Muscle Force-generating Capacity Research Articles

Acute Changes in Hamstring Injury Risk Factors After a Session of High-Volume Maximal Sprinting Speed Efforts in Soccer Players.

Maximal sprinting speed (MSS) overexposure is associated with increased risk of injury. This study aimed to describe changes in sprint performance-related factors and hamstring strain injury (HSI) risk factors after a high-volume sprinting session in soccer players. A high-volume sprinting session can induce acute changes in several sprint performance-related factors (sprint time and mechanical properties) and HSI risk factors (posterior chain muscle strength, hamstring range of motion, and dynamic lumbo-pelvic control [LPC], measured as changes in anterior pelvic tilt [APT] during maximal speed sprinting). Prospective observational case series. Level 4. Fifteen active male amateur soccer players participated. Changes in sprint performance-related factors and HSI risk factors were examined for 72 hours after high-volume MSS efforts (H-VMSSE) using a soccer-contextualized multifactorial approach. Muscle damage proxy markers (hamstring perceived soreness and creatine kinase) were also examined. H-VMSSE induced decrements in sprint performance-related factors. Significant reductions in theoretical maximal horizontal velocity (P < 0.01; effect size [ES], -0.71) and performance (P = 0.02; ES, -0.59) were observed for 48 and 72 hours after H-VMSSE. Small but significant reductions in posterior chain muscle force-generating capacity were detected for 48 and 72 hours after H-VMSSE for the nondominant (P < 0.03; ES, -0.60) and dominant (P < 0.04; ES, -0.40) leg. Finally, players exhibited persistent small, albeit nonsignificant (P = 0.06; ES, 0.53), decreases in dynamic LPC (APT increases) for 72 hours after H-VMSSE. H-VMSSE induced declines in both sprint performance-related factors and HSI risk factors. Sprinting can alter a player's anatomic structure by increasing APT during the maximum speed phase of the sprint. A soccer-contextualized multifactorial approach might allow for the regulation of MSS dosage depending on individual HSI risk factor status, thereby serving as a tailored "vaccine" for sprinting needs.

Fiber-type traps: revisiting common misconceptions about skeletal muscle fiber types with application to motor control, biomechanics, physiology, and biology.

Skeletal muscle is a highly complex tissue that is studied by scientists from a wide spectrum of disciplines, including motor control, biomechanics, exercise science, physiology, cell biology, genetics, regenerative medicine, orthopedics, and engineering. Although this diversity in perspectives has led to many important discoveries, historically, there has been limited overlap in discussions across fields. This has led to misconceptions and oversimplifications about muscle biology that can create confusion and potentially slow scientific progress across fields. The purpose of this synthesis paper is to bring together research perspectives across multiple muscle fields to identify common assumptions related to muscle fiber type that are points of concern to clarify. These assumptions include 1) classification by myosin isoform and fiber oxidative capacity is equivalent, 2) fiber cross-sectional area (CSA) is a surrogate marker for myosin isoform or oxidative capacity, and 3) muscle force-generating capacity can be inferred from myosin isoform. We address these three fiber-type traps and provide some context for how these misunderstandings can and do impact experimental design, computational modeling, and interpretations of findings, from the perspective of a range of fields. We stress the dangers of generalizing findings about "muscle fiber types" among muscles or across species or sex, and we note the importance for precise use of common terminology across the muscle fields.

Mechanisms of Estrogen Influence on Skeletal Muscle: Mass, Regeneration, and Mitochondrial Function.

