Longitudinal observations of sympathetic neural activity and hemodynamics during 6 months recovery from SARS-CoV-2 infection.

Cross-sectional data indicate that acute SARS-CoV-2 infection increases resting muscle sympathetic nerve activity (MSNA) and alters hemodynamic responses to orthostasis in young adults. However, the longitudinal impact of contracting SARS-CoV-2 on autonomic function remains unclear. The aim of this study was to longitudinally track MSNA, sympathetic transduction to blood pressure (BP), and hemodynamics over 6 months following SARS-CoV-2 infection. Young adults positive with SARS-CoV-2 reported to the laboratory three times over 6 months (V1:41 ± 17, V2:108 ± 21, V3:173 ± 16 days post-infection). MSNA, systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were measured at rest, during a cold pressor test (CPT), and at 30° head-up tilt (HUT). Basal SBP (p = 0.019) and DBP (p < 0.001) decreased throughout the 6 months, whereas basal MSNA and HR were not different. Basal sympathetic transduction to BP and estimates of baroreflex sensitivity did not change over time. SBP and DBP were lower during CPT (SBP: p = 0.016, DBP: p = 0.007) and HUT at V3 compared with V1 (SBP: p = 0.041, DBP: p = 0.017), with largely no changes in MSNA. There was a trend toward a visit-by-time interaction for burst incidence (p = 0.055) during HUT, wherein at baseline immediately prior to tilting, burst incidence was lower at V3 compared with V1 (p = 0.014), but there were no differences between visits in the 30 HUT position. These results support impairments to cardiovascular health, and potentially autonomic function, which may improve over time. However, the improvements in BP over 6 months recovery from mild SARS-CoV-2 infection are likely not a direct result of changes in sympathetic activity.

Muscle fatigability and post-acute COVID-19 syndrome: A case study.

The acute phase of COVID-19 has been well studied, however with increasing post-acute COVID-19 syndrome, much is unknown about its long-term effects. A common symptom in both the acute and post-acute phases has been fatigue, assessed predominantly qualitatively. Here we present a case study objectively assessing neuromuscular fatiguability in a young male (27 year, 1.85 m, 78 kg) who continues to experience COVID-19 related fatigue and cognitive dysfunction, including other symptoms, 12+ months post-infection. Prior to infection, he was part of a neuromuscular study forming the basis of our pre-COVID-19 results. The study was repeated 12 months post-COVID-19 infection. Muscle strength, endurance, torque steadiness, voluntary activation, twitch properties, electromyography, and compound muscle action potential were obtained and compared pre- and post-COVID-19. All measurements were done using a dorsiflexion dynamometer in which the participant also was asked to produce a one-minute fatiguing maximal voluntary contraction. Muscle strength, voluntary activation, and fatigability (slope of torque) showed no meaningful differences, suggesting intrinsic neuromuscular properties are not affected. However, torque steadiness was impaired three-fold in the post- compared with pre-COVID-19 test. The participant also reported a higher level of perceived exertion subjectively and a continued complaint of fatigue. These findings indicate that muscle fatiguability in post-acute COVID-19 syndrome may not be a limitation of the muscle and its activation, but a perceptual disconnect caused by cognitive impairments relating to physical efforts. This case report suggests the potential value of larger studies designed to assess these features in post-acute COVID-19 syndrome.

Advances in muscle health and nutrition: A toolkit for healthcare professionals.

Low muscle mass and malnutrition are prevalent conditions among adults of all ages, with any body weight or body mass index, and with acute or chronic conditions, including COVID-19. This article synthesizes the latest research advancements in muscle health and malnutrition, and their impact on immune function, and clinical outcomes. We provide a toolkit of illustrations and scientific information that healthcare professionals can use for knowledge translation, educating patients about the importance of identifying and treating low muscle mass and malnutrition. We focus on the emerging evidence of mitochondrial dysfunction in the context of aging and disease, as well as the cross-talk between skeletal muscle and the immune system. We address the importance of myosteatosis as a component of muscle composition, and discuss direct, indirect and surrogate assessments of muscle mass including ultrasound, computerized tomography, deuterated creatine dilution, and calf circumference. Assessments of muscle function are also included (handgrip strength, and physical performance tests). Finally, we address nutrition interventions to support anabolism, reduce catabolism, and improve patient outcomes. These include protein and amino acids, branched-chain amino acids, with a focus on leucine; ß-hydroxy-ß-methylbutyrate (HMB), vitamin D; n-3 polyunsaturated fatty acids (n-3 PUFA), polyphenols, and oral nutritional supplements. We concluded with recommendations for clinical practice and a call for action on research focusing on evaluating the impact of body composition assessments on targeted nutrition interventions, and consequently their ability to improve patient outcomes.

Prevention of Loss of Muscle Mass and Function in Older Adults during COVID-19 Lockdown: Potential Role of Dietary Essential Amino Acids.

