Stretch-shortening cycles protect against the age-related loss of power generation in rat single muscle fibres.

Aging is associated with impaired strength and power during isometric and shortening contractions, however, during lengthening (i.e., eccentric) contractions, strength is maintained. During daily movements, muscles undergo stretch-shortening cycles (SSCs). It is unclear whether the age-related maintenance of eccentric strength offsets age-related impairments in power generation during SSCs owing to the utilization of elastic energy or other cross-bridge based mechanisms. Here we investigated how aging influences SSC performance at the single muscle fibre level and whether performing active lengthening prior to shortening protects against age-related impairments in power generation. Single muscle fibres from the psoas major of young (∼8 months; n = 31 fibres) and old (∼32 months; n = 41 fibres) male F344BN rats were dissected and chemically permeabilized. Fibres were mounted between a force transducer and length controller and maximally activated (pCa 4.5). For SSCs, fibres were lengthened from average sarcomere lengths of 2.5 to 3.0 µm and immediately shortened back to 2.5 µm at both fast and slow (0.15 and 0.60 Lo/s) lengthening and shortening speeds. The magnitude of the SSC effect was calculated by comparing work and power during shortening to an active shortening contraction not preceded by active lengthening. Absolute isometric force was ∼37 % lower in old compared to young rat single muscle fibres, however, when normalized to cross-sectional area (CSA), there was no longer a significant difference in isometric force between age groups, meanwhile there was an ∼50 % reduction in absolute power in old as compared with young. We demonstrated that SSCs significantly increased power production (75-110 %) in both young and old fibres when shortening occurred at a fast speed and provided protection against power-loss with aging. Therefore, in older adults during everyday movements, power is likely 'protected' in part due to the stretch-shortening cycle as compared with isolated shortening contractions.

Time course changes in in vivo muscle mechanical function and Ca2+ regulation of force following experimentally induced gradual ovarian failure in mice.

The abrupt cessation of ovarian hormone release is associated with declines in muscle contractile function, yet the impact of gradual ovarian failure on muscle contractility across peri-, early- and late-stage menopause remains unclear. In this study, a 4-vinylcyclohexene diepoxide (VCD)-induced ovarian failure mouse model was used to examine time course changes in muscle mechanical function. Plantar flexors of female mice (VCD: n = 10; CON: n = 8) were assessed at 40 (early perimenopause), 80 (late perimenopause), 120 (menopause onset) and 176 (late menopause) days post-initial VCD injection. A torque-frequency relationship was established across a range of frequencies (10-200 Hz). Isotonic dynamic contractions were elicited against relative loads (10-80% maximal isometric torque) to determine the torque-velocity-power relationship. Mice then performed a fatigue task using intermittent 100 Hz isometric contractions until torque dropped by 60%. Recovery of twitch, 10 Hz and 100 Hz torque were tracked for 10 min post-task failure. Additionally, intact muscle fibres from the flexor digitorum brevis underwent a fatigue task (50 repetitions at 70 Hz), and 10 and 100 Hz tetanic [Ca2+] were monitored for 10 min afterward. VCD mice exhibited 16% lower twitch torque than controls across all time points. Apart from twitch torque, 10 Hz torque and 10 Hz tetanic [Ca2+], where VCD showed greater values relative to pre-fatigue during recovery, no significant differences were observed between control and VCD mice during recovery. These results indicate that gradual ovarian failure has minimal detriments to in vivo muscle mechanical function, with minor alterations observed primarily for low-frequency stimulation during recovery from fatigue.

Age-related blunting of serial sarcomerogenesis and mechanical adaptations following 4 wk of maximal eccentric resistance training.

