Journal of Applied Physiology

Autonomic nervous system (ANS) activity causes acute variations in the blood pressure. Blood pressure responds to high intensity interval exercise (HIIE) repeatedly during alternating intensities, however, ANS response to the changing intensities of HIIE is unknown. We characterized the response of beat-to-beat blood pressure variability (BTB BPV) to an acute bout of HIIE using coefficient of variation (CoV) and spectral low frequency [LF], and high frequency [HF] domains. Our hypotheses were mean arterial pressure BTB BPV, would increase during 1) high intensity and 2) active recovery of HIIE compared to baseline (BL). BTB BPV would reduce during 1) cool down 2) post HIIE 3) 30 minutes post HIIE compared to BL in young adults. HIIE included bouts of 1-minute high-intensity separated by 1-minute recovery ({square}70% and 10% estimated Wattmax) for total of 10 minutes on a recumbent stepper. A secondary analysis was performed using twenty-one datasets of young individuals (age 25{+/-}1.5, 48% female). During high intensity, LF and HF increased compared to BL (p < 0.05) indicating increased sympathetic activity and breathing. During active recovery, LF and HF remained elevated above BL and were greater than during high intensity (p [&le;] 0.02). Sympathetic activity reduced back to BL immediately post HIIE but returned to being higher than BL at 30 minutes after HIIE (p=0.001). BTB BPV CoV also increased during HIIE compared to BL (p<0.05). Results suggest that young healthy individuals have increased BTB BPV during HIIE suggesting cardiovascular system responds to ANS fluctuations during changing exercise intensity. New and NoteworthyThis novel study analyzed beat -to-beat blood pressure variability during high intensity interval exercise (HIIE) in young healthy adults. We found that blood pressure variability was highest during active recovery compared to resting or high intensity exercise. Moreover, variability increased during HIIE but returned to resting post-exercise. These findings provide valuable insights into the blood pressure and ANS responses to HIIE, contributing to our understanding of their impact on overall cardiovascular health in young adults.

Understanding skeletal muscle adaptation is key to optimizing training and rehabilitation strategies, yet the causal links between training stimuli and muscle response remain unclear. This gap reflects the difficulty of observing multi-scale adaptations within the same muscle in vivo. Calf muscles, critical for propulsion and postural control, remain relatively under-studied, and long-term outcomes with intermediate stages of adaptation are rarely documented. We investigated temporal and regional remodelling of the gastrocnemius medialis muscle during 12 weeks of eccentric training in six young, healthy adults. Participants trained on alternate days with progressive overload calf raise exercises. Muscle architecture and function were assessed at baseline, 6, and 12 weeks using 3D ultrasonography and dynamometry. Group-level analysis revealed a 38% increase in peak plantarflexion torque at 90{degrees} (p < 0.01), while muscle volume, PCSA, fascicle length, and pennation angle showed no consistent changes. Individual response profiles varied: some participants showed longitudinal growth with longer fascicles and smaller pennation angles, others displayed radial growth with increased PCSA, while some exhibited minimal architectural change despite torque gains. Trends suggested shifts in fascicle length-angle torque relationships and altered tendon compliance in certain individuals. By combining regional muscle morphology with functional outcomes over time, this study demonstrates the feasibility of tracking multi-scale adaptation in vivo. The pronounced inter-individual and region-specific variability highlights the need for tailored interventions that consider baseline architecture and regional strain patterns to optimize outcomes in training and rehabilitation.

RationaleMechanical ventilation rapidly induces slow and fast fiber contractile dysfunction in the human diaphragm, which could be attenuated by phrenic nerve stimulation. Here, we present data from a controlled trial of intraoperative phrenic stimulation to offset slow and fast fiber contractile dysfunction and myofilament protein derangements. ObjectivesIn this study, we tested the hypothesis that intraoperative hemidiaphragm stimulation would mitigate slow and fast fiber loss of contractile function in the human diaphragm. MethodsNineteen adults (9 females, age 59 {+/-}12 years) consented to participate. Unilateral phrenic twitch stimulation was applied for one minute, every 30 minutes during cardiothoracic surgery. Thirty minutes following the last stimulation bout, biopsies were obtained from the hemidiaphragms for single fiber force mechanics and quantitation of thin filament protein abundance. Effects of stimulation and fiber type on force mechanics were evaluated with linear mixed models with the subject treated as a random intercept effect. Measurements and Main ResultsSubjects underwent 6 {+/-}2 hemidiaphragm stimulations at 17 {+/-}6 mA, during 278 {+/-}68 minutes of mechanical ventilation. In slow-twitch fibers, cross-sectional area (p<0.0001) and specific force (p<0.0005) were significantly greater on the stimulated side. Longer-duration surgeries were associated with lower slow-twitch specific force (p<0.001). Stimulation did not alter contractile function of fast-twitch fibers or calcium-sensitivity in either fiber type. There were no differences in abundance or phosphorylation of myofilament proteins. ConclusionUnilateral phrenic stimulation during open chest surgery preserved contractile function of slow-twitch diaphragm fibers, but had no effect on relative abundance of sarcomeric proteins.

