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The use of electrical stimulation (ES) can contribute to our knowledge of how our neuromuscular system can adapt to physical stress or unloading. Although it has been recently challenged, the standard technique used to explore central modifications is the twitch interpolated method which consists in superimposing single twitches or high-frequency doublets on a maximal voluntary contraction (MVC) and to compare the superimposed response to the potentiated response obtained from the relaxed muscle. Alternative methods consist in (1) superimposing a train of stimuli (central activation ratio), (2) comparing the MVC response to the force evoked by a high-frequency tetanus or (3) examining the change in maximal EMG response during voluntary contractions, if this variable is normalized to the maximal M wave, i.e. EMG response to a single stimulus. ES is less used to examine supraspinal factors but it is useful for investigating changes at the spinal level, either by using H reflexes, F waves or cervicomedullary motor-evoked potentials. Peripheral changes can be examined with ES, usually by stimulating the muscle in the relaxed state. Neuromuscular propagation of action potentials on the sarcolemma (M wave, high-frequency fatigue), excitation–contraction coupling (e.g. low-frequency fatigue) and intrinsic force (high-frequency stimulation at supramaximal intensity) can all be used to non-invasively explore muscular function with ES. As for all indirect methods, there are limitations and these are discussed in this review. Finally, (1) ES as a method to measure respiratory muscle function and (2) the comparison between electrical and magnetic stimulation will also be considered.

To develop a simplified magnetic resonance imaging method (MRI) to assess total adipose tissue (AT) and adipose tissue free mass (ATFM) from three single MRI slices in people with overweight/obesity in order to implement body composition follow-up in a clinical research setting. Body composition of 310 participants (70 women and 240 men, age: 50.8 ± 10.6 years, BMI: 31.3 ± 5.6 kg.m −2 ) was assessed with 3 single slices (T6-T7, L4-L5 and at mid-thigh) MRI. Multiple regression analysis was used to develop equations predicting AT and ATFM from these three single slices. Then we implemented a longitudinal phase consisting in a 2-month exercise training program during which we tested the sensitivity of these equations in a subgroup of participants with overweight/obesity (n = 79) by comparing the exercise-induced variations between predicted and measured AT and ATFM. The following equations: total AT = − 12.74105 + (0.02919 × age) + (4.27634 × sex (M = 0, F = 1)) + (0.22008 × weight) + (26.92234 × AT T6-T7) + (23.70142 × AT L4-L5) + (37.94739 × AT mid-thigh) and total ATFM = − 33.10721 + (− 0.02363 × age) + (− 3.58052 × sex (M = 0, F = 1)) + (30.02252 × height) + (0.08549 × weight) + (11.36859 × ATFM T6-T7) + (27.82244 × ATFM L4-L5) + (58.62648 × ATFM mid-thigh) showed an excellent prediction (adjusted R 2  = 97.2% and R 2  = 92.5%; CCC = 0.986 and 0.962, respectively). There was no significant difference between predicted and measured methods regarding the AT variations (− 0.07 ± 2.02 kg, p = 0.70) and the ATFM variations (0.16 ± 2.41 kg, p = 0.49) induced by 2-months of exercise training. This simplified method allows a fully accurate assessment of the body composition of people with obesity in less than 20 min (10 min for images acquisition and analysis, respectively), useful for a follow-up.

