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

Abstract

Intense 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 the vastus lateralis to assess single fibre mechanical function. Neither MVC force nor twitch parameters were altered following intensified training (all p>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, all p<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 pCa50 value (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.

The addition of blood flow restriction during resistance exercise does not increase prolonged low‐frequency force depression

“…Investigating the acute neuromuscular adaptations, performance fatigue and PLFFD recovery within hours to days after BFR exercise versus traditional exercise can inform optimal training and rehabilitation strategies, including recovery period optimization. PLFFD may occur due to reduced calcium release from the sarcoplasmic reticulum or myofibrillar calcium sensitivity and is influenced by the exercise mode, recovery period, species and training status (Allen et al., 2008 ; Bruton et al., 2008 ; Olsson et al., 2020 ; Place et al., 2015 ; Roussel et al., 2023 ; Skurvydas et al., 2016 ; Watanabe & Wada, 2016 ). Reactive oxygen species (ROS) production has been implicated in the development of PLFFD (Andrade et al., 2001 ; Bruton et al., 2008 ; Gandra et al., 2018 ) and a reduction in muscle glycogen may be involved in some (Cheng et al., 2017 ; Duhamel et al., 2006 ; Gejl et al., 2014 ; Nielsen et al., 2014 ), but not all (Cheng et al., 2020 ), scenarios.…”

“…Investigating the acute neuromuscular adaptations, performance fatigue and PLFFD recovery within hours to days after BFR exercise versus traditional exercise can inform optimal training and rehabilitation strategies, including recovery period optimization. PLFFD may occur due to reduced calcium release from the sarcoplasmic reticulum or myofibrillar calcium sensitivity and is influenced by the exercise mode, recovery period, species and training status (Allen et al, 2008;Bruton et al, 2008;Olsson et al, 2020;Place et al, 2015;Roussel et al, 2023;Skurvydas et al, 2016;Watanabe & Wada, 2016). Reactive oxygen species (ROS) production…”