Older adults have difficulty maintaining balance when faced with postural disturbances, a task that is influenced by the stiffness of the triceps surae and Achilles tendon. Age-related changes in Achilles tendon stiffness have been reported at matched levels of effort, but measures typically have not been made at matched loads, which is important due to age-dependent changes in strength. Moreover, age-dependent changes in muscle stiffness have yet to be tested. Here, we investigate how age alters muscle and tendon stiffness and their influence on ankle stiffness. We hypothesized that age-related changes in muscle and tendon contribute to reduced ankle stiffness in older adults and evaluated this hypothesis when either load or effort were matched. We used B-mode ultrasound with joint-level perturbations to quantify ankle, muscle, and tendon stiffness across a range of loads and efforts in seventeen healthy younger and older adults. At matched loads, there was no significant difference in ankle, muscle, or tendon stiffness between groups (all p>0.13). However, at matched effort, older adults exhibited a significant decrease in ankle (27%; p=0.008), muscle (37%; p=0.02), and tendon stiffness (22%; p=0.03) at 30% of maximum effort. This is consistent with our finding that older adults were 36% weaker than younger adults in plantarflexion (p=0.004). Together these results indicate that, at the loads tested in this study, there are no age-dependent changes in the mechanical properties of muscle or tendon, only differences in strength that result in altered ankle, muscle, and tendon stiffness at matched levels of effort. NO_SCPLOWEWC_SCPLOWO_SCPCAP C_SCPCAPO_SCPLOWANDC_SCPLOW NO_SCPLOWOTEWORTHYC_SCPLOWWe provide the first simultaneous estimates of ankle, muscle, and tendon stiffness in younger and older adults. In contrast to earlier conclusions, we found that muscle and tendon mechanical properties are unaffected by age when compared at matched loads. However, due to age-related decreases in strength, mechanical properties do differ at matched efforts. As such, it is important to assess the relevance of the comparisons being made relative to the functional tasks under consideration.

Handgrip exercise (HGE) is a safe, accessible exercise modality shown to improve cardiovascular health and is particularly promising for individuals with limited mobility who cannot engage in traditional exercise. Given that contraction type and intensity influence systemic cardiorespiratory variables that affect cerebral blood flow regulation, this study examined the acute systemic hemodynamic and cerebrovascular responses to static and rhythmic HGE protocols at varying intensities. Thirty-three healthy young adults (17 males; 16 females age 22(1) years) performed four separate 5-minute HGE protocols in a randomized order: static HGE at 15% (S15) of maximal voluntary contraction (MVC), static HGE at 30% MVC, rhythmic HGE at 30% MVC, rhythmic HGE at 60% (R60) MVC. We hypothesized that rhythmic HGE at higher intensities would produce the greatest cerebrovascular responses due to enhanced venous return and cardiac output, while static HGE at higher intensities would elicit the greatest systemic (i.e., blood pressure, HR, ventilation) responses. Cerebral (middle cerebral artery blood velocity [MCAv] and cerebrovascular conductance index [MCACVCi], internal carotid artery [ICA] diameter, velocity, blood flow, and shear rate) and systemic hemodynamics (systolic [SBP], diastolic [DBP], mean arterial pressure [MAP], heart rate [HR], cardiac output [CO]), and end-tidal carbon dioxide (PETCO2) levels were averaged over the final 30s of each minute of exercise. There was a significant time and protocol interaction effect on HR (p<0.001). We found significant main effects of exercise protocol for MCAv (p<0.001), MCACVCi (p<0.001), ICA diameter (p=0.01) and blood flow (p=0.001), and PETCO2 (p=0.002). Greatest increases in MCAv alongside the largest reduction in ICA blood flow occurred in R60. The greatest increase in MCACVCi and ICA blood flow (from baseline) occurred in R30 compared to other protocols. In addition to the greater cerebrovascular responses, we also observed more modest systemic responses (lower HR, MAP, CO) and lower self-reported ratings of perceived exertion (p<0.001) in R30 compared to other protocols. Acute increases in MCACVCi and ICA blood flow observed in R30 (despite the lower perceived effort) may suggest that rhythmic HGE at low-moderate intensities can be a tolerable prescription for inducing exercise-related cerebrovascular adaptations (i.e., improved cerebral perfusion) in populations that may require adapted physical activity.

