Plantaris Research Articles

Morphofunctional assessment of muscles of the lower leg and foot after autoneuroplasty of resection defect of tibial portion of the sciatic nerve and single intraoperative electrical neurostimulation in adult rats

INTRODUCTION: There are no data in the literature on the effect of a single intraoperative electrical stimulation (IES) on the condition of the muscles of the lower leg and foot in the long-term period after autoplasty of the sciatic nerve in adult rats. AIM: To study morphofunctional characteristics of muscles of the lower leg and foot after autoneuroplasty of a resection defect of the tibial portion of the sciatic nerve and a single IES in adult rats. MATERIALS AND METHODS: The experiment was performed on 30 Wistar rats who underwent autoneuroplasty (AN) after resection of the tibial portion of the sciatic nerve. Fourteen rats underwent a 40-munite IES session (AN + IES series). In 16 rats IES was not conducted (AN series). At 4 and 6 months after the operation, the tibial nerve function index (TFI) was calculated by analyzing rats’ paw traces on a walking track. At the same time, light microscopy and histomorphometry of paraffin and epoxy sections of gastrocnemius and plantar interosseous muscles were performed. A conventional control was muscles of intact limbs. RESULTS: Atrophy and endomysial fibrosis were less expressed in the gastrocnemius of the AN + IES series in comparison with AN series, the effect was mediated by enhancement of vascularization. In plantar interosseous muscles at 4 months after the operation, the volume density of blood vessels in the AN + IES series was 7.35 (5.49; 8.69), which was greater than in the AN series — 3.43 (2.02; 5.59), р = 0.0196. Diameters of muscle fibers and volume density of endomysium were comparable. At 6 months after the operation, endomysial fibrosis progressed in both series, but in the AN + IES series, myopathically altered muscle fibers were less common. After 6-month observation, TFI increased (-47.95) in the AN + IES series and became higher (p = 0.0339) than in the AN series, in which TFI became even lower (-93.64) than it was after 4 months (-81.95) of the experiment. CONCLUSION: A single IES permits to reduce the denervation alterations in the gastrocnemius and plantar interosseous muscles conditioned by damage to the nerve and maturation, and also to improve the tibial nerve function index in the long term after autoneuroplasty.

Does force depression resulting from shortening against series elasticity contribute to the activation dependence of optimum length?

The optimum length for force generation (L0) increases as activation is reduced, challenging classic theories of muscle contraction. Although the activation dependence of L0 is seemingly consistent with length-dependent Ca2+ sensitivity, this mechanism can't explain the apparent force dependence of L0, or the effect of series compliance on activation-related shifts in L0. We have tested a theory proposing that the activation dependence of L0 relates to force depression resulting from shortening against series elasticity. This theory predicts that significant series compliance would cause tetanic L0 to be shorter than the length corresponding to optimal filament overlap, thereby increasing the activation dependence of L0. We tested this prediction by determining L0 and maximum tetanic force (P0) with (L0_spring, P0_spring) and without added compliance in bullfrog semitendinosus muscles. The activation dependence of L0 was characterised with the addition of twitch and doublet contractions. Springs attached to muscles gave added fixed-end compliances of 11-39% and induced force depression for tetanic fixed-end contractions (P0_spring < P0). We found strong, negative correlations between spring compliance and both P0_spring (r2 = 0.89-0.91) and L0_spring (r2 = 0.60-0.63; P < 0.001), while the activation dependence of L0 was positively correlated to added compliance (r2 = 0.45, P = 0.011). However, since the compliance-mediated reduction in L0 was modest relative to the activation-related shift reported for the bullfrog plantaris muscle, additional factors must be considered. Our demonstration of force depression under novel conditions adds support to the involvement of a stress-induced inhibition of cross-bridge binding.

Immediate Effects of Calf Tissue Flossing on Ankle Joint Torque and Dorsiflexion Range of Motion in Healthy Individuals: A Randomized Controlled Crossover Trial.

