The topic of unconscious influences on behavior has long been explored as a way of understanding human performance and the neurobiological correlates of intention, motivation and action. Previous research using transcranial magnetic stimulation has demonstrated that barely visible priming of an action concept, when combined with reward in the form of a consciously perceived positive stimulus, can alter the state of the motor system and enhance the maximal voluntary force level. One possible explanation is that positive stimulus-induced reward signals are processed by the dopaminergic system in the basal ganglia, motivating individuals to increase the effort they invest in particular behaviors, or to recruit the resources necessary for maintaining those behaviors. If so, given that the dopaminergic system has functionally and anatomically close connections with the noradrenergic system, we hypothesize that the state of the noradrenergic system may be enhanced by the same process. In accord with this hypothesis, we observed that barely visible goal priming with reward caused pupil dilation, suggesting that activity in the noradrenergic system increased. Importantly, this enhancement was accompanied by an unconscious increase in handgrip force. This is the first objective evidence that the pupil-linked neuromodulatory system is related to implicit learning of the link between physical exertion and reward, probably in the noradrenergic system, resulting in more forceful voluntary motor action in the absence of conscious awareness.

Low-to-moderate intensity resistance exercise with vascular occlusion induces increased<br />
muscle mass and strength, comparable to that after conventional heavy resistance training.<br />
Also, participants feel as if they require greater force (effort) to lift a weight when undergoing<br />
resistance exercise following vascular occlusion. Vascular occlusion of the proximal upper<br />
arm increased perceived magnitude of exerted hand-grip force without causing any accompanying<br />
changes either in electromyographic or efferent/afferent activity of the median nerve. There<br />
was also no effect on motor evoked potentials in the hand following resting-state transcranial<br />
magnetic stimulation (TMS) over the primary motor cortex (M1). Moreover, low-frequency,<br />
repetitive transcranial magnetic stimulation (lf-rTMS) over the left primary somatosensory cortex<br />
did not significantly affect estimations of right-hand grip force exertion. Thus, the primary<br />
factor responsible for the overestimation of force exertion with increased voluntary effort (“sense<br />
of effort”) during occlusion was the central signal related to motor command size. Brain imaging<br />
studies show that vascular occlusion increases M1 activi

Studies using force-matching tasks have suggested that when we feel a "sense of effort," cortical regions may act to increase motor commands, and thus recruit additional motor units, in order to compensate for the exerted force. We hypothesized that suppressing activity in the primary motor cortex (M1), which is the source of the motor commands, would initiate the same process, and induce the same sense of effort. In a force-matching task, grip force was applied to 'right' hand and 10 healthy participants were asked to try to exert the same amount by using 'left' hand, with no visual feedback. On some trials, low-frequency, repetitive transcranial magnetic stimulation (1f-rTMS) was used to suppress the M1 and the primary somatosensory cortex (SI) in the left hemisphere, separately. Results showed that participants tended to overestimate the level of exerted force by up to 24%. In contrast, sham stimulation of the M1 and If-rTMS over the SI did not significantly affect participants' estimations. Further, the M1 suppression resulted in a 42% reduction in motor-evoked potentials. Thus, the M1 suppression can affect our sense of effort, suggesting that compensatory neural mechanisms that increase the MI activity may play an important role in producing senses of effort. (C) 2014 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

The topic of unconscious influences on behaviour has long been explored as a means of understanding human performance and the neurobiological correlates of intention, motivation, and action. However, what is relatively unknown is whether subconsciously delivered priming stimuli, with or without rewards, can affect individuals' maximum level of force produced with their best effort. We demonstrated using transcranial magnetic stimulation that barely visible priming of an action concept, when combined with a reward in the form of a consciously visible positive stimulus, could alter the state of the motor system. In accordance with this neurophysiological alteration, the prime-plus-reward stimuli significantly increased the hand-grip force level of maximum voluntary contraction with little conscious awareness. This is the first objective evidence that the barely conscious presence of a behavioral goal can influence the state of the motor system and arouse latent ability for human force exertion.