During aging, muscles undergo atrophy, which is partly accounted for by a loss of sarcomeres in series. Serial sarcomere number (SSN) is associated with aspects of muscle mechanical function including the force-length and force-velocity-power relationships; hence, the age-related loss of SSN contributes to declining performance. Training emphasizing eccentric contractions increases SSN in young healthy rodents; however, the ability for eccentric training to increase SSN in old age is unknown. Ten young (8 mo) and 11 old (32 mo) male Fisher344/BN rats completed 4 wk of unilateral eccentric plantar flexion training. Pre- and posttraining, the plantar flexors were assessed for the torque-frequency, passive torque-angle, and torque-velocity-power relationships. The soleus, lateral gastrocnemius (LG), and medial gastrocnemius (MG) were harvested for SSN assessment via laser diffraction, with the untrained leg used as a control. In the untrained leg/pretraining, old rats had lower SSN in the soleus, LG, and MG, lower maximum torque, power, and shortening velocity, and greater passive torque than young. Young showed increased soleus and MG SSN following training. In contrast, old had no change in soleus SSN and experienced SSN loss in the LG. Pre- to posttraining, young experienced an increase in maximum isometric torque, whereas old had reductions in maximum torque, shortening velocity, and power, and increased passive torque. Our results show that although young muscle has the ability to add sarcomeres in response to maximal eccentric training, this stimulus could be not only ineffective, but also detrimental to aged muscle leading to dysfunctional remodeling.NEW & NOTEWORTHY The loss of sarcomeres in series with age contributes to declining muscle performance. The present study investigated whether eccentric training could improve performance via serial sarcomere addition in old muscle, like in young muscle. Four weeks of maximal eccentric training induced serial sarcomere addition in the young rat plantar flexors and improved in vivo performance, however, led to dysfunctional remodeling accompanied by further impaired performance in old rats.

Ultrasonographic measurements of fascicle length overestimate adaptations in serial sarcomere number.

Ultrasound-derived measurements of muscle fascicle length (FL) are often used to infer increases (chronic stretch or training) or decreases (muscle disuse or aging) in serial sarcomere number (SSN). Whether FL adaptations measured via ultrasound can truly approximate SSN adaptations has not been investigated. We casted the right hindlimb of 15 male Sprague-Dawley rats in a dorsiflexed position (i.e., stretched the plantar flexors) for 2 weeks, with the left hindlimb serving as a control. Ultrasound images of the soleus, lateral gastrocnemius (LG), and medial gastrocnemius (MG) were obtained with the ankle at 90° and full dorsiflexion for both hindlimbs pre and post-cast. Following post-cast ultrasound measurements, legs were fixed in formalin with the ankle at 90°, then muscles were dissected and fascicles were teased out for measurement of sarcomere lengths via laser diffraction and calculation of SSN. Ultrasound detected an 11% increase in soleus FL, a 12% decrease in LG FL, and an 8-11% increase in MG FL for proximal fascicles and at full dorsiflexion. These adaptations were partly reflected by SSN adaptations, with a 6% greater soleus SSN in the casted leg than the un-casted leg, but no SSN differences for the gastrocnemii. Weak relationships were observed between ultrasonographic measurements of FL and measurements of FL and SSN from dissected fascicles. Our results showed that ultrasound-derived FL measurements can overestimate an increase in SSN by ∼5%. Future studies should be cautious when concluding a large magnitude of sarcomerogenesis from ultrasound-derived FL measurements, and may consider applying a correction factor. NEW FINDINGS: What is the central question of this study? Measurements of muscle fascicle length via ultrasound are often used to infer changes in serial sarcomere number, such as increases following chronic stretch or resistance training, and decreases with ageing: does ultrasound-derived fascicle length accurately depict adaptations in serial sarcomere number? What is the main finding and its importance? Ultrasound detected an ∼11% increase in soleus fascicle length, but measurements on dissected fascicles showed the actual serial sarcomere number increase was only ∼6%; therefore, measurements of ultrasound-derived fascicle length can overestimate serial sarcomere number adaptations by as much as 5%.

The importance of serial sarcomere addition for muscle function and the impact of aging.

