Knee and Hip Isometric Force Steadiness Are Impaired in Women With Patellofemoral Pain.

ABSTRACT: Ferreira, AS, de Oliveira Silva, D, Ferrari, D, Magalhães, FH, Pappas, E, Briani, RV, Pazzinatto, MF, and de Azevedo, FM. Knee and hip isometric force steadiness are impaired in women with patellofemoral pain. J Strength Cond Res 35(10): 2878-2885, 2021-The purposes were as follows: to compare knee extension and hip abduction force steadiness and maximal strength between women with patellofemoral pain (PFP) and pain-free women; and to investigate whether maximal strength, self-reported pain during force-matching tasks, self-reported knee function, symptoms duration, and physical activity level are associated with knee extension and hip abduction force steadiness. Thirty women with PFP and 30 pain-free women were recruited. Knee extension and hip abduction maximal voluntary isometric contractions and submaximal isometric force-matching tasks were evaluated using an isokinetic dynamometer. Subjects were asked to match a target force corresponding to 10% of their maximal isometric voluntary contraction while force steadiness was computed as the coefficient of variation (CV) of the exerted force. Women with PFP had significant 36% lower knee extension and 33% lower hip abduction peak strength. They also had significant 70% lower knee extension force steadiness and 60% lower hip abduction force steadiness (i.e., higher CV) than pain-free women. Self-reported pain and self-reported knee function were significantly associated (r = 0.61, p < 0.001; r = -0.35, p = 0.05) and able to predict 41% of the variance of knee extensor force steadiness. Hip abductor maximum strength was significantly associated (r = -0.57; p = 0.001) and able to predict 32% of the variance of hip abductor force steadiness. These findings indicate that muscle impairments in PFP go beyond only low knee and hip muscle strength because women with PFP also present deficits in knee extension and hip abduction force steadiness. Evidence-based treatments aiming at improving force steadiness may be a promising addition to PFP rehabilitation programs.

Caffeine and Placebo Improved Maximal Exercise Performance Despite Unchanged Motor Cortex Activation and Greater Prefrontal Cortex Deoxygenation.

Caffeine (CAF) is an ergogenic aid used to improve exercise performance. Independent studies have suggested that caffeine may have the ability to increase corticospinal excitability, thereby decreasing the motor cortex activation required to generate a similar motor output. However, CAF has also been suggested to induce a prefrontal cortex (PFC) deoxygenation. Others have suggested that placebo (PLA) may trigger comparable effects to CAF, as independent studies found PLA effects on motor performance, corticospinal excitability, and PFC oxygenation. Thus, we investigated if CAF and CAF-perceived PLA may improve motor performance, despite the likely unchanged MC activation and greater PFC deoxygenation. Nine participants (26.4 ± 4.8 years old, VO2MAX of 42.2 ± 4.6 mL kg-1 min-1) performed three maximal incremental tests (MITs) in control (no supplementation) and ∼60 min after CAF and PLA ingestion. PFC oxygenation (near-infrared spectroscopy at Fp1 position), MC activation (EEG at Cz position) and vastus lateralis and rectus femoris muscle activity (EMG) were measured throughout the tests. Compared to control, CAF and PLA increased rectus femoris muscle EMG (P = 0.030; F = 2.88; d = 0.84) at 100% of the MIT, and enhanced the peak power output (P = 0.006; F = 12.97; d = 1.8) and time to exhaustion (P = 0.007; F = 12.97; d = 1.8). In contrast, CAF and PLA did not change MC activation, but increased the PFC deoxygenation as indicated by the lower O2Hb (P = 0.001; F = 4.68; d = 1.08) and THb concentrations (P = 0.01; F = 1.96; d = 0.7) at 80 and 100% the MIT duration. These results showed that CAF and CAF-perceived PLA had the ability to improve motor performance, despite unchanged MC activation and greater PFC deoxygenation. The effectiveness of CAF as ergogenic aid to improve MIT performance was challenged.

Cerebral Regulation in Different Maximal Aerobic Exercise Modes.

