Artificial oxygen carrier improves fatigue resistance in slow muscle but not in fast muscle in a rat in situ model

The effects of liposome‐encapsulated hemoglobin with high O2 affinity (h‐LEH), an artificial O2 carrier in skeletal muscle, were studied by in situ fatigue resistance test in fast‐type plantaris (PLT) and slow‐type soleus (SOL) muscles with or without ischemia in the rat. The distal tendons of PLT and SOL muscles were isolated in situ and individually attached to the force transducers to record the developed tension in response to stimuli (80 Hz tetanus train, 1.5 minutes) to the ipsilateral sciatic nerve. The fatigue resistance test (five sets separated by 2‐minute rests) was evaluated in terms of tension attenuation (fatigue) from the initial to the last tension (A) during each set, attenuation of the initial (B) or last tension (C) in each set, as compared to the first set in the presence or absence of ischemia or h‐LEH (10 mL/kg). While ischemia significantly enhanced fatigue only in PLT, h‐LEH showed no effect regardless of the perfusion pattern (normal/ischemia) or muscle‐type (PLT/SOL) during each set (A). In parameter (B), set‐by‐set fatigue development was observed in PLT, whereas h‐LEH‐SOL showed a trend of advanced fatigue resistance. Such trends became clear in the parameter C (last tension), because h‐LEH‐SOL exerted, rather than decreased, the tension enhancement regardless of the presence or absence of ischemia, whereas there were no h‐LEH effects in PLT. In addition, faster recovery of the nicotinamide adenine dinucleotide content in the muscle after 10 minutes of all fatigue tests was observed in h‐LEH‐SOL, while saline‐SOL still showed a significantly higher value than that of control. These results suggested that additional O2 supply by h‐LEH may accelerate the tricarboxylic acid cycle/electron transport chain in slow‐type aerobic SOL muscle containing abundant mitochondria and contribute to the faster removal of muscle fatigue substances such as lactate.