PurposeConsistently performing at the highest level in golf requires a complex interplay of physiological and psychological attributes, with success often defined by razor-thin margins. Sleep characteristics and cardiac autonomic function, reflected by resting heart rate (RHR) and heart rate variability (HRV), are key indicators of recovery and readiness to perform. Yet, their relevance to elite golf performance remains largely unexplored. MethodsWe analyzed wearable-derived longitudinal data from 389 professional tour-level golfers across 521 competitive events (2017-2025), encompassing 35,140 nights of sleep and biometric monitoring. Key metrics included sleep duration (7.2{+/-}0.7hrs), sleep consistency (69.1{+/-}6.9%), RHR (55.9{+/-}7.9bpm), HRV (64.2{+/-}28.1ms), and a composite Recovery score (59.1{+/-}9.9%). Golf performance (total score, great shots, poor shots, strokes gained) was extracted from a subscription-based database. Linear mixed-effects models assessed both between-person differences and within-person season-to-season changes, adjusting for age (34.1{+/-}9.1yrs), height (1.81{+/-}0.07m), and weight (83.2{+/-}10.6kg). ResultsGolfers with superior sleep and biometric profiles consistently performed better, both between and within individuals (Ps<0.05). Between individuals, each additional hour of sleep was associated with a lower score (b=-0.522), as was a 10-percentage point increase in sleep consistency (b=-0.382), a 1bpm lower RHR (b=-0.038), and a 10-percentage point increase in Recovery (b=-0.476). Within athletes, season-to-season improvements in sleep consistency (b=-0.193 per 10-percentage points), HRV (b=-0.016 per 1ms), and Recovery (b=-0.238 per 10 percentage points) were also associated with lower scores (Ps<0.05). ConclusionsSleep and measures of cardiac autonomic function are associated with performance in elite golf. Both individual differences and within-athlete improvements were linked to success, highlighting the potential role of sleep, resting heart rate, and heart rate variability in optimizing performance at the highest level of sport.

BackgroundAerobic training enhances VO2max, yet the contribution of peripheral microvascular remodeling to this improvement remains insufficiently understood. This research demonstrates how two distinct training modalities, high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT), influence oxygen transport dynamics and microvascular remodeling. MethodsTwenty-five healthy sedentary adults (15 women, 10 men; mean age 25 {+/-} 2 years; normal BMI) were randomly assigned to HIIT or MICT for 8 weeks. VO2max was assessed before and after the training program. 15 participants underwent non-invasive maximal cardiac output measurement (Qmax), while vastus lateralis muscle biopsies were obtained from 10 participants. Tissue samples were cleared and immunolabeled for VE-cadherin and alpha-smooth muscle actin to observe microvasculature architecture. A computational hemodynamic model integrating cardiac output and microvascular parameters was constructed to estimate flow dynamics. ResultsVO2max increased significantly in both training groups, with a greater improvement in HIIT (p = 0.024). Qmax increased similarly in both groups (p = 0.001), while calculated arteriovenous oxygen difference (a-vO2 diff) showed a trend toward improvement only in HIIT. No formation of new capillaries nor anastomoses (angiogenesis) was detected in either group; however, both HIIT and MICT induced significant capillary and venule dilation. Notably, only HIIT led to a significant increase in pericyte coverage (p = 0.047). Venules of both groups exhibited dilation accompanied by increased surrounding smooth muscle cells. No remodeling was found in arterioles. Hemodynamic modelisation estimated higher shear stress during HIIT than MICT and vasodilation tended to decrease shear stress over time during both training. Furthermore, pericyte recruitment was modelized to adapt to shear stress level limiting excessive capillary dilation during high effort intensity. ConclusionHIIT induces superior improvements in VO2max and distinct microvascular structural adaptations rather than angiogenesis. HIIT is supposed to stimulate a protective adaptation at the capillary level, limiting excessive dilation during maximal effort. Our hemodynamic model supports this shear stress-dependent mechanism. These findings underscore the role of exercise intensity and hemodynamics in shaping microvascular responses to endurance training. Clinical PerspectiveO_LIPeripheral adaptation to exercise is linked with the dilation of muscle capillaries and venules. C_LIO_LIMechanoadaptive responses, rather than growth factor-mediated angiogenesis, drive the remodeling of the muscle microvasculature. C_LIO_LIHigh-intensity interval training elicits higher shear stress than moderate continuous interval training, linking the adaptation of the microvasculature to increased blood flow as the primary factor that explains the superiority of HIIT compared to MICT in improving maximal oxygen consumption. C_LI Clinical implicationO_LITraining regimens should focus on increasing peripheral flow and shear stress to initiate microvasculature remodeling. C_LIO_LIPotentiating mechanoadaptative responses and microcirculation remodeling would provide a means to improve cardiovascular function and fitness C_LI

