Does Longer Leukocyte Telomere Length and Higher Physical Fitness Protect Master Athletes From Consequences of Coronavirus (SARS-CoV-2) Infection?

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ACE2 a double-edged sword?

Angiotensin-converting enzyme 2 (ACE2) is the binding protein/receptor used by the new SARS-CoV-2, which causes 2019 coronavirus disease (COVID-19), to enter host cells [1,2]. In 2003, Li and colleagues [3] at the Harvard Medical School, USA had previously described that a protein (spike proteins - S1 domain) da família do coronavirus binds efficiently to ACE2 [3,4]. From binding to ACE2, the virus envelope fuses into the host cell membrane allowing its genetic material entering the cell and replicate, triggering severe respiratory disease, including acute respiratory distress syndrome (ARDS), a devastating lung disease with high mortality rates (3060%).Sociedad Argentina de Fisiologí

The ACE2/Angiotensin-(1-7)/MAS axis of the renin-angiotensin system : focus on Angiotensin-(1-7).

The renin-angiotensin system (RAS) is a key player in the control of the cardiovascular system and hydroelectrolyte balance, with an influence on organs and functions throughout the body. The classical view of this system saw it as a sequence of many enzymatic steps that culminate in the production of a single biologically active metabolite, the octapeptide angiotensin (ANG) II, by the angiotensin converting enzyme (ACE). The past two decades have revealed new functions for some of the intermediate products, beyond their roles as substrates along the classical route. They may be processed in alternative ways by enzymes such as the ACE homolog ACE2. One effect is to establish a second axis through ACE2/ANG-(1?7)/MAS, whose end point is the metabolite ANG- (1?7). ACE2 and other enzymes can form ANG-(1?7) directly or indirectly from either the decapeptide ANG I or from ANG II. In many cases, this second axis appears to counteract or modulate the effects of the classical axis. ANG-(1?7) itself acts on the receptor MAS to influence a range of mechanisms in the heart, kidney, brain, and other tissues. This review highlights the current knowledge about the roles of ANG-(1?7) in physiology and disease, with particular emphasis on the brain

Master athletes have longer telomeres than age-matched non-athletes. A systematic review, meta-analysis and discussion of possible mechanisms.

The aim of this systematic review and meta-analysis was 1) to assess whether master athletes have longer telomeres than age-matched non-athletes and 2) discuss possible underlying mechanisms underlying telomere length preservation in master athletes. A literature search was performed in PubMed, Web of Science, Scopus and SPORTDiscus up to August 2020. Only original articles published in peer-reviewed journals that compared telomere length between master athletes and aged-matched non-athletes were included. Eleven studies fulfilled eligibility criteria and were included in the final analysis. Overall, 240 master athletes (51.9±7.5 years) and 209 age-matched non-athletes (50.1±9.1 years) were analyzed. Master athletes had been participating in high-level competitions for approximately 16.6 years. Pooled analyses revealed that master athletes had longer telomeres than aged-matched non-athletes (SMD=0.89; 95% CI=0.45 to 1.33; p<0.001). Master athletes showed lower pro-oxidant damage (SMD=0.59; 95% CI=0.26 to 0.91; p<0.001) and higher antioxidant capacity (SMD=-0.46; 95% CI=-0.89 to -0.03; p=0.04) than age-matched non-athletes. Further, greater telomere length in master athletes is associated with lower oxidative stress and chronic inflammation, and enhanced shelterin protein expression and telomerase activity. In conclusion, 1) master athletes have longer telomeres than age-matched non-athletes, which may be the result of 2) lower levels of oxidative stress and chronic inflammation, and elevated shelterin expression and telomerase activity

Lifetime overproduction of circulating angiotensin?(1?7) in rats attenuates the increase in skeletal muscle damage biomarkers after exhaustive exercise.

