Hyperbaric oxygen therapy at 1.3 ATA for 60 minutes significantly improved EEG and sEMG fatigue markers, and reduced lactate and perceived exertion compared to natural recovery (P<0.05).
RCT (n=34)
randomly assigned
Does hyperbaric oxygen therapy improve recovery from acute exercise-induced fatigue in college students?
Hyperbaric oxygen therapy at 1.3 ATA for 60 minutes accelerates recovery from central and peripheral fatigue induced by blood flow restriction exercise.
p-value: p=<0.05
Objective To evaluate the effect of hyperbaric oxygen therapy (HBOT) on acute exercise-induced fatigue via electroencephalogram (EEG) signal and surface electromyography (sEMG) signal, with the aim of providing a theoretical basis and methodological reference for promoting fatigue recovery. We hypothesized that HBOT for 60 min and natural recovery would reverse the changes in the indicators related to blood flow restriction (BFR) intervention, with HBOT demonstrating a superior restorative effect. Methods College students ( n = 34) majoring in physical education were randomly assigned to an experimental group ( n = 17) or control group ( n = 17). Fatigue was induced using four sets of weight-bearing squats (30 + 15 + 15 + 15 repetitions) combined with BFR intervention set to 80% of the arterial occlusion pressure (AOP) + 20% of the one repetition maximum (1RM) of the lower limbs. The control group naturally recovered for 60 min at ambient room temperature with 1.0 absolute atmospheres (ATA) and 20.9% oxygen concentration. The experimental group received 1.3 ATA hyperbaric oxygen therapy (HBOT) for 60 min. EEG signal, sEMG signal, heart rate, blood oxygen saturation, blood lactate accumulation (LA), and the Borg Subjective Fatigue Perception Assessment Scale (RPE) were assessed before exercise, immediately after exercise, and post-intervention. Results LA, RPE, alpha and theta waves in the central area and occipital lobe; alpha waves in the parietal lobe; and average values of RMS, MF, and MPF of the musculus femoris medialis, musculus rectus femoris, and external sural muscle had time-group interaction effects. After intervention, the experimental group exhibited significantly higher α wave amplitudes (central, occipital, and parietal lobes) and MF and MPF values (vastus medialis, rectus femoris, and lateral gastrocnemius), compared with the control group ( P < 0.05). By contrast, the experimental group demonstrated significantly lower β wave amplitudes in the central and occipital lobes, lower RMS values in the vastus medialis, rectus femoris, and lateral gastrocnemius muscles, and reduced LA levels and RPE scores, compared with the control group ( P < 0.05). Conclusion EEG and sEMG signal measurements indicate that BFR intervention induces central and peripheral fatigue simultaneously. After fatigue, 1.3 ATA-HBOT accelerates recovery from both types of fatigue within 60 min. Thus, this recovery method can be used as an effective strategy to accelerate recovery from BFR intervention-induced fatigue.
Fu et al. (Fri,) conducted a rct in Acute exercise-induced fatigue (n=34). Hyperbaric oxygen therapy (HBOT) vs. Natural recovery (1.0 ATA, 20.9% oxygen concentration) was evaluated on EEG signal, sEMG signal, heart rate, blood oxygen saturation, blood lactate accumulation (LA), and Borg Subjective Fatigue Perception Assessment Scale (RPE) (p=<0.05). Hyperbaric oxygen therapy at 1.3 ATA for 60 minutes significantly improved EEG and sEMG fatigue markers, and reduced lactate and perceived exertion compared to natural recovery (P<0.05).
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