The short-term scaling exponent of detrended fluctuation analysis (DFA1) applied to interbeat intervals may provide a method to identify ventilatory thresholds and indicate systemic perturbation during prolonged exercise. The purposes of this study were to i) confirm whether DFA1 values of 0.75 and 0.5 coincide with the gas exchange threshold (GET) and respiratory compensation point (RCP), ii) quantify DFA1 during constant-speed running near the maximal lactate steady state (MLSS), and iii) assess the repeatability of DFA1 between MLSS trials. Seventeen runners performed an incremental running test, and eleven and ten runners also performed constant-speed running 5% below, at, and 5% above the MLSS, and a repeat trial at MLSS, respectively. GET (bias [LOA]: -3.6 [-9.1 to 1.9] mL{middle dot}kg-1{middle dot}min-1) and RCP (-3.5 [-14.1 to 7.2] mL{middle dot}kg-1{middle dot}min-1) were overestimated using DFA1. DFA1 responses during 30-min running trials near MLSS were variable (i.e., 0.27 to 1.24), and affected by intensity (p=0.019) and duration (p=0.001). No difference in DFA1 was detected between MLSS trials (p=0.926). These results question whether DFA1 values can accurately delineate exercise thresholds, but the dependency of DFA1 on intensity and duration support its potential use to quantify systemic perturbations imposed by continuous exercise.

BackgroundIn patients with chronic coronary syndromes (CCS) increased ventilation/carbon dioxide production ([V]E/[V]CO2) slope has been found to predict disease progression and mortality similarly to patients with heart failure (HF), however, chemosensitivity has rarely been assessed in patients with CCS. MethodPatients with CCS, HF with reduced ejection fraction (EF<50%), old healthy (45+ years) and young adult healthy controls (<35 years) were recruited. For patients, a [V]E/[V]CO2 slope [&ge;]36 was an inclusion criterion. The Duffin rebreathing method was used to determine the resting end-expiratory partial pressure of carbon dioxide (PETCO2), ventilatory recruitment threshold (VRT) and slope (sensitivity) during a hyperoxic (150 mmHg O2) and hypoxic (50 mmHg O2) rebreathing test to determine central and peripheral chemosensitivity. ResultsIn patients with CCS, HF, and old and young controls, median [V]E/[V]CO2 slopes were 40.2, 41.3, 30.5 and 28.0, respectively. Both patient groups had similarly reduced hyperoxic VRT (at PETCO2 42.1 and 43.2 mmHg) compared to 46.0 and 48.8 mmHg in the old and young controls. Neither hypoxic VRT nor hyper- or hypoxic slopes were significantly different in patients compared to controls. Both patient groups had lower resting PETCO2 than controls, but only patients with HF had increased breathing frequency and rapid shallow breathing at rest. ConclusionIn patients with cardiac disease and excess ventilation, central chemoreflex VRT was reduced independently of the presence of heart failure. Low VRTs were related to resting excess ventilation in patients with CCS or HF, however, rapid shallow breathing was present only in patients with HF. Clinical perspectiveO_ST_ABSWhat is new?C_ST_ABSO_LIExcess ventilation during exercise and heightened chemosensory reflexes may be present not only in patients with HF but also in patients with CCS. This suggests that there is a gradual derangement of neurologic and/or hormonal factors leading to excess ventilation before the establishment of HF. C_LIO_LIIn patients with excess ventilation during exercise there is also excess ventilation at rest. C_LIO_LIExcess ventilation in patients with CCS does not show the rapid shallow breathing pattern that is typical for patients with HF. C_LI What are the clinical implications?O_LIWhile excess ventilation during exercise causes dyspnoea with associated negative effects on exercise tolerance and quality of life,1 excess ventilation at rest has been poorly investigated. More research is warranted as physiologic consequences may be substantial with the large time spent at rest compared to exercise. C_LIO_LIThe finding that the threshold of PETCO2 at which ventilation starts to increase rather than the [V]E/PETCO2 slope is increased in patients with inefficient ventilation suggests electrolyte derangement as an at least contributing cause which may stimulate alternative treatments such as intravenous iron therapy.2 C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=137 SRC="FIGDIR/small/24311710v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@149d9e2org.highwire.dtl.DTLVardef@17fc19dorg.highwire.dtl.DTLVardef@803364org.highwire.dtl.DTLVardef@ae18a7_HPS_FORMAT_FIGEXP M_FIG C_FIG