Human menopause is widely associated with impaired skeletal muscle quality and significant metabolic dysfunction. These observations pose significant challenges to the quality of life and mobility of the aging population, and are of relevance when considering the significantly greater losses in muscle mass and force-generating capacity of muscle from post-menopausal females relative to age-matched males. In this regard, the influence of estrogen on skeletal muscle has become evident across human, animal, and cell-based studies. Beneficial effects of estrogen have become apparent in mitigation of muscle injury and enhanced post-damage repair via various mechanisms, including prophylactic effects on muscle satellite cell number and function, as well as membrane stability and potential antioxidant influences following injury, exercise, and/or mitochondrial stress. In addition to estrogen replacement in otherwise deficient states, exercise has been found to serve as a means of augmenting and/or mimicking the effects of estrogen on skeletal muscle function in recent literature. Detailed mechanisms behind the estrogenic effect on muscle mass, strength, as well as the injury response are beginning to be elucidated and point to estrogen-mediated molecular cross talk amongst signalling pathways, such as apoptotic signaling, contractile protein modifications, including myosin regulatory light chain phosphorylation, and the maintenance of muscle satellite cells. This review discusses current understandings and highlights new insights regarding the role of estrogen in skeletal muscle, with particular regard to muscle mass, mitochondrial function, the response to muscle damage, and the potential implications for human physiology and mobility.

Whole-limb scaling of muscle mass and force-generating capacity in amniotes.

Skeletal muscle mass, architecture and force-generating capacity are well known to scale with body size in animals, both throughout ontogeny and across species. Investigations of limb muscle scaling in terrestrial amniotes typically focus on individual muscles within select clades, but here this question was examined at the level of the whole limb across amniotes generally. In particular, the present study explored how muscle mass, force-generating capacity (measured by physiological cross-sectional area) and internal architecture (fascicle length) scales in the fore- and hindlimbs of extant mammals, non-avian saurians (‘reptiles’) and bipeds (birds and humans). Sixty species spanning almost five orders of magnitude in body mass were investigated, comprising previously published architectural data and new data obtained via dissections of the opossum Didelphis virginiana and the tegu lizard Salvator merianae. Phylogenetic generalized least squares was used to determine allometric scaling slopes (exponents) and intercepts, to assess whether patterns previously reported for individual muscles or functional groups were retained at the level of the whole limb, and to test whether mammals, reptiles and bipeds followed different allometric trajectories. In general, patterns of scaling observed in individual muscles were also observed in the whole limb. Reptiles generally have proportionately lower muscle mass and force-generating capacity compared to mammals, especially at larger body size, and bipeds exhibit strong to extreme positive allometry in the distal hindlimb. Remarkably, when muscle mass was accounted for in analyses of muscle force-generating capacity, reptiles, mammals and bipeds almost ubiquitously followed a single common scaling pattern, implying that differences in whole-limb force-generating capacity are principally driven by differences in muscle mass, not internal architecture. In addition to providing a novel perspective on skeletal muscle allometry in animals, the new dataset assembled was used to generate pan-amniote statistical relationships that can be used to predict muscle mass or force-generating capacity in extinct amniotes, helping to inform future reconstructions of musculoskeletal function in the fossil record.

Low lysophosphatidylcholine induces skeletal muscle myopathy that is aggravated by high-fat diet feeding.

Obesity alters skeletal muscle lipidome and promotes myopathy, but it is unknown whether aberrant muscle lipidome contributes to the reduction in skeletal muscle contractile force-generating capacity. Comprehensive lipidomic analyses of mouse skeletal muscle revealed a very strong positive correlation between the abundance of lysophosphatidylcholine (lyso-PC), a class of lipids that is known to be downregulated with obesity, with maximal tetanic force production. The level of lyso-PC is regulated primarily by lyso-PC acyltransferase 3 (LPCAT3), which acylates lyso-PC to form phosphatidylcholine. Tamoxifen-inducible skeletal muscle-specific overexpression of LPCAT3 (LPCAT3-MKI) was sufficient to reduce muscle lyso-PC content in both standard chow diet- and high-fat diet (HFD)-fed conditions. Strikingly, the assessment of skeletal muscle force-generating capacity ex vivo revealed that muscles from LPCAT3-MKI mice were weaker regardless of diet. Defects in force production were more apparent in HFD-fed condition, where tetanic force production was 40% lower in muscles from LPCAT3-MKI compared to that of control mice. These observations were partly explained by reductions in the cross-sectional area in type IIa and IIx fibers, and signs of muscle edema in the absence of fibrosis. Future studies will pursue the mechanism by which LPCAT3 may alter protein turnover to promote myopathy.

