Supraspinal, spinal, and motor unit adjustments to fatiguing isometric contractions of the knee extensors at low and high submaximal intensities in males.

Contraction intensity is a key factor determining the development of muscle fatigue, and it has been shown to induce distinct changes along the motor pathway. The role of cortical and spinal inputs that regulate motor unit (MU) behavior during fatiguing contractions is poorly understood. We studied the cortical, spinal, and neuromuscular response to sustained fatiguing isometric tasks performed at 20% and 70% of the maximum isometric voluntary contraction (MVC), together with MU behavior of knee extensors in healthy active males. Neuromuscular function was assessed before and after performance of both tasks. Cortical and spinal responses during exercise were measured via stimulation of the motor cortex and spinal cord. High-density electromyography was used to record individual MUs from the vastus lateralis (VL). Exercise at 70%MVC induced greater decline in MVC (P = 0.023) and potentiated twitch force compared with 20%MVC (P < 0.001), with no difference in voluntary activation (P = 0.514). Throughout exercise, corticospinal responses were greater during the 20%MVC task (P < 0.001), and spinal responses increased over time in both tasks (P ≤ 0.042). MU discharge rate increased similarly after both tasks (P ≤ 0.043), whereas recruitment and derecruitment thresholds were unaffected (P ≥ 0.295). These results suggest that increased excitability of cortical and spinal inputs might be responsible for the increase in MU discharge rate. The increase in evoked responses together with the higher MU discharge rate might be required to compensate for peripheral adjustments to sustain fatiguing contractions at different intensities.NEW & NOTEWORTHY Changes in central nervous system and muscle function occur in response to fatiguing exercise and are specific to exercise intensity. This study measured corticospinal, neuromuscular, and motor unit behavior to fatiguing isometric tasks performed at different intensities. Both tasks increased corticospinal excitability and motor unit discharge rate. Our findings suggest that these acute adjustments are required to compensate for the exercise-induced decrements in neuromuscular function caused by fatiguing tasks.

Physical and Mental Fatigue Reduce Psychomotor Vigilance in Professional Football Players.

PURPOSE: Professional football players experience both physical and mental fatigue (MF). The main aims of this randomized crossover study were to investigate the effect of MF on repeated-sprint ability (RSA) and the effects of both physical fatigue and MF on psychomotor vigilance. METHODS: Seventeen male professional football players performed 10 maximal 20-m shuttle sprints interspaced by incomplete recovery (RSA test). Running speed, heart rate, brain oxygenation, and rating of perceived exertion were monitored during each sprint. The RSA test was preceded by either a 30-minute Stroop task to induce MF or by watching a documentary for 30 minutes (control [CON]) in a randomized counterbalanced order. Participants performed a psychomotor vigilance test at baseline, after the cognitive task (MF or CON), and after the RSA test. RESULTS: Heart rate and rating of perceived exertion significantly increased, while running speed and brain oxygenation significantly decreased over the repeated sprints (P < .001) with no significant differences between conditions. Response speed during the psychomotor vigilance test significantly declined after the Stroop task but not after CON (P = .001). Response speed during the psychomotor vigilance test declined after the RSA test in both conditions (P < .001) and remained lower in the MF condition compared to CON (P = .012). CONCLUSIONS: MF does not reduce RSA. However, the results of this study suggest that physical fatigue and MF have negative and cumulative effects on psychomotor vigilance. Therefore, strategies to reduce both physical fatigue and MF should be implemented in professional football players.

Ischemic preconditioning of the muscle reduces the metaboreflex response of the knee extensors.

PURPOSE: This study investigated the effect of ischemic preconditioning (IP) on metaboreflex activation following dynamic leg extension exercise in a group of healthy participants. METHOD: Seventeen healthy participants were recruited. IP and SHAM treatments (3 × 5 min cuff occlusion at 220 mmHg or 20 mmHg, respectively) were administered in a randomized order to the upper part of exercising leg's thigh only. Muscle pain intensity (MP) and pain pressure threshold (PPT) were monitored while administrating IP and SHAM treatments. After 3 min of leg extension exercise at 70% of the maximal workload, a post-exercise muscle ischemia (PEMI) was performed to monitor the discharge group III/IV muscle afferents via metaboreflex activation. Hemodynamics were continuously recorded. MP was monitored during exercise and PEMI. RESULTS: IP significantly reduced mean arterial pressure compared to SHAM during metaboreflex activation (mean ± SD, 109.52 ± 7.25 vs. 102.36 ± 7.89 mmHg) which was probably the consequence of a reduced end diastolic volume (mean ± SD, 113.09 ± 14.25 vs. 102.42 ± 9.38 ml). MP was significantly higher during the IP compared to SHAM treatment, while no significant differences in PPT were found. MP did not change during exercise, but it was significantly lower during the PEMI following IP (5.10 ± 1.29 vs. 4.00 ± 1.54). CONCLUSION: Our study demonstrated that IP reduces hemodynamic response during metaboreflex activation, while no effect on MP and PPT were found. The reduction in hemodynamic response was likely the consequence of a blunted venous return.

