Complex systems approaches to the adaptability of human functions and behavior in health, aging, and chronic diseases: protocol for a meta-narrative review.

BACKGROUND: Evaluating the adaptability of human functions and behavior has become a subject of growing interest due to aging populations and the increased prevalence of chronic diseases. Various research traditions, based on complex systems theories, have addressed the adaptability of human functions and behavior. However, despite the different research traditions, no review has so far compared them to provide a reliable and useful synthetic tool. Based on an adapted methodology, study objectives are to refine common and divergent traits in the way adaptability of the human functions and behavior has been studied via complex system approaches, with a special focus on aging and chronic diseases. In order to meet this objective, we will use the methodology of the meta-narrative review, and we present in this article the protocol that we will follow. METHODS: The meta-narrative review explores the contrasting and complementary ways in which researchers have studied a subject in order to synthesize information and extract theoretical and applied recommendations. In order to carry out this protocol, we detail our methodology of article extraction, coding, and synthesis. We present the six main stages of our review, from the planning stage to the recommendation stage, and the way we will implement the six principles that underpin the construction of a meta-narrative review. DISCUSSION: The use of a meta-narrative review methodology will yield greater visibility and comprehension of the adaptability of human functions and behavior studied via complex systems-based approaches. In a broader perspective, this paper is also geared to help future researchers carry out a meta-narrative review by highlighting the main challenges encountered and anticipated as well as elements to be taken into account before starting such a project.

High Prevalence of Non-Responders Based on Quadriceps Force after Pulmonary Rehabilitation in COPD.

Pulmonary rehabilitation (PR) in patients with COPD improves quality of life, dyspnea, and exercise tolerance. However, 30 to 50% of patients are "non-responders" (NRs) according to considered variables. Surprisingly, peripheral muscle force is never taken into account to attest the efficacy of PR, despite its major importance. Thus, we aimed to estimate the prevalence of force in NRs, their characteristics, and predictors of non-response. In total, 62 COPD patients were included in this retrospective study (May 2019 to December 2020). They underwent inpatient PR, and their quadriceps isometric maximal force (QMVC) was assessed. The PR program followed international guidelines. Patients with a QMVC increase <7.5 N·m were classified as an NR. COPD patients showed a mean improvement in QMVC after PR (10.08 ± 12.97 N·m; p < 0.001). However, 50% of patients were NRs. NRs had lower pre-PR values for body mass, height, body mass index, PaO2, and QMVC. Non-response can be predicted by low QMVC, high PaCO2, and gender (when male). This model has a sensitivity of 74% and specificity of 81%. The study highlights the considerable number of NRs and potential risk factors for non-response. To systematize the effects, it may be interesting to implement blood gas correction and/or optimize the programs to enhance peripheral and central effects.

Association between long-term oxygen therapy provided outside the guidelines and mortality in patients with COPD.

INTRODUCTION: Hypoxaemia is a frequent complication of chronic obstructive pulmonary disease (COPD). To prevent its consequences, supplemental oxygen therapy is recommended by international respiratory societies. However, despite clear recommendations, some patients receive long-term oxygen therapy (LTOT), while they do not meet prescription criteria. While evidence suggests that acute oxygen supply at high oxygenation targets increases COPD mortality, its chronic effects on COPD mortality remain unclear. Thus, the study will aim to evaluate through a systematic review and individual patient data meta-analysis (IPD-MA), the association of LTOT prescription outside the guidelines on survival over time in COPD. METHODS: Systematic review and IPD-MA will be conducted according to Preferred Reporting Items for a Systematic Review and Meta-Analyses IPD guidelines. Electronic databases (PubMed, Web of Science, EMBASE, Cochrane Central Register of Controlled Trials, ClinicalTrials.gov, OpenGrey and BioRxiv/MedRxix) will be scanned to identify relevant studies (cohort of stable COPD with arterial oxygen tension data available, with indication of LTOT filled out at the moment of the study and with a survival follow-up). The anticipated search dates are January-February 2022. The main outcome will be the association between LTOT and time to all-cause mortality according to hypoxaemia severity, after controlling for potential covariates and all available clinical characteristics. Quantitative data at the level of the individual patient will be used in a one-step approach to develop and validate a prognostic model with a Cox regression analysis. The one-step IPD-MA will be conducted to study the association and the moderators of association between supplemental oxygen therapy and mortality. Multilevel survival analyses using Cox-mixed effects models will be performed. ETHICS AND DISSEMINATION: As a protocol for a systematic review, a formal ethics committee review is not required. Only studies with institutional approval from an ethics committee and anonymised IPD will be included. Results will be disseminated through peer-reviewed publications and presentations in conferences. PROSPERO REGISTRATION NUMBER: CRD42020209823.

