Fabio Esposito

The surface mechanomyogram as a tool to describe the influence of fatigue on biceps brachii motor unit activation strategy. Historical basis and novel evidence.

The surface mechanomyogram (MMG) (detectable at the muscle surface as MMG by accelerometers, piezoelectric contact sensors or other transducers) is the summation of the activity of single motor units (MUs). Each MU contribution is related to the pressure waves generated by the active muscle fibres. The first part of this article will review briefly the results obtained by our group studying the possible role of motor unit recruitment and firing rate in determining the characteristics of the MMG during stimulated and voluntary contractions. The second part of this article will study the MMG and EMG during a short isometric force ramp from 0 to 90% of the maximal voluntary contraction (MVC) in fresh and fatigued biceps brachii. The aim is to verify whether changes in motor unit activation strategy in voluntarily fatigued muscle could be specifically reflected in the time and frequency domain parameters of the MMG. MMG-RMS vs. %MVC: at fatigue the MMG-RMS did not present the well known increment, when effort level increases, followed by a clear decrement at near-maximal contraction levels. MMG-MF vs. %MVC: compared to fresh muscle the fatigued biceps brachii showed an MF trend significantly shifted towards lower values and the steeper MF increment, from 65 to 85% MVC, was not present. The alteration in the MMG and EMG parameters vs. %MVC relationships at fatigue seems to be related to the impossibility of recruiting fast, but more fatigable MUs, and to the lowering of the global MUs firing during the short isometric force ramp investigated.

Limited maximal exercise capacity in patients with chronic heart failure: partitioning the contributors.

OBJECTIVES This study aimed to assess the factors limiting maximal exercise capacity in patients with chronic heart failure (CHF). BACKGROUND Maximal exercise capacity, an important index of health in CHF, might be limited by central and/or peripheral factors; however, their contributions remain poorly understood. METHODS We studied oxygen (O2) transport and metabolism at maximal cycle (centrally taxing) and knee-extensor (KE) (peripherally taxing) exercise in 12 patients with CHF and 8 healthy control subjects in normoxia and hyperoxia (100% O2). RESULTS Peak oxygen uptake (VO2) while cycling was 33% lower in CHF patients than in control subjects. By experimental design, peak cardiac output was reduced during KE exercise when compared with cycling (approximately 35%); although muscle mass specific peak leg VO2 was increased equally in both groups (approximately 70%), VO2 in the CHF patients was still 28% lower. Hyperoxia increased O2 carriage in all cases but only facilitated a 7% increase in peak leg VO2 in the CHF patients during cycling, the most likely scenario to benefit from increased O2 delivery. Several relationships, peak leg VO2 (KE + cycle) to capillary-fiber-ratio and capillaries around a fiber to mitochondrial volume, were similar in both groups (r = 0.6-0.7). CONCLUSIONS Multiple independent observations, including a significant skeletal muscle metabolic reserve, suggest skeletal muscle per se contributes minimally to limiting maximal cycle exercise in CHF or healthy control subjects. However, the consistent attenuation of the convective and diffusive components of O2 transport (25% to 30%) in patients with CHF during both cycle and even KE exercise compared with control subjects reveals an underlying peripheral O2 transport limitation from blood to skeletal muscle in this pathology.

Time and frequency domain analysis of electromyogram and sound myogram in the elderly

