Effects Of Muscle Atrophy Research Articles

The effect of muscle atrophy in people with unilateral transtibial amputation for three activities: Gait alone does not tell the whole story

Amputation imposes significant challenges in locomotion to millions of people with limb loss worldwide. The decline in the use of the residual limb results in muscle atrophy that affects musculoskeletal dynamics in daily activities. The aim of this study was to quantify the lower limb muscle volume discrepancy based on magnetic resonance (MR) imaging and to combine this with motion analysis and musculoskeletal modelling to quantify the effects in the dynamics of key activities of daily living. Eight male participants with traumatic unilateral transtibial amputation were recruited who were at least six months after receiving their definitive prostheses. The muscle volume discrepancies were found to be largest at the knee extensors (35 %, p = 0.008), followed by the hip abductors (17 %, p = 0.008). Daily activities (level walking, standing up from a chair and ascending one step) were measured in a motion analysis laboratory and muscle and joint forces quantified using a detailed musculoskeletal model for people with unilateral transtibial amputation which was calibrated in terms of the muscle volume discrepancies post-amputation at a subject-specific level. Knee extensor muscle forces were lower at the residual limb than the intact limb for all activities (p ≤ 0.008); residual limb muscle forces of the hip abductors (p ≤ 0.031) and adductors (p ≤ 0.031) were lower for standing-up and ascending one step. While the reduced knee extensor force has been reported by other studies, our results suggest a new biomechanically-based mitigation strategy to improve functional mobility, which could be achieved through strengthening of the hip abd/adductor muscles.

The Impact of Lower Extremity Skeletal Muscle Atrophy and Myosteatosis on Revascularization Outcomes in Patients with Peripheral Arterial Disease.

Background: This study investigated whether lower extremity muscle atrophy and myosteatosis in patients with peripheral arterial disease (PAD) are correlated to postoperative outcomes, such as reintervention or amputation-free survival. Methods: In this single-center retrospective cohort study of 462 patients treated for peripheral arterial disease scheduled for intervention, muscle mass and the presence of fattening of the lower extremity muscles were measured semiautomatically in a single computed tomography slice of the treated leg. Binary logistic regression models and Cox proportional hazards models were used to determine the effect of muscle atrophy and myosteatosis on reintervention and amputation. Results: Muscle atrophy and myosteatosis increased in PAD patients with Fontaine class IV compared with Fontaine class IIa. In PAD patients with muscle atrophy or myosteatosis, no association was found with the reintervention rate or reintervention-free survival, but an association was found with amputation-free survival, even after adjustment for patient-related, disease-severity, and comorbidities-related factors. Conclusion: Muscle atrophy and mysosteatosis increased in PAD patients with increasing disease severity. Lower extremity muscle atrophy and myosteatosis are associated with amputation rate and amputation-free survival in PAD patients. No association with reintervention rate or reintervention-free survival was found. Muscle atrophy and myosteatosis may serve as additional risk factors in decision making in the often frail vascular patient.

Effect of muscle atrophy and fatty infiltration on mid-term clinical, and functional outcomes after Achilles tendon repair

ObjectivesMuscle atrophy is one of the most common problems after Achilles tendon repair. The aim of this study was to evaluate the effect of gastrosoleus muscle atrophy and fatty infiltration on clinical, and functional outcomes after Achilles tendon repair. Material and methodsA total of 46 patients (mean age = 39.3 ± 7.4 years) who underwent open Achilles tendon repair were included in the study. During the clinical evaluation of muscle atrophy, ipsilateral and contralateral calf circumference (CC), maximum heel rise (HR), and ankle range of motion measurements were recorded. Functional outcomes were assessed via The Achilles tendon Total Rupture Score (ATRS), the American Orthopedic Foot and Ankle Society (AOFAS) ankle-hindfoot score, and the Leppilahti score. Muscle volume (MV), cross-sectional area (CSA), and percent of fatty infiltration (FI) were measured via magnetic image resonance. ResultsThe functional outcome scores were excellent: ATRS = 98.1 ± 2.2; AOFAS = 97.3 ± 4.1; Leppilahti score = 95.8 ± 5.1. There were significant differences detected between injured and non-injured legs regarding CC, HR, MV, CSA, and FI. Additionally, there were significant negative correlations between CSA and MV loss with all functional outcome scores. FI was correlated with only the AOFAS ankle-hindfoot score. ConclusionsSignificant muscle atrophy was measured after a mean follow-up period of 7.4 (range 2.0–12.6) years post-surgery and negatively correlated with clinical outcomes. CC is an easy and cost-effective measurement method to predict MV during the follow-up of Achilles tendon repairs.

The effect of high intensity interval training on some atrophic and anti-atrophic gene expression in rat skeletal muscle with diabetes

Summary Aims Muscle atrophy is one of the complications of people with diabetes. Exercise have reversing effect of muscle atrophy in various conditions, hence the aim of the study was to evaluate The effect of five weeks of high intensity interval training (HIIT) on the expression of Atrogin-1, miR-23a, miR-206 and myostatin in gastrocnemius muscles of diabetic rats. Methods For this purpose, diabetes was induced in 14 Wistar male rats with an average weight of 260 ± 10 g by injection of streptozotocin (50 mg/kg). They were randomly divided into two groups, controls (n = 7) and HIIT (n = 7). HIIT protocol included implementing four sets (3-minutes) at intensity of 85–90% VO2max and one minute recovery between each set with intensity of 30 to 35% VO2max. Twenty-four hours after the last training session, animals were anesthetized, gastrocnemius muscles were removed and Atrogin-1, miR-23a, miR-206 and myostatin genes expression was evaluated by quantitative REAL time PCR. Data were analyzed by Kolmogorov–Smirnov test and t-test (P Results In addition, the expression of myostatin and Atrogin-1 genes in the HIIT group was significantly lower than the control group (P ≤ 0.05). Conclusion It indicates that HIIT due to hyperglycemic healing can alter the expression of atrogin-1, miR-23a, miR-206 and myostatin genes, as an effective factors in reducing the complications of diabetes, including muscle atrophy.