Background Greater diaphragm fatigue has been reported after hypoxic versus normoxic exercise, but whether this is due to increased ventilation and therefore work of breathing or reduced blood oxygenation per se remains unclear. Hence, we assessed the effect of different blood oxygenation level on isolated hyperpnoea-induced inspiratory and expiratory muscle fatigue. Methods Twelve healthy males performed three 15-min isocapnic hyperpnoea tests (85% of maximum voluntary ventilation with controlled breathing pattern) in normoxic, hypoxic (SpO 2 = 80%) and hyperoxic (FiO 2 = 0.60) conditions, in a random order. Before, immediately after and 30 min after hyperpnoea, transdiaphragmatic pressure (P di,tw ) was measured during cervical magnetic stimulation to assess diaphragm contractility, and gastric pressure (P ga,tw ) was measured during thoracic magnetic stimulation to assess abdominal muscle contractility. Two-way analysis of variance (time x condition) was used to compare hyperpnoea-induced respiratory muscle fatigue between conditions. Results Hypoxia enhanced hyperpnoea-induced P di,tw and P ga,tw reductions both immediately after hyperpnoea (P di,tw : normoxia -22 ± 7% vs hypoxia -34 ± 8% vs hyperoxia -21 ± 8%; P ga,tw : normoxia -17 ± 7% vs hypoxia -26 ± 10% vs hyperoxia -16 ± 11%; all P < 0.05) and after 30 min of recovery (P di,tw : normoxia -10 ± 7% vs hypoxia -16 ± 8% vs hyperoxia -8 ± 7%; P ga,tw : normoxia -13 ± 6% vs hypoxia -21 ± 9% vs hyperoxia -12 ± 12%; all P < 0.05). No significant difference in P di,tw or P ga,tw reductions was observed between normoxic and hyperoxic conditions. Also, heart rate and blood lactate concentration during hyperpnoea were higher in hypoxia compared to normoxia and hyperoxia. Conclusions These results demonstrate that hypoxia exacerbates both diaphragm and abdominal muscle fatigability. These results emphasize the potential role of respiratory muscle fatigue in exercise performance limitation under conditions coupling increased work of breathing and reduced O 2 transport as during exercise in altitude or in hypoxemic patients.

Background Transcranial magnetic stimulation (TMS) is a widely-used investigative technique in motor cortical evaluation. Recently, there has been a surge in TMS studies evaluating lower-limb fatigue. TMS intensity of 120-130% resting motor threshold (RMT) and 120% active motor threshold (AMT) and TMS intensity determined using stimulus–response curves during muscular contraction have been used in these studies. With the expansion of fatigue research in locomotion, the quadriceps femoris is increasingly of interest. It is important to select a stimulus intensity appropriate to evaluate the variables, including voluntary activation, being measured in this functionally important muscle group. This study assessed whether selected quadriceps TMS stimulus intensity determined by frequently employed methods is similar between methods and muscles. Methods Stimulus intensity in vastus lateralis , rectus femoris and vastus medialis muscles was determined by RMT, AMT (i.e. during brief voluntary contractions at 10% maximal voluntary force, MVC) and maximal motor-evoked potential (MEP) amplitude from stimulus–response curves during brief voluntary contractions at 10, 20 and 50% MVC at different stimulus intensities. Results Stimulus intensity determined from a 10% MVC stimulus–response curve and at 120 and 130% RMT was higher than stimulus intensity at 120% AMT (lowest) and from a 50% MVC stimulus–response curve ( p  < 0.05). Stimulus intensity from a 20% MVC stimulus–response curve was similar to 120% RMT and 50% MVC stimulus–response curve. Mean stimulus intensity for stimulus–response curves at 10, 20 and 50% MVC corresponded to approximately 135, 115 and 100% RMT and 180, 155 and 130% AMT, respectively. Selected stimulus intensity was similar between muscles for all methods ( p  > 0.05). Conclusions Similar optimal stimulus intensity and maximal MEP amplitudes at 20 and 50% MVC and the minimal risk of residual fatigue at 20% MVC suggest that a 20% MVC stimulus–response curve is appropriate for determining TMS stimulus intensity in the quadriceps femoris . The higher selected stimulus intensities at 120-130% RMT have the potential to cause increased coactivation and discomfort and the lower stimulus intensity at 120% AMT may underestimate evoked responses. One muscle may also act as a surrogate in determining optimal quadriceps femoris stimulation intensity.

Both respiratory muscle endurance training (RMET) and inspiratory resistive training (IMT) seem to increase whole-body exercise performance, but direct comparisons between the two are scarce. We hypothesized that the similarity of RMET to exercise-induced ventilation would induce larger improvements compared to IMT. Twenty-six moderately-trained men performed either 4 weeks of RMET, IMT or SHAM training. Before and after the interventions, respiratory muscle endurance, 3-km running time-trial performance and leg muscle fatigue after intense constant-load cycling (assessed with femoral nerve magnetic stimulation) were measured. Both RMET (+ 59%) and IMT (+ 38%) increased respiratory muscle endurance (both p  < 0.01 vs. SHAM) but only IMT increased inspiratory strength (+ 32%, p  < 0.001 vs. SHAM). 3-km time improved showing a main effect of training ( p  = 0.026), however with no differences between groups. Leg fatigue after cycling was not attenuated with training ( p  = 0.088 for group-training interaction). All groups showed a significant (~ 0.3 l) increase in average tidal volume during cycling exercise combined with a concomitant reduction in respiratory exertion. While RMET and IMT improved specific aspects of respiratory muscles performance, no benefits beyond SHAM were seen during whole-body exercise. Changes in respiratory sensations might be a result of altered breathing pattern.