The aim of this work was to evaluate the influence of the ageing process on the time and frequency domain properties of the surface electrical and mechanical activity of muscle. In 20 healthy elderly subjects (10 men and 10 women, age range 65–78 years) and in 20 young controls, during isometric contractions of the elbow flexors in the 20%–100% range of the maximal voluntary contraction (MVC), estimations were made of the root mean square (rms) and the mean frequency (MF) of the power density spectrum distribution, from the surface electromyogram (EMG) and sound myogram (0SMG) signals, detected at the belly of the biceps brachii muscle. Compared to the young controls, the MVC was lower in the elderly subjects (P < 0.05); at the same %MVC the rms and the MF of EMG and SMG were lower (P < 0.05) in elderly subjects; the rms and MF of the two signals increased as a function of the effort level in all groups. Only in the 80%–100% MVC range did the EMG-MF level off and the SMG-rms decrease; in contrast the young controls, at 80% MVC the high frequency peak in the SMG power spectrum density distribution was not present in the elderly subjects. The results for MVC and %MVC can be related to the reduction in the numbers of muscle fibres in aged subjects. In particular, the lack of fast twitch fibre motor units (MU), attaining high firing rates, might also explain the result at 80% MVC. In 80%–100% MVC range the two signals rms and MF behaviour may have been related to the end of the recruitment of larger MU with high conduction velocity, and to the further increment of MU firing rate in the biceps brachii muscle beyond 80% MVC, respectively. Thus, the coupled analysis of the EMG and SMG with force suggests that in the elderly subjects the reduction of the number of muscle fibres may have co-existed with a MU activation pattern similar to that of the young subjects.

Electromyogram and mechanomyogram changes in fresh and fatigued muscle during sustained contraction in men

Abstract In surface electromyogram (EMG) and mechanomyogram (MMG) the electrical and mechanical activities of recruited motor units (MU) are summated. Muscle fatigue influences the electrical and mechanical properties of the active MU. The aim of this study was to evaluate fatigue-induced changes in the electrical and mechanical properties of MU after a short recovery period, using an analysis of force, surface EMG and MMG. In seven subjects the EMG and MMG were recorded from the biceps brachii muscle during sustained isometric effort at 80% of the maximal voluntary contraction (MVC), before (test 1) and 10 min after (test 2) a fatiguing exercise. From the time and frequency domain analysis of the signals, the root mean square (rms) and the mean frequency (f¯) of the power spectrum were calculated. The results were that the mean MVC was 412 (SEM 90) N and 304 (SEM 85) N in fresh and fatigued muscle, respectively; during tests 1 and 2 the mean EMG rms increased from 0.403 (SEM 0.07) mV to 0.566 (SEM 0.09) mV and from 0.476 (SEM 0.07) mV to 0.63 (SEM 0.09) mV, respectively; during test 1 the mean MMG rms decreased from 9.4 (SEM 0.8) mV to 5.7 (SEM 0.9) mV; in contrast, during test 2 constantly lower values were observed throughout contraction; during tests 1 and 2 the EMG f¯ declined from 122 (SEM 7) Hz to 74 (SEM 7) Hz and from 106 (SEM 8) Hz to 60 (SEM 7) Hz, respectively; during test 1 the MMG f¯ increased in the first 6 s from 19.3 (SEM 1.4) Hz to 23.9 (SEM 2.9) Hz, falling to 13.9 (SEM 1.3) Hz at the end of contraction; in contrast, during test 2 the MMG f¯ declined continuously from 18.7 (SEM 1) Hz to 12.4 (SEM 0.8) Hz. The lower MVC after the fatiguing exercise and the changes in the EMG parameters confirmed that 10 min after the fatiguing exercise, the mechanical and electrical activities of MU were altered. In addition, the MMG results suggested that after a 10-min recovery, some highly fatigable MU might not be recruitable.

Isolated quadriceps training increases maximal exercise capacity in chronic heart failure: The role of skeletal muscle convective and diffusive oxygen transport

