Twenty sedentary male university students were randomly assigned to an experimental or a control group. The experimental group trained the knee extensors of one leg by producing 30 isometric extension maximal voluntary contractions (MVC) per day, three times per week for 8 wk. After 8 wk of training, extensor MVC in the trained leg increased 32.8% (P less than 0.05), but there was no change in vastus lateralis maximal integrated electromyographic activity (IEMGmax). The most important finding was that the degree of hamstring coactivation during extension MVC decreased by approximately 20% (P less than 0.05) after the 1st wk of training. Less pronounced adaptations occurred in the untrained leg: extension MVC force increased 16.2% (P less than 0.05), hamstring coactivity decreased 13% (P less than 0.05) after 2 wk of training, and vastus lateralis IEMGmax was unchanged. The same measures in legs of the control group were not changed during the study. There were no changes in flexion MVC, biceps femoris IEMGmax, or the degree of quadriceps coactivity during flexion MVC in either leg of the control or experimental group. A reduction in hamstring coactivity in the trained and untrained legs indicates that these muscles provide less opposing force to the contracting quadriceps. We conclude that this small but significant decrease in hamstring coactivation that occurs during the early stages of training is a nonhypertrophic adaptation of the neuromuscular system in response to static resistance training of this type.
This study employed longitudinal measures of evoked spinal reflex responses (Hoffman reflex, V wave) to investigate changes in the activation of muscle and to determine if there are "linked" neural adaptations in the motor pathway following isometric resistance training. Twenty healthy, sedentary males were randomly assigned to either the trained (n = 10) or control group (n = 10). The training protocol consisted of 12 sessions of isometric resistance training of the plantar flexor muscles over a 4-wk period. All subjects were tested prior to and after the 4-wk period. To estimate changes in spinal excitability, soleus Hoffman (H) reflex and M wave recruitment curves were produced at rest and during submaximal contractions. Recruitment curves were analyzed using the slope method (Hslp/Mslp). Modulation of efferent neural drive was assessed through evoked V wave responses (V/Mmax) at 50, 75, and 100% maximal voluntary contraction (MVC). After 4 weeks, MVC torque increased 20.0 +/- 13.9% (mean +/- SD) in the trained group. The increase in MVC was accompanied by significant increases in the rate of torque development (42.5 +/- 13.3%), the soleus surface electromyogram (60.7 +/- 30.8%), voluntary activation (2.8 +/- 0.1%), and the rate of activation (48.7 +/- 24.3%). Hslp/Mslp was not altered by training; however, V/Mmax increased 57.3 +/- 34.2% during MVC. These results suggest that increases in MVC observed in the first few days of isometric resistance training can be accounted for by an increase in the rate of activation at the onset of muscle contraction. Augmentation of muscle activation may be due to increased volitional drive from supraspinal centers.
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.
Coactivation is antagonist muscle activity that occurs during voluntary contraction. Recently, we showed that the extent of coactivity in the knee flexors decreases after a short period of resistance training of the knee extensors (8). The purpose of the present experiment was to study the time course of coactivation in the knee flexors during fatigue of the knee extensors. Ten male subjects performed repeated submaximal static leg extensions in a low-intensity long-duration and a high-intensity short-duration fatigue protocol until they could no longer produce the required force [time limit of endurance (Tlim)]. Maximal voluntary contraction (MVC), submaximal force, and surface electromyographic (EMG) activity were measured periodically. Vastus lateralis EMG increased progressively during fatigue of the extensor muscles (P < 0.05), resulting in a 38% change from control at Tlim. Biceps femoris EMG, which was our measure of coactivation, also increased by approximately 60% at Tlim in each protocol (P < 0.05). These observations lead us to conclude that a small but significant force loss during repeated static contractions to Tlim is due to an increase in antagonist activity. Moreover, the close correlation between the antagonist and agonist EMG supports the notion of a "common drive" to both motoneuron pools (10).
Caffeine has known ergogenic effects, some of which have been observed during submaximal isometric contractions. We used 15 subjects in a randomized, double-blind, repeated-measures experiment to determine caffeine's ergogenic effects on neuromuscular variables that would contribute to increased endurance capacity. Subjects performed repeated submaximal (50% maximal voluntary contraction) isometric contractions of the right quadriceps to the limit of endurance (Tlim) 1 h after oral caffeine administration (6 mg/kg). Time to reach Tlim increased by 17 ± 5.25% ( P < 0.02) after caffeine administration compared with the placebo trial. The changes in contractile properties, motor unit activation, and M-wave amplitude that occurred as the quadriceps reached Tlim could not account for the prolonged performance after caffeine ingestion. In a separate experiment with the same subjects, we used a constant-sensation technique to determine whether caffeine influenced force sensation during 100 s of an isometric contraction of the quadriceps. The results of this experiment showed that caffeine reduced force sensation during the first 10–20 s of the contraction. The rapidity of this effect suggests that caffeine exerts its effects neurally. Based on these data, the caffeine-induced increase in Tlim may have been caused by a willingness to maintain near-maximal activation longer because of alterations in muscle sensory processes.
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