As the COVID-19 pandemic became a global emergency, social distancing, quarantine, and limitations in outdoor activities have resulted in an environment of enforced physical inactivity (EPI). A prolonged period of EPI in older individuals accelerates the deterioration of skeletal muscle health, including loss of muscle mass and function, commonly referred to as sarcopenia. Sarcopenia is associated with an increased likelihood of the progression of diabetes, obesity, and/or depression. Well-known approaches to mitigate the symptoms of sarcopenia include participation in resistance exercise training and/or intake of balanced essential amino acids (EAAs) and high-quality (i.e., containing high EEAs) protein. As the pandemic situation discourages physical exercise, nutritional approaches, especially dietary EAA intake, could be a good alternative for counteracting against EPI-promoted loss of muscle mass and function. Therefore, in the present review, we cover (1) the impact of EPI-induced muscle loss and function on health, (2) the therapeutic potential of dietary EAAs for muscle health (e.g., muscle mass and function) in the EPI condition in comparison with protein sources, and finally (3) practical guidelines of dietary EAA intake for optimal anabolic response in EPI.

The correlation between skeletal muscle index of the L3 vertebral body and malnutrition in patients with advanced lung cancer.

BACKGROUND: Studies have shown that the skeletal muscle index at the third lumbar vertebra (L3 SMI) had reasonable specificity and sensitivity in nutritional assessment and prognostic prediction in digestive system cancers, but its performance in lung cancer needs further investigation. METHODS: A retrospective study was performed on 110 patients with advanced lung cancer. The L3 SMI, the Patient-Generated Subjective Global Assessment score (PG-SGA score), body mass index (BMI), and serological indicators were analyzed. According to PG-SGA scores, patients were divided into severe malnutrition (≥9 points), mild to moderate malnutrition (≥3 points and ≤ 8 points), and no malnutrition (≤2 points) groups. Pearson correlation and logistic regression analysis were adopted to find factors related to malnutrition, and a forest plot was drawn. The receiver operating characteristic (ROC) curve was performed to compare the diagnostic values of malnutrition among factors, which were expressed by the area under curve (AUC). RESULTS: 1. The age of patients in the severe malnutrition group, the mild to moderate malnutrition group, and the no malnutrition group significantly differed, with mean ages of 63.46 ± 10.01 years, 60.42 ± 8.76 years, and 55.03 ± 10.40 years, respectively (OR = 1.062, 95%CI: 1.008 ~ 1.118, P = 0.024; OR = 1.100, 95%CI: 1.034 ~ 1.170, P = 0.002). Furthermore, the neutrophil to lymphocyte ratio (NLR) of the severe malnutrition group was significantly higher than that of the no malnutrition group, with statistical significance. The difference between the mild to moderate malnutrition group and the no malnutrition group were not statistically significant, with NLR of 4.07 ± 3.34 and 2.47 ± 0.92, respectively (OR = 1.657,95%CI: 1.036 ~ 2.649, P = 0.035). The L3 SMI of patients in the severe malnutrition and mild to moderate malnutrition groups were significantly lower than that of the patients in the no malnutrition group, with statistical significance. The L3 SMI of patients in the severe malnutrition group, mild to moderate malnutrition group, and no malnutrition group were 27.40 ± 4.25 cm2/m2, 38.19 ± 6.17 cm2/m2, and 47.96 ± 5.02 cm2/m2, respectively (OR = 0.600, 95%CI: 0.462 ~ 0.777, P < 0.001; OR = 0.431, 95%CI: 0.320 ~ 0.581, P < 0.001). 2. The Pearson correlation analysis showed that the PG-SGA score positively correlated with age (r = 0.296, P < 0.05) but negatively correlated with L3 SMI (r = - 0.857, P < 0.05). The L3 SMI was also negatively correlated with age (r = - 0.240, P < 0.05). 3. The multivariate analysis showed that the L3 SMI was an independent risk factor for malnutrition (OR = 0.446, 95%CI: 0.258 ~ 0.773, P = 0.004; OR = 0.289, 95%CI: 0.159 ~ 0.524, P < 0.001). CONCLUSION: 1. The differences in the L3 SMI was statistically significant among advanced lung cancer patients with different nutritional statuses. 2. In the nutritional assessment of patients with lung cancer, the L3 SMI was consistent with the PG-SGA. 3. The L3 SMI is an independent predictor of malnutrition in patients with advanced lung cancer.

Molecular Mechanisms of Muscle Fatigue.