Task-specific strength increases after lower-limb compound resistance training occurred in the absence of corticospinal changes in vastus lateralis.

NEW FINDINGS: What is the central question of the study? Are corticospinal responses to acute and short-term squat resistance training task-specific? What is the main finding and its importance? A single bout of resistance training increased spinal excitability, but no changes in corticospinal responses were noted following 4 weeks of squat training despite task-specific increases in strength. The present data suggest that processes along the corticospinal pathway of the knee extensors play a limited role in the task-specific increase in strength following resistance training. ABSTRACT: Neural adaptations subserving strength increases have been shown to be task-specific, but responses and adaptation to lower-limb compound exercises such as the squat are commonly assessed in a single-limb isometric task. This two-part study assessed neuromuscular responses to an acute bout (Study A) and 4 weeks (Study B) of squat resistance training at 80% of one-repetition-maximum, with measures taken during a task-specific isometric squat (IS) and non-specific isometric knee extension (KE). Eighteen healthy volunteers (25 ± 5 years) were randomised into either a training (n = 10) or a control (n = 8) group. Neural responses were evoked at the intracortical, corticospinal and spinal levels, and muscle thickness was assessed using ultrasound. The results of Study A showed that the acute bout of squat resistance training decreased maximum voluntary contraction (MVC) for up to 45 min post-exercise (-23%, P < 0.001). From 15-45 min post-exercise, spinally evoked responses were increased in both tasks (P = 0.008); however, no other evoked responses were affected (P ≥ 0.240). Study B demonstrated that following short-term resistance training, participants improved their one repetition maximum squat (+35%, P < 0.001), which was reflected by a task-specific increase in IS MVC (+49%, P = 0.001), but not KE (+1%, P = 0.882). However, no training-induced changes were observed in muscle thickness (P = 0.468) or any evoked responses (P = 0.141). Adjustments in spinal motoneuronal excitability are evident after acute resistance training. After a period of short-term training, there were no changes in the responses to central nervous system stimulation, which suggests that alterations in corticospinal properties of the vastus lateralis might not contribute to increases in strength.

Exercise intolerance and fatigue in chronic heart failure: is there a role for group III/IV afferent feedback?

Exercise intolerance and early fatiguability are hallmark symptoms of chronic heart failure. While the malfunction of the heart is certainly the leading cause of chronic heart failure, the patho-physiological mechanisms of exercise intolerance in these patients are more complex, multifactorial and only partially understood. Some evidence points towards a potential role of an exaggerated afferent feedback from group III/IV muscle afferents in the genesis of these symptoms. Overactivity of feedback from these muscle afferents may cause exercise intolerance with a double action: by inducing cardiovascular dysregulation, by reducing motor output and by facilitating the development of central and peripheral fatigue during exercise. Importantly, physical inactivity appears to affect the progression of the syndrome negatively, while physical training can partially counteract this condition. In the present review, the role played by group III/IV afferent feedback in cardiovascular regulation during exercise and exercise-induced muscle fatigue of healthy people and their potential role in inducing exercise intolerance in chronic heart failure patients will be summarised.

Brain stimulation and physical performance.

Non-invasive brain stimulation techniques have been used for decades to study brain function and for the treatment of various neurological disease. These techniques involve the passage of electrical current or magnetic field in a controlled manner to a targeted brain area. Recently, experimental studies explored the application of transcranial direct current stimulation (tDCS) for the improvement of physical performance in healthy individuals. In this chapter we reviewed and analyzed the current scientific literature, highlighted methodological limitations and also suggested possible neurophysiological mechanisms. The chapter also provides some technical and theoretical research-based principles for future research, to promote a better understanding of potential and caveats of this emerging field. Finally, ethical and regulatory issues related to performance enhancement via non-invasive brain stimulation are also discussed.