Adaptive Capacities and Complexity of Heart Rate Variability in Patients With Chronic Obstructive Pulmonary Disease Throughout Pulmonary Rehabilitation.

INTRODUCTION: The complexity of bio-signals, like R-R intervals, is considered a reflection of the organism's capacity to adapt. However, this association still remains to be consolidated. We investigated whether the complexity of R-R intervals at rest and during perturbation [6-minute walking test (6MWT)], yielded information regarding adaptive capacities in Chronic Obstructive Pulmonary Disease (COPD) patients during pulmonary rehabilitation (PR). METHODS: In total, 23 COPD patients (64 ± 8 years, with forced expiratory volume in 1 s of 55 ± 19% predicted) were tested three times at the start (T1), middle (T2), and end (T3) of 4 weeks PR. Each time, R-R intervals were measured at rest and during 6MWT. The complexity of R-R intervals was assessed by evenly spaced Detrended Fluctuations Analysis and evaluated by the fractal exponent α and deviation from maximal complexity |1-α|. RESULTS: The 6MWT distance was significantly increased at T2 and T3 compared to T1. Neither α nor |1-α| at rest and during perturbation significantly changed throughout PR, nor were they consistently associated with 6MWT distances at each time. Throughout the PR program, complexity during the 6MWT was significantly lower compared to the rest. The level of α during 6MWT at T1 was positively correlated with the improvement of the 6MWT distance throughout the PR program. DISCUSSION: Reduced complexity in COPD patients during acute perturbation at the beginning of PR supports a decreased improvement of the 6MWT distance throughout PR. This result seems consistent with the notion that the complexity reflects the patients' adaptive capacities and could therefore become a clinical indicator in an applied perspective.

Is bilateral corticospinal connectivity impaired in patients with chronic obstructive pulmonary disease?

KEY POINTS: During moderate and high levels of quadriceps force production, the ipsilateral motor cortex is concomitantly activated with the contralateral motor cortex throughout the corpus callosum to generate the motor command. Chronic obstructive pulmonary disease (COPD) patients display a structurally impaired corpus callosum that may explain the reduced motor command in this population, which in turn contributes to COPD-related muscle weakness of the knee extensors. The study aimed to determine whether bilateral connectivity was impaired and ipsilateral activation was lowered during unilateral strength production of the knee extensors. Our results indicate impaired bilateral connectivity but preserved ipsilateral activation in patients during unilateral isometric contractions of 50% of maximum voluntary strength. The preservation of ipsilateral activation during force production despite impaired bilateral connectivity is consistent with a reorganization of bilateral motor network function that drives unilateral strength production. ABSTRACT: The contralateral primary motor cortex (M1) is not the only brain area implicated in motor command generation. During moderate and high levels of quadriceps force production, the ipsilateral M1 is concomitantly activated. Such activation is mediated by the corpus callosum, the main component of bilateral connectivity. Structural damage to the corpus callosum has been observed in chronic obstructive pulmonary disease (COPD) patients, which might reduce ipsilateral activation and contribute to the lower motor command associated with COPD muscle weakness. We thus aimed to determine whether bilateral connectivity and ipsilateral activation were impaired in COPD. Twenty-two COPD patients and 21 healthy age-matched controls were evaluated by transcranial magnetic stimulation, at rest and during 50% of maximal voluntary isometric contraction (MVIC) of the dominant vastus lateralis muscle. Bilateral connectivity was determined by the ipsilateral silent period (iSP) during 50% MVIC. Ipsilateral activation was determined as the increase in ipsilateral excitability from rest to 50% MVIC. As expected, COPD patients had significantly lower MVIC (-25%, p = 0.03). These patients also showed a significantly lower iSP (-53%, p < 0.001) compared to controls. The ipsilateral excitability was increased in patients and controls (×2.5 and ×3.5, respectively, p < 0.001) but not differently between groups (p = 0.84). Despite impaired bilateral connectivity in COPD, ipsilateral activation was not increased. Reorganization in the patients' interhemispheric pathways could explain the preserved ipsilateral activation.

Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness.

BACKGROUND: Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness. METHODS: Twenty-two patients with quadriceps weakness (COPDMW), 18 patients with preserved quadriceps strength (COPDNoMW) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VAperipheral) and transcranial magnetic (VAcortical) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions. RESULTS: COPDMW exhibited lower VAcortical and lower MEP/Mmax compared with COPDNoMW (p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VAcortical and MEP/Mmax. CONCLUSIONS: COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.

Psychoactive medications in chronic obstructive pulmonary disease patients: From prevalence to effects on motor command and strength.

INTRODUCTION: In chronic-obstructive pulmonary disease (COPD) patients, the peripheral muscle weakness is partly due to reduced motor command. The psychoactive medications, which are often prescribed in COPD, are mainly inhibitory and thus may contribute to motor command reduction. The aims were to characterize and quantify the use of these drugs and determine their effects on cortical excitability and inhibition and thus on motor command and muscle weakness in these patients. METHODS: First, a prevalence study was conducted on 421 COPD patients. Second, cortical excitability, inhibition and voluntary activation were assessed in 40 patients (15 under psychoactive medications vs. 25 controls) by transcranial magnetic stimulation of the rectus femoris. Quadriceps maximal isometric strength was also assessed. RESULTS: About 48% of the patients were taking psychoactive medication. Benzodiazepines (21%) and antidepressants (13.5%) were the most prescribed. Patients with medications tended to be younger and isolated (p < 0.05). They also showed impaired cortical inhibition and decreased cortical excitability (+36%, p = 0.02). Voluntary activation was reduced (-3.6%, p = 0.04) but quadriceps strength was comparable between groups. CONCLUSIONS: Psychoactive medications are prevalent in COPD patients. Patients under these medications exhibited brain impairment and reduced motor command. Paradoxically, voluntary strength was unaltered.

Impact of Chronic Obstructive Pulmonary Disease on Cognitive and Motor Performances in Dual-Task Walking.

When two tasks are performed simultaneously, they compete for attentional resources, resulting in a performance decrement in one or both tasks. Patients with attention disorders have a reduced ability to perform several tasks simultaneously (e.g., talking while walking), which increases the fall risk and frailty. This study assessed the cognitive and motor performances of patients with COPD and healthy controls within a dual-task walking paradigm. A subobjective was to assess the impact of a pulmonary rehabilitation program on the dual-task performances in COPD. Twenty-five patients with COPD and 20 controls performed a cognitive task (subtraction) and a 15-m walking test separately (single-task; ST) and jointly (dual-task; DT). In addition, a subsample of 10 patients performed the same evaluations 5 weeks later after a pulmonary rehabilitation program following current recommendations. Cognitive and gait performances in ST showed no differences between patients with COPD and controls (all p > 0.05). However, COPD patients exhibited a greater increase in gait variability than controls in DT (4.07 ± 1.46% vs. 2.17 ± 0.7%, p < 0.001). The pulmonary rehabilitation program had no effect on the dual-task impairment for the subsample of patients (p = 0.87). This study provides evidence of insufficient attentional resources to successfully deal with DT in patients with COPD, and this was expressed through an exaggerated increase in gait variability in DT walking. Given the high risk of falls and disability associated with altered gait variability, dual-task training interventions should be considered in pulmonary rehabilitation programs.