In Vivo Fatigue Reduces In Vitro Performance In Human Skeletal Muscle Fibers

Muscle fatigue, the acute reduction in muscle force-generating capacity associated withrepeated or prolonged activation, derives from the accumulation of intracellular metabolites.However, reduced contractile performance (low-frequency force depression) persists long afterrecovery of metabolic homeostasis. Few studies have investigated in vivo fatigue on in vitromyofilament function in humans and the potential role of post-translational proteinmodification in this phenomenon. Therefore, the PURPOSE of this study was to examine theeffect of in vivo fatigue on the phosphorylation status of sarcomeric proteins and contractileperformance of human single muscle fibers. METHODS: In two separate studies, seven healthyadults performed repeated knee extensions until task failure with their dominant leg.Immediately following, bilateral, percutaneous biopsy of the vastus lateralis muscle wasperformed on the fatigued and non-fatigued (control) limbs. Tissue was divided and portionswere blotted, snap frozen, and stored at -80 °C until analysis by high resolution massspectrometry or prepared for single fiber mechanical analysis. Mass spec data were assessedusing edgeR while mechanical outcomes were assed via 2-way ANOVA using SPSS. RESULTS: Mass spectrometry confirmed differential phosphorylation of multiple residues in sarcomericproteins, including regulatory light chain and troponin I. We also observed phospho-enrichmentof myosin binding protein C (MyBP-C) and tropomyosin (β-Tm), and a reduction in titinphosphorylation. Mechanical analysis showed that fatigued fibers produced significantly lesspower (8.0 ± 6.2 mN/mm2) than controls (5.9 ± 3.9 mN/mm2; p = 0.05). Differences in tension(p = 0.11) or velocity (p = 0.11) relative to non-fatigued fibers were not significant. No MHCisoform by fatigue interactions were observed. CONCLUSION: These data suggest fatiguingcontractions alter phosphorylation of select sarcomeric proteins and alter contractileperformance in isolated single muscle fibers regardless of intracellular environment, supportingthe notion that altered contractile protein function potentiates in vivo fatigue and maycontribute to longer-lasting contractile deficits.

Strength training restores force-generating capacity in patients with schizophrenia.

Patients with schizophrenia spectrum disorders have impaired skeletal muscle force-generating capacity (FGC) of the lower extremities, that is, one repetition maximum (1RM) and rapid force development, and poor functional performance. We therefore investigated whether 12weeks of maximal strength training (MST) could (a) restore FGC and functional performance to the level of healthy references, (b) increase patient activation and quality of life, and (c) explore associations between symptom severity, defined daily dose of medication, illness duration, level of patient activation, and improvements in FGC and functional performance. Forty-eight outpatients were randomized to a training group (TG) or control group (CG). TG performed leg press MST 2day/week at~90% 1RM. The CG received two introductory training sessions and encouragement to train independently. Leg press 1RM, rapid force development, a battery of functional performance tests, Patient Activation Measure-13, and 36-Item Short Form Health Survey were tested. Healthy references performed baseline tests of FGC and functional performance. Thirty-six patients completed the study (TG: 17, CG: 19). TG improved 1RM (28%) and rapid force development (20%, both P<.01) to a level similar to healthy references, while no change was apparent in the CG. TG's improvement in rapid force development was negatively associated with defined daily dose of medication (r=-0.5, P=.05). Both TG and CG improved 30-second sit-to-stand test performance (P<.05) which was associated with improved rapid force development (r=0.6, P<.05). In conclusion, 12weeks of MST restored patients' lower extremity FGC to a level similar to healthy references and improved 30-second sit-to-stand test performance.

