Frequency-dependent coexistence of muscle fatigue and potentiation assessed by concentric isotonic contractions in human plantar flexors

Abstract

The purpose was to investigate whether post-activation potentiation (PAP) mitigates power (i.e., torque x angular velocity) loss during dynamic fatiguing contractions and subsequent recovery by enhancing either muscle torque or angular velocity in human plantar flexors. In 12 participants, electrically stimulated (1, 10 and 50 Hz) dynamic contractions were done during a voluntary isotonic fatiguing protocol (20 and 50% voluntary decreases) until a 75% loss in voluntary peak power, and throughout 30 minutes of recovery. At the initial portion of fatigue (20% decrease), power responses of evoked low frequencies (1 and 10 Hz) were enhanced due to PAP (156 and 137%, respectively, P<0.001), while voluntary maximal efforts were depressed due to fatiguing mechanisms. Following the fatiguing task, prolonged low-frequency force depression (PLFFD) was evident by reduced 10:50 Hz peak power ratios (21 - 24%) from 3-min onwards during the 30-min recovery (P<0.005). Inducing PAP with maximal voluntary contractions during PLFFD enhanced the peak power responses of low frequencies (1 and 10 Hz) by 128 - 160 %, P<0.01. This PAP response mitigated the effects of PLFFD as the 1:50 (P<0.05) and 10:50 (P>0.4) Hz peak power ratios were greater or not different from the pre-fatigue values. Additionally, PAP enhanced peak torque more than peak angular velocity during both baseline and fatigue measurements (P<0.03). These results indicate that PAP can ameliorate PLFFD acutely when evaluated during concentric isotonic contractions and that peak torque is enhanced to a greater degree compared to peak angular velocity at baseline and in a fatigued state.

Acute and prolonged competing effects of activation history on human motor unit firing rates during contractile impairment and recovery

“…Importantly here, when PAP is induced during the PLFFD period, the effects of PLFFD are mitigated due to presumed competing Ca 2+ -dependent mechanisms. Our results support prior reports showing that PAP can mitigate the effects of PLFFD by preferential enhancement of torque in response to low frequency stimulation (Fuglevand et al, 1999;Green & Jones, 1989;Vandenboom & Houston, 1996;Zero, Paris, et al, 2022).…”

“…The primary mechanisms for PLFFD following prolonged high‐intensity isometric contractions are impaired Ca 2+ release, Ca 2+ sensitivity, or both (Allen et al., 2008; Cheng et al., 2018). However, inducing PAP with acute high‐intensity contractions, which enhances Ca 2+ sensitivity (Persechini et al., 1985; Sweeney et al., 1993; Vandenboom, 2017), has been shown to acutely compensate for torque (Fuglevand et al., 1999; Green & Jones, 1989; Vandenboom & Houston, 1996) and power (Zero, Paris, et al., 2022) deficits observed during PLFFD. These reports of PAP mitigating PLFFD have been assessed with electrically evoked contractions.…”

Electrically Evoked Isotonic Plantar Flexion Contractions Are Impaired Less than Voluntary After a Dynamic Fatiguing Task

“…However, reductions in power for the 40% load were more related to impaired velocity generating capacity rather than dynamic torque, whereas for the 20% load, power was affected equally by reductions in both dynamic torque and velocity. In support of this, using a similar fatiguing task in the plantar flexors but assessing velocity and dynamic torque with an “unloaded” (weight of dynamometer arm only) contraction, we previously reported that impairments in power were more due to velocity than dynamic torque (30). Thus, the contributions of dynamic torque and velocity for reductions in power generating capacity after the fatiguing task are load dependent but likely depend on various related factors, including the muscle group evaluated and the ROM used in the task (10).…”