OBJECTIVES This study sought to elucidate the mechanisms responsible for the benefits of small muscle mass exercise training in patients with chronic heart failure (CHF). BACKGROUND How central cardiorespiratory and/or peripheral skeletal muscle factors are altered with small muscle mass training in CHF is unknown. METHODS We studied muscle structure, and oxygen (O(2)) transport and metabolism at maximal cycle (whole-body) and knee-extensor exercise (KE) (small muscle mass) in 6 healthy controls and 6 patients with CHF who then performed 8 weeks of KE training (both legs, separately) and repeated these assessments. RESULTS Pre-training cycling and KE peak leg O(2) uptake (Vo(2peak)) were ~17% and ~15% lower, respectively, in the patients compared with controls. Structurally, KE training increased quadriceps muscle capillarity and mitochondrial density by ~21% and ~25%, respectively. Functionally, despite not altering maximal cardiac output, KE training increased maximal O(2) delivery (~54%), arterial-venous O(2) difference (~10%), and muscle O(2) diffusive conductance (D(M)O(2)) (~39%) (assessed during KE), thereby increasing single-leg Vo(2peak) by ~53%, to a level exceeding that of the untrained controls. Post-training, during maximal cycling, O(2) delivery (~40%), arterial-venous O(2) difference (~15%), and D(M)O(2) (~52%) all increased, yielding an increase in Vo(2peak) of ~40%, matching the controls. CONCLUSIONS In the face of continued central limitations, clear improvements in muscle structure, peripheral convective and diffusive O(2) transport, and subsequently, O(2) utilization support the efficacy of local skeletal muscle training as a powerful approach to combat exercise intolerance in CHF.

Surface mechanomyogram reflects the changes in the mechanical properties of muscle at fatigue

Abstract The contractile properties of muscle are usually investigated by analysing the force signal recorded during electrically elicited contractions. The electrically stimulated muscle shows surface oscillations that can be detected by an accelerometer; the acceleration signal is termed the surface mechanomyogram (MMG). In the study described here we compared, in the human tibialis anterior muscle, changes in the MMG and force signal characteristics before, and immediately after fatigue, as well as during 6 min of recovery, when changes in the contractile properties of muscle occur. Fatigue was induced by sustained electrical stimulation. The final aim was to evaluate the reliability of the MMG as a tool to follow the changes in the mechanical properties of muscle caused by fatigue. Because of fatigue, the parameters of the force peak, the peak rate of force production and the peak of the acceleration of force production (d2F/dt2) decreased, while the contraction time and the half-relaxation time (½-RT) increased. The MMG peak-to-peak (p-p) also decreased. The attenuation rate of the force oscillation amplitude and MMG p-p at increasing stimulation frequency was greater after fatigue. With the exception of ½-RT, all of the force and MMG parameters were restored within 2 min of recovery. A high correlation was found between MMG and d2F/dt2 in un-fatigued muscle and during recovery. In conclusion, the MMG reflects specific aspects of muscle mechanics and can be used to follow the changes in the contractile properties of muscle caused by localised muscle fatigue.

Effects of temperature and fatigue on the electromechanical delay components

Introduction: Neuromuscular activation can be influenced by both muscle temperature (Tm) and fatigue. Methods: To assess the effects of Tm and fatigue on the electromechanical delay (EMD), 15 participants performed voluntary isometric contractions of different intensities under neutral (TmN), low (TmL), and high (TmH) Tm, before and after a fatiguing exercise. During contraction, electromyogram (EMG), mechanomyogram (MMG), and force (F) were recorded from the biceps brachii muscle. The EMD and the latencies between EMG and MMG (Δt EMG‐MMG, which includes the electrochemical processes of EMD) and between MMG and F (Δt MMG‐F, which includes the mechanical processes of EMD) were calculated. Results: TmL increased only Δt EMG‐MMG, both before and after fatigue. Fatigue lengthened EMD, Δt EMG‐MMG, and Δt MMG‐F under all Tm to a similar extent. Conclusions: While fatigue increased all EMD components, muscle cooling affected only the electrochemical but not the mechanical processes of EMD. Muscle Nerve, 2013

Acute passive stretching in a previously fatigued muscle: Electrical and mechanical response during tetanic stimulation