How to build a dinosaur: Musculoskeletal modeling and simulation of locomotor biomechanics in extinct animals

AbstractThe intersection of paleontology and biomechanics can be reciprocally illuminating, helping to improve paleobiological knowledge of extinct species and furthering our understanding of the generality of biomechanical principles derived from study of extant species. However, working with data gleaned primarily from the fossil record has its challenges. Building on decades of prior research, we outline and critically discuss a complete workflow for biomechanical analysis of extinct species, using locomotor biomechanics in the Triassic theropod dinosaurCoelophysisas a case study. We progress from the digital capture of fossil bone morphology to creating rigged skeletal models, to reconstructing musculature and soft tissue volumes, to the development of computational musculoskeletal models, and finally to the execution of biomechanical simulations. Using a three-dimensional musculoskeletal model comprising 33 muscles, a static inverse simulation of the mid-stance of running shows thatCoelophysisprobably used more upright (extended) hindlimb postures and was likely capable of withstanding a vertical ground reaction force of magnitude more than 2.5 times body weight. We identify muscle force-generating capacity as a key source of uncertainty in the simulations, highlighting the need for more refined methods of estimating intrinsic muscle parameters such as fiber length. Our approach emphasizes the explicit application of quantitative techniques and physics-based principles, which helps maximize results robustness and reproducibility. Although we focus on one specific taxon and question, many of the techniques and philosophies explored here have much generality to them, so they can be applied in biomechanical investigation of other extinct organisms.

12 Weeks Of Maximal Strength Training Restores Muscle Force-generating Capacity In Patients With Schizophrenia

Patients with schizophrenia spectrum disorders (ICD-10) suffer from impaired muscle force-generating capacity (MFGC) and functional performance of the lower extremities. PURPOSE: To investigate if 12 weeks of maximal strength training (MST) would restore MFGC and functional performance. METHODS: Forty-eight outpatients (28 men, 35±10 yrs; 20 women, 35±12 yrs) were randomized to a training group (TG) or control group (CG). Forty-eight age and gender matched healthy controls (28 men/20 women, 35±11 yrs) were tested to establish reference values. TG performed leg press MST (4x4 repetitions) 2d/week for 12 weeks at ~90% one repetition maximum (1RM). CG received two sessions of MST and encouragement to follow traditional physical activity guidelines. RESULTS: 17/24 patients in the TG (12 men/5 women, 34±11 years) completed 79% of training sessions and 19/22 patients in the CG (9 men/10 women, 37±12 years) completed the study. TG improved 1RM (28%, 12.6±4.1 to 16.2±5.0 Kg·mb-0.67, p<0.01) and rapid force development (20%, 18.6±8.6 to 22.4±10.8 N·m·s-1·mb-0.67,p<0.01), reaching 106% and 85% of healthy reference values, respectively. TG improvements differed from CG (p<0.01) where no changes occurred (1RM; 11.4±3.0 to 12.0±2.7 Kg·mb-0.67, rapid force development 16.4±6.9 to 17.3±6.5 N·m·s-1·mb-0.67). Both TG and CG improved 30-second sit-to-stand test (30sSTS) performance (15±3 to 17±4 stands and 13±3 to 14±3 stands, respectively, p<0.05). Changes were not apparent as between group difference nor close the gap to reference levels (27±5 stands). CONCLUSION: MST restored the patients’ lower extremity MFGC and improved 30sSTS performance. Supported by grants from the Norwegian ExtraFoundation for Health and Rehabilitation, The Liaison Committee between the Central Norway Regional Health Authority and the Norwegian University of Science and Technology, and The Norwegian Directorate of Health.