Implicit attitudes and the improvement of exercise capacity during pulmonary rehabilitation.

The aim of this study was to examine the role of explicit and implicit attitudes in the improvement of exercise capacity during a 5-week pulmonary rehabilitation (PR). A total of 105 patients performed walking tests at baseline and at the end of PR. Change between performances was computed at the end of PR, and Minimal-Clinically-Important-Difference (MCID) were used to categorize patients as responders (i.e. change above MCID, N = 54) or non-responders (i.e. change below MCID, N = 51). At baseline, implicit attitudes were measured through a physical activity versus sedentary behavior Implicit Association Test; explicit attitudes toward physical activity and sedentary behavior were measured by questionnaires. Only implicit attitudes significantly differed between the two groups (p = .015), responders displaying implicit attitudes significantly more in favor of physical activity (M = .91, SD = .54) than non-responders (M = .60, SD = .71) at baseline. Measuring implicit attitudes in PR could help to accurately estimate patients' motivation, and design more individualized rehabilitation programs.

Change in explicit and implicit motivation toward physical activity and sedentary behavior in pulmonary rehabilitation and associations with postrehabilitation behaviors.

OBJECTIVE: The aim of this study was twofold: (a) to determine whether Theory of Planned Behavior (TPB) variables and implicit attitudes toward physical activity and sedentary behavior would change during a 5-week pulmonary rehabilitation (PR) program, and (b) to investigate the relationships between behavioral intentions, implicit attitudes, physical activity, and sedentary behavior in postrehabilitation. DESIGN: Out of 142 patients with respiratory disease included in this study, 119 completed 2 questionnaires measuring TPB variables with regard to physical activity and sedentary behavior, and an Implicit Association Test (IAT) measuring implicit attitudes toward physical activity in contrast to sedentary behavior. The TPB questionnaires and the IAT were administered at the beginning (Time 1) and the end of the program (Time 2). Six months after the program (Time 3), 62 patients provided self-reported measures of their recreational physical activity and screen-based, leisure-time sedentary behavior. RESULTS: Over the course of pulmonary rehabilitation, perceived behavioral control and intentions toward physical activity increased, as did social norms and perceived behavioral control toward sedentary behavior; implicit attitudes were also more positive toward physical activity. Implicit attitudes at the end of PR (Time 2) were significantly associated with postrehabilitation physical activity (Time 3). CONCLUSIONS: TPB variables toward physical activity and sedentary behavior as well as implicit attitudes were enhanced during PR. At 6 months, implicit attitudes were significantly associated with physical activity. These results suggest that motivation, particularly implicit attitudes, should be targeted in future behavioral interventions in order to optimize the effects of rehabilitation on physical activity maintenance. (PsycINFO Database Record

The self-perception of dyspnoea threshold during the 6-min walk test: a good alternative to estimate the ventilatory threshold in chronic obstructive pulmonary disease.

To determine and/or adjust exercise training intensity for patients when the cardiopulmonary exercise test is not accessible, the determination of dyspnoea threshold (defined as the onset of self-perceived breathing discomfort) during the 6-min walk test (6MWT) could be a good alternative. The aim of this study was to evaluate the feasibility and reproducibility of self-perceived dyspnoea threshold and to determine whether a useful equation to estimate ventilatory threshold from self-perceived dyspnoea threshold could be derived. A total of 82 patients were included and performed two 6MWTs, during which they raised a hand to signal self-perceived dyspnoea threshold. The reproducibility in terms of heart rate (HR) was analysed. On a subsample of patients (n=27), a stepwise regression analysis was carried out to obtain a predictive equation of HR at ventilatory threshold measured during a cardiopulmonary exercise test estimated from HR at self-perceived dyspnoea threshold, age and forced expiratory volume in 1 s. Overall, 80% of patients could identify self-perceived dyspnoea threshold during the 6MWT. Self-perceived dyspnoea threshold was reproducibly expressed in HR (coefficient of variation=2.8%). A stepwise regression analysis enabled estimation of HR at ventilatory threshold from HR at self-perceived dyspnoea threshold, age and forced expiratory volume in 1 s (adjusted r=0.79, r=0.63, and relative standard deviation=9.8 bpm). This study shows that a majority of patients with chronic obstructive pulmonary disease can identify a self-perceived dyspnoea threshold during the 6MWT. This HR at the dyspnoea threshold is highly reproducible and enable estimation of the HR at the ventilatory threshold.