Tissue flossing involves wrapping a rubber band around a muscle group for a few minutes while performing joint motion, enhancing ankle joint torque and range of motion. As limited ankle dorsiflexion range of motion and plantar flexion muscle weakness are risk factors for sports injury, assessing the therapeutic effects of tissue flossing is important. This study aimed to evaluate the immediate effects of calf tissue flossing on enhancing ankle joint torque and dorsiflexion range of motion. We conducted a randomized controlled crossover trial involving 19 healthy adult males who received two interventions (low and high-pressure tissue flossing bands) and a control condition (underwrap). Each intervention was applied for 2 minutes on the non-dominant calf, with 5-10 days between sessions. A pressure sensor placed on the posterior calf monitored the wrapping compression force. The intervention exercise comprised six voluntary isometric contractions of the ankle at three angles (20° plantar flexion, neutral 0°, and 10° dorsiflexion) for 3 seconds each using a dynamometer. The maximal isometric ankle plantar flexion torque and dorsiflexion range of motion were evaluated pre- and post-intervention. Significant interactions were observed in ankle plantar flexion torque at 10° dorsiflexion (p < 0.01) but not at 0° or 20° plantar flexion. The low- and high-pressure bands significantly enhanced ankle plantar flexion torque by 4.3 Nm (effect size [ES]: 0.14, p = 0.02) and 4.9 Nm (ES: 0.15, p < 0.05), respectively, and also enhanced the ankle dorsiflexion range of motion by 1.7° (ES: 0.43, p < 0.01) and 1.3° (ES: 0.35, p = 0.02), respectively, compared to the control. The low- and high-pressure band conditions had comparable effects on torque and range of motion. A few minutes of the calf tissue flossing intervention significantly enhanced ankle plantar flexion torque and dorsiflexion range of motion, although the effect sizes were trivial to small.

Torque-angle relationships of human toe flexor muscles highlight their capacity for propulsion in gait.

Human proficiency for bipedal locomotion relies on the structure and function of our feet, including the interplay between active muscles and passive structures acting on the toes during the propulsive phase of gait. However, our understanding of the relative contributions of these different structures remains incomplete. We aimed to determine the distinct toe-flexion torque-angle relationships of the plantar intrinsic muscles (PIMs), extrinsic muscles, and passive structures, therefore offering insight into their force-generating capabilities and importance for walking and running. Torque-angle data were twice collected from nine healthy individuals (6 males, 3 females; 28±5 years) using supramaximal transcutaneous electrical stimuli applied at two tibial nerve sites to distinguish between muscle-driven and passive toe-flexion torque about the metatarsophalangeal (MTP) joint. Innervating extrinsic muscles and PIMs concurrently produced peak torques (Hallux=3.05±0.70 Nm, MTP angle=48.0°±13.6°; Lesser Digits=3.19±0.98 Nm, MTP angle=42.6°±13.4°) exceeding by 208% (Hallux) and 150% (Lesser Digits), respectively, those from PIM stimulation alone. Notably, MTP joint angles pertinent to gait corresponded to the ascending limb of the active torque-angle relationship, with active muscle joint torques the dominant contributor over passive torques. The latter finding suggests that human toe flexors are well-adapted to generate the MTP joint torques that are necessary for walking and running. This further supports the notion that muscles acting within the foot play an important role in the foot's mechanical function and our ability to walk and run in an upright posture.

Symmetry of Shank Muscle Strength, Passive Stiffness and Plantar Pressure Following IASTM Accompanied by Electrotherapy in a Case with Severe Ankle Stiffness

Excessive ankle stiffness can greatly impact mobility, leading to discomfort, difficulty in walking, and limited Range of Motion (ROM). We aimed to identify and address the symmetry of shank muscle strength, ankle passive stiffness, and plantar pressure distribution, in a patient with unilateral excessive ankle stiffness, utilizing Instrument-Assisted Soft Tissue Mobilization (IASTM) accompanied by Faradic Electrical Stimulation (FES). The patient’s muscle strength and ROM which had diminished due to 3.5 years of ankle immobilization post-rescue from amputation, underwent a 12-week program involving IASTM and FES. The plantar and dorsiflexion muscles’ torque, ROM, and plantar pressure were measured using an isokinetic and plantar distribution system before and after the intervention. Symmetry of muscle torque, ROM, and plantar pressure between two limbs were calculated for pre and post-test. Results indicated improvement in the ratio index of the concentric/eccentric dorsi- and plantar-flexion peak torque and dorsi- and plantar-flexion work, ROM, gait line length, and contact time after a 12-week intervention. The study suggests that IASTM and FES are effective interventions for restoring symmetry in a patient with post-operation complications, highlighting the need for further research on similar cases.

Curcumin Mitigates Muscle Atrophy Potentially by Attenuating Calcium Signaling and Inflammation in a Spinal Nerve Ligation Model.

