Aim. To verify salivary biochemical parameters (pH, NO2–/NOS, –SH groups, protein carbonyls – aldehyde and ketone phenylhydrazones (APH, KPH)) and heart rate variability (HRV) indices (SDNN, SI, LF/HF, TP, PARS) according to etiopathogenetic LPR phenotypes in young adult men.

Materials and methods. A single-center, cross-sectional, comparative observational study was conducted focusing on salivary biochemical parameters (pH, NOx/NOS, –SH groups, protein carbonyls) and HRV indices as tools for phenotype-oriented stratification. Two groups of young men were formed: the main LPR group (MG; n = 91) and a conditionally healthy control group without LPR signs (CG; n = 64). Examinations were performed between July 2024 and June 2025.

Results. In the MG, sympathetic predominance (28.6 %) and vagotonia / parasympathetic predominance (24.2 %) prevailed, whereas 13.2 % exhibited a breakdown of autonomic regulation – an indicator of depleted reserves – unlike the CG. No statistically significant differences between autonomic subtypes (by HRV) were found within the CG, whereas the MG showed significant inter-subgroup differences in salivary biochemical parameters; subsequent analyses were performed within subgroups (SG1–SG5).

Compared with controls, LPR patients demonstrated significantly higher salivary pH, –SH groups, NOS activity, NO2–, total protein, and protein carbonyls. Salivary pH varied by autonomic regulation type: SG1 remained close to control; SG2 showed acidification; SG3–SG4 exhibited an alkaline shift, maximal in SG4. The greatest increases in NOS activity and NO2– were observed in SG3–SG4, indicating hyperactivation of NO-dependent processes. These subgroups also showed maximal –SH groups and protein carbonyls, reflecting enhancement of thiol-dependent antioxidant defense and oxidative protein modification. SG2 displayed signs of adaptive strain – low pH with moderate increases in NOS and APH/KPH. SG5 tended toward reduced NOx and –SH, interpreted as depletion of antioxidant potential and transition of nitrosative stress to a destructive phase. The observed changes support saliva’s role as an indicator of oxidative – antioxidant balance and the barrier function of the upper airways.

Conclusions. Patients with LPR exhibit elevated salivary pH, NOS activity, NO2–, –SH, APH/KPH, and total protein, indicating nitrosative stress with strained antioxidant mechanisms. The magnitude of changes depends substantially on the autonomic regulation type: the most pronounced shifts occur in parasympathetic and humoral-metabolic phenotypes, which show maximal increases in NOS activity, NO2–, protein carbonyls, and salivary pH, whereas regulation breakdown features decreases in NO-related and antioxidant markers, reflecting enzymatic exhaustion and a transition from compensatory to destructive nitrosative stress. LPR patients thus display distinct biochemical phenotypes determined by autonomic profile, which should be considered for proper interpretation of results and for forecasting the adaptive reserves of the antioxidant system.