Angiotensin?(1?7) (Ang?[1?7]) can modulate glucose metabolism and protect against muscular damage. The aim of this study was to investigate the influence of lifetime increase of circulating levels of Ang?(1?7) at exhaustive swimming exercise (ESE). Sprague?Dawley (SD) and transgenic rats TGR(A1?7)3292 (TR) which overproduce Ang?(1?7) (2.5?fold increase) were submitted to ESE. The data showed no differences in time to exhaustion (SD: 4.90 ? 1.37 h vs. TR: 5.15 ? 1.15 h), creatine kinase, and transforming growth factor beta (TGF-?). Lactate dehydrogenase (SD: 219.9 ? 12.04 U/L vs. TR: 143.9 ? 35.21 U/L) and ??actinin (SD: 336.7 ? 104.5 U/L vs. TR: 224.6 ? 82.45 U/L) values were significantly lower in TR. There was a significant decrease in the range of blood glucose levels (SD: ?41.4 ? 28.32 mg/dl vs. TR: ?13.08 ? 39.63 mg/dl) in SD rats. Muscle (SD: 0.06 ? 0.02 mg/g vs. TR: 0.13 ? 0.01 mg/g) and hepatic glycogen (SD: 0.66 ? 0.36 mg/g vs. TG: 2.24 ? 1.85 mg/g) in TR were higher. The TR presented attenuation of the increase in skeletal muscle damage biomarkers and of the changes in glucose metabolism after ESE

Eccentric overload muscle damage is attenuated by a novel angiotensin- (1-7) treatment.

The development of new strategies to attenuate exercise-induced muscle damage may be helpful for training regimens. The aim of this study was to determine whether a oral formulation of angiotensin Ang-(1-7)[HP?CD/Ang-(1-7)] is effective to reduce pain, and muscle damage markers after eccentric-overload exercise. HP?CD (Placebo) and HP?CD/Ang-(1-7) (Ang-(1-7) group were treated for 7 days (one capsule/day). The pain was measured by visual analogue scale, maximal strength (MS) using force platform. Blood samples were collected for cytokines and creatine kinase (CK) analysis. The Ang-(1-7)-treated group reported less pain immediately (3.46? 0.64 vs. placebo 3.80? 0.77 cm) and 24h after exercise (3.07?0.71 vs. 3.73?0.58cm placebo) and higher MS at 24h (24?12N) and 48h (30?15N) vs. placebo (-8 ? 9 N and -10 ? 9 N). The CK for Ang-(1-7) (0.5 ? 0.1 and 0.9?0.2 U/L) were lower at 48 and 72h vs. placebo (fold changes of 1.7?0.5 and 1.5?0.3 U/L). The TNF-? level was lower in the treated group post-exercise (38 ? 2.5 pg/ml) vs. placebo (45 ? 2.9 pg/ml) but no significant changes were observed for IL-6 and IL-10. Our data indicate that treatment with Ang-(1-7) may attenuate pain, some of the muscle damage markers and improves performance following eccentric exercise

High-intensity aerobic training lowers blood pressure and modulates the renal renin-angiotensin system in spontaneously hypertensive rats

Background: This study aimed to verify the effects of high-intensity aerobic training (HIAT) on BP control and renin-angiotensin system (RAS) components in renal tissue of SHR. Ten SHRs received HIAT or control for 8-weeks. At the end of the training, the SBP showed a reduction of ~ 30mmHg (p < .01) in HIAT and increased by ~ 15 mmHg in the  control group. HIAT resulted in a higher release of nitrite, IL-6, ACE2 and ATR2. These results indicated an association between BP, NO and renal RAS. Abbreviations: JAA: writing, carried out all experimental procedures, performed statistical analysis, original draft and revised manuscript DMS: data interpretation, formal analysis, writing, editing and revised manuscript BAP: carried all experimental procedures, revised manuscritpt CPCG: carried all experimental procedures, revised manuscritpt MEN: experimental procedures, revised manuscript and data interpretation RWP: drafted and revised manuscript RCA: writing, experimental procedures, revised manuscript JP: writing, data interpretation and revised manuscript OLF: writing, original draft and revised manuscript