Ankle and knee extensor muscle effort during locomotion in young and older athletes: Implications for understanding age-related locomotor decline

Age-related reduction in muscle force generation capacity is similarly evident across different lower limb muscle groups, yet decline in locomotor performance with age has been shown to depend primarily on reduced ankle extensor muscle function. To better understand why ageing has the largest detrimental effect on ankle joint function during locomotion, we examined maximal ankle and knee extensor force development during a two-leg hopping test in older and young men, and used these forces as a reference to calculate relative operating efforts for the knee and ankle extensors as participants walked, ran and sprinted. We found that, across locomotion modes in both age groups, ankle extensors operated at a greater relative effort compared to knee extensors; however, slightly less pronounced differences between ankle and knee extensor muscle efforts were present among older men, mainly due to a reduction in the ankle extensor force generation during locomotion modes. We consider these findings as evidence that reduced ankle push-off function in older age is driven by a tendency to keep ankle extensor effort during locomotion lower than it would otherwise be, which, in turn, may be an important self-optimisation strategy to prevent locomotor-induced fatigue of ankle extensor muscles.

Skeletal muscle mitochondrial function and exercise capacity are not impaired in mice with knockout of STAT3.

Signal transducer and activator of transcription 3 (STAT3) was recently found to be localized to mitochondria in a number of tissues and cell types, where it modulates oxidative phosphorylation via interactions with the electron transport proteins, complex I and complex II. Skeletal muscle is densely populated with mitochondria although whether STAT3 contributes to skeletal muscle oxidative capacity is unknown. In the present study, we sought to elucidate the contribution of STAT3 to mitochondrial and skeletal muscle function by studying mice with muscle-specific knockout of STAT3 (mKO). First, we developed a novel flow cytometry-based approach to confirm that STAT3 is present in skeletal muscle mitochondria. However, contrary to findings in other tissue types, complex I and complex II activity and maximal mitochondrial respiratory capacity in skeletal muscle were comparable between mKO mice and floxed/wild-type littermates. Moreover, there were no genotype differences in endurance exercise performance, skeletal muscle force-generating capacity, or the adaptive response of skeletal muscle to voluntary wheel running. Collectively, although we confirm the presence of STAT3 in skeletal muscle mitochondria, our data establish that STAT3 is dispensable for mitochondrial and physiological function in skeletal muscle.NEW & NOTEWORTHY Whether signal transducer and activator of transcription 3 (STAT3) can regulate the activity of complex I and II of the electron transport chain and mitochondrial oxidative capacity in skeletal muscle, as it can in other tissues, is unknown. By using a mouse model lacking STAT3 in muscle, we demonstrate that skeletal muscle mitochondrial and physiological function, both in vivo and ex vivo, is not impacted by the loss of STAT3.

Obesity, but not metabolic control, is associated with muscle strength and endurance in diabetic older adults

The objective of this study is to investigate the association between muscle function, body composition, and metabolic control in adults with type 2 diabetes mellitus (DM2). Forty-eight individuals with DM2 were divided into four groups according to the severity of obesity (body mass index [BMI]: lean [LN, n = 10], overweight [OW, n = 16], obese class I [OBI, n = 15], and obese class II [OBII, n = 7]). Absolute peak torque (TQ), relative peak torque (TQ/body weight [BW]), total work (TW), and fatigue index (FI) were assessed by means of an isokinetic dynamometer during concentric knee extensor contraction. Spearman's correlation coefficients were used to estimate the association between measurements. Although OBII had higher insulin levels than both LN and OW groups, no significant differences were found between groups for TQ, TQ/BW, TW, and FI, as well as between metabolic variables and muscle measurements. There was a positive correlation between BMI and TQ (rs = .45) and resistance tests, between BMI and TQ (rs = .43), and TW (rs = .37). Metabolic variables do not correlate with muscle strength and endurance in DM2. However, severity of obesity measured by the BMI is positively associated with muscle force-generating capacity and endurance.

Patients with schizophrenia have impaired muscle force-generating capacity and functional performance.