Hypnosis often leads people to obey a suggestion of movement and to lose perceived voluntariness. This inexplicable phenomenon suggests that the state of the motor system may be altered by hypnosis; however, objective evidence for this is still lacking. Thus, we used transcranial magnetic stimulation of the primary motor cortex (M1) to investigate how hypnosis, and a concurrent suggestion that increased motivation for a force exertion task, influenced the state of the motor system. As a result, corticospinal excitability was enhanced, producing increased force exertion, only when the task-motivating suggestion was provided during hypnotic induction, showing that the hypnotic suggestion actually altered the state of M1 and the resultant behavior. (C) 2014 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

We previously observed that transient vascular occlusion in volunteers increased the estimation of force exertion with no change in peripheral nerves or muscles. We hypothesized that the primary factor responsible for the overestimation of force exertion during occlusion was the centrally generated motor command, as hypothesized by McCloskey et al. (1974) and McCloskey (1978, 1981). In the present study, we tested the hypothesis that transient vascular occlusion increases the excitability of the primary motor cortex (M1) during force exertion. Healthy human volunteers lay on a bed and squeezed a dynamometer in their right hand. Repetitive gripping forces were exerted at 20%, 40%, or 60% of maximum force, with or without transient (20s) vascular occlusion of the proximal portion of the right upper arm. During the task, single-pulse transcranial magnetic stimulation was applied to the contralateral M1 to induce motor evoked potentials (MEPs) in the flexor carpi ulnaris (FCU) muscle. The MEP amplitudes were enhanced with occlusion under all conditions, with the exception of 60% contraction. In contrast, no significant difference was observed between the MEP amplitudes obtained from the occluded or non-occluded, relaxed FCU muscle. These results suggest that transient vascular occlusion increases the excitability of M1 only during force exertion. (C) 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

Avascular occlusion by a tourniquet inflated at the proximal end of the upper arm is Suggested to affect the estimation of exertion force level. In the first part of this study, subjects were asked to estimate the isometric force exerted by the occluded hand with that of the other hand (matching experiment). We found that the perceived force with arterial occlusion was always overestimated. To examine the underlying neural mechanism for this phenomenon, in the second part, the somatosensory evoked potentials (SEPs) and nerve action potential (NAP) were recorded following electrical median nerve stimulation with or without arterial occlusion. Moreover, the maximum motor response (M response) to median nerve stimuli at the axilla was recorded from the skin surface of the thenar eminence muscle of the hand during with arterial occlusion. The N20 of SEP and NAP at Erb's point were unaffected by the arterial occlusion, and the M response was also unchanged. These results suggest that the tourniquet-induced transient occlusion of the brachial artery does not seriously affect median nerve function. Thus, it is likely that the primary responsible factor for the overestimation of perceived force exertion during arterial occlusion is the centrally generated motor command as previously hypothesized by McCloskey [McCloskey, D.I., Ebeling, P., Goodwin, G.M.. 1974. Estimation of weights and tensions and apparent involvement of a "sense of effort". Exp Neurol. 42, 220-232; McCloskey, D.I., 1978. Kinesthetic sensibility. Physiol, Rev. 58, 763-820; McCloskey. D.I., 1981. Corollary discharge and motor commands and perception. In: Brookhart, J.M., Mountcastle. V.B. (Eds.), Handhook of Physiology. American Physiological Society, Bethesda, pp. 1415-1447]. (c) 2005 Elsevier Ireland Ltd and the Japan Neuroscience Society. All fights reserved.

To obtain insight into the relative contributions of exercise and occlusive stimuli to these muscular adaptations, the present study investigated the short- and long-term effects of varied combinations of low-intensity exercise and vascular occlusion. The subjects were separated into 3 groups (n = 6 for each group): low-intensity with vascular occlusion (LIO), low-intensity without vascular occlusion (LI), and vascular occlusion without exercise (VO). LIO and LI groups performed bilateral knee extension exercises in seated positions with an isotonic extension machine. In the LIO group, both sides of the thigh were pressure-occluded at the proximal end by means of a tourniquet during the entire session of exercise (similar to 10 min), whereas only the occlusion with the same pressure and duration was given in the VO group. The mean occlusion pressure was 218 +/- 8.1 mmHg (mean +/- SE). The exercise session consisted of five sets of exercise at an intensity of 10-20% 1 RM and was performed twice a week for 8 wk. After the period of exercise training, isometric and isokinetic strengths at all velocities examined increased significantly in the LIO group (p &lt; 0.05), whereas no significant change in strength was seen in the LI and VO groups. The increase in muscular strength in LIO was associated with a significant increase in the cross-sectional area of knee extensor muscles by 10.3 +/- 1.6%. The plasma growth hormone concentration measured 15 min after the session of exercise showed a marked increase only in LIO. The results showed that the low-intensity exercise and occlusive stimuli have cooperative effects in the long-term adaptation of muscle and an acute response to growth hormone.

