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The steady-state isometric force following active muscle shortening or lengthening is smaller (force depression; FD) or greater (residual force enhancement; RFE) than a purely isometric contraction at the corresponding length. The mechanisms behind these phenomena remain not fully understood, with few studies investigating the effects of FD and RFE in stretch-shortening cycles (SSC). The purpose of this study was to investigate the influence of RFE and peak force at the end of the stretch phase on the steady-state isometric force following shortening. Isometric thumb adduction force measurements were preceded by an isometric, a shortening contraction to induce FD, and SSCs at different stretch speeds (15°/s, 60°/s, and 120°/s). The different peak force values at the end of stretch and the different amounts of work performed during shortening did not influence the steady-state isometric force at the end of the SSC. We conclude that the FD following SSC depends exclusively on the amount of RFE established in the initial stretch phase in situations where the timing and contractile conditions of the shortening phase are kept constant .

Background Osteoarthritis (OA) is a chronic and painful condition where the articular cartilage surfaces progressively degenerate, resulting in loss of function and progressive disability. Obesity is a primary risk factor for the development and progression of knee OA, defined as the “metabolic OA” phenotype. Metabolic OA is associated with increased fat deposits that release inflammatory cytokines/adipokines, thereby resulting in systemic inflammation which can contribute to cartilage degeneration. There is currently no cure for OA. Prebiotics are a type of dietary fiber that can positively influence gut microbiota thereby reducing systemic inflammation and offering protection of joint integrity in rodents. However, no human clinical trials have tested the effects of prebiotics in adults with obesity suffering from knee OA. Therefore, the purpose of this double-blind, placebo-controlled, randomized trial is to determine if prebiotic supplementation can, through positive changes in the gut microbiota, improve knee function and physical performance in adults with obesity and knee OA. Methods Adults ( n  = 60) with co-morbid obesity (BMI > 30 kg/m 2 ) and knee OA (Kellgren-Lawrence grade II–III) will be recruited from the Alberta Hip and Knee Clinic and the Rocky Mountain Health Clinic and surrounding community of Calgary, Canada, and randomized (stratified by sex, BMI, and age) to prebiotic (oligofructose-enriched inulin; 16 g/day) or a calorie-matched placebo (maltodextrin) for 6 months. Anthropometrics, performance-based tests, knee pain, serum inflammatory markers and metabolomics, quality of life, and gut microbiota will be assessed at baseline, 3 months, 6 months (end of prebiotic supplementation), and 3 months following the end of the prebiotic supplementation. Clinical significance There is growing pressure on health care systems for aggressive OA treatment such as total joint replacement. Less aggressive, yet effective, conservative treatment options have the potential to address the growing prevalence of co-morbid obesity and knee OA by delaying the need for joint replacement or ideally preventing its need altogether. The results of this clinical trial will provide the first evidence regarding the efficacy of prebiotic supplementation on knee joint function and pain in adults with obesity and knee OA. If successful, the results may provide a simple, safe, and easy to adhere to intervention to reduce knee joint pain and improve the quality of life of adults with co-morbid knee OA and obesity. Trial registration Clinical Trials.gov NCT04172688 . Registered on 21 November 2019.

Botulinum toxin type-A (BTX-A) injections have become a common treatment modality for patients suffering from muscle spasticity. Despite its benefits, BTX-A treatments have been associated with adverse effects on target muscles. Currently, application of BTX-A is largely based on clinical experience, and research quantifying muscle structure following BTX-A treatment has not been performed systematically. The purpose of this study was to evaluate strength, muscle mass, and contractile material six months following a single or repeated (2 and 3) BTX-A injections into the quadriceps femoris of New Zealand white rabbits. Twenty three skeletally mature rabbits were divided into four groups: experimental group rabbits received 1, 2, or 3 injections at intervals of 3 months (1-BTX-A, 2-BTX-A, 3-BTX-A, respectively) while control group rabbits received volume-matched saline injections. Knee extensor strength, quadriceps muscle mass, and quadriceps contractile material of the experimental group rabbits were expressed as a percentage change relative to the control group rabbits. One-way ANOVA was used to determine group differences in outcome measures (α=0.05). Muscle strength and contractile material were significantly reduced in experimental compared to control group rabbits but did not differ between experimental groups. Muscle mass was the same in experimental BTX-A and control group rabbits. We concluded from these results that muscle strength and contractile material do not fully recover within six months of BTX-A treatment.

The steady-state isometric force following active muscle shortening or lengthening is smaller (force depression; FD) or greater (residual force enhancement; RFE) than a purely isometric contraction at the corresponding length. The mechanisms underlying these phenomena are not explained within the context of the cross-bridge theory and are rarely studied in concert. Previous studies have shown RFE to be speed-independent. In the present study, we investigated if RFE preceded by active shortening is time-dependent by electrically evoking RFE in the human adductor pollicis muscle. The results shown that a slow stretch following FD fully re-established RFE compared to higher speeds of stretch. The mechanism(s) responsible for the recovery of RFE following a preceding shortening contraction (FD) might be associated with the recovery of cross-bridge based force and/or the re-engagement of a passive structural element (titin). Voluntary interaction with one’s environment involves highly coordinated shortening and lengthening muscle contractions. Therefore comprehending these history-dependent muscle properties in the context of movement control is paramount in understanding the behavior of in vivo motor control.