Abstract The aim of this study was to assess the effects of acute passive stretching on the electrical and mechanical response of a previously fatigued muscle. Eleven participants underwent maximal tetanic stimulations (50 Hz) of the medial gastrocnemius, before and after a fatiguing protocol and after a bout of passive stretching of the fatigued muscle. During contraction, surface electromyography (EMG), mechanomyography (MMG), and force were recorded. The following parameters were calculated: (1) the EMG root mean square (RMS), mean frequency, and fibre conduction velocity; (2) MMG peak-to-peak and RMS; (3) the peak force, contraction time, half-relaxation time, peak rate of force development (dF/dt) and its acceleration (d2 F/dt 2). Fatigue reduced peak force by 18% (P < 0.05) and affected the other force, EMG, and MMG parameters. After stretching: (1) all EMG parameters recovered to pre-fatigue values; (2) MMG peak-to-peak remained depressed, while RMS recovered to pre-fatigue values; (3) the peak force, peak rate of force development and its acceleration were further reduced by 22, 18, and 51%, respectively, and half-relaxation time by 40% (P < 0.05). In conclusion, acute passive stretching, when applied to a previously fatigued muscle, further depresses the maximum force-generating capacity. Although stretching does not alter the electrical parameters of the fatigued muscle, it does affect the mechanical behaviour of the muscle–tendon unit.

The effects of breathing He-O2 mixtures on maximal oxygen consumption in normoxic and hypoxic men.

1 The hypothesis that the ventilatory resistance to O2 flow (RV) does limit maximal O2 consumption (V̇O2 max) in hypoxia, but not in normoxia, at least in non‐athletic subjects, was tested. RV was reduced by using He–O2 mixtures. 2 V̇O2, max was measured during graded cyclo‐ergometric exercise in eight men (aged 30 ± 3 years) who breathed N2–O2 and He–O2 mixtures in normoxia (inspired oxygen fraction (FI,O2= 0.21) and hypoxia (FI,O2= 0.11). O2 consumption, expired and alveolar ventilations (V̇E and V̇A, respectively), blood lactate and haemoglobin concentrations, heart rate and arterial oxygen saturation (Sa,O2) were determined at the steady state of each work load. Arterial O2 and CO2 partial pressures (Pa,O2) and Pa,CO2, respectively) were measured at rest and at the end of the highest work load. 3 Maximal V̇E and V̇A were significantly increased by He—O2 breathing in normoxia (+27 and +18%, respectively), without significant changes in Pa, O2, Sa, O2V̇O2, max In hypoxia, V̇E and V̇A increased (+31 and +24%, respectively), together with Pa,O2 (+17%), Sa, O2 (+6%) and V̇O2, max (+14%). 4 The results support the hypothesis that the role of RV in limiting V̇O2,max is negligible in normoxia. In hypoxia, the finding that higher V̇E and V̇A values during He–O2 breathing led to higher V̇O2,max values suggests a greater role of RV as a limiting factor. It is unclear whether the finding that the V̇O2 max values were the same during He–O2 and N2–O2 breathing in normoxia is due to a non‐linear response of the O2 transfer system, as previously proposed.

Moderate exercise training induces ROS-related adaptations to skeletal muscles.

Aim of the present work was the evaluation of the effects of moderate exercise training on 2 skeletal muscles differing in fibre-type composition, Tibialis Anterior (TA) and Soleus (SOL). Fibre adaptations, including their metabolic shift and mechanisms underlying proliferation and differentiation, oxidative stress markers, antioxidant and cytoprotective molecules, activity of Ca2+-handling molecules were examined. 6 male 2-month-old rats trained on a treadmill for 1 h/day, 3 days/week, for 14 weeks, reaching 30 m/min at the end of training. 6 age-matched sedentary rats served as controls. Rats were sacrificed 24 h after the last training session. Muscle regulatory factors increased in both muscles, activating satellite cell proliferation, which led to moderate hypertrophy in SOL and to moderate hyperplasia in TA, where the upregulation of desmin and TNFR2 expression suggests that myotube formation by proliferating myoblasts is somehow delayed. Changes leading to a more oxidative metabolism together with the upregulation of a number of antioxidant enzymes occurred in TA. HSP70i protein was upregulated in both SOL and TA, while oxidative stress markers increased in SOL alone. The status of ionic channels and pumps was preserved. We suggest that the increase in ROS, known to be associated with exercise, underlies most observed results.