The Effect of Anodal Transcranial Direct Current Stimulation Over Left and Right Temporal Cortex on the Cardiovascular Response: A Comparative Study.

Background: Stimulation of the right and left anterior insular cortex, increases and decreases the cardiovascular response respectively, thus indicating the brain's lateralization of the neural control of circulation. Previous experiments have demonstrated that transcranial direct current stimulation (tDCS) modulates the autonomic cardiovascular control when applied over the temporal cortex. Given the importance of neural control for a normal hemodynamic response, and the potential for the use of tDCS in the treatment of cardiovascular diseases, this study investigated whether tDCS was capable of modulating autonomic regulation. Methods: Cardiovascular response was monitored during a post-exercise muscle ischemia (PEMI) test, which is well-documented to increase sympathetic drive. A group of 12 healthy participants performed a PEMI test in a control (Control), sham (Sham) and two different experimental sessions where the anodal electrode was applied over the left temporal cortex and right temporal cortex with the cathodal electrode placed over the contralateral supraorbital area. Stimulation lasted 20 min at 2 mA. The hemodynamic profile was measured during a PEMI test. The cardiovascular parameters were continuously measured with a transthoracic bio-impedance device both during the PEMI test and during tDCS. Results: None of the subjects presented any side effects during or after tDCS stimulation. A consistent cardiovascular response during PEMI test was observed in all conditions. Statistical analysis did not find any significant interaction and any significant main effect of condition on cardiovascular parameters (all ps > 0.316) after tDCS. No statistical differences regarding the hemodynamic responses were found between conditions and time during tDCS stimulation (p > 0.05). Discussion: This is the first study comparing the cardiovascular response after tDCS stimulation of left and right TC both during exercise and at rest. The results of the current study suggest that anodal tDCS of the left and right TC does not affect functional cardiovascular response during exercise PEMI test and during tDCS. In light of the present and previous findings, the effect of tDCS on the cardiovascular response remains inconclusive.

The Ergogenic Effects of Transcranial Direct Current Stimulation on Exercise Performance.

The physical limits of the human performance have been the object of study for a considerable time. Most of the research has focused on the locomotor muscles, lungs, and heart. As a consequence, much of the contemporary literature has ignored the importance of the brain in the regulation of exercise performance. With the introduction and development of new non-invasive devices, the knowledge regarding the behavior of the central nervous system during exercise has advanced. A first step has been provided from studies involving neuroimaging techniques where the role of specific brain areas have been identified during isolated muscle or whole-body exercise. Furthermore, a new interesting approach has been provided by studies involving non-invasive techniques to manipulate specific brain areas. These techniques most commonly involve the use of an electrical or magnetic field crossing the brain. In this regard, there has been emerging literature demonstrating the possibility to influence exercise outcomes in healthy people following stimulation of specific brain areas. Specifically, transcranial direct current stimulation (tDCS) has been recently used prior to exercise in order to improve exercise performance under a wide range of exercise types. In this review article, we discuss the evidence provided from experimental studies involving tDCS. The aim of this review is to provide a critical analysis of the experimental studies investigating the application of tDCS prior to exercise and how it influences brain function and performance. Finally, we provide a critical opinion of the usage of tDCS for exercise enhancement. This will consequently progress the current knowledge base regarding the effect of tDCS on exercise and provides both a methodological and theoretical foundation on which future research can be based.

Effects of caffeine on neuromuscular fatigue and performance during high-intensity cycling exercise in moderate hypoxia.

PURPOSE: To investigate the effects of caffeine on performance, neuromuscular fatigue and perception of effort during high-intensity cycling exercise in moderate hypoxia. METHODS: Seven adult male participants firstly underwent an incremental exercise test on a cycle ergometer in conditions of acute normobaric hypoxia (fraction inspired oxygen = 0.15) to establish peak power output (PPO). In the following two visits, they performed a time to exhaustion test (78 ± 3% PPO) in the same hypoxic conditions after caffeine ingestion (4 mg kg-1) and one after placebo ingestion in a double-blind, randomized, counterbalanced cross-over design. RESULTS: Caffeine significantly improved time to exhaustion by 12%. A significant decrease in subjective fatigue was found after caffeine consumption. Perception of effort and surface electromyographic signal amplitude of the vastus lateralis were lower and heart rate was higher in the caffeine condition when compared to placebo. However, caffeine did not reduce the peripheral and central fatigue induced by high-intensity cycling exercise in moderate hypoxia. CONCLUSION: The caffeine-induced improvement in time to exhaustion during high-intensity cycling exercise in moderate hypoxia seems to be mediated by a reduction in perception of effort, which occurs despite no reduction in neuromuscular fatigue.

