Electrically evoked force loss of the knee extensors is equivalent for young and old females and males

Data are scant on sex-related differences for electrically evoked contractions, which assess intrinsic contractile properties while limiting spinal and supraspinal adaptations to mitigate fatigue. Furthermore, the few studies that exist use stimulus frequencies considerably higher than the natural motor unit discharge rate for the target force. The purpose of this study was to compare force loss to electrically evoked contractions at a physiological stimulus frequency among young females (n = 12), young males (n = 12), old females (n = 11), and old males (n = 11). The quadriceps of the dominant leg were fatigued by 3 min of intermittent transcutaneous muscle belly stimulation (15 Hz stimulus train to initially evoke 25% of maximal voluntary force). Impairment of tetanic contractile impulse (area under the curve) did not differ between sexes for young or old adults or between age groups, with a pooled value of 55.2% ± 12.4% control at the end of fatigue. These data contrast with previous findings at 30 Hz, when the quadriceps of females had greater fatigue resistance than males for young and old adults. The present results highlight the impact stimulus frequency has on intrinsic fatigability of muscle; the findings have implications for future fatigue paradigms and treatment approaches when utilizing electrical stimulation for rehabilitation. Novelty Fatigue was not different between sexes with a stimulation frequency comparable to discharge rates during voluntary contractions. These results highlight that stimulus frequency not only influences fatigue development but also between-group differences.

The influence of preceding activity and muscle length on voluntary and electrically evoked contractions

Muscle length and preceding activity independently influence rate of torque development (RTD) and electromechanical delay (EMD), but it is unclear whether these parameters interact to optimize RTD and EMD. The purpose of this study was to determine the influence of muscle length and preceding activity on RTD and EMD during voluntary and electrically stimulated (e-stim) contractions. Participants (n = 17, males, 24 ± 3 years) performed isometric knee extensions on a dynamometer. Explosive maximal contractions were performed at 2 knee angles (35° and 100° referenced to a 0° straight leg) without preceding activity (unloaded, UNL) and with preceding activities of 20%, 40%, 60%, and 80% of maximal voluntary contraction (MVC) torque. Absolute and normalized voluntary RTD were slowed with preceding activities ≥40% MVC for long muscle lengths and all preceding activities for short muscle lengths compared with UNL (p < 0.001). Absolute and normalized e-stim RTD were slower with preceding activities ≥40% MVC compared with UNL (p < 0.001) for both muscle lengths. Normalized RTD was faster at short muscle lengths than at long muscle lengths (p < 0.001) for e-stim (∼50%) and voluntary (∼32%) UNL contractions, but this effect was not present for absolute RTD. Muscle length did not affect EMD (p > 0.05). EMD was shorter at 80% MVC compared with UNL (∼35%; p < 0.001) for both muscle lengths during voluntary but not e-stim contractions. While RTD is limited by preceding activity at both muscle lengths, long muscle lengths require greater preceding activity to limit RTD than short muscle lengths, which indicates long muscle lengths may offer a “protective effect” for RTD against preceding activity.

Neuromuscular manifestations of work-related myalgia in women specific to extensor carpi radialis brevis

This study assessed neuromuscular function in the extensor carpi radialis brevis (ECRB) of female workers diagnosed with work-related myalgia (WRM, n = 14, age 45.2 ± 1.9 years) and the ECRB of healthy controls (CON, n = 10, age 34.6 ± 2.5 years). Groups were compared on voluntary and electrically evoked functional responses at rest (Pre), immediately following a 5 min repetitive task (Post-0) performed at 60% maximal voluntary contraction (MVC), and after 5 min of recovery (Post-5). Despite near complete motor unit activation (MUA) (CON 98% ± 1% vs. WRM 99% ± 1%), at Pre, WRM produced 26% less (P < 0.05) MVC force than CON. Following an MVC, twitch force was increased (P < 0.05) by 94% ± 13% and 54% ± 11% in CON and WRM, respectively (CON vs. WRM; P < 0.05). The peak force and the maximal rates of force development and decline of electrically evoked contractions (10–100 Hz) were generally depressed (P < 0.05) at Post-0 and Post-5 relative to Pre. The response pattern to increasing frequencies of stimulation was not different (P > 0.05) between groups and MUA was not impaired (CON 97% ± 1% vs. WRM 97% ± 1%; P > 0.05). In conclusion, the peripheral weakness observed in the ECRB in WRM at rest does not result in abnormal fatigue or recovery responses after performing a task controlled for relative demand (60% MVC).

Accessibility of Targeted DHPR Sites to Streptavidin and Functional Effects of Binding on EC Coupling

In skeletal muscle, the dihydropyridine receptor (DHPR) in the plasma membrane (PM) serves as a Ca2+ channel and as the voltage sensor for excitation–contraction (EC coupling), triggering Ca2+ release via the type 1 ryanodine receptor (RyR1) in the sarcoplasmic reticulum (SR) membrane. In addition to being functionally linked, these two proteins are also structurally linked to one another, but the identity of these links remains unknown. As an approach to address this issue, we have expressed DHPR α1S or β1a subunits, with a biotin acceptor domain fused to targeted sites, in myotubes null for the corresponding, endogenous DHPR subunit. After saponin permeabilization, the ∼60-kD streptavidin molecule had access to the β1a N and C termini and to the α1S N terminus and proximal II–III loop (residues 671–686). Steptavidin also had access to these sites after injection into living myotubes. However, sites of the α1S C terminus were either inaccessible or conditionally accessible in saponin- permeabilized myotubes, suggesting that these C-terminal regions may exist in conformations that are occluded by other proteins in PM/SR junction (e.g., RyR1). The binding of injected streptavidin to the β1a N or C terminus, or to the α1S N terminus, had no effect on electrically evoked contractions. By contrast, binding of streptavidin to the proximal α1S II–III loop abolished such contractions, without affecting agonist-induced Ca2+ release via RyR1. Moreover, the block of EC coupling did not appear to result from global distortion of the DHPR and supports the hypothesis that conformational changes of the α1S II–III loop are necessary for EC coupling in skeletal muscle.