We investigated cerebral responses, simultaneously with peripheral and ratings of perceived exertion (RPE) responses, during different VO2MAX-matched aerobic exercise modes. Nine cyclists (VO2MAX of 57.5 ± 6.2 ml·kg(-1)·min(-1)) performed a maximal, controlled-pace incremental test (MIT) and a self-paced 4 km time trial (TT4km). Measures of cerebral (COX) and muscular (MOX) oxygenation were assessed throughout the exercises by changes in oxy- (O2Hb) and deoxy-hemoglobin (HHb) concentrations over the prefrontal cortex (PFC) and vastus lateralis (VL) muscle, respectively. Primary motor cortex (PMC) electroencephalography (EEG), VL, and rectus femoris EMG were also assessed throughout the trials, together with power output and cardiopulmonary responses. The RPE was obtained at regular intervals. Similar motor output (EMG and power output) occurred from 70% of the duration in MIT and TT4km, despite the greater motor output, muscle deoxygenation (↓ MOX) and cardiopulmonary responses in TT4km before that point. Regarding cerebral responses, there was a lower COX (↓ O2Hb concentrations in PFC) at 20, 30, 40, 50 and 60%, but greater at 100% of the TT4km duration when compared to MIT. The alpha wave EEG in PMC remained constant throughout the exercise modes, with greater values in TT4km. The RPE was maximal at the endpoint in both exercises, but it increased slower in TT4km than in MIT. Results showed that similar motor output and effort tolerance were attained at the closing stages of different VO2MAX-matched aerobic exercises, although the different disturbance until that point. Regardless of different COX responses during most of the exercises duration, activation in PMC was preserved throughout the exercises, suggesting that these responses may be part of a centrally-coordinated exercise regulation.

Influences of premotoneuronal command statistics on the scaling of motor output variability during isometric plantar flexion.

This study focuses on neuromuscular mechanisms behind ankle torque and EMG variability during a maintained isometric plantar flexion contraction. Experimentally obtained torque standard deviation (SD) and soleus, medial gastrocnemius, and lateral gastrocnemius EMG envelope mean and SD increased with mean torque for a wide range of torque levels. Computer simulations were performed on a biophysically-based neuromuscular model of the triceps surae consisting of premotoneuronal spike trains (the global input, GI) driving the motoneuron pools of the soleus, medial gastrocnemius, and lateral gastrocnemius muscles, which activate their respective muscle units. Two types of point processes were adopted to represent the statistics of the GI: Poisson and Gamma. Simulations showed a better agreement with experimental results when the GI was modeled by Gamma point processes having lower orders (higher variability) for higher target torques. At the same time, the simulations reproduced well the experimental data of EMG envelope mean and SD as a function of mean plantar flexion torque, for the three muscles. These results suggest that the experimentally found relations between torque-EMG variability as a function of mean plantar flexion torque level depend not only on the intrinsic properties of the motoneuron pools and the muscle units innervated, but also on the increasing variability of the premotoneuronal GI spike trains when their mean rates increase to command a higher plantar flexion torque level. The simulations also provided information on spike train statistics of several hundred motoneurons that compose the triceps surae, providing a wide picture of the associated mechanisms behind torque and EMG variability.

Vibration-induced extra torque during electrically-evoked contractions of the human calf muscles.

BACKGROUND: High-frequency trains of electrical stimulation applied over the lower limb muscles can generate forces higher than would be expected from a peripheral mechanism (i.e. by direct activation of motor axons). This phenomenon is presumably originated within the central nervous system by synaptic input from Ia afferents to motoneurons and is consistent with the development of plateau potentials. The first objective of this work was to investigate if vibration (sinusoidal or random) applied to the Achilles tendon is also able to generate large magnitude extra torques in the triceps surae muscle group. The second objective was to verify if the extra torques that were found were accompanied by increases in motoneuron excitability. METHODS: Subjects (n = 6) were seated on a chair and the right foot was strapped to a pedal attached to a torque meter. The isometric ankle torque was measured in response to different patterns of coupled electrical (20-Hz, rectangular 1-ms pulses) and mechanical stimuli (either 100-Hz sinusoid or gaussian white noise) applied to the triceps surae muscle group. In an additional investigation, Mmax and F-waves were elicited at different times before or after the vibratory stimulation. RESULTS: The vibratory bursts could generate substantial self-sustained extra torques, either with or without the background 20-Hz electrical stimulation applied simultaneously with the vibration. The extra torque generation was accompanied by increased motoneuron excitability, since an increase in the peak-to-peak amplitude of soleus F waves was observed. The delivery of electrical stimulation following the vibration was essential to keep the maintained extra torques and increased F-waves. CONCLUSIONS: These results show that vibratory stimuli applied with a background electrical stimulation generate considerable force levels (up to about 50% MVC) due to the spinal recruitment of motoneurons. The association of vibration and electrical stimulation could be beneficial for many therapeutic interventions and vibration-based exercise programs. The command for the vibration-induced extra torques presumably activates spinal motoneurons following the size principle, which is a desirable feature for stimulation paradigms.