LAUSR

Objective: A decline in protein homeostasis is associated with the development and progression of several cardiovascular diseases, including hypertension. Physical exercise is a promising intervention to counter defects in protein quality control. Isometric resistance training (IRT) promotes clinically relevant reductions in blood pressure (BP), however, its effects on protein homeostasis are not clearly defined. We determined the general proteomic profile in human plasma of older adults with high normal BP to hypertension and how it changes in response to IRT. Design and method: Older adults (n = 11, age: 73 ± 3 years) with high normal BP to hypertension participated in 8-weeks of IRT. IRT consisted of 4x45 sec contractions, alternatively with both hands, at an intensity of 50% of the maximum voluntary contraction, with a 1-min interval between sets, performed 3 times per week. Fourier-transform infrared (FTIR) spectroscopy assessed changes in the plasma after versus before IRT in the region of the spectra attributed to the secondary structure of proteins (1700–1600 cm-1). Results: Samples showed an excellent discrepancy before versus after IRT in the 1700–1600 cm-1 region. IRT induced a shift in the peak in the in the spectra region of 1622 cm-1; this region is attributed to intermolecular beta-sheets, which are common structures found in mature fibrils. Mature fibrils are prone to form toxic protein aggregates, especially amyloid aggregates. After IRT, participants appeared to have lower levels of intermolecular beta-sheets and samples were enriched with antiparallel beta-sheets (1696 cm-1) and beta-turns (1665 cm-1). Conclusions: The decrease in intermolecular beta-sheets may represent an improvement in the protein turnover and a better protein quality control in hypertension as a result of IRT. The differences in the antiparallel beta-sheets and beta-turns after IRT indicate IRT is modifying the protein profile. Further studies are needed to confirm these results and to address how exercise is influencing protein homeostasis.