Patients with schizophrenia have impaired physical health. However, evidence of how skeletal muscle force-generating capacity (FGC), a key component of functional performance, may contribute to the impairment is scarce. Thus, the aim of this study was to investigate the patient groups' skeletal muscle FGC and its association with functional performance. Leg-press FGC was assessed along with a battery of functional performance tests in 48 outpatients (28 men, 34±10years; 20 women, 36±12years) with schizophrenia spectrum disorder (ICD-10, F20-29), and compared with 48 healthy age- and gender-matched references. Results revealed reduced one-repetition maximum (1RM) in men (-19%, P<.01) and a trend toward reduction in women (-13%, P=.067). The ability to develop force rapidly was also impaired (men: -30%; women: -25%, both P<.01). Patients scored worse than healthy references on all physical performance tests (stair climbing: -63%; 30-second sit-to-stand (30sSTS): -48%; six-minute walk test (6MWT): -22%; walking efficiency: -14%; and unipedal stance eyes open: -20% and closed: -73%, all P<.01). 1RM correlated with 6MWT (r=.45), stair climbing (r=-.44), 30sSTS (r=.43), walking efficiency (r=.26), and stance eyes open (r=.33) and closed (r=.45), all P<.01. Rapid force development correlated with 6MWT (r=.54), stair climbing (r=-.49), 30sSTS (r=.45), walking efficiency (r=.26), and stance eyes open (r=.44) and closed (r=.51), all P<.01. In conclusion, skeletal muscle FGC and functional performance are reduced in patients with schizophrenia and should be recognized as important aspects of the patient groups' impaired health. Resistance training aiming to improve these components should be considered an important part of clinical treatment.

Functional Performance With Age: The Role of Long-Term Strength Training.

Physical function is shown to decline with age. However, how long-term strength training may attenuate the age-related limitation in functional tasks with various force demands is unclear. In a cross-sectional study, we assessed maximal muscle strength, initial and late phase rate of force development (RFD), as well as 4 tests of functional performance in 11 strength-trained master athletes (MAs), 11 recreationally active older adults (AEs), 10 sedentary older adults (SOAs), and 9 moderately active young controls. Functional performance was divided into 2 categories: more force-demanding (chair-rising ability and stair-climbing power) and less force-demanding (habitual walking speed and 1-leg standing) tasks. MA exhibited 75%, 45%, and 26% higher leg press maximal strength compared with SOA, AE, and young, respectively (P < .01). MA leg press RFD was not different from young, but was higher compared to AE and SOA during both the initial (0-50 ms: 104%-177%, P < .05) and late phase (100-200 ms: 37%-52%, P < .05) of muscle contraction. MA also showed better mean (SD) performance compared with AE and SOA (P < .05) in more force-demanding functional tasks; chair-rising ability (MA: 6.2 (1.2) seconds; AE: 8.6 (1.8) seconds; SOA: 9.7 (3.0) seconds; young: 6.5 (1.0) seconds) and stair-climbing power (MA: 701 (161) W; AE: 556 (104) W; SOA: 495 (116) W; young: 878 (126) W). No differences (mean (SD)) were observed between MA and AE in less force-demanding tasks, but both groups were superior (P < .05) compared with SOA in walking speed (MA: 1.49 (0.21) m·s; AE: 1.56 (0.17) m·s; SOA: 1.27 (0.22) m·s; young: 1.62 (0.22) m·s) and balance test completion (MA: 45%; AE: 45%; SOA: 0%; young: 100%). Our results reveal that maintaining a high muscle force-generating capacity into older age is related to beneficial effects on functional performance, which may not be achieved with recreational activity, thus highlighting strength training as an important contribution to healthy aging.

Using musculoskeletal modelling to clarify the effect of wrist posture on muscle force-generating capacities and maximal grip force during a power grip task

Using musculoskeletal modelling to clarify the effect of wrist posture on muscle force-generating capacities and maximal grip force during a power grip task

Genioglossus activation during maximal sniff manoeuvres: Is upper airway function relevant in the clinical assessment of inspiratory and expiratory muscle strength?

Genioglossus activation during maximal sniff manoeuvres: Is upper airway function relevant in the clinical assessment of inspiratory and expiratory muscle strength?

Force-Length Relationship Modeling of Wrist and Finger Flexor Muscles.

