Effects of intensified training with insufficient recovery on joint level and single muscle fibre mechanical function: The role of myofibrillar Ca2+sensitivity

Abstract

AbstractIntense exercise training with insufficient recovery is associated with reductions in neuromuscular performance. However, it is unclear how single muscle fibre mechanical function and myofibrillar Ca2+sensitivity contribute to these impairments. We investigated the effects of overload training on joint-level neuromuscular performance and cellular-level mechanical function. Fourteen athletes (4 female, 10 male) underwent a 3-week intensified training protocol consisting of ∼140% of their regular training hours with three additional high-intensity training sessions per week. Neuromuscular performance of the knee extensors was assessed via maximum voluntary contraction (MVC) force, electrically evoked twitch contractions, and a force-frequency relationship. Muscle biopsies were taken from thevastus lateralisto assess single fibre mechanical function. Neither MVC force nor twitch parameters were altered following intensified training (allp>0.05), but a rightward shift in the force-frequency curve was observed with a 6-27% reduction in force at low-frequencies (5-20Hz, allp<0.05). In single fibres, maximal force output was not reduced following intensified training, but there was a rightward shift in the force-pCa curve driven by a 6% reduction in Ca2+sensitivity as indicated by a lower pCa50value (i.e., higher [Ca2+]) across fibre types (Pre=6.477±0.157, Post=6.088±0.480,p<0.05). These data indicate intensified training leads to impaired Ca2+sensitivity at the single fibre level, which in part explains impaired neuromuscular function at the joint level during lower frequencies of activation. This is an important consideration for athletes, as performance is often assessed at maximal levels of activation, and these underlying impairments in force generation may be less obvious.New & NoteworthyIntense exercise training with insufficient recovery leads to impaired muscle contractile performance. These impairments often manifest at lower frequencies of muscle stimulation, termed prolonged low-frequency force depression. Impaired myofibrillar calcium sensitivity has been suggested as a potential mechanism of prolonged low-frequency force depression. Our work shows that impaired calcium sensitivity of single muscle fibres coincided with joint level prolonged low-frequency force depression after intense exercise training with insufficient recovery.