The steady‐state isometric force following active muscle shortening or lengthening is smaller (force depression, FD) or greater (residual force enhancement, RFE) than a purely isometric contraction at the corresponding length. The mechanism underlying these phenomena is not explained within the context of the cross‐bridge theory, with few studies investigating the effects of FD and RFE in stretching–shortening cycle (SSC). The purpose of this study was to perform SSC, where the time between the end of stretch and the end of shortening was manipulated by (1) adding a pause between stretch and shortening (protocol 1) or (2) performing the shortening contraction at different speeds (protocol 2). The results show that, in protocol 1, FD was reduced for SSC with a 0‐sec and 0.5‐sec interval between stretching and shortening, but was the same for SSC with a 1‐sec interval compared to the pure FD condition. In protocol 2, FD was reduced for SSC with shortening speeds of 30 and 60°/sec, but was the same for shortening speeds of 15 and 20°/sec compared to the pure FD condition. These findings provide evidence that stretch preceding shortening affects FD in a time‐ and speed‐dependent manner, providing new information on the potential mechanism of FD and RFE. The results show that force depression (FD) was reduced for stretching–shortening cycle (SSC) with a >0.5‐sec interval between stretching and shortening, but was the same for SSC with a 1‐sec interval compared to the pure FD condition. Additionally, FD was reduced for SSC at shortening speeds of 30 and 60°/sec, but was the same for shortening speeds of 15 and 20°/sec compared to pure FD condition. These findings provide evidence that stretch preceding shortening affects FD in a time‐ and speed‐dependent manner, providing new information on the potential mechanism of FD and residual force enhancement.

Studies on residual force enhancement (rFE) and residual force depression (rFD) of the muscle‐tendon unit (MTU) have typically been conducted independent of each other, with little information available on how stretch‐induced rFE affects the shortening phase and the steady‐state MTU isometric force at the end of stretch‐shortening cycles (SSCs). We showed previously that when rFE is kept constant, but the force at the end of the stretch is varied by changing the stretch speed, the steady‐state forces at the end of SSCs were the same. These results led to the hypothesis that the amount of rFE of the MTU established in the initial stretch phase of SSCs determines the steady‐state force following the shortening phase of SSCs. This study was aimed at testing this hypothesis. Steady‐state MTU isometric thumb adduction forces were measured for pure isometric contractions, following pure shortening contractions, following pure stretch contractions, and following SSCs with constant shortening speed and magnitude. However, two stretch magnitudes (30° and 10° thumb abduction) and stretch speeds (15°/sec and ~ 60°/sec, respectively) were chosen such that forces at the end of the stretch phase of the SSCs were the same, while rFE differed substantially. As hypothesized, the steady‐state isometric MTU forces following SSCs were positively related to the stretch‐magnitude dependent amount of rFE established in the stretch phase and were independent of the force reached at the end of the stretch phase in SSCs. Among many competing theories, these results can potentially be explained with the idea that there is a length‐specific engagement of a passive structural element at the initial length of muscle activation. Mean (±SD) values of force depression for FD30°, SSC10°‐60°/sec, and SSC30°–15°/sec (protocol 2) and residual force enhancement for the RFE10°–60°/sec and RFE30°–15°/sec (protocol 1) normalized to the isometric reference contraction. As hypothesized, the steady‐state isometric force following SSCs were positively related to the amount of RFE established in the stretch phase.

Purpose Obesity is a primary risk factor for knee osteoarthritis (OA). Prebiotics enhance beneficial gut microbes and can reduce body fat and inflammation. Our objective was to examine if a 6-month prebiotic intervention improved physical function in adults with knee osteoarthritis and obesity. We also measured knee pain, body composition, quality of life, gut microbiota, inflammatory markers, and serum metabolomics. Methods Adults (n = 54, mostly women) with co-morbid obesity (BMI > 30 kg/m 2 ) and unilateral/bilateral knee OA were randomly assigned to prebiotic (oligofructose-enriched inulin; 16 g/day; n = 31) or isocaloric placebo (maltodextrin; n = 21) for 6 months. Performance based-tests, knee pain, quality of life, serum metabolomics and inflammatory markers, and fecal microbiota and short-chain fatty acids were assessed. Results Significant between group differences were detected for the change in timed-up-and-go test, 40 m fast paced walk test, and hand grip strength test from baseline that favored prebiotic over placebo. Prebiotic also reduced trunk fat mass (kg) at 6 months and trunk fat (%) at 3 months compared to placebo. There was a trend (p = 0.059) for reduced knee pain at 6 months with prebiotic versus placebo. In gut microbiota analysis, a total of 37 amplicon sequence variants differed between groups. Bifidobacterium abundance was positively correlated with distance walked in the 6-min walk test and hand grip strength. At 6 months, there was a significant separation of serum metabolites between groups with upregulation of phenylalanine and tyrosine metabolism with prebiotic. Conclusion Prebiotics may hold promise for conservative management of knee osteoarthritis in adults with obesity and larger trials are warranted. Clinical Trial Registration Clinicaltrials.gov/study/NCT04172688.

