Assessment of fatigue-related biochemical alterations in a rat swimming model under hypoxia

It is well known that exercise-induced fatigue is exacerbated following hypoxia exposure and may arise from central and/or peripheral mechanisms. To assess the relative contribution of peripheral and central factors to exercise-induced fatigue under hypoxia, a rat model of fatigue by a bout of exhaustive swimming was established and fatigue-related biochemical changes in normoxic and severe hypoxic conditions were compared. Rats were randomly divided into four groups, normoxia resting (NR), exhaustive swimming (NE), hypoxia resting (HR) and exhaustive swimming (HE) groups. The swimming time to exhaustion with a weight equal to 2.5% of their body weight reduced under hypoxia (HE 37±9 min vs. NE 91±16 min, p<0.05). There were lower blood lactate levels (HE 10.9±2.1 mmol/L vs. NE 14.1±1.4 mmol/L, p<0.05), lower gastrocnemius pAMPK/AMPK ratios (HE 0.9±0.2 vs. NE 1.3±0.3, p<0.05) and higher gastrocnemius glycogen contents (HE 1.6±0.4 mg/g tissue vs. NE 1.1±0.3 mg/g tissue, p<0.05) in HE than in NE, which all suggested a lower degree of peripheral fatigue in HE group than in NE group. Meanwhile, there was a significant increase in striatal DOPAC caused by exhaustive swimming under normoxia, while this increase was almost blunted under severe hypoxia, indicating that hypoxia might exacerbate exercise-induced central fatigue. These biochemical changes suggest that from normoxia to severe hypoxia, the relative contribution of peripheral and central factors to exercise-induced fatigue alters, and central fatigue may play a predominant role in the decline in exercise performance under hypoxia.