The addition of blood flow restriction during resistance exercise does not increase prolonged low-frequency force depression.

At a given exercise intensity, blood flow restriction (BFR) reduces the volume of exercise required to impair post-exercise neuromuscular function. Compared to traditional exercise, the time course of recovery is less clear. After strenuous exercise, force output assessed with electrical muscle stimulation is impaired to a greater extent at low versus high stimulation frequencies, a condition known as prolonged low-frequency force depression (PLFFD). It is unclear if BFR increases PLFFD after exercise. This study tested if BFR during exercise increases PLFFD and slows recovery of neuromuscular function compared to regular exercise. Fifteen physically active participants performed six low-load sets of knee-extensions across four conditions: resistance exercise to task failure (RETF), resistance exercise to task failure with BFR applied continuously (BFRCONT) or intermittently (BFRINT), and resistance exercise matched to the lowest exercise volume condition (REVM). Maximal voluntary contraction (MVC) force output, voluntary activation and a force-frequency (1-100 Hz) curve were measured before and 0, 1, 2, 3, 4 and 24 h after exercise. Exercise to task failure caused similar reductions at 0 h for voluntary activation (RETF = 81.0 ± 14.2%, BFRINT = 80.9 ± 12.4% and BFRCONT = 78.6 ± 10.7%) and MVC force output (RETF = 482 ± 168 N, BFRINT = 432 ± 174 N, and BFRCONT = 443 ± 196 N), which recovered to baseline values between 4 and 24 h. PLFFD occurred only after RETF at 1 h supported by a higher frequency to evoke 50% of the force production at 100 Hz (1 h: 17.5 ± 4.4 vs. baseline: 15 ± 4.1 Hz, P = 0.0023), BFRINT (15.5 ± 4.0 Hz; P = 0.03), and REVM (14.9 ± 3.1 Hz; P = 0.002), with a trend versus BFRCONT (15.7 ± 3.5 Hz; P = 0.063). These findings indicate that, in physically active individuals, using BFR during exercise does not impair the recovery of neuromuscular function by 24 h post-exercise.

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.

The effect of gradual ovarian failure on dynamic muscle function and the role of high-intensity interval training on mitigating impairments.

Skeletal muscle contractile function is impaired in menopause and exercise may mitigate this decline. We used the 4-vinylcyclohexene diepoxide (VCD) model of menopause to investigate the effects of gradual ovarian failure on skeletal muscle contractile function and whether high-intensity interval training (HIIT) can mitigate impairments. Sexually mature female CD-1 mice were assigned to one of three groups: control sedentary (n = 5), VCD-sedentary (n = 5), or VCD-training (n = 5). Following ovarian failure (a 4-mo process), the VCD-training group underwent 8 wk of uphill HIIT. Mice were euthanized 8 wk after ovarian failure, representing late menopause. Single fibers from the soleus (SOL) and extensor digitorum longus (EDL) muscles were dissected, chemically permeabilized, and mechanically tested. Single muscle fibers were maximally activated (pCa 4.5), then isotonic load clamps were performed to evaluate force-velocity-power relationships. Absolute force and peak power were 31.0% and 32.2% lower in VCD-sedentary fibers compared with control fibers, respectively, in both SOL and EDL muscles. Despite reductions in absolute force, there were no concomitant increases in contractile velocity to preserve power production. HIIT attenuated force loss in the VCD-training group such that peak force was not different from the control group across muscles and was partially effective at mitigating power loss (21.7% higher peak power in VCD-training compared with VCD-sedentary) but only in fast-type SOL fibers. These findings indicate that ovarian failure impairs dynamic contractile function-likely through a combination of lower force-generating capacity and slower shortening velocity-and that HIIT may be insufficient to completely counteract the deleterious effects of menopause at the cellular level.NEW & NOTEWORTHY We used the VCD model of menopause to investigate the effects of gradual ovarian failure on skeletal muscle contractile function and whether high-intensity interval training (HIIT) can mitigate impairments. Our findings indicate that ovarian failure impairs dynamic contractile function-likely through a combination of lower force-generating capacity and slower shortening velocity-and that HIIT may be insufficient to completely counteract the deleterious effects of menopause at the cellular level.