The effect of transcranial direct current stimulation of the motor cortex on exercise-induced pain.

PURPOSE: Transcranial direct current stimulation (tDCS) provides a new exciting means to investigate the role of the brain during exercise. However, this technique is not widely used in exercise science, with little known regarding effective electrode montages. This study investigated whether tDCS of the motor cortex (M1) would elicit an analgesic response to exercise-induced pain (EIP). METHODS: Nine participants completed a VO2max test and three time to exhaustion (TTE) tasks on separate days following either 10 min 2 mA tDCS of the M1, a sham or a control. Additionally, seven participants completed 3 cold pressor tests (CPT) following the same experimental conditions (tDCS, SHAM, CON). Using a well-established tDCS protocol, tDCS was delivered by placing the anodal electrode above the left M1 with the cathodal electrode above dorsolateral right prefrontal cortex. Gas exchange, blood lactate, EIP and ratings of perceived exertion (RPE) were monitored during the TTE test. Perceived pain was recorded during the CPT. RESULTS: During the TTE, no significant differences in time to exhaustion, RPE or EIP were found between conditions. However, during the CPT, perceived pain was significantly (P < 0.05) reduced in the tDCS condition (7.4 ± 1.2) compared with both the CON (8.6 ± 1.0) and SHAM (8.4 ± 1.3) conditions. CONCLUSION: These findings demonstrate that stimulation of the M1 using tDCS does not induce analgesia during exercise, suggesting that the processing of pain produced via classic measures of experimental pain (i.e., a CPT) is different to that of EIP. These results provide important methodological advancement in developing the use of tDCS in exercise.

Central alterations of neuromuscular function and feedback from group III-IV muscle afferents following exhaustive high-intensity one-leg dynamic exercise.

The aims of this investigation were to describe the central alterations of neuromuscular function induced by exhaustive high-intensity one-leg dynamic exercise (OLDE, study 1) and to indirectly quantify feedback from group III-IV muscle afferents via muscle occlusion (MO, study 2) in healthy adult male humans. We hypothesized that these central alterations and their recovery are associated with changes in afferent feedback. Both studies consisted of two time-to-exhaustion tests at 85% peak power output. In study 1, voluntary activation level (VAL), M-wave, cervicomedullary motor evoked potential (CMEP), motor evoked potential (MEP), and MEP cortical silent period (CSP) of the knee extensor muscles were measured. In study 2, mean arterial pressure (MAP) and leg muscle pain were measured during MO. Measurements were performed preexercise, at exhaustion, and after 3 min recovery. Compared with preexercise values, VAL was lower at exhaustion (-13 ± 13%, P < 0.05) and after 3 min of recovery (-6 ± 6%, P = 0.05). CMEP area/M area was lower at exhaustion (-38 ± 13%, P < 0.01) and recovered after 3 min. MEP area/M area was higher at exhaustion (+25 ± 27%, P < 0.01) and after 3 min of recovery (+17 ± 20%, P < 0.01). CSP was higher (+19 ± 9%, P < 0.01) only at exhaustion and recovered after 3 min. Markers of afferent feedback (MAP and leg muscle pain during MO) were significantly higher only at exhaustion. These findings suggest that the alterations in spinal excitability and CSP induced by high-intensity OLDE are associated with an increase in afferent feedback at exhaustion, whereas central fatigue does not fully recover even when significant afferent feedback is no longer present.

Improvement in hemodynamic responses to metaboreflex activation after one year of training in spinal cord injured humans.

Spinal cord injured (SCI) individuals show an altered hemodynamic response to metaboreflex activation due to a reduced capacity to vasoconstrict the venous and arterial vessels below the level of the lesion. Exercise training was found to enhance circulating catecholamines and to improve cardiac preload and venous tone in response to exercise in SCI subjects. Therefore, training would result in enhanced diastolic function and capacity to vasoconstrict circulation. The aim of this study was to test the hypothesis that one year of training improves hemodynamic response to metaboreflex activation in these subjects. Nine SCI individuals were enrolled and underwent a metaboreflex activation test at the beginning of the study (T0) and after one year of training (T1). Hemodynamics were assessed by impedance cardiography and echocardiography at both T0 and T1. Results show that there was an increment in cardiac output response due to metaboreflex activity at T1 as compared to T0 (545.4 ± 683.9 mL · min(-1) versus 220.5 ± 745.4 mL · min(-1), P < 0.05). Moreover, ventricular filling rate response was higher at T1 than at T0. Similarly, end-diastolic volume response was increased after training. We concluded that a period of training can successfully improve hemodynamic response to muscle metaboreflex activation in SCI subjects.