The supraspinatus is the most frequently injured rotator cuff muscle, but its anatomical characteristics such as larger size, complex fiber architecture, and a single exposed tendon have limited the development of reproducible ex vivo contractility assays. In this study, we establish a robust method for ex vivo assessment of murine supraspinatus contractile function and characterize its physiological properties across age and injury conditions. We additionally adapt a barium chloride (BaCl2)-induced injury protocol for the supraspinatus, an approach not previously described, to evaluate how acute myofiber degeneration affects muscle performance. Male C57BL/6 mice (4 months) underwent 1.2% BaCl2 injection directly into the supraspinatus to induce controlled myofiber necrosis, allowing comparison of contractile behavior between injured and uninjured muscles. Using our injury ex vivo physiological testing protocol, we quantified optimal length (L0), twitch kinetics, force-frequency responses, peak tetanic force, and preliminary fatigue-recovery dynamics. Our protocol consistently generated fused tetanic contractions and reproducible force-frequency curves in the supraspinatus. We observed differences in supraspinatus contractility between young and old mice, consistent with well-established age-related changes in hindlimb muscle contractility. In addition, BaCl2 injury produced significant impairments in contractility 48 hours post-injection, demonstrating the sensitivity of this method to acute muscle damage. This study provides a novel and reliable method for evaluating the contractile function of the murine supraspinatus muscle ex vivo, overcoming previous anatomical challenges.

ObjectiveExamine the association of ectopic adipose tissue (AT) with skeletal muscle (SM) mitochondrial bioenergetics in older adults. MethodsCross-sectional data from 829 older adults [&ge;]70 years was used. Total abdominal, subcutaneous, and visceral AT; and thigh muscle fat infiltration (MFI) was quantified by MRI. SM mitochondrial energetics were characterized using in vivo 31P-MRS (ATPmax) and ex vivo high-resolution respirometry (maximal oxidative phosphorylation (OXPHOS)). ActivPal was used to measure PA (step count). Linear regression models adjusted for covariates were applied, with sequential adjustment for BMI and PA. ResultsIndependent of BMI, total abdominal (standardized (Std.) {beta}=-0.21; R2=0.09) and visceral AT (Std. {beta}=-0.16; R2=0.09) were associated with ATPmax (p<0.01), but not after further adjustment for PA (p[&ge;]0.05). Visceral AT (Std. {beta}=-0.16; R2=0.25) and thigh MFI (Std. {beta}=-0.11; R2=0.24) were negatively associated with carbohydrate-supported maximal OXPHOS independent of BMI and PA (p<0.05). Total abdominal AT (Std. {beta}=-0.19; R2=0.24) and visceral AT (Std. {beta}=-0.17; R2=0.24) were associated with fatty acid-supported maximal OXPHOS independent of BMI and PA (p<0.05). ConclusionsSkeletal MFI and abdominal visceral, but not subcutaneous AT, are inversely associated with SM mitochondrial bioenergetics in older adults independent of BMI. Associations between ectopic AT and in vivo mitochondrial bioenergetics are attenuated by PA.

Mouse models of chronic intermittent hypoxia are widely used in research to understand the role of sleep apnea in disease pathogenesis. Mice exposed to periodic reductions in FIO2 model arterial desaturations observed in humans and recapitulate many comorbidities of sleep apnea. Here, we perform a detailed characterization and confirm reports that mice in room air experience spontaneous, periodic desaturation events. We measured peripheral oxygen saturation in the four mouse strains most commonly used in intermittent hypoxia research (C57BL/6J, CD1, BALB/c, and 129S1) and subjected them to conscious barometric plethysmography to measure oxygen desaturations and apneas simultaneously and took measurements across a range of fractional inspired oxygen (FIO2). As expected, all strains experienced periodic apneas that were followed by desaturations and decreasing FIO2 resulted in a reduction of spontaneous apneic events (p = 0.001). Surprisingly, most oxygen desaturations were not preceded by apneas or hypopneas, and mice experienced more desaturations at lower FIO2 (p < 0.001), despite less frequent apneas. Furthermore, we found strain differences in ventilatory response consistent with prior findings and a novel strain difference in 129S1 mice. These data suggest that spontaneous desaturations are caused not only by apneas and hypopneas but also by other mechanisms, independent of respiration. Our findings provide important context for mouse models of sleep apnea and associated diseases, and future work should explore the extent to which these findings are relevant in humans.