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%.

Eccentric exercise-induced muscle weakness amplifies the history dependence of force.

INTRODUCTION: Following active lengthening or shortening contractions, isometric steady-state torque is increased (residual force enhancement; rFE) or decreased (residual force depression; rFD), respectively, compared to fixed-end isometric contractions at the same muscle length and level of activation. Though the mechanisms underlying this history dependence of force have been investigated extensively, little is known about the influence of exercise-induced muscle weakness on rFE and rFD. PURPOSE: Assess rFE and rFD in the dorsiflexors at 20%, 60%, and 100% maximal voluntary torque (MVC) and activation matching, and electrically stimulated at 20% MVC, prior to, 1 h following, and 24 h following 150 maximal eccentric dorsiflexion contractions. METHODS: Twenty-six participants (13 male, 24.7 ± 2.0y; 13 female, 22.5 ± 3.6y) were seated in a dynamometer with their right hip and knee angle set to 110° and 140°, respectively, with an ankle excursion set between 0° and 40° plantar flexion (PF). MVC torque, peak twitch torque, and prolonged low frequency force depression were used to assess eccentric exercise-induced neuromuscular impairments. History-dependent contractions consisted of a 1 s isometric (40°PF or 0°PF) phase, a 1 s shortening or lengthening phase (40°/s), and an 8 s isometric (0°PF or 40°PF) phase. RESULTS: Following eccentric exercise; MVC torque was decreased, prolonged low frequency force depression was present, and both rFE and rFD increased for all maximal and submaximal conditions. CONCLUSIONS: The history dependence of force during voluntary torque and activation matching, and electrically stimulated contractions is amplified following eccentric exercise. It appears that a weakened neuromuscular system amplifies the magnitude of the history-dependence of force.

The relationship between single muscle fibre and voluntary rate of force development in young and old males.

PURPOSE: It is suggested that the early phase (< 50 ms) of force development during a muscle contraction is associated with intrinsic contractile properties, while the late phase (> 50 ms) is associated with maximal force. There are no direct investigations of single muscle fibre rate of force development (RFD) as related to joint-level RFD METHODS: Sixteen healthy, young (n = 8; 26.4 ± 1.5 yrs) and old (n = 8; 70.1 ± 2.8 yrs) males performed maximal voluntary isometric contractions (MVC) and electrically evoked twitches of the knee extensors to assess RFD. Then, percutaneous muscle biopsies were taken from the vastus lateralis and chemically permeabilized, to assess single fibre function. RESULTS: At the joint level, older males were ~ 30% weaker and had ~ 43% and ~ 40% lower voluntary RFD values at 0-100 and 0-200 ms, respectively, than the younger ones (p ≤ 0.05). MVC torque was related to every voluntary RFD epoch in the young (p ≤ 0.001), but only the 0-200 ms epoch in the old (p ≤ 0.005). Twitch RFD was ~ 32% lower in the old compared to young (p < 0.05). There was a strong positive relationship between twitch RFD and voluntary RFD during the earliest time epochs in the young (≤ 100 ms; p ≤ 0.01). While single fibre RFD was unrelated to joint-level RFD in the young, older adults trended (p = 0.052-0.055) towards significant relationships between joint-level RTD and Type I single fibre RFD at the 0-30 ms (r2 = 0.48) and 0-50 ms (r2 = 0.49) time epochs. CONCLUSION: Electrically evoked twitches are good predictors of early voluntary RFD in young, but not older adults. Only the older adults showed a potential relationship between single fibre (Type I) and joint-level rate of force development.

Muscle quality indices separately associate with joint-level power-related measures of the knee extensors in older males.