Validity of mid-arm muscular area measured by anthropometry in nonobese patients with increased muscle atrophy and variation of subcutaneous fat thickness

The anthropometric measurement of mid-arm muscular area (MAMA) involves overestimation because of various assumptions, this overestimation being progressive with increasing adiposity. However, the effects of muscle atrophy and variation of the subcutaneous fat thickness have remained uncertain. The validity of MAMA estimated by anthropometry was examined by comparing with MAMA measured by computed tomography (CT) in a nonobese population. The effects of muscle atrophy and variation of the subcutaneous fat thickness on the validity of MAMA were examined by new indices. The relative MAMA was compared between the anthropometric and CT methods in 45 patients. New indices were introduced for assessing muscle deformity (muscle deformity index, MDI) and subcutaneous fat variation (SFVI). The effects of MDI, SFVI and age on the difference of MAMA between the anthropometric and CT methods were investigated. MDIs were positively correlated with age in males (r=0.47, P<0.05) and females (r=0.66, P<0.001). SFVI was positively correlated with age only in females (r=0.54, P<0.01). Even in these patients, the relative MAMA estimated by anthropometry was significantly associated with that measured by CT (r=0.85, P<0.0001 in males and r=0.90, P<0.0001 in females). A Bland-Altman plot indicated that the difference between both methods was relatively small, although increased adiposity might be a source of overestimation for anthropometric MAMA measurement. MAMA estimated by anthropometry was a reliable indicator of muscle mass in patients with muscle atrophy and varying thickness of subcutaneous fat in lean patients.

Exercise Training in Heart Failure: How?

Patients with congestive heart failure (CHF) reach a lower peak oxygen uptake (peak VO2) than that attained by ageand sex-matched healthy subjects [1,2]. In CHF patients, there has been no relationship observed between left ventricular ejection fraction (LVEF) and peak exercise performance [1,2]. Furthermore, peak VO2 is not related to the change in LVEF from rest to peak exercise. Also, acute improvements of central hemodynamics have not been found to acutely improve exercise performance, while longterm improvements do result in a signi~cant increase in peak VO2 [1,2]. These ~ndings suggest that the reduction in exercise capacity experienced by CHF patients may be more signi~cantly in_uenced by factors other than poor ventricular function. Patients with CHF have been found to have reduced maximum muscle strength compared to healthy individuals, greater fatigue at a given workload, and a lower peak VO2. Skeletal muscle atrophy has been observed and can occur early in the course of the disease [1,2]. Furthermore, signi~cant positive linear relationships have been found between peak VO2 and measures of skeletal muscle mass, suggesting that muscle atrophy contributes to effort intolerance. Muscle atrophy is not the only factor responsible for reduced performance since the results from a number of studies would suggest that the impairment of skeletal muscle blood _ow may also play at least a partial role. A number of potential mechanisms underlie the reduction in vasodilatory capacity, including a reduction in endothelium-derived relaxing factor, salt retention, and increases in various vasoconstrictive neurohormones such as endothelin, norepinephrine, renin, angiotensin II, and vasopressin [1,2]. Abnormalities in skeletal muscle metabolism have been observed in CHF patients that could impair exercise capacity. The abnormalities of metabolism are independent of the effects of muscle atrophy and reductions in blood _ow observed in these patients. Finally, abnormalities of skeletal muscle histology and biochemistry have been observed that could contribute to the impairment of exercise capacity found in CHF patients [1,2]. These ~ndings in the skeletal muscle have led to the development of the skeletal muscle hypothesis to explain exercise intolerance in CHF patients [3]. This theory suggests that left ventricular dysfunction sets in motion a series of events that leads to abnormalities of skeletal muscle metabolism, function, and atrophy. In response to these changes, the patient experiences both muscle fatigue and dyspnea, as well as excessive vasoconstrictor drive to nonexercising vascular beds. The theory suggests that after instituting treatment to correct hemodynamics, there will be a delay in the improvement of exercise capacity until there has been resolution of the skeletal muscle abnormalities. Exercise training would potentially speci~cally reverse the changes found in the skeletal muscles of CHF patients. Standardized guidelines for exercise training of CHF patients have not been established, although some recommendations have been made for this patient population [4]. These recommendations have been based on the results of previous studies or on experience from rehabilitation of coronary patients without CHF and have been modi~ed for the CHF population [1,4]. Furthermore, these recommendations have not taken into consideration the results of more recent studies outlining alternative strategies for exercise training of CHF patients. Any recommendations for exercise training should be based on the underlying pathophysiology found in CHF patients. Accordingly, the documented pathophysiology would support the use of an exercise training program designed to improve the aerobic and strength capacities of these patients. The purpose of this article is to review training techniques used in CHF patients and to provide direction as to the type of exercise training program that could be used by these individuals.