“Exercise starts and ends in the brain”: this was the title of a review article authored by Dr. Bengt Kayser back in 2003. In this piece of work, the author highlights that pioneer studies have primarily focused on the cardiorespiratory-muscle axis to set the human limits to whole-body exercise tolerance. In some circumstances, however, exercise cessation may not be solely attributable to these players: the central nervous system is thought to hold a relevant role as the ultimate site of exercise termination. In fact, there has been a growing interest relative to the “brain” response to exercise in chronic cardiorespiratory diseases, and its potential implication in limiting the tolerance to physical exertion in patients. To reach these overarching goals, non-invasive techniques, such as near-infrared spectroscopy and transcranial magnetic stimulation, have been successfully applied to get insights into the underlying mechanisms of exercise limitation in clinical populations. This review provides an up-to-date outline of the rationale for the “brain” as the organ limiting the tolerance to physical exertion in patients with cardiorespiratory diseases. We first outline some key methodological aspects of neuromuscular function and cerebral hemodynamics assessment in response to different exercise paradigms. We then review the most prominent studies which explored the influence of major cardiorespiratory diseases on these outcomes. After a balanced summary of existing evidence, we finalize by detailing the rationale for investigating the “brain” contribution to exercise limitation in hitherto unexplored cardiorespiratory diseases, an endeavor that might lead to innovative lines of applied physiological research.

Chronic mountain sickness is a maladaptive syndrome that affects individuals living permanently at high altitude and is characterized primarily by excessive erythrocytosis (EE). Recent results concerning the impact of EE in Andean highlanders on clotting and the possible promotion of hypercoagulability, which can lead to thrombosis, were contradictory. We assessed the coagulation profiles of Andeans highlanders with and without excessive erythrocytosis (EE+ and EE−). Blood samples were collected from 30 EE+ and 15 EE− in La Rinconada (Peru, 5100–5300 m a.s.l.), with special attention given to the sampling pre‐analytical variables. Rotational thromboelastometry tests were performed at both native and normalized (40%) haematocrit using autologous platelet‐poor plasma. Thrombin generation, dosages of clotting factors and inhibitors were measured in plasma samples. Data were compared between groups and with measurements performed at native haematocrit in 10 lowlanders (LL) at sea level. At native haematocrit, in all rotational thromboelastometry assays, EE+ exhibited hypocoagulable profiles (prolonged clotting time and weaker clot strength) compared with EE− and LL (all P < 0.01). At normalized haematocrit, clotting times were normalized in most individuals. Conversely, maximal clot firmness was normalized only in FIBTEM and not in EXTEM/INTEM assays, suggesting abnormal platelet activity. Thrombin generation, levels of plasma clotting factors and inhibitors, and standard coagulation assays were mostly normal in all groups. No highlanders reported a history of venous thromboembolism based on the dedicated survey. Collectively, these results indicate that EE+ do not present a hypercoagulable profile potentially favouring thrombosis. What is the central question of this study? Are Andean highlanders with excessive erythrocytosis (EE+) exhibiting a hypercoagulable profile compared with highlanders without erythrocytosis (EE−) and lowlanders (LL)? What is the main finding and its importance? Despite normal plasma coagulation (thrombinography and levels of clotting factors and inhibitors), EE+ exhibited a hypocoagulable rotational thromboelastometry profile (prolonged clotting time and weaker clot strength) compared with EE− and LL. In EE+, haematocrit normalization at 40% corrected maximal clot firmness in rotational thromboelastometry FIBTEM tests, but not in EXTEM and INTEM tests, suggesting that platelets play a role in the native hypocoagulable profile.