PURPOSE: The purpose of this study was to investigate associations of muscle quality indices with joint-level power-related measures in the knee extensors of thirty-two older males (65-88 years). METHODS: Muscle quality indices included: echo intensity, ratio of intracellular- to total water content (ICW/TW), and specific muscle strength. Echo intensity was acquired from the rectus femoris (EIRF) and vastus lateralis (EIVL) by ultrasonography. ICW/TW was computed from electrical resistance of the right thigh obtained by bioelectrical impedance spectroscopy. Specific muscle strength was determined as the normalized maximal voluntary isometric knee extension (MVIC) torque to estimated knee extensor volume. Isotonic maximal effort knee extensions with a load set to 20% MVIC torque were performed to obtain the knee extension power-related measures (peak power, rate of power development [RPD], and rate of velocity development [RVD]). Power and RPD were normalized to MVIC. RESULTS: There were no significant correlations between muscle quality indices except between EIRF and EIVL (|r|≤ 0.253, P ≥ 0.162). EIRF was negatively correlated with normalized RPD and RVD (r ≤ - 0.361, P ≤ 0.050). ICW/TW was positively correlated with normalized peak power (r = 0.421, P = 0.020). Specific muscle strength was positively correlated with absolute peak power and RPD (r ≥ 0.452, P ≤ 0.012). CONCLUSION: Knee extension power-related measures were lower in participants with higher EI, lower ICW/TW, and lower specific muscle strength, but the muscle quality indices may be determined by independent physiological characteristics.

Trade-Off Between Maximal Power Output and Fatigue Resistance of the Knee Extensors for Older Men.

This study investigated associations of fatigue resistance determined by an exercise-induced decrease in neuromuscular power with prefatigue neuromuscular strength and power of the knee extensors in 31 older men (65-88 years). A fatigue task consisted of 50 consecutive maximal effort isotonic knee extensions (resistance: 20% of prefatigue isometric maximal voluntary contraction torque) over a 70° range of motion. The average of the peak power values calculated from the 46th to 50th contractions during the fatigue task was normalized to the prefatigue peak power value, which was defined as neuromuscular fatigue resistance. Neuromuscular fatigue resistance was negatively associated with prefatigue maximal power output (r = -.530) but not with prefatigue maximal voluntary contraction torque (r = -.252). This result highlights a trade-off between prefatigue maximal power output and neuromuscular fatigue resistance, implying that an improvement in maximal power output might have a negative impact on neuromuscular fatigue resistance.

Age-related reductions in the number of serial sarcomeres contribute to shorter fascicle lengths but not elevated passive tension.

We investigated age-related changes to fascicle length, sarcomere length and serial sarcomere number (SSN), and how this affects passive force. Following mechanical testing to determine passive force, the medial gastrocnemius muscle of young (n=9) and old (n=8) Fisher 344BN hybrid rats was chemically fixed at the optimal muscle length for force production; individual fascicles were dissected for length measurement, and laser diffraction was used to assess sarcomere length. Old rats had ∼14% shorter fascicle lengths than young rats, which was driven by a ∼10% reduction in SSN, with no difference in sarcomere length (∼4%). Passive force was greater in the old than in the young rats at long muscle lengths. Shorter fascicle lengths and reduced SSN in the old rats could not entirely explain increased passive forces for absolute length changes, owing to a slight reduction in sarcomere length in old rats, resulting in similar sarcomere length at long muscle lengths.

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.

Perception of effort during an isometric contraction is influenced by prior muscle lengthening or shortening.

PURPOSE: Following a shortening or lengthening muscle contraction, torque produced in the isometric steady state is lower (residual torque depression; rTD) or higher (residual torque enhancement; rTE), respectively, compared to a purely isometric contraction at the same final muscle length and level of activation. This is referred to as the history dependence of force. When matching a given torque level, there is greater muscle activation (electromyography; EMG) following shortening and less activation following lengthening. Owing to these differences in neuromuscular activation, it is unclear whether perception of effort is altered by the history dependence of force during plantar-flexion. METHODS: Experiment 1 tested whether perception of effort differed between the rTD and rTE state when torque was matched. Experiment 2 tested whether perception of effort differed between the rTD and rTE state when EMG was matched. Finally, experiment 3 tested whether EMG differed between the rTD and rTE state when perception of effort was matched. RESULTS: When torque was matched, both EMG and perception of effort were higher in the rTD compared to rTE state. When EMG was matched, torque was lower in the rTD compared to rTE state while perception of effort did not differ between the two states. When perception of effort was matched, torque was lower in the rTD compared to rTE state and EMG did not differ between the two states. CONCLUSION: The combined results from these experiments indicate that the history dependence of force alters one's perception of effort, dependent on the level of motor command.