Brain Damage and Motor Cortex Impairment in Chronic Obstructive Pulmonary Disease: Implication of Nonrapid Eye Movement Sleep Desaturation.

STUDY OBJECTIVES: Nonrapid eye movement (NREM) sleep desaturation may cause neuronal damage due to the withdrawal of cerebrovascular reactivity. The current study (1) assessed the prevalence of NREM sleep desaturation in nonhypoxemic patients with chronic obstructive pulmonary disease (COPD) and (2) compared a biological marker of cerebral lesion and neuromuscular function in patients with and without NREM sleep desaturation. METHODS: One hundred fifteen patients with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] grades 2 and 3), resting PaO2 of 60-80 mmHg, aged between 40 and 80 y, and without sleep apnea (apnea-hypopnea index < 15) had polysomnographic sleep recordings. In addition, twenty-nine patients (substudy) were assessed i) for brain impairment by serum S100B (biological marker of cerebral lesion), and ii) for neuromuscular function via motor cortex activation and excitability and maximal voluntary quadriceps strength measurement. RESULTS: A total of 51.3% patients (n = 59) had NREM sleep desaturation (NREMDes). Serum S100B was higher in the NREMDes patients of the substudy (n = 14): 45.1 [Q1: 37.7, Q3: 62.8] versus 32.9 [Q1: 25.7, Q3: 39.5] pg.ml(-1) (P = 0.028). Motor cortex activation and excitability were lower in NREMDes patients (both P = 0.03), but muscle strength was comparable between groups (P = 0.58). CONCLUSIONS: Over half the nonhypoxemic COPD patients exhibited NREM sleep desaturation associated with higher values of the cerebral lesion biomarker and lower neural drive reaching the quadriceps during maximal voluntary contraction. The lack of muscle strength differences between groups suggests a compensatory mechanism(s). Altogether, the results are consistent with an involvement of NREM sleep desaturation in COPD brain impairment. CLINICAL TRIAL REGISTRATION: The study was registered at www.clinicaltrials.gov as NCT01679782.

Is nocturnal desaturation a trigger for neuronal damage in chronic obstructive pulmonary disease?

Patients with chronic obstructive pulmonary disease (COPD) present many neurological disorders of unknown origin. Although hypoxemia has long been thought to be responsible, several studies have shown evidence of neuronal damage and dysfunction even in non-hypoxemic patients with COPD. Adaptive mechanisms protect the brain from hypoxia: when arterial oxygen tension (PaO2) decreases, the cerebral blood flow (CBF) increases, ensuring continuously adequate oxygen delivery to the brain. However, this mechanism is abolished during non-rapid eye movement (NREM) sleep. Any drop in PaO2 during NREM sleep is therefore not compensated by increased CBF, causing decreased cerebral oxygen delivery with subsequent brain hypoxia. Patients with may therefore be exposed to neuronal damage during this critical time. This mechanism is of vital importance for patients with COPD because of the potentially deleterious cortical effects. Nocturnal desaturation is quite frequent in COPD and affects approximately one out of two patients who are not hypoxemic during wakefulness. Although the prevalence of NREM sleep desaturation has never been specifically assessed in COPD, current data suggest that at least half of the nocturnal desaturation in desaturating patients occurs during NREM sleep. This review presents the rationale for the hypothesis that nocturnal desaturation during NREM sleep promotes neuronal damage and dysfunction in COPD.

Cortical implication in lower voluntary muscle force production in non-hypoxemic COPD patients.