Objective: To investigate blood indices of muscle damage after a competitive rugby match.
Methods: Fifteen elite amateur rugby players volunteered to participate (mean (SE) age 26.6 (0.7) years, height 179.8 (1.0) cm, weight 87.4 (2.2) kg, and VO(2)MAX 58.5 (1.2) ml/kg/min). The study was conducted after two competitive matches during the 1999-2000 season. Plasma concentrations of lactate, potassium (K+), sodium (Na+), and myoglobin, and the activity of creatine kinase were measured before and after the matches. In addition, the number of tackles by and on each subject and the average duration of the work and rest periods were analysed using video recordings of the matches.
Results: Myoglobin concentration and creatine kinase activity showed appreciable transient increases after the match. Peak values for myoglobin concentration (980 (166) mu g/l) and creatine kinase activity (1081 ( 159) U/l) were observed 45 minutes and 24 hours after the match respectively. Positive and significant correlations were observed between the number of tackles and both peak myoglobin concentration (r = 0.85, p&lt; 0.01; n = 14) and peak creatine kinase activity (r = 0.92, p&lt; 0.01; n = 14). Plasma lactate and K+ concentrations also showed appreciable increases after the match, whereas plasma Na+ concentration showed a gradual decrease. The mean duration of the work and rest periods were 21.5 (2.2) and 24.3 (3.1) seconds respectively.
Conclusions: The rugby matches resulted in serious structural damage to the muscles, the extent of which was highly dependent on the number of tackles.

The effects of resistance exercise combined with vascular occlusion on muscle function were investigated in highly trained athletes. Elite rugby players (n = 17) took part in an 8 week study of exercise training of the knee extensor muscles. in which low-intensity [about 50% of one repetition maximum] exercise combined with an occlusion pressure of about 200 mmHg (LIO. n=6). low-intensity exercise without the occlusion (LI. n = 6), and no exercise training (untrained control. it = 5) were included. The exercise in the LI group was of the same intensity and amount as in the LIO group. The LIO group showed a significantly larger increase in isokinetic knee extension torque than that in the other two groups (P &lt; 0.05) at all the velocities studied. On the other hand. no significant difference was seen between LI and the control group. In the LIO group, the cross-sectional area of knee extensors increased significantly (P&lt;0.01). suggesting that the increase in knee extension strength was mainly caused by muscle hypertrophy. The dynamic endurance of knee extensors estimated from the decreases in mechanical work production and peak force after 50 repeated concentric contractions was also improved after LIO. whereas no significant change was observed in the LI and control groups. The results indicated that low-intensity resistance exercise causes, in almost fully trained athletes. increases in muscle size. strength and endurance, when combined with vascular occlusion.

We investigated the effect of low-intensity resistance exercise training on muscular size and strength where the interset rest period was shortened so as to reduce the metabolite clearance. Female subjects (aged 45.4 +/- 9.5 years, n = 10) performed bilateral knee extension exercises in a seated position on an isotonic leg extension machine. The exercise sessions consisted of 3 sets of exercise at a mean intensity of similar to50% 1RM with an interset rest period of 30 seconds and was performed twice a week for a period of 12 weeks. The strength and the cross-sectional area (CSA) of the knee extensors and flexors were examined with an isokinetic dynamometer and magnetic resonance imaging (MRI), respectively. The CSAs of the knee extensors and flexors increased by 7.1 +/- 1.6% (p &lt; 0.01, Wilcoxon signed rank test) and 2.5 +/- 1.4% (not significant), respectively. Isometric and isokinetic strengths increased significantly (p &lt; 0.01) at all velocities examined, whereas no significant change was observed in those of knee flexors. These results indicate that a low-intensity resistance exercise with a short interset rest period is substantially effective in inducing muscular hypertrophy and concomitant increase in strength.

Purpose: We have previously shown that the combination of low-intensity resistive exercise and moderate vascular occlusion induces in humans a marked increase in growth hormone secretion and muscular hypertrophy. The present study investigated the effects of vascular occlusion on the size of thigh muscles in patients who underwent an operation for the reconstruction of the anterior cruciate ligament to see whether it attenuates the disuse muscular atrophy without any exercise combined. Methods: Two sessions of occlusive stimulus, each consisting of five repetitions of vascular occlusion (mean maximal pressure, 238 mm Hg) for 5 min and the release of occlusion for 3 min, were applied daily to the proximal end of the thigh from 3rd to 14th days after the operation. Changes in the cross-sectional area (CSA) of thigh muscles were analyzed with magnetic resonance images taken on the 3rd and 14th day after the operation. Results: Without occlusive stimulus (control), the CSAs of knee extensors and flexors decreased by 20.7 +/- 2.2% and 11.3 +/- 2.6% (mean +/- SEM, N = 8), whereas with the occlusive stimulus, they decreased by 9.4 +/- 1.6% and 9.2 +/- 2.6% (N = 8), respectively. The relative decrease in CSA of knee extensors was significantly (P &lt; 0.05) larger in the control group than in the experimental group. Conclusion: The results indicate that the occlusive stimulus effectively diminishes the postoperation disuse atrophy of knee extensors.