The mechanisms for the loss in limb muscle power in old (60-79 years) and very old ([&ge;]80 years) adults and whether the mechanisms differ between men and women are not well-understood. We compared maximal power of the knee extensor muscles between young, old, and very old men and women and identified the neural and muscular factors contributing to the age-related loss of power. 31 young (22.9{+/-}3.0 years, 15 women), 83 old (70.4{+/-}4.9 years, 39 women), and 16 very old adults (85.8{+/-}4.2 years, 9 women) performed maximal isokinetic contractions at 14 different velocities (30- 450{degrees}/s) to identify peak power. Voluntary activation (VA) and contractile properties were assessed with transcranial magnetic stimulation to the motor cortex and electrical stimulation of the femoral nerve. The age-related loss in power was [~]6.5 W{middle dot}year-1 for men (R2=0.62, p<0.001), which was a greater rate of decline (p=0.002) than the [~]4.2 W{middle dot}year-1 for women (R2=0.77, p<0.001). Contractile properties were the most closely associated variables with power output for both sexes, such as the rate of torque development of the potentiated twitch (men: R2=0.69, p<0.001; women: R2=0.57, p<0.001). VA was weakly associated with power in women (R2=0.13, p=0.012) but not men (p=0.191), whereas neuromuscular activation (EMG amplitude) during the maximal power contraction was not associated with power in men (p=0.347) or women (p=0.106). These data suggest that the age-related loss in power of the knee extensor muscles is due primarily to factors within the muscle for both sexes, although neural factors may play a minor role in older women. NEW & NOTEWORTHYThe accelerated age-related loss in power relative to the loss in muscle mass of the knee extensors was primarily due to factors altering the contractile properties of the muscle for both old and very old ([&ge;]80 yr) adults. The mechanisms for the decrements in power with aging appear largely similar for men and women, although neural factors may play more of a role in older women.

Ultrasound shear wave elastography can be used to characterize mechanical properties of unstressed tissue by measuring shear wave velocity (SWV), which increases with increasing tissue stiffness. Measurements of SWV have often been assumed to be directly related to the stiffness of muscle. Some have also used measures of SWV to estimate stress, since muscle stiffness and stress covary during active contractions. However, few have considered the direct influence of muscle stress on SWV, independent of the stress-dependent changes in muscle stiffness, even though it is well known that stress alters shear wave propagation. The objective of this study was to determine how well the theoretical dependency of SWV on stress can account for measured changes of SWV in passive and active muscle. Data were collected from six isoflurane-anesthetized cats; three soleus muscles and three medial gastrocnemius muscles. Muscle stress and stiffness were measured directly along with SWV. Measurements were made across a range of passively and actively generated stresses, obtained by varying muscle length and activation, which was controlled by stimulating the sciatic nerve. Our results show that SWV depends primarily on the stress in a passively stretched muscle. In contrast, the SWV in active muscle is higher than would be predicted by considering only stress, presumably due to activation-dependent changes in muscle stiffness. Our results demonstrate that while SWV is sensitive to changes in muscle stress and activation, there is not a unique relationship between SWV and either of these quantities when considered in isolation.

BackgroundOlder adults exhibit a slower recovery of muscle mass following disuse atrophy than young adults. At a smaller scale, muscle fibre cross-sectional area (i.e., sarcomeres in parallel) exhibits this same pattern. Less is known, however, about age-related differences in the recovery of muscle fibre length, driven by increases in serial sarcomere number (SSN), following disuse. The purpose of this study was to investigate age-related differences in SSN adaptations and muscle mechanical function during and following muscle immobilization. We hypothesized that old rats would experience a similar magnitude of SSN loss during immobilization, however, take longer to recover SSN than young following cast removal, which would limit the recovery of muscle mechanical function. MethodsWe casted the plantar flexors of young (8 months) and old (32 months) male rats in a shortened position for 2 weeks, and assessed recovery during 4 weeks of voluntary ambulation. Following sacrifice, legs were fixed in formalin for measurement of soleus wet weight and SSN with the un-casted soleus acting as a control. Ultrasonographic measurements of pennation angle (PA) and muscle thickness (MT) were also conducted weekly. In-vivo active and passive torque-angle relationships were constructed pre-cast, post-cast, and following 4 weeks of recovery. ResultsFrom pre- to post-cast, young and old rats experienced similar decreases in SSN (-20%, P<0.001), muscle wet weight (-25%, P<0.001), MT (-30%), PA (-15%, P<0.001), and maximum isometric torque (-40%, P<0.001), but there was a greater increase in passive torque in old (+180%, P<0.001) compared to young rats (+68%, P=0.006). Following cast removal, young exhibited quicker recovery of SSN, PA, and MT than old, but SSN recovered sooner than PA and MT in both young and old. Muscle wet weight recovered 90% and active torque fully recovered in young rats, whereas in old these remained unrecovered at 75% and 72%, respectively. ConclusionsThis study showed that old rats retain a better ability to recover longitudinal compared to parallel muscle morphology following cast removal, making SSN a highly adaptable, appealing mechanism for restoration of functional capacity following disuse in elderly populations.