During natural aging, skeletal muscle experiences impairments in mechanical performance due, in part, to changes in muscle architecture and size, notably with a loss of muscle cross-sectional area (CSA). Another important factor that has received less attention is the shortening of fascicle length (FL), potentially reflective of a decrease in serial sarcomere number (SSN). Interventions that promote the growth of new serial sarcomeres, such as chronic stretching and eccentric-biased resistance training, have been suggested as potential ways to mitigate age-related impairments in muscle function. Although current research suggests it is possible to stimulate serial sarcomerogenesis in muscle in old age, the magnitude of sarcomerogenesis may be less than in young muscle. This blunted effect may be partly due to age-related impairments in the pathways regulating mechanotransduction, muscle gene expression, and protein synthesis, as some have been implicated in SSN adaptation. The purpose of this review was to investigate the impact of aging on the ability for serial sarcomerogenesis and elucidate the molecular pathways that may limit serial sarcomerogenesis in old age. Age-related changes in mechanistic target of rapamycin (mTOR), insulin-like growth factor 1 (IGF-1), myostatin, and serum response factor signaling, muscle ring finger protein (MuRFs), and satellite cells may hinder serial sarcomerogenesis. In addition, our current understanding of SSN in older humans is limited by assumptions based on ultrasound-derived fascicle length. Future research should explore the effects of age-related changes in the identified pathways on the ability to stimulate serial sarcomerogenesis, and better estimate SSN adaptations to gain a deeper understanding of the adaptability of muscle in old age.

Physiological and clinical responses to cycling 7850 km over 85 days in a physically active middle-aged man with idiopathic Parkinson's disease.

This case characterizes the clinical motor, perceived fatigue, gait and balance, cardiovascular, neuromuscular, and cardiopulmonary responses after cycling 7850 km over 85 days in a physically active 57-year-old male with idiopathic Parkinson's disease (PD). The participant cycled 73/85 days (86%); averaging 107.5 ± 48.9 km/day over 255.4 ± 108.8 min. Average cycling heart rate was 117 ± 11 bpm. The Unified Parkinson Disease Rating Scale (UPDRS) Part III motor score decreased from 46 to 26 (-44%), while the mean Parkinson Fatigue Scale (PFS-16) score decreased from 3.4 to 2.3 (-32%). Peak power output on a maximal aerobic exercise test increased from 326 to 357 W (+10%), while peak isotonic power of single-leg knee extension increased from 312 to 350 W (+12%). Maximal oxygen uptake following the trip was 53.1 mL/min/kg or 151% of predicted. Resting heart rate increased from 48 to 71 bpm (+48%). The systolic and diastolic blood pressure responses to a 2-min submaximal static handgrip exercise were near absent at baseline (∆2/∆2 mm Hg) but appeared normal post-trip (∆17/∆9 mm Hg). Gait and static balance measures were unchanged. This case report demonstrates the capacity for physiological and clinical adaptations to a high-volume, high-intensity cycling regiment in a physically active middle-aged male with PD.

Eccentric exercise-induced muscle weakness abolishes sex differences in fatigability during sustained submaximal isometric contractions.

BACKGROUND: Females are typically less fatigable than males during sustained isometric contractions at lower isometric contraction intensities. This sex difference in fatigability becomes more variable during higher intensity isometric and dynamic contractions. While less fatiguing than isometric or concentric contractions, eccentric contractions induce greater and longer lasting impairments in force production. However, it is not clear how muscle weakness influences fatigability in males and females during sustained isometric contractions. METHODS: We investigated the effects of eccentric exercise-induced muscle weakness on time to task failure (TTF) during a sustained submaximal isometric contraction in young (18-30 years) healthy males (n = 9) and females (n = 10). Participants performed a sustained isometric contraction of the dorsiflexors at 35° plantar flexion by matching a 30% maximal voluntary contraction (MVC) torque target until task failure (i.e., falling below 5% of their target torque for ≥2 s). The same sustained isometric contraction was repeated 30 min after 150 maximal eccentric contractions. Agonist and antagonist activation were assessed using surface electromyography over the tibialis anterior and soleus muscles, respectively. RESULTS: Males were ∼41% stronger than females. Following eccentric exercise both males and females experienced an ∼20% decline in maximal voluntary contraction torque. TTF was ∼34% longer in females than males prior to eccentric exercise-induced muscle weakness. However, following eccentric exercise-induced muscle weakness, this sex-related difference was abolished, with both groups having an ∼45% shorter TTF. Notably, there was ∼100% greater antagonist activation in the female group during the sustained isometric contraction following exercise-induced weakness as compared to the males. CONCLUSION: This increase in antagonist activation disadvantaged females by decreasing their TTF, resulting in a blunting of their typical fatigability advantage over males.