Denervation-induced calcium/calmodulin-dependent protein kinase II (CaMKII) activation and inflammation can result in muscle atrophy. Curcumin and bisdemethoxycurcumin are well known to exhibit an anti-inflammatory effect. In addition, curcumin has been shown to attenuate CaMKII activation in neuronal cells. This study aimed to examine the effect of curcumin or bisdemethoxycurcumin on CaMKII activation, inflammation, and muscle cross-sectional area (CSA) in spinal nerve ligated rats. Sixteen female rats were assigned to sham (CON), spinal nerve ligation (SNL), SNL+ curcumin 100 mg/kg BW (100CUR), and SNL+ bisdemethoxycurcumin 50 mg/kg BW (50CMO) for 4 weeks. Ipsilateral (surgical) soleus and tibialis anterior (TA) muscles was stained for dystrophin to measure CSA. Ipsilateral and contralateral (non-surgical) plantaris muscles were analyzed for protein content for acetylcholine receptor (AChR), CaMKII, CaMKIIThr286, nuclear factor-κB (NF-κB), NF-κBSer536, and interleukin-1β (IL-1β) and normalized to α-tubulin and then CON. A significant (p < 0.050) group effect was observed for TA CSA where CON (11,082.25 ± 1617.68 μm2; p < 0.001) and 100CUR (9931.04 ± 2060.87 μm2; p = 0.018) were larger than SNL (4062.25 ± 151.86 μm2). In the ipsilateral plantaris, the SNL (4.49 ± 0.69) group had greater CaMKII activation compared to CON (1.00 ± 0.25; p = 0.010), 100CUR (1.12 ± 0.45; p = 0.017), and 50CMO (0.78 ± 0.19; p = 0.009). The ipsilateral plantaris (2.11 ± 0.66) had greater IL-1β protein content than the contralateral leg (0.65 ± 0.14; p = 0.041) in the SNL group. In plantaris, the SNL (1.65 ± 0.51) group had greater NF-κB activation compared to CON (1.00 ± 0.29; p = 0.021), 100CUR (0.61 ± 0.10; p = 0.003), 50CMO (0.77 ± 0.25; p = 0.009) groups. The observed reduction in Ca2+ signaling and inflammation in type II plantaris muscle fibers might reflect the changes within the type II TA muscle fibers which may contribute to the mitigation of TA mass loss with curcumin supplementation.

Decreased number of satellite cells-derived myonuclei in both fast- and slow-twitch muscles in HeyL-KO mice during voluntary running exercise

BackgroundSkeletal muscles possess unique abilities known as adaptation or plasticity. When exposed to external stimuli, such as mechanical loading, both myofiber size and myonuclear number increase. Muscle stem cells, also known as muscle satellite cells (MuSCs), play vital roles in these changes. HeyL, a direct target of Notch signaling, is crucial for efficient muscle hypertrophy because it ensures MuSC proliferation in surgically overloaded muscles by inhibiting the premature differentiation. However, it remains unclear whether HeyL is essential for MuSC expansion in physiologically exercised muscles. Additionally, the influence of myofiber type on the requirement for HeyL in MuSCs within exercised muscles remains unclear.MethodsWe used a voluntary wheel running model and HeyL-knockout mice to investigate the impact of HeyL deficiency on MuSC-derived myonuclei, MuSC behavior, muscle weight, myofiber size, and myofiber type in the running mice.ResultsThe number of new MuSC-derived myonuclei was significantly lower in both slow-twitch soleus and fast-twitch plantaris muscles from exercised HeyL-knockout mice than in control mice. However, expect for the frequency of Type IIb myofiber in plantaris muscle, exercised HeyL-knockout mice exhibited similar responses to control mice regarding myofiber size and type.ConclusionsHeyL expression is crucial for MuSC expansion during physiological exercise in both slow and fast muscles. The frequency of Type IIb myofiber in plantaris muscle of HeyL-knockout mice was not significantly reduced compared to that of control mice. However, the absence of HeyL did not affect the increased size and frequency of Type IIa myofiber in plantaris muscles. In this model, no detectable changes in myofiber size or type were observed in the soleus muscles of either control or HeyL-knockout mice. These findings imply that the requirement for MuSCs in the wheel-running model is difficult to observe due to the relatively low degree of hypertrophy compared to surgically overloaded models.