Effects of acute vasodilation on the hemodynamic response to muscle metaboreflex.

The aim of the present study was to test the contribution of stroke volume (SV) in hemodynamic response to muscle metaboreflex activation in healthy individuals. We hypothesized that an acute decrease in cardiac afterload and preload due to the administration of a vasodilating agent could reduce postexercise muscle ischemia (PEMI)-induced SV response. Ten healthy males (age 33.6 ± 1.3 yr) were enrolled and randomly assigned to the following study protocol: 1) PEMI session, 2) control exercise recovery (CER) session, 3) PEMI after sublingual administration of 5 mg of isosorbide dinitrate (ISDN), and 4) CER after ISDN. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were a blunted SV response during metaboreflex following acute arterial and venous vasodilation, associated with a reduction in cardiac diastolic time and filling, and a decrement of systemic vascular resistance. These hemodynamic changes restrain blood pressure response during metaboreflex activation. Our results indicate that hemodynamic response to metaboreflex activation is a highly integrated phenomenon encompassing complex interplay between heart rate, cardiac performance, preload, and afterload and that impairment of one or more of these parameters leads to altered hemodynamic response to metaboreflex.

Progressive improvement in hemodynamic response to muscle metaboreflex in heart transplant recipients.

Exercise capacity remains lower in heart transplant recipients (HTRs) following transplant compared with normal subjects, despite improved cardiac function. Moreover, metaboreceptor activity in the muscle has been reported to increase. The aim of the present investigation was to assess exercise capacity together with metaboreflex activity in HTR patients for 1 yr following heart transplant, to test the hypothesis that recovery in exercise capacity was paralleled by improvements in response to metaboreflex. A cardiopulmonary test for exercise capacity and Vo(2max) and hemodynamic response to metaboreflex activation obtained by postexercise ischemia were gathered in six HTRs and nine healthy controls (CTL) four times: at the beginning of the study (T0, 42 ± 6 days after transplant), at the 3rd, 6th, and 12th month after TO (T1, T2, and T3). The main results were: 1) exercise capacity and Vo(2max) were seen to progressively increase in HTRs; 2) at T0 and T1, HTRs achieved a higher blood pressure response in response to metaboreflex compared with CTL, and this difference disappeared at T2 and T3; and 3) this exaggerated blood pressure response was the result of a systemic vascular resistance increment. This study demonstrates that exercise capacity progressively improves in HTRs after transplant and that this phenomenon is accompanied by a progressive reduction of the metaboreflex-induced increase in blood pressure and systemic vascular resistance. These facts indicate that, despite improved cardiac function, resetting of cardiovascular regulation in HTRs requires months.

Altered hemodynamics during muscle metaboreflex in young type 1 diabetes patients.

A reduction in catecholamine levels during exercise has been described in young subjects with type 1 diabetes mellitus (DM1). It has been suggested that type 1 diabetes per se is associated with the loss of sympathetic response before any clinical evidence. Considering that an increase in sympathetic drive is required for normal cardiovascular response to muscle metaboreflex, the aim of this study was to assess the hemodynamics during metaboreflex in DM1 patients. Impedance cardiography was used to measure hemodynamics during metaboreflex activation, obtained through postexercise ischemia in 14 DM1 patients and in 11 healthy controls (CTL). Principal results were: 1) blunted blood pressure response during metaboreflex was observed in DM1 patients compared with the CTL; 2) reduced capacity to increase systemic vascular resistance was also witnessed in DM1 subjects; 3) DM1 subjects reported higher stroke volumes as a consequence of reduced cardiac afterload compared with the CTL, which led to a more evident cardiac output response, which partially compensated for the lack of vasoconstriction. These facts suggest that cardiovascular regulation was altered in DM1 patients and that there was a reduced capacity to increase sympathetic tone, even in the absence of any overt clinical sign. The metaboreflex test appears to be a valid tool to detect early signs of this cardiovascular dysregulation.