The day-to-day reliability of residual force enhancement during voluntary and electrically stimulated contractions.

Residual force enhancement (rFE) is characterized by increased steady-state isometric force following active muscle lengthening compared with a fixed-end isometric contraction at the same muscle length and level of neuromuscular activation. Many studies have characterized rFE in humans; however, the day-to-day reliability of rFE is unclear. We aimed to examine day-to-day reliability of rFE across various contraction types in the dorsiflexors in males and females. Twenty-five recreationally active young adults completed two visits, 1 week apart. Following determination of maximum voluntary contraction (MVC) strength, rFE was assessed during maximal voluntary effort, 20% MVC electrically stimulated, and 20% MVC torque-matching conditions. Each rFE condition was completed at two joint excursions: 0°-20° plantar flexion (PF) and 0°-40° PF. Intraclass correlation coefficients (ICC) assessed relative reliability and typical error of measurement (TEM), and the correlation variability of TEM (CVTEM) assessed absolute reliability. Electrically stimulated contractions demonstrated the highest reliability at 40° PF (ICC: 0.9; CVTEM: 22.8%) and 20° PF (ICC: 0.8; CVTEM: 34.3%), followed by maximal voluntary contractions at 40° PF (ICC: 0.7; CVTEM: 55.1%) and 20° PF (ICC: 0.1; CVTEM: 81.1%). The torque-matching trials showed poor reliability for 20° and 40° PF (ICC: -0.1 to 0.3; CVTEM: 118.1%-155.2%). Our results demonstrate higher reliability of rFE when stretching to the descending limb of the torque-angle relationship compared with the plateau region, and in electrically stimulated compared with voluntary contractions in the dorsiflexors for both males and females.

Influence of 4 weeks of downhill running on calcium sensitivity of rat single muscle fibers.

Improved Ca2+ sensitivity has been suggested as a mechanism behind enhancements in muscle mechanical function following eccentric training. However, little is known regarding the effects of eccentric training on single muscle fiber Ca2+ sensitivity. Adult male Sprague-Dawley rats (sacrificial age ~18 weeks; mass = 400.1 ± 34.8 g) were assigned to an eccentric training (n = 5) or sedentary control group (n = 6). Eccentric training consisted of 4 weeks of weighted downhill running 3×/week at a 15° decline and 16 m/min for 35 min per day in 5-min bouts. After sacrifice, vastus intermedius single muscle fibers were dissected, chemically permeabilized, and stored until testing. Fibers (n = 63) were isolated, and standard Ca2+ sensitivity, force, rate of force redevelopment (ktr ), and active instantaneous stiffness tests were performed using [Ca2+ ] ranging from 7.0 to 4.5. Following all mechanical testing, fiber type was determined using SDS-PAGE. There was no difference in pCa50 (i.e., [Ca2+ ] needed to elicit half of maximal force) between groups or between fiber types. However, when comparing normalized force across pCa values, fibers from the control group produced greater forces than fibers from the trained group at lower Ca2+ concentrations (p < 0.05), and this was most evident for Type I fibers (p = 0.002). Type II fibers produced faster (p < 0.001) ktr than Type I fibers, but there were no differences in absolute force, normalized force, or other measures of mechanical function between fibers from the trained and control groups. These findings indicate that eccentric training does not appear to improve single muscle fiber Ca2+ sensitivity.

Influence of weighted downhill running training on serial sarcomere number and work loop performance in the rat soleus.