Motor unit contributions to activation reduction and torque steadiness following active lengthening: a study of residual torque enhancement.

Following active lengthening, steady-state isometric (ISO) torque is greater than a purely ISO contraction at the same muscle length, this is referred to as residual torque enhancement (rTE). A phenomenon of rTE is activation reduction, characterized by reduced electromyography (EMG) amplitude for a given torque output. We hypothesized that lower motor unit discharge rates would contribute to activation reduction and lessening torque steadiness. Ten young male subjects performed ISO dorsiflexion contractions at 10 and 20% of maximal voluntary contraction (MVC) torque. During rTE trials, the muscle was activated at 10° of plantar flexion, then the ankle was rotated to the ISO position at 40°. Fine wire electrodes recorded motor unit (MU)-discharge rates and variability from the tibialis anterior. Surface EMG quantified activation reduction, and steadiness was determined as the coefficient of variation of torque. The activation reduction was 44 and 24% at 10 and 20% MVC, respectively (P < 0.05). Fewer MUs were recorded in the rTE than ISO condition at 10% (~47%) and 20% (~36%) MVC (P < 0.05). Discharge rates were 19 and 26% lower in the rTE compared with the ISO condition for 10 and 20% MVC, respectively (P < 0.05), with no difference in variability between conditions (P > 0.05). Steadiness was ~22 and 18% lower for the rTE than ISO condition at 10 and 20% MVC (P < 0.05). Our findings indicate that activation reduction may be attributed to lower MU discharge rate and fewer detectable MUs and that this theoretically contributes to a reduction in steadiness in the rTE condition.NEW & NOTEWORTHY Our findings indicate that lower electromyographic activity during the torque enhanced condition following active lengthening compared with a purely isometric contraction arises from fewer active motor units and a lower discharge rate of those that are active. We used an acute condition of increased torque capacity to induce a decrease in net output of the motor neuron pool during a submaximal task to demonstrate, in humans, the impact of motor unit activity on torque steadiness.

The influence of training-induced sarcomerogenesis on the history dependence of force.

The increase or decrease in isometric force following active muscle lengthening or shortening, relative to a reference isometric contraction at the same muscle length and level of activation, are referred to as residual force enhancement (rFE) and residual force depression (rFD), respectively. The purpose of these experiments was to investigate the trainability of rFE and rFD on the basis of serial sarcomere number (SSN) alterations to history-dependent force properties. Maximal rFE/rFD measures from the soleus and extensor digitorum longus (EDL) of rats were compared after 4 weeks of uphill or downhill running with a no-running control. SSN adapted to the training: soleus SSN was greater with downhill compared with uphill running, while EDL demonstrated a trend towards more SSN for downhill compared with no running. In contrast, rFE and rFD did not differ across training groups for either muscle. As such, it appears that training-induced SSN adaptations do not modify rFE or rFD at the whole-muscle level.

Fiber Type and Size as Sources of Variation in Human Single Muscle Fiber Passive Elasticity.

Studies on single muscle fiber passive material properties often report relatively large variation in elastic modulus (or normalized stiffness), and it is not clear where this variation arises. This study was designed to determine if the stiffness, normalized to both fiber cross-sectional area and length, is inherently different between types 1 and 2 muscle fibers. Vastus lateralis fibers (n = 93), from ten young men, were mechanically tested using a cumulative stretch-relaxation protocol. SDS-PAGE classified fibers as types 1 or 2. While there was a difference in normalized stiffness between fiber types (p = 0.0019), an unexpected inverse relationship was found between fiber diameter and normalized stiffness (r = -0.64; p < 0.001). As fiber type and diameter are not independent, a one-way analysis of covariance (ANCOVA) including fiber diameter as a covariate was run; this eliminated the effect of fiber type on normalized stiffness (p = 0.1935). To further explore the relationship between fiber size and elastic properties, we tested whether stiffness was linearly related to fiber cross-sectional area, as would be expected for a homogenous material. Passive stiffness was not linearly related to fiber area (p < 0.001), which can occur if single muscle fibers are better represented as composite materials. The rule of mixtures for composite materials was used to explore whether the presence of a stiff perimeter-based fiber component could explain the observed results. The model (R2 = 0.38) predicted a perimeter-based normalized stiffness of 8800 ± 2600 kPa/µm, which is within the range of basement membrane moduli reported in the literature.

