The results revealed that shouting significantly increased the handgrip force level of sustained MVC, caused by a reduction of the silent period. Such an enhancing effect of shouting on handgrip MVC is generally consistent with the results of previous studies (1,2,5). Our findings indicate that the motor system was more excitable during sustained muscular contraction paired with shouting, leading to the generation of additional muscular force in maximal exertion effort. These results show that the muscular force-potentiating effect of shouting in maximal force exertion is relevant to the potentiation of motor system activity, via the additional drive of shouting operating on M1.
The main finding was the remarkable potentiation effect of shouting on the handgrip maximal voluntary force during a 2-min period of sustained MVC, with an average increase of approximately 30% in the handgrip force. This increase rate is greater than the effect of shouting on the maximal voluntary force (15%) during a brief MVC reported in our previous study (5). One potential reason for this discrepancy is a difference in the experimental period of muscular force exertion between the present study (2 min) and the previous study (within 5 s). It is conceivable that maximal force exertion for 2 min induces both peripheral and central fatigue, resulting in a marked decline in force production during a 2-min sustained MVC. Indeed, handgrip maximal voluntary force declined to approximately 70% of pre-MVC. This could be caused by a progressive, exercise-induced decline in voluntary activation of a muscle during sustained maximal effort, which attributes to impairment at sites proximal to the neuromuscular junction (6). Thus, the differences in the potentiating effects on MVC mentioned above may be relevant to the experimental period and fatigue of human voluntary contractions.
The muscular force-enhancing effect of shouting was accompanied by a reduced silent period. Changes in silent periods of longer than 100 ms in the hand muscles of healthy participants (19) are considered to reflect cortical inhibition (15). The cortical silent period originates largely from the M1 (15), in which GABAergic circuits are believed to produce the cortical silent period (20–22). The cortical silent period is used as a measure for assessing motor excitability (23). Thus, shouting transiently may enhance the activity of motor cortical neurons. At the same time, we must keep in mind that shouting may enhance the activity of spinal motor neurons, because bEMG during handgrip MVC significantly increased when combined with shouting. However, we were convinced that such an enhancement of the spinal motor neuronal activity may by caused by the enhancing effect of shouting on motor cortical neurons. Because analysis of covariance for continuous measurements adjusted for bEMG revealed that there was no significant interaction, between set (1–5 sets) and bEMG (F [9,140] = 1.25; p = 0.26; effect size: partial η2 = 0.075); however, there was a significant difference of y-intercept (p < 0.001): there was a significant reduction of SP between with and without shouting, irrespective of changes in bEMG. This notion is supported by recent evidence that shouting increases handgrip MVC through the reduction of motor cortical inhibition with no significant changes in bEMG (5).
We found that shouting led to a reduced silent period, and increased handgrip maximal voluntary force. Increased maximal voluntary force may have been brought about by the reduced motor cortical inhibition. These enhancement effects of shouting on handgrip MVC and motor system activity were observed when participants shouted while exerting the handgrip muscular force during maximal effort: shouting never occurred immediately prior to or almost simultaneously with force exertion. Thus, the additional drive of shouting operating on the motor system led to a reduced silent period, and increased maximal voluntary force. This result supported the present finding that producing a shout without handgrip muscular contraction enhanced the motor system state, indicating that the motor command for shouting is transmitted to the motor cortex, and in the final cortical stage of the motor execution program the motor command of shouting is devoted to M1. Therefore, shouting-induced excitatory input to M1 contributes to the muscular force-enhancing effect of shouting during maximal force exertion.
In spite of the reduced silent period, we never observed any changes in MEP amplitude during MVC; there were no statistically significant differences in MEP amplitudes between with and without shouting during handgrip MVC (Fig. 5B). The reason for this failure to detect any changes is because most of the M1 neurons may have already been recruited (24), leaving fewer neurons available to respond to TMS. Thus, the level of M1 neuron recruitment reaching a plateau during MVC might have overshadowed any differences in MEP amplitudes during MVC between with and without shouting.
No consistent enhancing effects of shouting during handgrip MVC on pupil area were observed in the present study (see Pupil area in Results for details). A recent study reported that shouting significantly increased the handgrip force level of a brief MVC for 1–2 s, followed by an increase in pupil size (5). One reason for this discrepancy is a difference in an experimental protocol concerning MVC between the present study (continuous) and the previous study (momentary). It is conceivable that there is no room for pupil dilation when shouting is performed throughout the maximal force exertion for 2 min. In the current study, pupil area markedly increased immediately after the appearance of the word “squeeze” on the display, and remained at a high level until the end of squeezing; there was no significant difference in pupil area between the pre-MVC and the sustained MVC without shouting (Fig. 6; Table 1: Set 1 no-shout in order of shouting [first]) (t[7] = 0.96, d = 0.34; p = 0.36). Thus, the differences in the influence of shouting on pupil area may be related to experimental force exertion protocol in maximal effort. It should be noted, however, that the current results do not necessarily imply that shouting never affects the pupil-linked neuromodulatory system state. The level of pupillary dilation reaching a plateau during MVC (25) might have overshadowed any differences in the pupil-linked neuromodulatory system state between with and without shouting.
We found that shouting led to a reduced silent period during MVC, and increased handgrip maximal voluntary force. Increased handgrip maximal force may have been brought about by the reduced motor cortical inhibition during maximal effort, through the additional drive of shouting operating on the motor system. These results indicate that the muscular force-potentiating effect of shouting in maximal force exertion is relevant to the potentiation of motor system activity, caused by the transmitted motor command of shouting to M1. In turn, this suggests that maximum volition does not cause the motor system to generate maximum activity. This is an active characteristic of the neural systems in the human brain. However, we do not know to what exact extent that spinal motor neuronal excitability involves in neural activity of the force-enhancing effect of shouting, a puzzle that remains to be solved. From the perspective of accessing the latent ability for human force exertion, it may be useful for future studies to examine whether devoting an additional motor command, such as shouting, to M1 improves the characteristics of neural system activity.