Impact of long‐term high‐altitude residence on cardiopulmonary function in asymptomatic men: A cross‐sectional study

To evaluate altitude-stratified differences in static lung function, aerobic capacity, and exercise physiology under standardized normoxic conditions, and identify multiple predictors of peak oxygen uptake (VO₂) reduction among asymptomatic men after prolonged residence at varying altitudes. We conducted a cross-sectional study of 103 asymptomatic men stratified by residential altitude: low (<2500 m; n = 35), high (2500-3500 m; n = 32), and very high (>3500 m; n = 36). All underwent spirometry, fasting blood tests, and symptom-limited cardiopulmonary exercise testing (CPET) in normoxia. Multiple linear regression identified independent predictors of peak VO₂/kg. Very high-altitude residents had significantly lower peak VO₂/kg (-13.4 mL·min⁻¹·kg⁻¹ vs. low altitude, p < 0.001), reduced oxygen pulse, and impaired small-airway function (MMEF, FEF₇₅; p < 0.05), despite preserved ventilatory efficiency (VE/VCO₂ slope, p = 0.782). Hemoglobin was elevated at higher altitudes; triglycerides were higher only above 3500 m. Age (β = -0.285), regular exercise (≥3 sessions/week; β = +3.648), and very high-altitude residence (β = -13.370) independently predicted peak VO₂/kg (all p < 0.001; R² = 0.739). Residence above 3500 m causes persistent cardiopulmonary impairment driven by circulatory limitations and smoking, despite preserved ventilatory efficiency. Normoxic assessment identifies regular exercise (≥3 sessions/week) as a key countermeasure against altitude-induced deconditioning. Prioritizing smoking cessation and mandatory exercise programs is therefore recommended for long-term health in high-altitude personnel.