Increased serial sarcomere number (SSN) has been observed in rats following downhill running training due to the emphasis on active lengthening contractions; however, little is known about the influence on dynamic contractile function. Therefore, we employed 4 weeks of weighted downhill running training in rats, then assessed soleus SSN and work loop performance. We hypothesised trained rats would produce greater net work output during work loops due to a greater SSN. Thirty-one Sprague-Dawley rats were assigned to a training or sedentary control group. Weight was added during downhill running via a custom-made vest, progressing from 5-15% body mass. Following sacrifice, the soleus was dissected, and a force-length relationship was constructed. Work loops (cyclic muscle length changes) were then performed about optimal muscle length (LO) at 1.5-3-Hz cycle frequencies and 1-7-mm length changes. Muscles were then fixed in formalin at LO. Fascicle lengths and sarcomere lengths were measured to calculate SSN. Intramuscular collagen content and crosslinking were quantified via a hydroxyproline content and pepsin-solubility assay. Trained rats had longer fascicle lengths (+13%), greater SSN (+8%), and a less steep passive force-length curve than controls (P<0.05). There were no differences in collagen parameters (P>0.05). Net work output was greater (+78-209%) in trained than control rats for the 1.5-Hz work loops at 1 and 3-mm length changes (P<0.05), however, net work output was more related to maximum specific force (R2=0.17-0.48, P<0.05) than SSN (R2=0.03-0.07, P=0.17-0.86). Therefore, contrary to our hypothesis, training-induced sarcomerogenesis likely contributed little to the improvements in work loop performance. This article has an associated First Person interview with the first author of the paper.

The influence of longitudinal muscle fascicle growth on mechanical function.

Skeletal muscle has the remarkable ability to remodel and adapt, such as the increase in serial sarcomere number (SSN) or fascicle length (FL) observed after overstretching a muscle. This type of remodeling is termed longitudinal muscle fascicle growth, and its impact on biomechanical function has been of interest since the 1960s due to its clinical applications in muscle strain injury, muscle spasticity, and sarcopenia. Despite simplified hypotheses on how longitudinal muscle fascicle growth might influence mechanical function, existing literature presents conflicting results partly due to a breadth of methodologies. The purpose of this review is to outline what is currently known about the influence of longitudinal muscle fascicle growth on mechanical function and suggest future directions to address current knowledge gaps and methodological limitations. Various interventions indicate longitudinal muscle fascicle growth can increase the optimal muscle length for active force, but whether the whole force-length relationship widens has been less investigated. Future research should also explore the ability for longitudinal fascicle growth to broaden the torque-angle relationship's plateau region, and the relation to increased force during shortening. Without a concurrent increase in intramuscular collagen, longitudinal muscle fascicle growth also reduces passive tension at long muscle lengths; further research is required to understand whether this translates to increased joint range of motion. Finally, some evidence suggests longitudinal fascicle growth can increase maximum shortening velocity and peak isotonic power; however, there has yet to be direct assessment of these measures in a neurologically intact model of longitudinal muscle fascicle growth.

Power attenuation from restricting range of motion is minimized in subjects with fast RTD and following isometric training.

Time-dependent measures consisting of rate of torque development (RTD), rate of velocity development (RVD), and rate of neuromuscular activation can be used to evaluate explosive muscular performance, which becomes critical when performing movements throughout limited ranges of motion (ROM). In this study, we investigated how restricting ROM influences power production while also exploring the relationship with time-dependent measures before and after isometric resistance training. Using a HUMAC NORM dynamometer, seven males (27 ± 7 yr) and six females (22 ± 3 yr) underwent 8 wk of maximal isometric dorsiflexion training 3 days/wk. One leg was trained at 0° [short-muscle tendon unit (MTU) length] and the other at 40° of plantar flexion (long-MTU length). RTD and rate of neuromuscular activation were evaluated during "fast" maximal isometric contractions. Power, RVD, and rate of neuromuscular activation were assessed during maximal isotonic contractions in four conditions [small (40°-30° of plantar flexion) ROM at 10% and 50% MVC; large (40°-0° of plantar flexion) ROM at 10% and 50% MVC] for both legs, pre- and posttraining. Despite no change in rate of neuromuscular activation following training, peak power, RTD, and RVD increased at both MTU lengths (P < 0.05). Strong relationships (R2 = 0.73) were observed between RTD and peak power in the small ROM, indicating that fast time-dependent measures are critical for optimal performance when ROM is constrained. Meanwhile, strong relationships (R2 = 0.90) between RVD and power were observed at the 50% load, indicating that RVD is critical when limited by load and ROM is not confined. Maximal isometric dorsiflexion training can be used to improve time-dependent measures (RTD, RVD) to minimize power attenuation when ROM is restricted.NEW & NOTEWORTHY Power output was greater in the unrestricted than restricted ROM, and there were strong relationships between rate of torque development (RTD) and velocity development (RVD) with peak power. RTD and RVD had the strongest relationships with power when ROM was restricted and unrestricted, respectively. Following 8 wk of isometric training, discrepancies in power between restricted and unrestricted ROM were reduced. Increasing RTD through isometric training increased power in dynamic movements, especially when ROM was restricted.