Muscle fatigue (MF) declines the capacity of muscles to complete a task over time at a constant load. MF is usually short-lasting, reversible, and is experienced as a feeling of tiredness or lack of energy. The leading causes of short-lasting fatigue are related to overtraining, undertraining/deconditioning, or physical injury. Conversely, MF can be persistent and more serious when associated with pathological states or following chronic exposure to certain medication or toxic composites. In conjunction with chronic fatigue, the muscle feels floppy, and the force generated by muscles is always low, causing the individual to feel frail constantly. The leading cause underpinning the development of chronic fatigue is related to muscle wasting mediated by aging, immobilization, insulin resistance (through high-fat dietary intake or pharmacologically mediated Peroxisome Proliferator-Activated Receptor (PPAR) agonism), diseases associated with systemic inflammation (arthritis, sepsis, infections, trauma, cardiovascular and respiratory disorders (heart failure, chronic obstructive pulmonary disease (COPD))), chronic kidney failure, muscle dystrophies, muscle myopathies, multiple sclerosis, and, more recently, coronavirus disease 2019 (COVID-19). The primary outcome of displaying chronic muscle fatigue is a poor quality of life. This type of fatigue represents a significant daily challenge for those affected and for the national health authorities through the financial burden attached to patient support. Although the origin of chronic fatigue is multifactorial, the MF in illness conditions is intrinsically linked to the occurrence of muscle loss. The sequence of events leading to chronic fatigue can be schematically denoted as: trigger (genetic or pathological) -> molecular outcome within the muscle cell -> muscle wasting -> loss of muscle function -> occurrence of chronic muscle fatigue. The present review will only highlight and discuss current knowledge on the molecular mechanisms that contribute to the upregulation of muscle wasting, thereby helping us understand how we could prevent or treat this debilitating condition.

Impact of Lockdown during COVID-19 Pandemic on Central Activation, Muscle Activity, Contractile Function, and Spasticity in People with Multiple Sclerosis.

BACKGROUND: People with multiple sclerosis (MS) suffer from symptoms related to neural control, such as reduced central activation, lower muscle activity, and accentuated spasticity. A forced 9-week home confinement related to COVID-19 in Spain may have worsened these symptoms. However, no study has demonstrated the impact of home confinement on neuromuscular mechanisms in the MS population. This study was aimed at analyzing the effects of a 9-week home confinement on central activation, muscle activity, contractile function, and spasticity in MS patients. METHODS: Eighteen participants were enrolled in the study. Left and right knee extensor maximum voluntary isometric contraction (MVIC), maximal neural drive via peak surface electromyography (EMG) of the vastus lateralis, central activation ratio (CAR), and muscle contractile function via electrical stimulation of the knee extensor muscles, as well as spasticity using the pendulum test, were measured immediately before and after home confinement. RESULTS: Seventeen participants completed the study. CAR significantly decreased after lockdown (ES = 1.271, p < 0.001). Regarding spasticity, there was a trend to decrease in the number of oscillations (ES = 0.511, p = 0.059) and a significant decrease in the duration of oscillations (ES = 0.568, p = 0.038). Furthermore, in the left leg, there was a significant decrease in the first swing excursion (ES = 0.612, p = 0.027) and in the relaxation index (ES = 0.992, p = 0.001). Muscle contractile properties, MVIC, and EMG variables were not modified after confinement. CONCLUSIONS: The results suggest that a home confinement period of 9 weeks may lead to an increase in lower limb spasticity and a greater deficit in voluntary activation of the knee extensors.

Prognostic Implication of Baseline Sarcopenia for Length of Hospital Stay and Survival in Patients With Coronavirus Disease 2019.

BACKGROUND: The impact of sarcopenia on clinical outcomes of coronavirus disease 2019 (COVID-19) is not clearly determined yet. We aimed to investigate the association between baseline sarcopenia and clinical outcomes in patients with COVID-19. METHODS: All hospitalized adult patients with COVID-19 who had baseline chest computed tomography (CT) scans at a Korean university hospital from February 2020 to May 2020 were included. The main outcome was time from hospital admission to discharge. Death was considered as a competing risk for discharge. Baseline skeletal muscle cross-sectional area at the level of the 12th thoracic vertebra was measured from chest CT scans. The lowest quartile of skeletal muscle index (skeletal muscle cross-sectional area divided by height-squared) was defined as sarcopenia. RESULTS: Of 121 patients (median age, 62 years; 44 men; 29 sarcopenic), 7 patients died and 86 patients were discharged during the 60-day follow-up. Patients with sarcopenia showed a longer time to discharge (median, 55 vs 28 days; p < .001) and a higher incidence of death (17.2% vs 2.2%; p = .004) than those without sarcopenia. Baseline sarcopenia was an independent predictor of delayed hospital discharge (adjusted hazard ratio [aHR], 0.47; 95% confidence interval [95% CI], 0.23-0.96), but was not independently associated with mortality in patients with COVID-19 (aHR, 3.80; 95% CI, 0.48-30.26). The association between baseline sarcopenia and delayed hospital discharge was consistent in subgroups stratified by age, sex, comorbidities, and severity of COVID-19. CONCLUSIONS: Baseline sarcopenia was independently associated with a prolonged hospital stay in patients with COVID-19. Sarcopenia could be a prognostic marker in COVID-19.

COVID-19 pandemic is an urgent time for older people to practice resistance exercise at home.

Social distancing measures have been used to contain the COVID-19 pandemic; nevertheless, it causes unintended greater time at home and consequently a reduction in general physical activity and an increase in sedentary time, which is harmful to older people. A decrease in daily physical activities and an increase in sedentary time culminates in an impactful skeletal muscle disuse period and reduction in neuromuscular abilities related to functional capacity. Home-based resistance training is a strategy to mitigate physical inactivity and improve or retain muscle function and functional performance. Therefore, it is an urgent time to encourage older people to perform resistance exercises at home to avoid a harmful functional decline and promote physical health.