Acute and long-term effects of resistance exercise combined with vascular occlusion on muscular function were investigated. Changes in integrated electromyogram with respect to time (iEMG), vascular resistive index, and plasma lactate concentration were measured in five men either during or after elbow flexion exercises with the proximal end of the arm occluded at 0-100 mmHg. The mean iEMG, postexercise hyperemia, and plasma lactate concentration were all elevated with the increase in occlusion pressure at a low-intensity exercise, whereas they were unchanged with the increase in occlusion pressure at high-intensity exercise. To investigate the long-term effects of low-intensity exercise with occlusion, older women (n = 24) were subjected to a 16-wk exercise training for elbow flexor muscles, in which low-intensity [similar to 50-30% one repetition maximum (1 RM)] exercise with occlusion at similar to 110 mmHg (LIO), low-intensity exercise without occlusion (LI), and high- to medium-intensity (similar to 80-50% 1 RM) exercise without occlusion (HI) were performed. Percent increases in both cross-sectional area and isokinetic strength of elbow flexor muscles after LIO were larger than those after LI (P &lt; 0.05) and similar to those after HI. The results suggest that resistance exercise at an intensity even lower than 50% 1 RM is effective in inducing muscular hypertrophy and concomitant increase in strength when combined with vascular occlusion.

Hormonal and inflammatory responses to low-intensity resistance exercise with vascular occlusion were studied. Subjects (n = 6) performed bilateral leg extension exercise in the seated position, with the proximal end of their thigh compressed at 214 +/- 7.7 (SE) mmHg throughout the session of exercise by means of a pressure tourniquet. Mean intensity and quantity of the exercise were 20% of 1 repetition maximum and 14 repetitions x 5 sets, respectively. In each set, the subjects repeated the movement until exhaustion. Plasma concentrations of growth hormone (GH), norepinephrine (NE), lacate (La), lipid peroxide (LP), interleukin-6 (IL-6), and activity of creatine phosphokinase (CPK) were measured before and after the exercise was finished and the tourniquet was released. Concentrations of GH, NE, and La consistently showed marked, transient increases after the exercise with occlusion, whereas they did not change a great deal after the exercise without occlusion (control) done at the same intensity and quantity. Notably, concentration of GH reached a level -290 times as high as that of the resting level 15 min after the exercise. IL-6 concentration showed a much more gradual increase and was maintained at a slightly higher level than in the control even 24 h after exercise. Concentrations of LP and CPK showed no significant change. The results suggest that extremely light resistance exercise combined with occlusion greatly stimulates the secretion of GH through regional accumulation of metabolites without considerable tissue damage.

The relations between the velocity of prestretch and the mechanical energy liberated during the subsequent isovelocity release were studied in contractions of frog single fibers and human muscles. During isometric contractions of frog single fibers, a ramp stretch of varied velocity (amplitude, 0.02 fiber length; velocity, 0.08-1.0 fiber length/s) followed by a release (amplitude, 0.02 fiber length; velocity, 1.0 fiber length/s) was given, and the amount of work liberated during the release was measured. For human muscles, elbow flexions were performed with a prestretch of varied velocity (range, 40 degrees; velocity, 30-180 degrees/s) followed by an isokinetic shortening (velocity, 90 degrees/s). In both frog single fibers and human muscles, the work production increased with both the velocity of stretch and the peak of force attained before the release up to a certain level; thereafter it declined with the further increases of these variables. In human muscles, the enhancement of work production was not associated with a significant increase in integrated electromyogram. This suggests that changes in intrinsic mechanical properties of muscle fibers play an important role in the stretch-induced enhancement of work production.

The relation between the eccentric force developed during a countermovement and the mechanical power output was studied in squatting exercises under nominally isotonic load (50% of 1-repetition maximum). The subjects (n = 5) performed squatting exercises with a countermovement at varied deceleration rates before lifting the load. The ground reaction force and video images were recorded to obtain the power output of the body. Net muscle moments acting at hip, knee, and ankle joints were calculated from video recordings by using inverse dynamics. When an intense deceleration was taken at the end of downward movement, large eccentric force was developed, and the mechanical power subsequently produced during the lifting movement was consistently larger than that produced without the countermovement. Both maximal and mean power outputs during concentric actions increased initially with the eccentric force, whereas they began to decline when the eccentric force exceeded similar to 1.4 times the sum of load and body weight. Video-image analysis showed that this characteristic relation was predominantly determined by the torque around the knee joint. Electromyographic analyses showed no consistent increase in time-averaged integrated electromyograph from vastus lateralis with the power output, suggesting that the enhancement of power output is primarily caused by the prestretch-induced improvement of an intrinsic force-generating capability of the agonist muscle.