The torque-frequency relationship is impaired similarly following two bouts of eccentric exercise: No evidence of a protective repeated bout effect.

High-intensity eccentric exercise can lead to muscle damage and weakness. The 'repeated bout effect' (RBE) can attenuate these impairments when performing a subsequent bout. The influence of eccentric exercise-induced muscle damage on low-frequency force production is well-characterized; however, it is unclear how eccentric exercise and the RBE affect torque production across a range of stimulation frequencies (i.e., the torque-frequency relationship). We investigated the influence of an initial (Bout 1) and repeated bout (Bout 2) of eccentric exercise on the elbow flexor torque-frequency relationship. Eleven males completed two bouts of high-intensity eccentric elbow flexions, 4 weeks apart. Torque-frequency relationships were constructed at baseline and 0.5, 24, 48, 72, 96, and 168 h following both bouts via percutaneous stimulation at 1, 6, 10, 20, 30, 40, 50, and 100 Hz. Serum creatine kinase activity, self-reported muscle soreness, and isometric maximum voluntary contraction torque indirectly inferred the presence of muscle damage following Bout 1, and attenuation of muscle damage following Bout 2. Torque amplitude at all stimulation frequencies was impaired 30 min following eccentric exercise, however, torque at lower (1-10 Hz) and higher frequencies (40-100 Hz) recovered within 24 h while torque across the middle frequency range (20-30 Hz) recovered by 48 h. No between-bout differences were detected in absolute or normalized torque at any stimulation frequency, indicating no protective RBE on the elbow flexor torque-frequency relationship.

Power loss is attenuated following a second bout of high-intensity eccentric contractions due to the repeated bout effect's protection of rate of torque and velocity development.

High-intensity unaccustomed eccentric contractions result in weakness and power loss because of fatigue and muscle damage. Through the repeated bout effect (RBE), adaptations occur, then damage and weakness are attenuated following a subsequent bout. However, it is unclear whether the RBE protects peak power output. We investigated the influence of the RBE on power production and estimated fatigue- and damage-induced neuromuscular impairments following repeated high-intensity eccentric contractions. Twelve healthy adult males performed 5 sets of 30 maximal eccentric elbow flexions and repeated an identical bout 4 weeks later. Recovery was tracked over 7 days following both bouts. Reduced maximum voluntary isometric contraction torque, and increased serum creatine kinase and self-reported soreness indirectly inferred muscle damage. Peak isotonic power, time-dependent measures - rate of velocity development (RVD) and rate of torque development (RTD) - and several electrophysiological indices of neuromuscular function were assessed. The RBE protected peak power, with a protective index of 66% 24 h after the second eccentric exercise bout. The protection of power also related to preserved RVD (R2 = 0.61, P < 0.01) and RTD (R2 = 0.39, P < 0.01). Furthermore, the RBE's protection against muscle damage permitted the estimation of fatigue-associated neuromuscular performance decrements following eccentric exercise. Novelty: The repeated bout effect protects peak isotonic power. Protection of peak power relates to preserved rates of torque and velocity development, but more so rate of velocity development. The repeated bout effect has little influence on indices of neuromuscular fatigue.

Influence of isometric training at short and long muscle-tendon unit lengths on the history dependence of force.