Recent studies have shown that muscle alterations cannot totally explain peripheral muscle weakness in COPD. Cerebral abnormalities in COPD are well documented but have never been implicated in muscle torque production. The purpose of this study was to assess the neural correlates of quadriceps torque control in COPD patients. Fifteen patients (FEV1 54.1±3.6% predicted) and 15 age- and sex-matched healthy controls performed maximal (MVCs) and submaximal (SVCs) voluntary contractions at 10, 30 and 50% of the maximal voluntary torque of the knee extensors. Neural activity was quantified with changes in functional near-infrared spectroscopy oxyhemoglobin (fNIRS-HbO) over the contralateral primary motor (M1), primary somatosensory (S1), premotor (PMC) and prefrontal (PFC) cortical areas. In parallel to the lower muscle torque, the COPD patients showed lower increase in HbO than healthy controls over the M1 (p<0.05), PMC (p<0.05) and PFC areas (p<0.01) during MVCs. In addition, they exhibited lower HbO changes over the M1 (p<0.01), S1 (p<0.05) and PMC (p<0.01) areas during SVCs at 50% of maximal torque and altered motor control characterized by higher torque fluctuations around the target. The results show that low muscle force production is found in a context of reduced motor cortex activity, which is consistent with central nervous system involvement in COPD muscle weakness.

Neuromuscular fatigue is not different between constant and variable frequency stimulation.

This study compared fatigue development of the triceps surae induced by two electrical stimulation protocols composed of constant and variable frequency trains (CFTs, VFTs, 450 trains, 30 Hz, 167 ms ON, 500 ms OFF and 146 ms ON, 500 ms OFF respectively). For the VFTs protocol a doublet (100 Hz) was used at the beginning of each train. The intensity used evoked 30% of a maximal voluntary contraction (MVC) and was defined using CFTs. Neuromuscular tests were performed before and after each protocol. Changes in excitation-contraction coupling were assessed by analysing the M-wave [at rest (Mmax) and during MVC (Msup)] and associated peak twitch (Pt). H-reflex [at rest (Hmax) and during MVC (Hsup)] and the motor evoked potential (MEP) during MVC were studied to assess spinal and corticospinal excitability of the soleus muscle. MVC decrease was similar between the protocols (-8%, P<0.05). Mmax, Msup and Pt decreased after both protocols (P<0.01). Hmax/Mmax was decreased (P<0.05), whereas Hsup/Msup and MEP/Msup remained unchanged after both protocols. The results indicate that CFTs and VFTs gave rise to equivalent neuromuscular fatigue. This fatigue resulted from alterations taking place at the muscular level. The finding that cortical and spinal excitability remained unchanged during MVC indicates that spinal and/or supraspinal mechanisms were activated to compensate for the loss of spinal excitability at rest.

A new method for muscle fatigue assessment: Online model identification techniques.

INTRODUCTION: The purpose of this study was to propose a method that allows extraction of the current muscle state under electrically induced fatigue. METHODS: The triceps surae muscle of 5 subjects paralyzed by spinal cord injury was fatigued by intermittent electrical stimulation (5 × 5 trains at 30 Hz). Classical fatigue indices representing muscle contractile properties [peak twitch (Pt) and half-relaxation time (HRT)] were assessed before and after each 5-train series and were used to identify 2 relevant parameters (Fm , Ur ) of a previously developed mathematical model using the Sigma-Point Kalman Filter. RESULTS: Pt declined significantly during the protocol, whereas HRT remained unchanged. Identification of the model parameters with experimental data yielded a model-based fatigue assessment that gave a more stable evaluation of fatigue than classical parameters. CONCLUSIONS: This work reinforces clinical research by providing a tool that clinicians can use to monitor fatigue development during stimulation.

Does central fatigue exist under low-frequency stimulation of a low fatigue-resistant muscle?