The Effect of a Stretch-Shortening Cycle on Muscle Activation and Muscle Oxygen Consumption: A Study of History-Dependence.

Caron, KE, Burr, JF, and Power, GA.. The effect of a stretch-shortening cycle on muscle activation and muscle oxygen consumption: a study of history-dependence. J Strength Cond Res 34(11): 3139-3148, 2020-Stretch-shortening cycles (SSCs) are observed in a variety of human movements and are associated with increases in performance. Few studies have considered the effects of stretch-induced residual force enhancement (rFE) and shortening-induced residual force depression (rFD) during an SSC, and none have considered these properties during voluntary contractions. With force matched via a robotically resisted Smith machine, we hypothesized that in the isometric steady-state following an SSC (a) muscle activation (electromyography) of the knee and hip extensors would be greater and (b) muscle oxygen consumption be higher than the reference isometric condition (ISO), but less than the rFD condition. Subjects (n = 20, male, 24.9 ± 3.9 year) performed a squat exercise over 100-140° knee angle and a matched ISO at the top and bottom of the squat. After active shortening, the vastus medialis (VM), vastus lateralis (VL), and gluteus maximus (GM) showed activation increase in the rFD-state compared with ISO (∼15%, ∼11%, and ∼25% respectively). During the isometric steady-state following the SSC, there was no difference in activation as compared with ISO for VM, VL, but GM showed an activation increase of ∼15%. VM and VL showed an activation increase in the rFD-state compared with the isometric steady-state following SSC (∼16 and ∼10% respectively). Muscle oxygen consumption (tissue saturation index) was not different during the isometric steady-states following rFD and SSC compared with ISO. During a voluntary SSC exercise, the activation increase expected in the FD-state was attenuated, with no change in muscle oxygen consumption. The concomitant role of rFE and rFD during a voluntary position-matched SSC seems to counteract shortening-induced activation increase and may optimize movement economy.

Central contributions to torque depression: an antagonist perspective.

Torque depression (TD) is the reduction in steady-state isometric torque following active muscle shortening when compared to an isometric reference contraction at the same muscle length and activation level. Central nervous system excitability differs in the TD state. While torque production about a joint is influenced by both agonist and antagonist muscle activation, investigations of corticospinal excitability have focused on agonist muscle groups. Hence, it is unknown how the TD state affects spinal and supraspinal excitability of an antagonist muscle. Eight participants (~ 24y, three female) performed 14 submaximal dorsiflexion contractions at the intensity needed to maintain a level of integrated electromyographic activity in the soleus equivalent to 15% of that recorded during a maximum plantar flexion contraction. The seven contractions of the TD protocol included a 2 s isometric phase at an ankle angle of 140°, a 1 s shortening phase at 40°/s, and a 7 s isometric phase at an angle of 100°. The seven isometric reference contractions were performed at an ankle angle of 100° for 10 s. Motor evoked potentials (MEPs), cervicomedullary motor evoked potentials (CMEPs), and maximal M-waves (Mmax) were recorded from the soleus in both conditions. In the TD compared to isometric reference state, a 13% reduction in dorsiflexor torque was accompanied by 10% lower spinal excitability (normalized CMEP amplitude; CMEP/Mmax), and 17% greater supraspinal excitability (normalized MEP amplitude; MEP/CMEP) for the soleus muscle. These findings demonstrate a neuromechanical coupling following active muscle shortening and indicate that the underlying mechanisms of TD influence antagonist activation during voluntary force production.

The sag response in human muscle contraction.