A Natural History Study of Hindlimb Physiology and Histopathology in a Heterozygous OPMD Mouse Model

ABSTRACTBackgroundOculopharyngeal muscular dystrophy (OPMD) is an adult‐onset autosomal dominant myopathy. OPMD is caused by a short alanine expansion in the gene encoding for poly(A) binding protein nuclear 1 (PABPN1) forming insoluble nuclear aggregates. OPMD patients are predominantly heterozygous, and the knock‐in Pabpn1+/A17 mouse, which expresses one copy of the expanded Pabpn1 gene under the PABPN1 promoter genetically, mimics OPMD. Insights into the A17/+ mouse model are necessary to evaluate its preclinical value and test therapeutics for OPMD. Here, we performed a natural disease history study for the A17/+ model.MethodsWe combined muscle force measurements of the tibialis anterior with magnetic resonance imaging (MRI) measurements of the calf muscles made in 4‐, 8‐ and 12‐month‐old wild‐type and A17/+ mice. These measures were complemented by muscle histopathology staining and image quantification to detect PABPN1 aggregates and to assess muscle wasting. Statistical significance between genotypes over the three time points was assessed using ANOVA or Student's t test.ResultsPABPN1 nuclear aggregates were found in the 12‐month‐old A17/+ mice at similar quantities of ~2% across hindlimb muscles. We did not observe changes in muscle strength of the tibialis anterior in A17/+ mice. MRI analyses of hindlimb muscles revealed no metabolic difference, no fatty infiltration and limited muscle atrophy between A17/+ and +/+ mice. The plantaris muscle in A17/+ showed 30% atrophy at 12 months of age, which was corroborated by a 30% myofiber shift in the myosin heavy chain −2A to −2B ratio. Histopathologic staining did not reveal muscle wasting in the hindlimb muscles.ConclusionsDespite the presence of PABPN1 insoluble aggregates in hindlimb muscles, muscle involvement in the 12‐month‐old A17/+ mice was limited. Our results query the usefulness of A17/+ hindlimb muscles for preclinical studies.

Differential Responses To Heat Stress On The Regeneration Of Injured Rat Soleus And Plantaris Muscles

Differential Responses To Heat Stress On The Regeneration Of Injured Rat Soleus And Plantaris Muscles

Allogenic Vertebral Body Adherent Mesenchymal Stromal Cells Promote Muscle Recovery in Diabetic Mouse Model of Limb Ischemia

Chronic limb-threatening ischemia (CLTI) carries a significant risk for amputation, especially in diabetic patients with poor options for revascularization. Phase I trials have demonstrated efficacy of allogeneic mesenchymal stromal cells (MSC) in treating diabetic CLTI. Vertebral bone-adherent mesenchymal stromal cells (vBA-MSC) are derived from vertebral bodies of deceased organ donors, which offer the distinct advantage of providing a 1,000x greater yield compared to that of living donor bone aspiration. This study describes the effects of intramuscular injection of allogenic vBA-MSC in promoting limb perfusion and muscle recovery in a diabetic CLTI mouse model. A CLTI mouse model was created through unilateral ligation of the femoral artery in male polygenic diabetic TALLYHO mice. The treated mice were injected with vBA-MSC into the gracilis muscle of the ischemic limb 7days post ligation. Gastrocnemius or tibialis muscle was assessed postmortem for fibrosis by collagen staining, capillary density via immunohistochemistry, and mRNA by quantitative real-time polymerase chain reaction (PCR). Laser Doppler perfusion imaging and plantar flexion muscle testing (MT) were performed to quantify changes in limb perfusion and muscle function. Compared to vehicle (Veh) control, treated mice demonstrated indicators of muscle recovery, including decreased fibrosis, increased perfusion, muscle torque, and angiogenesis. PCR analysis of muscle obtained 7 and 30 days post vBA-MSC injection showed an upregulation in the expression of MyoD1 (P=0.03) and MyH3 (P=0.008) mRNA, representing muscle regeneration, vascular endothelial growth factor A (VEGF-A) (P=0.002; P=0.004) signifying angiogenesis as well as interleukin (IL-10) (P<0.001), T regulatory cell marker Foxp3 (P=0.04), and M2-biased macrophage marker Mrc1 (CD206) (P=0.02). These findings indicate human allogeneic vBA-MSC ameliorate ischemic muscle damage and rescue muscle function. These results in a murine model will enable further studies to develop potential therapies for diabetic CLTI patients.

A three-headed plantaris muscle with a bipartite insertion of its two accessory heads.