The history dependence of force is an intrinsic property of muscle whereby a muscle actively shortened or lengthened to an isometric steady-state produces less (residual force depression; rFD) or more force (residual force enhancement; rFE), respectively, than a purely isometric contraction at the same muscle length and level of activation. Previous studies on the modifiability of the history dependence of force have been inconclusive, and none have attempted to modify rFD and rFE through isometric resistance training biased to short vs long muscle-tendon unit (MTU) lengths. We tested maximal voluntary rFD and rFE in seven males and six females before and after 8 weeks of maximal isometric dorsiflexion training 3 days/wk. Participants trained one leg at 0° of plantar flexion (short-MTU training) and one at 40° of plantar flexion (long-MTU training). Ultrasonography of the tibialis anterior assessed resting muscle architecture. Tibialis anterior fascicle length decreased by ~3% following short-MTU training (P = .03) and increased by ~4% following long-MTU training (P = .01). rFD did not change following training at either MTU length (absolute rFD: P = .53; percent rFD: P = .51), nor did rFE (absolute rFE: P = .78; percent rFE: P = .80), with no relationships between the change in fascicle length and the change in percent rFD (R2  = .01, P = .62) nor rFE (R2  = .001, P = .88). Our data indicate that voluntary rFD and rFE were not modified by isometric training and not related to the fascicle length adaptations we observed.

Differential changes in muscle architecture and neuromuscular fatigability induced by isometric resistance training at short and long muscle-tendon unit lengths.

We evaluated the effects of differential muscle architectural adaptations on neuromuscular fatigue resistance. Seven young males and six females participated in this study. Using a longitudinal within-subject design, legs were randomly assigned to perform isometric training of the tibialis anterior (TA) three times per week for 8 wk at a short (S-group) or long muscle-tendon unit length (L-group). Before and following training, fascicle length (FL) and pennation angle (PA) of the TA were assessed. As well, fatigue-related time course changes in isometric maximal voluntary contraction (MVC) torque and isotonic peak power (20% MVC resistance) were determined before, immediately after, and 1, 2, 5, and 10 min following task failure. The fatiguing task consisted of repeated maximal effort isotonic (20% MVC resistance) contractions over a 40° range of motion until the participant reached a 40% reduction in peak power. Although there was no clear improvement in neuromuscular fatigue resistance following training in either group (P = 0.081; S-group: ∼20%; L-group: ∼51%), the change in neuromuscular fatigue resistance was related positively to the training-induced increase in PA (∼6%, P < 0.001) in the S-group (r = 0.739, P = 0.004) and negatively to the training-induced increase in FL (∼4%, P = 0.001) in the L-group (r = -0.568, P = 0.043). Both groups recovered similarly for MVC torque and peak power after the fatiguing task as compared with before training. We suggest that the relationships between the changes in muscle architecture and neuromuscular fatigue resistance depend on the muscle-tendon unit lengths at which the training is performed.NEW & NOTEWORTHY Eight weeks of isometric training at a long or short muscle-tendon unit length increased and did not change fascicle length, respectively. The "width" of the torque-angle relationship plateau became broader following isometric training at the long length. Despite marked differences in muscle architecture and functional adaptations between the groups, there was only a small-magnitude improvement in neuromuscular fatigue resistance, which was surprisingly negatively related to increased fascicle length in the long length-training group.

Differential contributions of fatigue-induced strength loss and slowing of angular velocity to power loss following repeated maximal shortening contractions.

The purpose of this study was to investigate the relationship between fatigue-induced reductions in isometric torque and isotonic power and to quantify the extent to which the decreases in angular velocity and dynamic torque can explain the power loss immediately following an isotonic fatiguing task and throughout recovery in seven young males and six young females. All measurements were performed with both legs. For dorsiflexion, fatigue-related time-course changes in isometric maximal voluntary contraction (MVC) torque, angular velocity, dynamic torque, and power production following repeated maximal isotonic contractions (load: 20% MVC) were investigated before, immediately after, and 1, 2, 5 and 10 min after a fatiguing task. There were no relationships between the fatigue-related reductions in isometric MVC torque and peak power at any timepoint, suggesting that fatigue-induced reductions in isometric MVC torque does not entirely reflect fatigue-induced changes in dynamic performance. The relative contribution of fatigue-related reduction in dynamic torque on power loss was greater immediately following the task, and lower throughout recovery than the corresponding decrease in angular velocity. Thus, power loss immediately following the task was more strongly related to the decline in dynamic torque; however, this relationship shifted throughout recovery to a greater dependence on slowing of angular velocity for power loss.