PURPOSE: We examined how muscle length and time between stimuli (inter-pulse interval, IPI) influence declines in force (sag) seen during unfused tetani in the human adductor pollicis muscle. METHODS: A series of 16-pulse contractions were evoked with IPIs between 1 × and 5 × the twitch time to peak tension (TPT) at large (long muscle length) and small (short muscle length) thumb adduction angles. Unfused tetani were mathematically deconstructed into a series of overlapping twitch contractions to examine why sag exhibits length- and IPI-dependencies. RESULTS: Across all IPIs tested, sag was 62% greater at short than long muscle length, and sag increased as IPI was increased at both muscle lengths. Force attributable to the second stimulus increased as IPI was decreased. Twitch force declined from maximal values across all IPI tested, with the greatest reductions seen at short muscle length and long IPI. At IPI below 2 × TPT, the twitch with highest force occurred earlier than the peak force of the corresponding unfused tetani. Contraction-induced declines in twitch duration (TPT + half relaxation time) were only observed at IPI longer than 1.75 × TPT, and were unaffected by muscle length. CONCLUSIONS: Sag is an intrinsic feature of healthy human adductor pollicis muscle. The length-dependence of sag is related to greater diminution of twitch force at short relative to long muscle length. The dependence of sag on IPI is related to IPI-dependent changes in twitch duration and twitch force, and the timing of peak twitch force relative to the peak force of the associated unfused tetanus.

Mitigating the bilateral deficit: reducing neural deficits through residual force enhancement and activation reduction.

PURPOSE: The bilateral deficit (BLD) is characterized by a reduction in maximal voluntary torque during a bilateral contraction relative to the sum of left and right unilateral contractions. The BLD has been attributed to interhemispheric inhibition as a result of unilateral torque differences between limbs. If the BLD is the result of interhemispheric inhibition, lowering activation for a torque matching task, as shown in residual force enhancement (RFE), may help overcome the decrease in neural drive during bilateral contractions. Therefore, the purpose of the present study was to determine whether RFE could reduce the BLD. METHODS: Participants (n = 12) performed both isometric and RFE MVCs of the elbow flexors under three conditions: (1) unilateral-left; (2) unilateral-right; and (3) bilateral. To directly address the purpose of the study, a sub-group of participants that displayed both RFE and a BLD ("Responders", n = 6) were selected from the participant pool. RESULTS: "Responders" displayed RFE (7.1 ± 5.3%) and an isometric BLD (BI: - 9.9 ± 3.2%). In the RFE state, the BLD was no longer significant (- 5.8 ± 7.9%), accompanied by the elimination of differences in biceps brachii EMG between arms (left: - 11.7 ± 10.3%; right: - 11.5 ± 13.2%), as seen during isometric contractions (left: - 12.0 ± 23.2%; right: - 21.1 ± 16.6%). CONCLUSION: Residual force enhancement appears to mitigate the BLD, alleviating the effects of a decrease in neural drive by allowing more force for a given level of muscle activation when compared to a purely isometric contraction.

Reduction in single muscle fiber rate of force development with aging is not attenuated in world class older masters athletes.

Normal adult aging is associated with impaired muscle contractile function; however, to what extent cross-bridge kinetics are altered in aging muscle is not clear. We used a slacken restretch maneuver on single muscle fiber segments biopsied from the vastus lateralis of young adults (∼23 yr), older nonathlete (NA) adults (∼80 yr), and age-matched world class masters athletes (MA; ∼80 yr) to assess the rate of force redevelopment (ktr) and cross-bridge kinetics. A post hoc analysis was performed, and only the mechanical properties of "slow type" fibers based on unloaded shortening velocity (Vo) measurements are reported. The MA and NA were ∼54 and 43% weaker, respectively, for specific force compared with young. Similarly, when force was normalized to cross-sectional area determined via the fiber shape angularity data, both old groups did not differ, and the MA and NA were ∼43 and 48% weaker, respectively, compared with young (P < 0.05). Vo for both MA and NA old groups was 62 and 46% slower, respectively, compared with young. Both MA and NA adults had approximately two times slower values for ktr compared with young. The slower Vo in both old groups relative to young, coupled with a similarly reduced ktr, suggests impaired cross-bridge kinetics are responsible for impaired single fiber contractile properties with aging. These results challenge the widely accepted resilience of slow type fibers to cellular aging.