The plantaris muscle consists of a small muscular and a long tendinous part and is located at the superficial compartment of the posterior leg. The purpose of the current cadaveric report is to describe a rare variant of the plantaris muscle. During a routine dissection, a three-headed plantaris with two accessory heads was identified with a variant insertion of the two accessory heads. All heads originated from the femur popliteal surface, independently the one from the other. The first head contributed to the long and thin calcaneal tendon, and the two accessory heads were mainly inserted via their musculoaponeurotic expansion into the medial femoral condyle. The plantaris muscle morphological variability has been extensively studied lately. The incidence of the two-headed muscle has been estimated at 1.6%, while the three-headed muscle corresponds to an even rarer variation. This is the third case reported in the English literature, while the insertion of the two accessory heads has never been described before.

Differences in the Size of Individual Plantar Intrinsic Foot Muscles Between Ballet Dancers and Non-Dancers.

In classic ballet, choreography often involves tiptoe standing. Tiptoe standing requires a high and stable foot arch structure, which is achieved by contraction of the plantar intrinsic foot muscles (PIFMs). Long-term repetitive loading with a specific movement can induce hypertrophic adaptation of the associated muscles. For dancers, however, limited information on the size of individual PIFMs is available from previous studies. The purpose of this study was to determine the differences in the sizes of 10 individual PIFMs between dancers and non-dancers. Muscle volumes (MVs) of 10 individual PIFMs were measured using magnetic resonance imaging in 15 female dancers and 15 female non-dancers. Muscles analyzed included abductor hallucis, flexor digitorum brevis, abductor digiti minimi, quadratus plantae, lumbricals, flexor hallucis brevis, adductor hallucis oblique head, adductor hallucis transverse head, flexor digiti minimi, plantar/dorsal interossei. In addition to absolute MVs, relative MVs normalized to body mass (rMVBM) and the percentage of individual MVs relative to the sum of 10 individual PIFM MVs (%MVWHOLE) were calculated. The absolute MVs of 6 individual PIFMs, including the flexor digitorum brevis and lumbricals, were +16% to 59% larger in dancers than in non-dancers (P ≤ .048). The rMVBM of all individual PIFMs were +35% to 95% larger in dancers than in non-dancers (P ≤ .019). The %MVWHOLE of the flexor digitorum brevis and lumbricals were +10% to 36% higher (P ≤ .014) and those of the abductor digiti minimi and adductor hallucis oblique head were +8% to 11% lower (P ≤ .037) in dancers than in non-dancers. For all 3 MV measures, only the flexor digitorum brevis and lumbricals, which are functionally specialized for flexion of the second to fifth metatarsophalangeal joints, were consistently larger in dancers than in non-dancers. This may be due to long-term repetitive loading on these PIFMs during ballet training involving tiptoe standing.

Comparing the effectiveness of robotic plantarflexion resistance and biofeedback between overground and treadmill walking

Individuals with diminished walking performance caused by neuromuscular impairments often lack plantar flexion muscle activity. Robotic devices have been developed to address these issues and increase walking performance. While these devices have shown promise in their ability to increase musculature engagement of the lower limbs when used on a treadmill, most have not been developed or validated for overground walking and community use. Overground walking may limit the effectiveness of robotic devices due to differences in gait characteristics between walking terrains and reduced user engagement. The purpose of this study was to validate our multimodal robotic gait training system for overground walking in individuals with neuromuscular gait impairments. This untethered wearable robotic device can provide an ankle resistive torque proportional to the users’ biological ankle torque. The device can also provide audio biofeedback based on users’ plantar pressure intending to increase ankle power and muscle activity of the plantar flexors. Seven individuals with cerebral palsy participated. Participants walked overground and on a treadmill with our robotic gait training system in a single testing session. Results showed all seven participants to increase peak plantar flexor muscle activity, 10.3% on average, when walking with the gait trainer overground compared to treadmill. When compared to typical baseline overground walking, overground gait trainer use caused individuals to have slightly less knee joint excursion (3°) and moderately more ankle joint excursion (7°). This work supports our vision of using the wearable robotic device as a gait aid and rehabilitation tool in the home and community settings.

Different outcomes of endurance and resistance exercise in skeletal muscles of Oculopharyngeal muscular dystrophy.