During an unexpected loss of balance, avoiding a fall requires people to readjust their footing rapidly and effectively. We investigated the activation patterns of the ankle and knee muscles, and muscle fiber type recruitment resulting from unannounced, medio-lateral (i.e., right/left) horizontal-surface walking perturbations in twenty healthy adults (27.00{+/-}2.79 years, 10 females). Surface electromyography (sEMG) total spectral power for specific frequency bands (40-60Hz, 60-150Hz, 150-250Hz, 250-400Hz and 400-1000Hz), from tibialis anterior (TA) and vastus lateralis (VL) muscles were analyzed. Compared to non-perturbed walking, we found a significant increase in the total spectral power of lower-extremity muscles during the first 3 seconds after perturbation. When two feet were on the ground in time of perturbation we found a different muscle fiber type recruitment pattern between VL and TA muscles. This was not significant for perturbations implemented when one foot was on the ground. Our findings suggest that muscle operating frequency is modulated in real time to fit body state and somatosensory input in the context of functional goal requirements such as a rapid change of footing in response to unexpected loss of balance in single and double-support phases of gait. New & NoteworthyTo study muscle spectral profiles in response to loss of balance, we investigated the dynamics of muscle spectral power changes, across different frequency bands after unannounced mechanical perturbations during walking. We showed increased activation of high-frequency motor units of the lower-limb muscles, subside 3 seconds after perturbation. Differences in power increase of specific frequency bands suggest that muscle activation is modulated in real time to fit body state in the context of functional goal requirements.

Abstract Purpose: MyotonPRO (MTP) and time-harmonic elastography (THE) are increasingly used to assess muscle mechanical properties, yet they operate on fundamentally different physical principles. MTP measures composite MTP stiffness (N/m) through surface oscillations, while THE quantifies intrinsic shear modulus (THE stiffness, kPa) via propagating shear waves. This study aimed at systematically compare MTP and THE measurements in the vastus lateralis muscle across different contraction intensities and examine how the skin layer and subcutaneous fat (SLSF) thickness influence their relationship. Methods: Twenty-six healthy adults (15 males, 11 females; age 25 [SD 4] years) underwent MTP and THE measurements of the vastus lateralis at rest and during isometric contractions at 15% and 30% maximal voluntary contraction (MVC). Effects of contraction intensities on tissue properties were assessed using univariate analyses of variance with repeated measures. Associations between the different outcomes of THE and MTP technologies were explored using Pearson's correlations and partial correlation coefficients separately for each contraction intensity with adjustment of the SLSF thickness of participants. Results: Both technologies detected contraction intensity-dependent stiffening across all outcomes (p < 0.001). THE stiffness increased from 5.3 [1.2] kPa at rest to 15.6 [6.1] kPa at 30% MVC; THE wave attenuation increased from 0.83 [0.19] to 1.42 [0.36] s/m while MTP stiffness increased from 337.3 [49.3] N/m at rest to 529.4 [160.7] N/m at 30% MVC. Correlations between modalities were weak and condition-dependent. THE wave attenuation did not significantly correlate with any MTP outcome across conditions. Conclusion: MTP and THE detect contraction-induced stiffening through fundamentally different physical mechanisms and should not be regarded as interchangeable. Their correlation is modest at rest and breaks down (or reverses) during active contraction, with subcutaneous fat as a key modifying factor. Clinical trial number: Not applicable.

