BACKGROUND: Physical exercise is a well-established strategy to control blood pressure. Nonetheless, its effects on protein homeostasis in individuals with hypertension are not clearly defined. AIMS: Evaluate proteostasis, quality of life, and inflammation, oxidative stress, and vasoactive biomarkers in adults with hypertension regarding reported exercise habits. METHODS: Twenty individuals were recruited in a health-care centre, 10 regular exercisers (age: 68.3 ± 4.2 years) and 10 age-matched individuals without regular exercise participation (age: 67.7 ± 5.1 years). Proteostasis and the levels of ubiquitin, heat shock protein 70 (Hsp70), endothelial nitric oxide synthase (eNOS), matrix metalloproteinases 2 (MMP-2), tissue inhibitor of MMP-2 (TIMP-2), connexin 43 (Cx43) and extracellular superoxide dismutase-3 (SOD-3) were assessed in plasma using immunoblotting techniques (western blot or slot blot) and Fourier-transform infrared spectroscopy (FTIR). Quality of life was assessed using the Short Form 36 (SF-36) version 2.0 questionnaire. RESULTS: Significant higher levels of interleukin (IL)-6 (P = 0.014), eNOS (P = 0.011), Cx43 (P = 0.020), TIMP-2 (P = 0.038), and SOD-3 (P = 0.001), with a fold increase of 1.5, 1.2, 2.1, 1.3, and 1.2, respectively, were found in the exercise group. The overall quality of life (60.1 ± 4.3 vs. 53.2 ± 5.9, P = 0.009), as well as mental health domain (59.4 ± 7.9 vs. 50.7 ± 7.2, P = 0.024) were significantly higher in the exercise group. Multivariate analysis by FTIR showed that the age-matched group is characterized by peaks related with antiparallel β-sheet, whereas exercise group is characterized by peaks related to random coils, β-sheet, and α-helix. CONCLUSIONS: Individuals with regular exercise participation showed better proteostasis, quality of life, inflammatory profile, antioxidant defenses, and eNOS levels.

Endothelial dysfunction has been suggested as a potential mechanism contributing to the development and progression of heart failure (HF). Levels of circulating endothelial cells (CECs), endothelial progenitor cells (EPCs), and hematopoietic stem and progenitor cells (HSPCs) have been recognized as useful markers of vascular damage and endothelial repair in response to tissue injury. To evaluate the circulating levels of EPCs, CECs, and HSPCs among patients with HF with reduced ejection fraction (HFrEF). In 82 individuals (42 patients with HFrEF and 42 age-matched subjects without established cardiovascular disease), peripheral blood was drawn and levels of EPCs, CECs, and HSPCs were quantified by flow cytometry. Patients with HFrEF showed lower levels of circulating EPCs (5.28 × 10^-3 ± 6.83 × 10^-4% vs. 7.76 × 10^-3 ± 4.91 × 10^-4%, p ≤0.001) and CECs (5.11 × 10^-3 ± 7.87 × 10^-4% vs. 6.51 × 10^-3 ± 5.21 × 10^-4%, p = 0.005) when compared to the age-matched group. Circulating levels of HSPCs were not significantly different between groups (p = 0.590). Additionally, the number of EPCs and CECs was significantly higher in HFrEF patients with overweight/obesity (n = 24) compared to patients with normal weight (n = 17). Circulating levels of EPCs and CECs were significantly decreased in patients with HFrEF in comparison to age-matched subjects without established cardiovascular disease, suggesting that the levels of CECs and EPCs may be potential biomarkers of the cellular response to vascular injury in patients with HFrEF.

Hypertension is the most determinant risk factor for cardiovascular diseases. Early intervention and future therapies targeting hypertension mechanisms may improve the quality of life and clinical outcomes. Hypertension has a complex multifactorial aetiology and was recently associated with protein homeostasis (proteostasis). This work aimed to characterize proteostasis in easy-to-access plasma samples from 40 individuals, 20 with controlled hypertension and 20 age- and gender-matched normotensive individuals. Proteostasis was evaluated by quantifying the levels of protein aggregates through different techniques, including fluorescent probes, slot blot immunoassays and Fourier-transform infrared spectroscopy (FTIR). No significant between-group differences were observed in the absolute levels of various protein aggregates (Proteostat or Thioflavin T-stained aggregates; prefibrillar oligomers and fibrils) or total levels of proteostasis-related proteins (Ubiquitin and Clusterin). However, significant positive associations between Endothelin 1 and protein aggregation or proteostasis biomarkers (such as fibrils and ubiquitin) were only observed in the hypertension group. The same is true for the association between the proteins involved in quality control and protein aggregates. These results suggest that proteostasis mechanisms are actively engaged in hypertension as a coping mechanism to counteract its pathological effects in proteome stability, even when individuals are chronically medicated and presenting controlled blood pressure levels.

It is widely accepted that exercise training has beneficial effects on vascular health. Although a dose-dependent relation has been suggested, little is known about the effects of different exercise durations on endothelial markers. This study aimed to assess the effect of single exercise sessions with different durations in the circulating levels of endothelial progenitor cells (EPCs) and endothelial cells (CECs) among adults with cardiovascular risk factors. Ten participants performed two multicomponent exercise sessions, one week apart, lasting 30 and 45 min (main exercise phase). Before and after each exercise session, blood samples were collected to quantify EPCs and CECs by flow cytometry. The change in EPCs was significantly different between sessions by 3.0% (95% CI: 1.3 to 4.7), being increased by 1.8 ± 1.7% (p = 0.009) in the 30 min session vs. −1.2 ± 2.0% (p > 0.05) in the 45 min session. No significant change was observed in CECs [−2.0%, 95%CI: (−4.1 to 0.2)] between the sessions. In conclusion, a multicomponent exercise session of 30 min promotes an acute increase in the circulating levels of EPCs without increasing endothelial damage (measured by the levels of CECs) among adults with cardiovascular risk factors.