Cellular mechanisms underlying overreaching in skeletal muscle following excessive high-intensity interval training.

Abstract

Overreaching (OR) can be defined as a decline in physical performance resulting from excessive exercise training, necessitating days to weeks recovery. Impairments in the contractile function of skeletal muscle are believed to be a primary factor contributing to OR. However, the cellular mechanism triggering OR remains unclear. The purpose of this study was to elu idate the mechanisms underlying OR. Rats' plantar flexor muscles were subjected to repeated electrical stimulations mimicking excessive high-intensity interval training (HIIT) daily for 13 consecutive days, and isometric torques were monitored. The torque was measured one day after HIIT, and subsequently, the physiological function of type II fibers was analyzed by using mechanically-skinned-fiber technique. Eleven out of 17 rats exhibited torque decline, while others did not. Thus, the rats were divided into OR and non-overreaching (NOR) groups. Skinned fibers from the gastrocnemius (GAS) muscles of both groups showed decreased depolarization-induced force and increased myofibrillar Ca²⁺ sensitivity.However, the fibers from the OR group, but not the NOR group, exhibited a decrease in myofibrillar maximal force. Biochemical analyses of a superficial region of GAS muscle revealed that α-actinin 2 content was increased in the NOR group, but not the OR group, whereas calpain-3 autolysis was increased in the OR group, but not the NOR group. These findings shed light on the cellular mechanism underlying OR: OR following excessive HIIT was induced by a decreased myofibrillar maximal force, while Ca²⁺ sensitivity was increased.