Successful reactive balance control requires coordinated modulation of hip, knee, and ankle torques. Stabilizing joint torques arise from feedforward neural signals that modulate the musculoskeletal systems intrinsic mechanical properties, namely muscle short-range stiffness, and neural feedback pathways that activate muscles in response to sensory input. Although feedforward and feedback pathways are known to modulate the torque at each joint, the role of each pathway to the balance-correcting response across joints is poorly understood. Since the feedforward and feedback torque responses act at different delays following perturbations to balance, we modified the sensorimotor response model (SRM), previously used to analyze the muscle activation response to perturbations, to consist of parallel feedback loops with different delays. Each loop within the model is driven by the same information, center of mass (CoM) kinematics, but each loop has an independent delay. We evaluated if a parallel loop SRM could decompose the reactive torques into the feedforward and feedback contributions during balance-correcting responses to backward support surface translations at four magnitudes. The SRM accurately reconstructed reactive joint torques at the hip, knee, and ankle, across all perturbation magnitudes (R2>0.84 & VAF>0.83). Moreover, the hip and knee exhibited feedforward and feedback components, while the ankle only exhibited feedback components. The lack of a feedforward component at the ankle may occur because the compliance of the Achilles tendon attenuates muscle short-range stiffness. Our model may provide a framework for evaluating changes in the feedforward and feedback contributions to balance that occur due to aging, injury, or disease. NEWS AND NOTEWORTHYReactive balance control requires coordination of neurally-mediated feedforward and feedback pathways to generate stabilizing joint torques at the hip, knee, and ankle. Using a sensorimotor response model, we decomposed reactive joint torques into feedforward and feedback contributions based on delays relative to center of mass kinematics. Responses across joints were driven by the same signals, but contributions from feedforward versus feedback pathways differed, likely due to differences in musculotendon properties between proximal and distal muscles.

It is unclear whether muscle functional adaptations to concentric (CON-RT) and eccentric (ECC-RT) resistance training are most specific to their exercise characteristics or the structural adaptations they evoke. In this study, the effects of effort- and volume-matched CON-RT and ECC-RT on regional hypertrophy, muscle architecture, and function were compared, and associations between the outcomes were explored. Twelve trained young men (25.5{+/-}3.6y) completed 18 isokinetic ankle-dorsiflexion exercise sessions over 6 weeks: CON-RT in one leg and ECC-RT in the other (2-4 sets, 6-10 maximal repetitions, 10{degrees}/s). Tibialis anterior size and architecture (ultrasound imaging) and maximum voluntary dorsiflexion function (isokinetic dynamometry) were assessed. Muscle thickness increased similarly between conditions and across proximal-distal regions (8%), pennation angle increased more in CON-RT (8%) than ECC-RT (4%), and fascicle length increased only after ECC-RT (7%). Functional adaptations were more closely associated with specific structural adaptations than with contraction mode, velocity, or angle. Isometric torque increased similarly in both conditions overall (8%) but CON-RT improved only at shorter muscle lengths and shifted the peak-torque angle leftward, whereas ECC-RT improved at both shorter and longer lengths and broadened the torque-angle plateau, which was associated with fascicle length increases. ECC-RT produced greater increases in both eccentric (13%) and concentric torques (17%) than CON-RT (3%, 9%, respectively), and changes were similar across velocities - contrary to the training specificity theory. Changes in pennation angle were associated with dynamic strength changes. These findings suggest that muscle function adapts to the structural changes induced by training, regardless of the training scheme used.

Cardiovascular dysfunction significantly contributes to morbidity and mortality following cervical spinal cord injury (SCI). Unfortunately, only a limited number of preclinical models have been developed for investigating cardiovascular dysfunction following cervical SCI. Furthermore, the broader consequences of cervical SCI on aerobic capacity and muscle endurance during physiological stress testing also remains understudied preclinically. Therefore, in this study we assessed potential deficits across multiple physiological systems in a rat model of cervical SCI using a battery of stress tests. Female Sprague-Dawley rats (n = 20) received either a C8 midline contusion (cSCI) or laminectomy alone as a control (LAM). Exercise stress testing was conducted to evaluate cardiorespiratory fitness and recovery using a metabolic treadmill, or forelimb fitness using the isometric pull task. Orthostatic stress testing and pharmacological stress testing were also performed to more directly challenge the cardiovascular system. Our findings demonstrate a decline in aerobic fitness in cSCI rats, as evidenced by dysregulated excess post-exercise oxygen consumption. cSCI rats also exhibited impaired muscle endurance compared to LAM. During orthostatic stress testing, 70% of cSCI rats experienced an approximately 25 mmHg decrease in systolic blood pressure and 20 mmHg decrease in diastolic blood pressure, in addition to modest but significant decreases in heart rate, myocardial contractility index, stroke volume index, and cardiac output index. During dobutamine infusion, cardiac output index and stroke volume index were significantly reduced following cSCI compared to LAM. Overall, these stress testing results suggest that preclinical cervical SCI in rats can lead to, and therefore model, clinically relevant impairments in cardiopulmonary exercise performance, muscle endurance, and cardiovascular function.