Maximal central motor drive is known to decrease during prolonged exercise although it remains to be determined whether a supraspinal deficit exists, and if so, when it appears. The purpose of this study was to evaluate corticospinal excitability and muscle voluntary activation before, during and after a 4-h cycling exercise. Ten healthy subjects performed three 80-min bouts on an ergocycle at 45% of their maximal aerobic power. Before exercise and immediately after each bout, neuromuscular function was evaluated in the quadriceps femoris muscles under isometric conditions. Transcranial magnetic stimulation was used to assess voluntary activation at the cortical level (VATMS), corticospinal excitability via motor-evoked potential (MEP) and intracortical inhibition by cortical silent period (CSP). Electrical stimulation of the femoral nerve was used to measure voluntary activation at the peripheral level (VAFNES) and muscle contractile properties. Maximal voluntary force was significantly reduced after the first bout (13 ± 9%, P<0.01) and was further decreased (25 ± 11%, P<0.001) at the end of exercise. CSP remained unchanged throughout the protocol. Rectus femoris and vastus lateralis but not vastus medialis MEP normalized to maximal M-wave amplitude significantly increased during cycling. Finally, significant decreases in both VATMS and VAFNES (∼ 8%, P<0.05 and ∼ 14%, P<0.001 post-exercise, respectively) were observed. In conclusion, reductions in VAFNES after a prolonged cycling exercise are partly explained by a deficit at the cortical level accompanied by increased corticospinal excitability and unchanged intracortical inhibition. When comparing the present results with the literature, this study highlights that changes at the cortical and/or motoneuronal levels depend not only on the type of exercise (single-joint vs. whole-body) but also on exercise intensity and/or duration.

Vascular aging involves reduced endothelial function, a key factor in cardiovascular diseases. Intermittent hypoxia may improve endothelial function and cardiorespiratory fitness (CRF), but its effects in elderly individuals, especially in the mid‐term, have not yet been studied. This randomized, single‐blind controlled trial aimed to investigate whether an 8‐week intermittent hypoxic conditioning (IHC) program may enhance flow‐mediated dilation (FMD) and CRF in elderly individuals. Twenty‐six participants (60–80 year‐old) were assigned to either the IHC (n = 12) or the control group (CTL: n = 14). The IHC group underwent 24 passive intermittent hypoxia sessions (3/week). Brachial artery FMD, cardiopulmonary exercise testing (CPET), and ambulatory 24‐h blood pressure were assessed at baseline (Pre), immediately post‐intervention (Post 1), and 2 months later (Post 2). FMD showed a trend toward improvement in the IHC group, being significant when normalized for baseline artery diameter (p = 0.023; ηp2 = 0.150) between Pre and Post 2. Peak ventilation during CPET increased from Pre to Post 1 (p = 0.021), with no other significant CRF changes. Daytime systolic blood pressure decreased by 6 mmHg (p = 0.070, ηp2 = 0.105). No significant alterations in these outcomes were observed in the CTL group (p > 0.05). Moderate IHC enhanced mid‐term endothelial function, suggesting potential to mitigate age‐related vascular decline.

Severe obstructive sleep apnoea (OSA) can lead to neurocognitive alterations, including gait impairments. The beneficial effects of continuous positive airway pressure (CPAP) on improving excessive daytime sleepiness and daily functioning have been documented. However, a demonstration of CPAP treatment efficacy on gait control is still lacking. This study aims to test the hypothesis that CPAP improves gait control in severe OSA patients. In this prospective controlled study, twelve severe OSA patients (age = 57.2±8.9 years, body mass index = 27.4±3.1 kg·m-2, apnoea-hypopnoea index = 46.3±11.7 events·h-1) and 10 healthy matched subjects were included. Overground gait parameters were recorded at spontaneous speed and stride time variability, a clinical marker of gait control, was calculated. To assess the role of executive functions in gait and postural control, a dual-task paradigm was applied using a Stroop test as secondary cognitive task. All assessments were performed before and after 8 weeks of CPAP treatment. Before CPAP treatment, OSA patients had significantly larger stride time variability (3.1±1.1% vs 2.1±0.5%) and lower cognitive performances under dual task compared to controls. After CPAP treatment, stride time variability was significantly improved and no longer different compared to controls. Cognitive performance under dual task also improved after CPAP treatment. Eight weeks of CPAP treatment improves gait control of severe OSA patients, suggesting morphological and functional cerebral improvements. Our data provide a rationale for further mechanistic studies and the use of gait as a biomarker of OSA brain consequences.