Because the hand joints possess a broad range of motion, the muscle length can vary importantly which might result in significant variations of the muscle force-generating capacities. However, facing the complexity of this musculoskeletal system, no study has examined the effect of hand muscle length change on muscle force. This study aimed to characterize the force-length relationship of muscles involved in wrist and metacarpophalangeal flexion. Eleven participants performed two sessions: (i) one for the wrist flexor muscles and (ii) one for the finger flexor muscles. For each session, the participants performed two maximal voluntary contractions and then two progressive isometric ramps from 0% to 100% of their maximal force capacity at five different wrist/metacarpophalangeal angles. Torque, kinematic, and electromyographic data were recorded. An ultrasound scanner was used to measure the myotendinous junction displacement of flexor carpi radialis (FCR) and flexor digitorum superficialis (FDS) during isometric contractions. A three-dimensional relationship between muscle length, force, and activation level was modeled using optimization procedure. Globally, the FCR was stronger and shorter compared with FDS. The results showed that the three-dimensional relationships fitted well the experimental data (mean R = 0.92 ± 0.07 and 0.87 ± 0.11 for FCR and FDS, respectively). Using joint angle and EMG data, this approach allows to estimate the muscle force with low estimation errors (<9% of Fmax). This study proposes a new method to investigate the force-length relationship by combining ultrasound measurement, musculoskeletal modeling and optimization procedures. The data and relationships provide a new insight into hand biomechanics and muscle function that could be useful for designing hand tools or surgical operations.

Maximal strength training: the impact of eccentric overload.

The search for the most potent strength training intervention is continuous. Maximal strength training (MST) yields large improvements in force-generating capacity (FGC), largely attributed to efferent neural drive enhancement. However, it remains elusive whether eccentric overload, before the concentric phase, may augment training-induced neuromuscular adaptations. A total of 53 23 ± 3 (SD)-yr-old untrained males were randomized to either a nontraining control group (CG) or one of two training groups performing leg press strength training with linear progression, three times per week for 8 wk. The first training group carried out MST with four sets of four repetitions at ~90% one-repetition maximum (1RM) in both action phases. The second group performed MST with an augmented eccentric load of 150% 1RM (eMST). Measurements were taken of 1RM and rate of force development (RFD), countermovement jump (CMJ) performance, and evoked potentials recordings [V-wave (V) and H-reflex (H) normalized to M-wave (M) in musculus soleus]. 1RM increased from 133 ± 16 to 157 ± 23 kg and 123 ± 18 to 149 ± 22 kg and CMJ by 2.3 ± 3.6 and 2.2 ± 3.7cm for MST and eMST, respectively (all P < 0.05). Early, late, and maximal RFD increased in both groups [634-1,501 N/s (MST); 644-2,111 N/s (eMST); P < 0.05]. These functional improvements were accompanied by increased V/M-ratio (MST: 0.34 ± 0.11 to 0.42 ± 14; eMST: .36 ± 0.14 to 0.43 ± 13; P < 0.05). Resting H/M-ratio remained unchanged. Training-induced improvements did not differ. All increases, except for CMJ, were different from the CG. MST is an enterprise for large gains in FGC and functional performance. Eccentric overload did not induce additional improvements, suggesting firing frequency and motor unit recruitment during MST may be maximal. NEW & NOTEWORTHY This is the first study to apply evoked potential recordings to investigate effects on efferent neural drive following high-intensity strength training with and without eccentric overload in a functionally relevant lower extremity exercise. We document that eccentric overload does not augment improvements in efferent neural drive or muscle force-generating capacity, suggesting that high-intensity concentric loads may maximally tax firing frequency and motor unit recruitment.

Neural Plasticity with Age: Unilateral Maximal Strength Training Augments Efferent Neural Drive to the Contralateral Limb in Older Adults.

