.3% (PL) and 99.8+/-0.3% (CF) to 94.8+/-3.5% (PL) and 95.3+/-5.0% (CF), indicating the presence of central activation failure. Caffeine offset the decline in H(slp)/M(slp )observed in the placebo trial (P<0.05), but it did not prevent the decline in maximal voluntary activation or MVC torque. Furthermore, although the decline in spinal excitability was correlated to the decline in EMG(max) (r=0.55, P<0.05) it was not correlated with the decline in % activation or MVC torque. Thus a fatigue-induced decline in spinal excitability did not limit maximal activation.

Central excitability does not limit postfatigue voluntary activation of quadriceps femoris.

After fatigue, motor evoked potentials (MEP) elicited by transcranial magnetic stimulation and cervicomedullary evoked potentials elicited by stimulation of the corticospinal tract are depressed. These reductions in corticomotor excitability and corticospinal transmission are accompanied by voluntary activation failure, but this may not reflect a causal relationship. Our purpose was to determine whether a decline in central excitability contributes to central fatigue. We hypothesized that, if central excitability limits voluntary activation, then a caffeine-induced increase in central excitability should offset voluntary activation failure. In this repeated-measures study, eight men each attended two sessions. Baseline measures of knee extension torque, maximal voluntary activation, peripheral transmission, contractile properties, and central excitability were made before administration of caffeine (6 mg/kg) or placebo. The amplitude of vastus lateralis MEPs elicited during minimal muscle activation provided a measure of central excitability. After a 1-h rest, baseline measures were repeated before, during, and after a fatigue protocol that ended when maximal voluntary torque declined by 35% (Tlim). Increased prefatigue MEP amplitude (P=0.055) and cortically evoked twitch (P<0.05) in the caffeine trial indicate that the drug increased central excitability. In the caffeine trial, increased MEP amplitude was correlated with time to task failure (r=0.74, P<0.05). Caffeine potentiated the MEP early in the fatigue protocol (P<0.05) and offset the 40% decline in placebo MEP (P<0.05) at Tlim. However, this was not associated with enhanced maximal voluntary activation during fatigue or recovery, demonstrating that voluntary activation is not limited by central excitability.

Effects of caffeine on neuromuscular function.

This double-blind, repeated-measures study examined the effects of caffeine on neuromuscular function. Eleven male volunteers [22.3 +/- 2.4 (SD) yr] came to the laboratory for control, placebo, and caffeine (6 mg/kg dose) trials. Each trial consisted of 10 x 1-ms stimulation of the tibial nerve to elicit maximal H reflexes of the soleus, four attempts at a maximal voluntary contraction (MVC) of the right knee extensors, six brief submaximal contractions, and a 50% MVC held to fatigue. Isometric force and surface electromyographic signals were recorded continuously. The degree of maximal voluntary activation was assessed with the twitch-interpolation technique. Single-unit recordings were made with tungsten microelectrodes during the submaximal contractions. Voluntary activation at MVC increased by 3.50 +/- 1.01 (SE) % (P < 0. 01), but there was no change in H-reflex amplitude, suggesting that caffeine increases maximal voluntary activation at a supraspinal level. Neither the force-EMG relationship nor motor unit firing rates were altered by caffeine. Subjects were able to hold a 50% MVC for an average of 66.1 s in the absence of caffeine. Time to fatigue (T(lim)) increased by 25.80 +/- 16.06% after caffeine administration (P < 0.05). There was no significant change in T(lim) from pretest to posttest in the control or placebo trials. The increase in T(lim) was associated with an attenuated decline in twitch amplitude, which would suggest that the mechanism is, at least in part, peripheral.