The aim of this study was to analyze changes in oxidative stress and muscle damage markers during a 36-h survival training combined with sleep deprivation. The study included 23 male students of physical education (specialty: Physical Education for Uniformed Services), randomly divided into the survival or control group. The students in the survival group completed a 36-h survival training with moderate to low physical activity, without the possibility to sleep. The students in the control group performed only physical activity included in daily routines and had a normal sleep pattern. No significant changes in measured parameters were seen in the control group throughout the study period. In the survival group, plasma lipid hydroperoxides (LHs) and creatine kinase (CK) activity increased at 24 h and remained elevated up to 36 h (main effects for LHs: time, p
= 0.006 and group × time, p
= 0.00008; main effects for CK: time, p
= 0.000001, group, p
= 0.005, and group × time, p
= 0.000001). A 12-h recovery was sufficient to normalize both LHs and CK to the pre-training level; in fact, the post-recovery LHs and CK levels were even lower than at baseline. Residual total antioxidant capacity (TAC) of plasma (without the major constituents: uric acid and albumin) was elevated at both 24 h and 36 h of survival training, but not following a 12-h recovery (main effects: group, p
= 0.001 and group × time, p
= 0.04). In turn, the activity of glutathione peroxidase (GPx) in whole blood and superoxide dismutase (SOD) in erythrocytes decreased between 24 h and 36 h of survival training (main group effect for GPx, p
= 0.038 and SOD, p
= 0.045). In conclusion, these findings imply that a 36-h survival training with sleep deprivation impairs enzymatic antioxidant defense, increases lipid peroxidation, and induces muscle damage. Our findings also indicate that at least in the case of young physically active men, a 12-h recovery after the 36-h period of physical activity with sleep deprivation may be sufficient for the normalization of oxidative and muscle damage markers and restoration of blood prooxidant-antioxidant homeostasis.
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