Carbohydrate Ingestion Increases Interstitial Glucose and Mitigates Neuromuscular Fatigue During Single-Leg Knee Extensions.

INTRODUCTION: We aimed to investigate the neuromuscular contributions to enhanced fatigue resistance with carbohydrate ingestion, and to identify whether fatigue is associated with changes in interstitial glucose levels assessed using a continuous glucose monitor (CGM). METHODS: Twelve healthy participants (6 males, 6 females) performed isokinetic single-leg knee extensions (90°/s) at 20% of the maximal voluntary contraction (MVC) torque until MVC torque reached 60% of its initial value (i.e, task failure). Central and peripheral fatigue were evaluated every 15 min during the fatigue task using the interpolated twitch technique (ITT), and electrically evoked torque. Using a single-blinded cross-over design, participants ingested carbohydrates (CHO) (85 g sucrose/h), or a placebo (PLA), at regular intervals during the fatigue task. Minute-by-minute interstitial glucose levels measured via CGM, and whole blood glucose readings were obtained intermittently during the fatiguing task. RESULTS: CHO ingestion increased time to task failure over PLA (113 ± 69 vs. 81 ± 49 min; mean ± SD; p < 0.001) and was associated with higher glycemia as measured by CGM (106 ± 18 vs 88 ± 10 mg/dL, p < 0.001) and whole blood glucose sampling (104 ± 17 vs 89 ± 10 mg/dL, p < 0.001). When assessing the values in the CHO condition at a similar timepoint to those at task failure in the PLA condition (i.e., ~81 min), MVC torque, % voluntary activation, and 10 Hz torque were all better preserved in the CHO vs. PLA condition (p < 0.05). CONCLUSIONS: Exogenous CHO intake mitigates neuromuscular fatigue at both the central and peripheral levels by raising glucose concentrations rather than by preventing hypoglycemia.

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.

Home-based resistance training performed at either fast or slow speeds improves power output in older adults.

PURPOSE: We investigated the effect of an unsupervised, body mass- home-based resistance training program in older adults performed at either a fast or slow contractile speed on changes to muscle-power, -volume, -architecture, and fatigue resistance of the knee extensors. METHODS: Thirty-two male older adults (age 65-88 years) were separated into 1) fast-speed exercise (Fast-group), 2) slow-speed exercise (Slow-group), and 3) no exercise (Control-group) groups. Participants in the exercise groups performed 30-45 repetitions of knee-extension and sit-to-stand exercises 3 times a week for 8 weeks with different exercise speed between the groups. Before and after the intervention period, the following variables were measured: Isotonic power, isometric strength, twitch contractile properties, muscle-activity, -architecture, and -quality, neuromuscular fatigue resistance of the knee extensors, and thigh muscle volume. RESULTS: Peak power was increased in both the Fast-group (+24 %, P < 0.01, d = 0.65) and Slow-group (+12 %, P < 0.05, d = 0.33) but not in the Control-group. Training increased pennation angle of the vastus lateralis in both the Fast-group (+8 %, P < 0.01, d = 0.42) and Slow-group (+8 %, P < 0.01, d = 0.42), while only the Fast-group showed increase in pennation angle of the rectus femoris (+12 %, P < 0.01, d = 0.64) and thigh muscle volume (+16 %, P < 0.01, d = 0.52). There was no time × group interaction effect for the other neuromuscular measures. CONCLUSIONS: Unsupervised, body mass- and home-based resistance training performed at either fast or slow speeds can improve muscle power in older adults, while fast-speed exercise may be preferable over slow-speed owing to the relatively greater improvement of muscle-power, -volume, -architecture, and better time efficiency.

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.

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.

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.

Effects of chemically induced ovarian failure on single muscle fiber contractility in a mouse model of menopause.

OBJECTIVE: Menopause is associated with impaired skeletal muscle contractile function. The temporal and mechanistic bases of this dysfunction are unknown. Using a mouse model of menopause, we identified how gradual ovarian failure affects single muscle fiber contractility. STUDY DESIGN: Ovarian failure was chemically induced over 120 days, representing the perimenopausal transition. Mice were sacrificed and soleus and extensor digitorum longus muscles were dissected and chemically permeabilized for single fiber mechanical testing. MAIN OUTCOME MEASURES: Muscle fiber contractility was assessed via force, rate of force redevelopment, instantaneous stiffness, and calcium sensitivity. RESULTS: Peak force and cross-sectional area of the soleus were, respectively, ~33 % and ~24 % greater following ovarian failure compared with controls (p < 0.05) with no differences in force produced by the extensor digitorum longus across groups (p > 0.05). Upon normalizing force to cross-sectional area there were no differences across groups (p > 0.05). Following ovarian failure, rate of force redevelopment of single fibers from the soleus was ~33 % faster compared with controls. There was no shift in the midpoint of the force­calcium curve between groups or muscles (p > 0.05). However, following ovarian failure, Type I fibers from the soleus had a higher calcium sensitivity between pCa values of 4.5 and 6.2 compared with controls (p < 0.05), with no differences for Type II fibers or the extensor digitorum longus (p > 0.05). CONCLUSIONS: In our model of menopause, alterations to muscle contractility were less evident than in ovariectomized models. This divergence across models highlights the importance of better approximating the natural trajectory of menopause during and after the transitional phase of ovarian failure on neuromuscular function.