Efferent neural drive during strong muscle contractions is attenuated with age, even after life-long strength training. However, it is unknown if this deterioration may impede contralateral neural plasticity, and limit the clinical value of unilateral strength training. We assessed muscle force-generating capacity, evoked potentials recordings (V-wave and H-reflex normalized to M-wave; V/M-ratio and H/M-ratio) and voluntary activation (VA) in the plantar flexors of the contralateral limb following unilateral maximal strength training (MST) with the dominant limb for 3 weeks (nine sessions). Twenty-three 73 ± 4(SD) year old males were randomized to a MST group (N = 11), exercising with an intensity of ~90% of maximal strength, or a control group (CG, N = 12). MST improved contralateral maximal strength (107.6 ± 27.0 to 119.1 ± 34.8 Nm; 10%) and rate of force development (197.3 ± 54.1 to 232.8 ± 77.7 Nm s-1; 18%) (both p < .05). These strength gains were associated with (r = 0.465-0.608) an enhanced soleus V/M-ratio (0.12 ± 0.09 to 0.21 ± 0.17) and VA (79.5 ± 5.1 to 83.3 ± 5.2%) (all p < .05). H/M-ratio (10% maximal strength) remained unaltered after MST, and no changes were apparent in the CG. In conclusion, cross-limb effects in older adults are regulated by efferent neural drive enhancement, and advocate the clinical relevance of MST to improve neuromuscular function in individuals with conditions that results in unilateral strength reductions.

Sensorimotor control of breathing in the mdx mouse model of Duchenne muscular dystrophy.

Respiratory failure is a leading cause of mortality in Duchenne muscular dystrophy (DMD), but little is known about the control of breathing in DMD and animal models. We show that young (8weeks of age) mdx mice hypoventilate during basal breathing due to reduced tidal volume. Basal CO2 production is equivalent in wild-type and mdx mice. We show that carotid bodies from mdx mice have blunted responses to hyperoxia, revealing hypoactivity in normoxia. However, carotid body, ventilatory and metabolic responses to hypoxia are equivalent in wild-type and mdx mice. Our study revealed profound muscle weakness and muscle fibre remodelling in young mdx diaphragm, suggesting severe mechanical disadvantage in mdx mice at an early age. Our novel finding of potentiated neural motor drive to breathe in mdx mice during maximal chemoactivation suggests compensatory neuroplasticity enhancing respiratory motor output to the diaphragm and probably other accessory muscles. Patients with Duchenne muscular dystrophy (DMD) hypoventilate with consequential arterial blood gas derangement relevant to disease progression. Whereas deficits in DMD diaphragm are recognized, there is a paucity of knowledge in respect of the neural control of breathing in dystrophinopathies. We sought to perform an analysis of respiratory control in a model of DMD, the mdx mouse. In 8-week-old male wild-type and mdx mice, ventilation and metabolism, carotid body afferent activity, diaphragm muscle force-generating capacity, and muscle fibre size, distribution and centronucleation were determined. Diaphragm EMG activity and responsiveness to chemostimulation was determined. During normoxia, mdx mice hypoventilated, owing to a reduction in tidal volume. Basal CO2 production was not different between wild-type and mdx mice. Carotid sinus nerve responses to hyperoxia were blunted in mdx, suggesting hypoactivity. However, carotid body, ventilatory and metabolic responses to hypoxia were equivalent in wild-type and mdx mice. Diaphragm force was severely depressed in mdx mice, with evidence of fibre remodelling and damage. Diaphragm EMG responses to chemoactivation were enhanced in mdx mice. We conclude that there is evidence of chronic hypoventilation in young mdx mice. Diaphragm dysfunction confers mechanical deficiency in mdx resulting in impaired capacity to generate normal tidal volume at rest and decreased absolute ventilation during chemoactivation. Enhanced mdx diaphragm EMG responsiveness suggests compensatory neuroplasticity facilitating respiratory motor output, which may extend to accessory muscles of breathing. Our results may have relevance to emerging treatments for human DMD aiming to preserve ventilatory capacity.