Exercise is widely considered to have beneficial impact on skeletal muscle aging. In addition, there are also several studies demonstrating a positive effect of exercise on muscular dystrophies. Oculopharyngeal muscular dystrophy (OPMD) is a late-onset autosomal dominant inherited neuromuscular disorder caused by mutations in the PAPBN1 gene. These mutations consist in short (1-8) and meiotically stable GCN trinucleotide repeat expansions in its coding region responsible for the formation of PAPBN1 intranuclear aggregates. This study aims to characterize the effects of two types of chronic exercise, resistance and endurance, on the OPMD skeletal muscle phenotype using a relevant murine model of OPMD. In this study, we tested two protocols of exercise. In the first, based on endurance exercise, FvB (wild-type) and A17 (OPMD) mice underwent a 6-week-long motorized treadmill protocol consisting in three sessions per week of running 20cm/s for 20min. In the second protocol, based on resistance exercise generated by chronic mechanical overload (OVL), surgical removal of gastrocnemius and soleus muscles was performed, inducing hypertrophy of the plantaris muscle. In both types of exercise, muscles of A17 and FvB mice were compared with those of respective sedentary mice. For all the groups, force measurement, muscle histology, and molecular analyses were conducted. Following the endurance exercise protocol, we did not observe any major changes in the muscle physiological parameters, but an increase in the number of PABPN1 intranuclear aggregates in both tibialis anterior (+24%, **P=0.0026) and gastrocnemius (+18%, ****P<0.0001) as well as enhanced collagen deposition (+20%, **P=0.0064 in the tibialis anterior; +35%, **P=0.0042 in the gastrocnemius) in the exercised A17 OPMD mice. In the supraphysiological resistance overload protocol, we also observed an increased collagen deposition (×2, ****P<0.0001) in the plantaris muscle of A17 OPMD mice which was associated with larger muscle mass (×2, ****P<0.0001) and fibre cross sectional area (×2, ***P=0.0007) and increased absolute maximal force (×2, ****P<0.0001) as well as a reduction in PABPN1 aggregate number (-16%, ****P<0.0001). Running exercise and mechanical overload led to very different outcome in skeletal muscles of A17 mice. Both types of exercise enhanced collagen deposition but while the running protocol increased aggregates, the OVL reduced them. More importantly OVL reversed muscle atrophy and maximal force in the A17 mice. Our study performed in a relevant model gives an indication of the effect of different types of exercise on OPMD muscle which should be further evaluated in humans for future recommendations as a part of the lifestyle of individuals with OPMD.

Effects of a 12-week intrinsic foot muscle strengthening training (STIFF) on gait in older adults: a parallel randomized controlled trial protocol

BackgroundFalling is highly prevalent among older adults and has serious impact. Age-induced mobility impairments, such as gait modifications, are strongly associated with increased fall risk. Among fall prevention interventions, those including exercises are most effective. However, there is an urgent need to further improve these kinds of interventions. Strengthening the plantar intrinsic foot muscles might benefit mobility in older adults, which may contribute to the reduction of fall risk. The aim of this paper is to provide a protocol to investigate the effect of a plantar intrinsic foot muscle strengthening training versus no training on gait and intrinsic foot muscle function in older adults who are involved in a functional exercise program.MethodsFor this assessor-blinded RCT, older adults (> 65 years) are recruited who are involved in a group-based functional exercise program. Eligibility criteria include: being able to ambulate 10 m barefoot without using a walking aid and reporting to have either fear of falling or experienced a fall in the previous 12 months or have difficulties with mobility, gait, or balance in daily life. Participants are randomly assigned to an intervention and a control group. The intervention group follows a 12-week plantar intrinsic foot muscle strengthening training. The training consists of isolated and functional foot exercises to be performed 5 times a week, each session lasting approximately 20 min. The training is supervised once a week and the intensity gradually increases based on the participant’s progression. Both groups keep a diary to report physical activities, fall incidents and movement related discomfort. The control condition is limited to keeping this diary. Data are collected at baseline and post-intervention. The trial outcomes are the between group differences in the mean change from baseline in maximum gait speed (primary outcome measure), capacity and strength of the plantar intrinsic foot muscles, foot and ankle biomechanics during gait, and various other fall risk-related variables. ANCOVA’s are used to analyze the trial outcomes.DiscussionThe results of this RCT will offer recommendations, related to plantar intrinsic foot muscle strengthening, to existing fall preventive exercise programs.Trial registrationThe trial is registered in the United States National Library of Medicine through ClinicalTrials.gov (NCT05531136, 07/26/2022).