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%.

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.

Blood Pressure Responses to Postexercise Circulatory Occlusion Are Attenuated After Exercise-Induced Muscle Weakness.

PURPOSE: Exercise blood pressure (BP) responses are thought to be determined by relative exercise intensity (percent maximal voluntary contraction (MVC) strength). However, cross-sectional studies report that during a static contraction, higher absolute force is associated with greater BP responses to relative intensity exercise and subsequent muscle metaboreflex activation with postexercise circulatory occlusion (PECO). We hypothesized that a bout of unaccustomed eccentric exercise would reduce knee extensor MVC and subsequently attenuate BP responses to PECO. METHODS: Continuous BP, heart rate, muscle oxygenation, and knee extensor electromyography were recorded in 21 young healthy individuals (female, n = 10) during 2 min of 20% MVC static knee extension exercise and 2 min of PECO, performed before and 24 h after 300 maximal knee extensor eccentric contractions to cause exercise-induced muscle weakness. As a control, 14 participants repeated the eccentric exercise 4 wks later to test whether BP responses were altered when exercise-induced muscle weakness was attenuated via the protective effects of the repeated bout effect. RESULTS: Eccentric exercise reduced MVC in all participants (144 ± 43 vs 110 ± 34 N·m, P < 0.0001). BP responses to matched relative intensity static exercise (lower absolute force) were unchanged after eccentric exercise ( P > 0.99) but were attenuated during PECO (systolic BP: 18 ± 10 vs 12 ± 9 mm Hg, P = 0.02). Exercise-induced muscle weakness modulated the deoxygenated hemoglobin response to static exercise (64% ± 22% vs 46% ± 22%, P = 0.04). When repeated after 4 wks, exercise-induced weakness after eccentric exercise was attenuated (-21.6% ± 14.3% vs -9.3 ± 9.7, P = 0.0002) and BP responses to PECO were not different from control values (all, P > 0.96). CONCLUSIONS: BP responses to muscle metaboreflex activation, but not exercise, are attenuated by exercise-induced muscle weakness, indicating a contribution of absolute exercise intensity on muscle metaboreflex activation.

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.

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.

Heating the Skin Over the Knee Improves Kinesthesia During Knee Extension.

To determine how heating affects dynamic joint position sense at the knee, participants (n = 11; F = 6) were seated in a HUMAC NORM dynamometer. The leg was passively moved through extension and flexion, and participants indicated when the 90° reference position was perceived, both at baseline (28.74 ± 2.43 °C) and heated (38.05 ± 0.16 °C) skin temperatures. Day 2 of testing reduced knee skin feedback with lidocaine. Directional error (actual leg angle-target angle) and absolute error (AE) were calculated. Heating reduced extension AE (baseline AE = 5.46 ± 2.39°, heat AE = 4.10 ± 1.97°), but not flexion. Lidocaine did not significantly affect flexion AE or extension AE. Overall, increased anterior knee-skin temperature improves dynamic joint position sense during passive knee extension, where baseline matching is poorer. Limited application of lidocaine to the anterior thigh, reducing some skin input, did not influence dynamic joint position sense, suggesting cutaneous receptors may play only a secondary role to spindle information during kinesthetic tasks. Importantly, cutaneous input from adjacent thigh regions cannot be ruled out as a contributor.

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.

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.

Age-related performance fatigability: a comprehensive review of dynamic tasks.

Adult aging is associated with a myriad of changes within the neuromuscular system, leading to reductions in contractile function of old adults. One of the consequences of these age-related neuromuscular adaptations is altered performance fatigability, which can limit the ability of old adults to perform activities of daily living. Whereas age-related fatigability during isometric tasks has been well characterized, considerably less is known about fatigability of old adults during dynamic tasks involving movement about a joint, which provides a more functionally relevant task compared with static contractions. This review provides a comprehensive summary of age-related fatigability during dynamic contractions, where the importance of task specificity is highlighted with a brief discussion of the potential mechanisms responsible for differences in fatigability between young and old adults. The angular velocity of the task is critical for evaluating age-related fatigability, as tasks that constrain angular velocity (i.e., isokinetic) produce equivocal age-related differences in fatigability, whereas tasks involving unconstrained velocity (i.e., isotonic-like) consistently induce greater fatigability for old compared with young adults. These unconstrained velocity tasks, which are more closely associated with natural movements, offer an excellent model to uncover the underlying age-related mechanisms of increased fatigability. Future work evaluating the mechanisms of increased age-related fatigability during dynamic tasks should be evaluated using contraction modes that are specific to the task (i.e., dynamic), rather than isometric, particularly for the assessment of spinal and supra spinal components. Advancing our understanding of age-related fatigability is likely to yield novel insights and approaches for improving mobility limitations in old adults.

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.