Botulinum toxin type A (BTX-A) is a frequently used therapeutic tool to denervate muscles in the treatment of neuromuscular disorders. Although considered safe by the US Food and Drug Administration, BTX-A can produce adverse effects in target and non-target muscles. With an increased use of BTX-A for neuromuscular disorders, the effects of repeat injections of BTX-A on strength, muscle mass and structure need to be known. Therefore, the purpose of this study was to investigate the changes in strength, muscle mass and contractile material in New Zealand White (NZW) rabbits. Twenty NZW rabbits were divided into 4 groups: control and 1, 3 and 6 months of unilateral, repeat injections of BTX-A into the quadriceps femoris. Outcome measures included knee extensor torque, muscle mass and the percentage of contractile material in the quadriceps muscles of the target and non-injected contralateral hindlimbs. Strength in the injected muscles was reduced by 88%, 89% and 95% in the 1, 3 and 6 months BTX-A injected hindlimbs compared to controls. Muscle mass was reduced by 50%, 42% and 31% for the vastus lateralis (VL), rectus femoris (RF) and vastus medialis (VM), respectively, at 1 month, by 68%, 51% and 50% at 3 months and by 76%, 44% and 13% at 6 months. The percentage of contractile material was reduced for the 3 and 6 months animals to 80–64%, respectively, and was replaced primarily by fat. Similar, but less pronounced results were also observed for the quadriceps muscles of the contralateral hindlimbs, suggesting that repeat BTX-A injections cause muscle atrophy and loss of contractile tissue in target muscles and also in non-target muscles that are far removed from the injection site.

Onabotulinum toxin A (BTX-A) is a frequently used treatment modality to relax spastic muscles by preventing acetylcholine release at the motor nerve endings. Although considered safe, previous studies have shown that BTX-A injections cause muscle atrophy and deterioration in target and non-target muscles. Ideally, muscles should fully recover following BTX-A treatments, so that muscle strength and performance are not affected in the long-term. However, systematic, long-term data on the recovery of muscles exposed to BTX-A treatments are not available, thus practice guidelines on the frequency and duration of BTX-A injections, and associated recovery protocols, are based on clinical experience with little evidence-based information. Therefore, the purpose of this study was to investigate muscle recovery following a six months, monthly BTX-A injection (3.5U/kg) protocol. Twenty seven skeletally mature NZW rabbits were divided into 5 groups: Control (n=5), zero month recovery – BTX-A+0M (n=5), one month recovery – BTX-A+1M (n=5), three months recovery – BTX-A+3M (n=5), and six months recovery – BTX-A+6M (n=7). Knee extensor strength, muscle mass and percent contractile material in injected and contralateral non-injected muscles was measured at each point of recovery. Strength and muscle mass were partially and completely recovered in injected and contralateral non-injected muscles for BTX-A+6M group animals, respectively. The percent of contractile material partially recovered in the injected, but did not recover in the contralateral non-injected muscles. We conclude from these results that neither target nor non-target muscles fully recover within six months of a BTX-A treatment protocol and that clinical studies on muscle recovery should be pursued.

Purpose The menisci are thought to modulate load transfer and to absorb shocks in the knee joint. No study has experimentally measured the meniscal functions in the intact, in vivo joint loaded by physiologically relevant muscular contractions. Methods Right knee joints of seven New Zealand white rabbits were loaded using isometric contractions of the quadriceps femoris muscles controlled by femoral nerve stimulation. Isometric knee extensor torques at the maximal and two submaximal force levels were performed at knee angles of 70°, 90°, 110°, and 130°. Patellofemoral and tibiofemoral contact areas and pressure distributions were measured using Fuji Presensor film inserted above and below the menisci and also with the menisci removed. Results Meniscectomy was associated with a decrease in tibiofemoral contact area ranging from 30 to 70 % and a corresponding increase in average contact pressures. Contact areas measured below the menisci were consistently larger than those measured on top of the menisci. Contact areas in the patellofemoral joint (PFJ), and peak pressures in tibiofemoral and PFJs, were not affected by meniscectomy. Contact areas and peak pressures in all joints depended crucially on knee joint angle and quadriceps force: The more flexed the knee joint was, the larger were the contact areas and the higher were the peak pressures. Conclusions In agreement with the literature, removal of the menisci was associated with significant decreases in tibiofemoral contact area and corresponding increases in average contact pressures, but surprisingly, peak pressures remained unaffected, indicating that the function of the menisci is to distribute loads across a greater contact area.