The influence of foot muscles exercises and minimalist shoes on lactate threshold velocity in long-distance amateur runners: a randomized controlled trial

The exercises of plantar foot muscles may have beneficial effects on the performance of the lower extremity muscles. The aim of this study was to compare two methods of foot muscle strengthening: direct short foot muscle exercises and indirect activation through training in minimalist footwear in regard to influence on lactate threshold velocity in long-distance runners. 55 recreational runners aged 21–45 years took part in that study. They were randomly divided into 2 groups: Group 1 (n = 25) with short foot muscle exercises, and Group 2 (n = 30) with training in minimalist shoes. The progressive running test was performed to determine heart rate (HR) and running velocity corresponding to lactate threshold (VLT). Two-way ANOVA was used to determine the significance of the differences regarding the evaluated variables. After the 8-week training program, higher values of VLT were observed in both groups. This change was significant only in Group 1 (p < 0.05). In Group 2, the higher value was noted but the changes were non-significant. Strengthening of the short foot muscles may improve lactate threshold velocity which is connected with running performance. Considering the obtained results, it is worth contemplating the implementation of these methods in the training of long-distance runners.

Differential Mitochondrial Adaptation of the Slow and Fast Skeletal Muscles by Endurance Running Exercise in Streptozotocin-Induced Diabetic Mice.

The skeletal muscle is the main organ responsible for insulin action, and glucose disposal and metabolism. Endurance and/or resistance training raises the number of mitochondria in diabetic muscles. The details of these adaptations, including mitochondrial adaptations of the slow and fast muscles in diabetes, are unclear. This study aimed to determine whether exercise training in streptozotocin (STZ)-induced mice leads to differential adaptations in the slow and fast muscles, and improving glucose clearance. Eight-week-old mice were randomly distributed into normal control (CON), diabetes (DM), and diabetes and exercise (DM+Ex) groups. In the DM and DM+Ex groups, mice received a freshly prepared STZ (100 mg/kg) intraperitoneal injection on two consecutive days. Two weeks after the injection, the mice in the groups ran on a treadmill for 60 min at 20 m/min for a week and subsequently at 25 m/min for 5 weeks (5 days/week). The analyses indicated that running training at low speed (25 m/min) enhanced mitochondrial enzyme activity and expression of lactate and glucose transporters in the plantaris (low-oxidative) muscle that improved whole-body glucose metabolism in STZ-induced diabetic mice. There were no differences in glucose transporter expression levels in the soleus (high-oxidative) muscle. The endurance running exercise at 20-25 m/min was sufficient to induce mitochondrial adaptation in the low-oxidative muscles, but not in the high-oxidative muscles, of diabetic mice. In conclusion, the present study indicated that running training at 25 m/min improved glucose metabolism by increasing the mitochondrial enzyme activity and glucose transporter 4 and monocarboxylate transporter 4 protein contents in the low-oxidative muscles in STZ-induced diabetic mice.

Predicting muscle function and mass with electrical impedance myography: A study in rat analogs of micro- and partial gravity

IntroductionSpaceflight results in marked muscle atrophy and a corresponding loss in muscle strength. Methods to evaluate spaceflight-induced changes to muscle size and strength are difficult to achieve within the tight confines of spacecrafts. Therefore, convenient methods to non-invasively monitor muscle that are predictive of actual muscle function are critical for future missions to ensure the health and safety of crew members. PurposeEvaluate the ability of non-invasive in vivo electrical impedance myography (EIM) combined with statistical models to predict muscle size and strength in rodent models of micro- and partial gravity. MethodsMale and female Fisher rats (N = 120), half gonadectomized, were divided into three different weightbearing (WB) conditions of 40 animals each, including 0%WB (0 % of weight-bearing, simulated microgravity), 40%WB (40 % of weight-bearing, simulated Martian gravity), and 100%WB (100 % of weight-bearing, full weight-bearing controls). Rats remained in designated interventions for 28 days. Afterward, rats underwent a series of musculoskeletal strength assessments and measurement of EIM. Rats were then euthanized and gastrocnemius tissues collected. Machine-learning (ML) algorithms were applied to full spectrum EIM data to predict various muscle parameters. Results40%WB and 0%WB rats had lower grip strength and plantar flexion compared to 100%WB. Correspondingly, 40%WB and 0%WB also had reduced gastrocnemius mass compared to 100%WB. EIM resistance values demonstrated a dose-dependency response, with greater resistance values associated with reduced gravitational load. ML-enhanced EIM yielded strong predictions of muscle plantar flexion force and muscle mass, with root mean squared errors of 18.4 % of 22.0 %, and R2 values of 0.87 an 0.88, respectively. ConclusionML-enhanced EIM may be a helpful tool to non-invasively monitor muscle changes predictive of muscle force production and mass during exposure to reduced gravity.

Treadmill running and mechanical overloading improved the strength of the plantaris muscle in the dystrophin-desmin double knockout (DKO) mouse.