The aim of the present study was to determine whether central fatigue occurs when fatigue is electrically induced in the abductor pollicis brevis muscle. Three series of 17 trains (30 Hz, 450 µs, 4 s on/6 s off, at the maximal tolerated intensity) were used to fatigue the muscle. Neuromuscular tests consisting of electrically evoked and voluntary contractions were performed before and after every 17-train series. Both the force induced by the stimulation trains and maximal voluntary force generation capacity significantly decreased throughout the protocol (-27 and -20%, respectively, at the end of the protocol, P < 0.001). These decreases were accompanied by failure in muscle excitability (P < 0.01), as assessed by the muscle compound action potential (M-wave or Mmax), leading to significant impairment in the muscle contractile properties (P < 0.05), as assessed by the muscle mechanical response (Pt). Central fatigue indices (level of activation, RMS/Mmax and H reflex) were not significantly changed at any point in the protocol. This gives evidence of preserved motor command reaching the motor neurons and preserved spinal excitability. The results indicate that this low-frequency stimulation protocol entails purely peripheral fatigue development when applied to a low fatigue-resistant muscle.

Kinetics of neuromuscular changes during low-frequency electrical stimulation.

The purpose of the study was to examine the time course of neuromuscular fatigue components during a low-frequency electrostimulation (ES) session. Three bouts of 17 trains of stimulation at 30 HZ (4 s on, 6 s off) were used to electrically induce fatigue in the plantar flexor muscles. Before and after every 17-train bout, torque, electromyographic activity [expressed as root mean square (RMS) and median frequency (MF) values], evoked potentials (M-wave and H-reflex), and the level of voluntary activation (LOA, using twitch interpolation technique) were assessed. Torque during maximal voluntary contraction decreased significantly from the very first stimulation bout (-6.6 +/- 1.11%, P < 0.001) and throughout the session (-10.32 +/- 1.68% and -11.53 +/- 1.27%, for the second and third bouts, respectively). The LOA and RMS/Mmax values were significantly decreased during the ES session (-2.9 +/- 1.07% and -17.5 +/- 6.14%, P < 0.01 and P< 0.001, respectively, at the end of the protocol), while MF showed no changes. The Hmax/Mmax ratio and Mmax were not significantly modified during the session. All twitch parameters were significantly potentiated after the first bout and throughout the session (P < 0.001). The maximal torque decrease was evident from the early phase of a low-frequency ES protocol, with no concomitant inhibition of motoneuron excitability or depression of muscle contractile properties. These results are consistent with an early failure of the central drive to the muscle.

Recurrence quantification analysis of surface electromyographic signal: sensitivity to potentiation and neuromuscular fatigue.

This study aimed to assess the capacity of recurrence quantification analysis (RQA) to detect potentiation and to determine the fatigue components to which RQA is sensitive. Fifteen men were divided in two groups [8 endurance-trained athletes (END) and 7 power-trained athletes (POW)]. They performed a 10-min intermittent (5s contraction, 5s rest) knee extension exercise at 50% of their maximal voluntary isometric contraction. Muscular fatigue and potentiation were evaluated with neurostimulation technique. Mechanical (peak torque, Pt) and electrophysiological (M-wave) responses following electrical stimulation of the femoral nerve were measured at rest and every 10s throughout exercise. Vastus lateralis muscle activity (root mean square, RMS) was recorded during each contraction, and RMS was normalized to M-wave area (RMS/M). During contraction, muscle activity was analyzed with RQA to obtain the percentage of determinism (%Det). At the beginning of exercise, a significant Pt increase (+52%, P<0.001) was observed in both groups, indicating potentiation. At this time, %Det remained constant in both groups, indicating that RQA did not detect potentiation. Thereafter, Pt decreased in POW from 5min 30s of exercise (-30%, P<0.001), reflecting impairment in excitation-contraction coupling, and %Det increased from 3min 30s (P<0.01). In END, Pt remained high and %Det was unchanged. These two results indicated that RQA detected the peripheral component of fatigue. Conversely, RQA did not detect central adaptation to fatigue since %Det remained constant when a significant increase in RMS/M (P<0.01) appeared in END.