No abstract

Creatine (Cr), one of the most popular nutritional supplements among athletes, has been recently shown to prevent the cytotoxicity caused by different oxidative stressors in various mammalian cell lines, including C2C12 myoblasts, via a direct antioxidant activity. Here, the effect of Cr on the differentiating capacity of C2C12 cells exposed to H(2)O(2) has been investigated. Differentiation into myotubes was monitored using morphological, ultrastructural, and molecular techniques. Treatment with H(2)O(2) (1 h) not only caused a significant (30%) loss of cell viability, but also abrogated the myogenic ability of surviving C2C12. Cr-supplementation (24 h prior to H(2)O(2) treatment) was found to prevent these effects. Interestingly, H(2)O(2)-challenged cells preconditioned with the established antioxidants trolox or N-acetyl-cysteine, although cytoprotected, did not display the same differentiating ability characterizing oxidatively-injured, Cr-supplemented cells. Besides acting as an antioxidant, Cr increased the level of muscle regulatory factors and IGF1 (an effect partly refractory to oxidative stress), the cellular availability of phosphocreatine and seemed to exert some mitochondrially-targeted protective activity. It is concluded that Cr preserves the myogenic ability of oxidatively injured C2C12 via a pleiotropic mechanism involving not only its antioxidant capacity, but also the contribution to cell energy charge and effects at the transcriptional level which common bona fide antioxidants lack.

Infection with the SARS-CoV-2 virus causes cardiopulmonary and vascular complications, ranging in severity. Understanding the pathogenic mechanisms of the novel SARS-CoV2 infection and progression can provide potential novel targets for its prevention and/or treatment. Virus microbiota reciprocal interactions have been studied in a variety of viral infections. For example, the integrity of Coronavirus particles can be disrupted by surfactin, a bacterial surface molecule that targets other viruses, including that of influenza A. In this light, intestinal microbiota likely influences COVID-19 virulence, while from its side SARS-CoV-2 may affect the intestinal microbiome promoting dysbiosis and other deleterious consequences. Hence, the microbiota pre-existing health status and its alterations in the course of SARS-CoV-2 infection, are likely to play an important, still underscored role in determining individual susceptibility and resilience to COVID-19. Indeed, the vast majority of COVID-19 worst clinical conditions and fatalities develop in subjects with specific risk factors such as aging and the presence of one or more comorbidities, which are intriguingly characterized also by unhealthy microbiome status. Moreover, these comorbidities require complex pharmacological regimens known as “polypharmacy” that may further affect microbiota integrity and worsen the resilience to viral infections. This complex situation may represent a further and underestimated risk with regard to COVID-19 clinical burden for the elderly and comorbid people. Here, we discuss the possible biological, physiopathological, and clinical implications of gut microbiota in COVID-19 and the strategies to improve/maintain its healthy status as a simple and adjunctive strategy to reduce COVID-19 virulence and socio-sanitary burden.

Social isolation has adverse effects on mental health, physical exercise, and dietary habits. This longitudinal observational study aimed to investigate the effects of mood states and exercise on nutritional choices, on 176 college students (92 males, 84 females; 23 ± 4 years old) during the COVID-19 lockdown. During 21 days, nutrition and exercise were daily monitored, and the mood states assessed. A factor analysis was used to reduce the number of nutritional variables collected. The relationships between exercise, mood and nutrition were investigated using a multivariate general linear model and a mediation model. Seven factors were found, reflecting different nutritional choices. Exercise was positively associated with fruit, vegetables and fish consumption (p = 0.004). Depression and quality of life were, directly and inversely, associated with cereals, legumes (p = 0.005; p = 0.004) and low-fat meat intake (p = 0.040; p = 0.004). Exercise mediated the effect of mood states on fruit, vegetables and fish consumption, respectively, accounting for 4.2% and 1.8% of the total variance. Poorer mood states possibly led to unhealthy dietary habits, which can themselves be linked to negative mood levels. Exercise led to healthier nutritional choices, and mediating the effects of mood states, it might represent a key measure in uncommon situations, such as home-confinement.

Menopause is an age-dependent physiological condition associated with a natural decline in oestrogen levels, which causes a progressive decrease of muscle mass and strength and bone density. Sarcopenia and osteoporosis often coexist in elderly people, with a prevalence of the latter in elderly women. The profound interaction between muscle and bone induces a negative resonance between the two tissues affected by these disorders worsening the quality of life in the postmenopausal period. It has been estimated that at least 1 in 3 women over age 50 will experience osteoporotic fractures, often requiring hospitalisation and long-term care, causing a large financial burden to health insurance systems. Hormonal replacement therapy is effective in osteoporosis prevention, but concerns have been raised with regard to its safety. On the whole, the increase in life expectancy for postmenopausal women along with the need to improve their quality of life makes it necessary to develop specific and safe therapeutic strategies, alternative to hormonal replacement therapy, targeting both sarcopenia and osteoporosis progression. This review will examine the rationale and the effects of dietary protein, vitamin D and calcium supplementation combined with a specifically-designed exercise training prescription as a strategy to counteract these postmenopausal-associated disorders.