Limited knowledge exists regarding the chronic effect of muscular exercise on muscle function in a murine model of severe Duchenne muscular dystrophy (DMD). Here we determined the effects of 1month of voluntary wheel running (WR), 1month of enforced treadmill running (TR) and 1month of mechanical overloading resulting from the removal of the synergic muscles (OVL) in mice lacking both dystrophin and desmin (DKO). Additionally, we examined the effect of activin receptor administration (AR). DKO mice, displaying severe muscle weakness, atrophy and greater susceptibility to contraction-induced functional loss, were exercised or treated with AR at 1month of age and in situ force production of lower leg muscle was measured at the age of 2months. We found that TR and OVL increased absolute maximal force and the rate of force development of the plantaris muscle in DKO mice. In contrast, those of the tibialis anterior (TA) muscle remained unaffected by TR and WR. Furthermore, the effects of TR and OVL on plantaris muscle function in DKO mice closely resembled those in mdx mice, a less severe murine DMD model. AR also improved absolute maximal force and the rate of force development of the TA muscle in DKO mice. In conclusion, exercise training improved plantaris muscle weakness in severely affected dystrophic mice. Consequently, these preclinical results may contribute to fostering further investigations aimed at assessing the potential benefits of exercise for DMD patients, particularly resistance training involving a low number of intense muscle contractions. KEY POINTS: Very little is known about the effects of exercise training in a murine model of severe Duchenne muscular dystrophy (DMD). One reason is that it is feared that chronic muscular exercise, particularly that involving intense muscle contractions, could exacerbate the disease. In DKO mice lacking both dystrophin and desmin, characterized by severe lower leg muscle weakness, atrophy and fragility in comparison to the less severe DMD mdx model, we found that enforced treadmill running improved absolute maximal force of the plantaris muscle, while that of tibialis anterior muscle remained unaffected by both enforced treadmill and voluntary wheel running. Furthermore, mechanical overloading, a non-physiological model of chronic resistance exercise, reversed plantaris muscle weakness. Consequently, our findings may have the potential to alleviate concerns and pave the way for exploring the prescription of endurance and resistance training as a viable therapeutic approach for the treatment of dystrophic patients. Additionally, such interventions may serve in mitigating the pathophysiological mechanisms induced by physical inactivity.

High-intensity interval training using electrical stimulation ameliorates muscle fatigue in chronic kidney disease-related cachexia by restoring mitochondrial respiratory dysfunction.

Exercise, especially high-intensity interval training (HIIT), can increase mitochondrial respiratory capacity and enhance muscular endurance, but its systemic burden makes it difficult to safely and continuously prescribe for patients with chronic kidney disease (CKD)-related cachexia who are in poor general condition. In this study, we examined whether HIIT using electrical stimulation (ES), which does not require whole-body exercise, improves muscle endurance in the skeletal muscle of 5/6 nephrectomized rats, a widely used animal model for CKD-related cachexia. Male Wistar rats (10weeks old) were randomly assigned to a group of sham-operated (Sham) rats and a group of 5/6 nephrectomy (Nx) rats. HIIT was performed on plantar flexor muscles in vivo with supramaximal ES every other day for 4weeks to assess muscle endurance, myosin heavy-chain isoforms, and mitochondrial respiratory function in Nx rats. A single session was also performed to identify upstream signaling pathways altered by HIIT using ES. In the non-trained plantar flexor muscles from Nx rats, the muscle endurance was significantly lower than that in plantar flexor muscles from Sham rats. The proportion of myosin heavy chain IIa/x, mitochondrial content, mitochondrial respiratory capacity, and formation of mitochondrial respiratory supercomplexes in the plantaris muscle were also significantly decreased in the non-trained plantar flexor muscles from Nx rats than compared to those in plantar flexor muscles from Sham rats. Treatment with HIIT using ES for Nx rats significantly improved these molecular and functional changes to the same degrees as those in Sham rats. Furthermore, a single session of HIIT with ES significantly increased the phosphorylation levels of AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (MAPK), pathways that are essential for mitochondrial activation signaling by exercise, in the plantar muscles of both Nx and Sham rats. The findings suggest that HIIT using ES ameliorates muscle fatigue in Nx rats via restoration of mitochondrial respiratory dysfunction with activation of AMPK and p38 MAPK signaling. Our ES-based HIIT protocol can be performed without placing a burden on the whole body and be a promising intervention that is implemented even in conditions of reduced general performance status such as CKD-related cachexia.