Burn injuries can be devastating, with life-long impacts including an increased risk of hospitalization for a wide range of secondary morbidities. One area that remains not fully understood is the impact of burn trauma on the central nervous system (CNS). This review will outline the current findings on the physiological impact that burns have on the CNS and how this may contribute to the development of neural comorbidities including mental health conditions. This review highlights the damaging effects caused by burn injuries on the CNS, characterized by changes to metabolism, molecular damage to cells and their organelles, and disturbance to sensory, motor and cognitive functions in the CNS. This damage is likely initiated by the inflammatory response that accompanies burn injury, and it is often long-lasting. Treatments used to relieve the symptoms of damage to the CNS due to burn injury often target inflammatory pathways. However, there are non-invasive treatments for burn patients that target the functional and cognitive damage caused by the burn, including transcranial magnetic stimulation and virtual reality. Future research should focus on understanding the mechanisms that underpin the impact of a burn injury on the CNS, burn severity thresholds required to inflict damage to the CNS, and acute and long-term therapies to ameliorate deleterious CNS changes after a burn.

Multiple neuromuscular processes contribute to the loss of force production following repeated, high-intensity muscular efforts; however, the relative contribution of each process is unclear. In Experiment 1, 16 resistance trained men performed six sets of unilateral isometric plantar flexor contractions of the right leg (3 s contraction/2 s rest; 85% maximal voluntary contraction torque; 90-s inter-set rest) until failure with and without caffeine ingestion (3 mg kg^-1) on two separate days. Corticospinal excitability and cortical silent period (cSP) were assessed before and immediately, 10 and 20 min after the exercise. In Experiment 2, electrically evoked tetanic force and persistent inward current (PIC)-mediated facilitation of the motor neuron pool (estimated using neuromuscular electrical stimulation with tendon vibration) were assessed before and after the same exercise intervention in 17 resistance trained men. Results showed decreases in peak plantar flexion torque (Experiment 1: -12.2%, Experiment 2: -16.9%), electrically evoked torque (20 Hz -15.3%, 80 Hz -15.3%, variable-frequency train -17.9%), and cSP (-3.8%; i.e., reduced inhibition) post-exercise which did not recover by 20 min. Electromyographic activity (EMG; -6%), corticospinal excitability (-9%), and PIC facilitation (-24.8%) were also reduced post-exercise but recovered by 10 min. Caffeine ingestion increased torque and EMG but did not notably affect corticospinal excitability, PIC amplification, or electrically evoked torque. The data indicate that a decrease in muscle function largely underpins the loss of force after repeated, high-intensity muscular efforts, but that the loss is exacerbated immediately after the exercise by simultaneous decreases in corticospinal excitability and PIC amplitudes at the motor neurons.

Purpose: Resistance exercise increases blood flow, induces osmotic and hydrostatic fluid shifts during and immediately after exercise, and may trigger inflammatory responses for several days in the working muscle. The resultant muscle swelling can subsequently affect muscle size and quality assessments. However, the effects of muscle swelling on x-ray attenuation of adipose estimate errors are unknown. Methods: Peripheral quantitative computed tomography (pQCT) and ultrasonography were used to assess muscle and adipose tissue properties of both upper arms before, 24, 48, and 72 h after unilateral resistance exercise. Recreationally active participants (n = 17) completed the exercise while their contralateral limb served as a control. Results: Resistance exercise resulted in a significant increase in pQCT-derived muscle cross-sectional area (includes intermuscular adipose tissue [IMAT] area), muscle area (excludes IMAT area) and IMAT area, and ultrasound-derived muscle thickness at 24, 48, and 72 h. A significant decrease in pQCT-derived muscle density was also detected as well as an increase in ultrasound-derived echo intensity at 48 and 72 h. The changes in muscle area, IMAT area, and muscle density were significantly correlated with changes in echo intensity, whereas the changes in muscle cross-sectional area and IMAT area were significantly correlated with changes in muscle thickness. Conclusion: Unaccustomed resistance exercise can cause errors in pQCT- and ultrasound-based muscle and adipose estimates for at least 72 h. These errors are the result of muscle swelling likely caused by muscle blood flow and inflammation-dependent fluid shifts in muscle. These findings may have implications for measurements in other inflammatory conditions.

Background: Burn injuries cause significant motor and sensory dysfunctions that can negatively impact burn survivors’ quality of life. The underlying mechanisms of these burn-induced dysfunctions have primarily been associated with damage to the peripheral neural architecture, however, evidence points to a systemic influence of burn injury. Central nervous system (CNS) reorganizations due to inflammation, afferent dysfunction, and pain could contribute to persistent motor and sensory dysfunction in burn survivors. Recent evidence shows that the capacity for neuroplasticity is associated with self-reported functional recovery in burn survivors. Objective: This review first outlines motor and sensory dysfunctions following burn injury and critically examines recent literature investigating the mechanisms mediating CNS reorganization following burn injury. The review then provides recommendations for future research and interventions targeting the CNS such as non-invasive brain stimulation to improve functional recovery. Conclusions: Directing focus to the CNS following burn injury, alongside the development of non-invasive methods to induce functionally beneficial neuroplasticity in the CNS, could advance treatments and transform clinical practice to improve quality of life in burn survivors.

Purpose: Unilateral strength training may attenuate the decline in muscle strength and size in homologous, contralateral muscles. This study aimed to determine whether the cross-education of strength could specifically attenuate the effects of detraining immediately after a short (prehabilitation-type) period of strength training. Methods: Twenty-six strength-trained participants were assigned to either four weeks of unilateral strength training of the stronger arm (UNI) or detraining (Detrain). Motor evoked potential (MEP) and cortical silent period (cSP) responses, muscle cross-sectional area (CSA_Flexor; peripheral quantitative computed tomography) and maximal strength, rate of force development (RFD) and muscle activation (EMG) were examined in both elbow flexors before and after the intervention period. Results: In UNI, one-repetition maximum (1-RM) strength improved in both the trained (∆ = 2.0 ± 0.9 kg) and non-trained (∆ = 0.8 ± 0.9 kg) arms despite cessation of training of the weaker arm, whereas 1-RM strength was unchanged in Detrain. Maximal voluntary isometric contraction, isokinetic peak torque, and RFD did not change in either group. No neural changes were detected in UNI, but cSP increased in Detrain (∆ = 0.010 ± 0.015 s). CSA_Flexor increased in the trained arm (∆ = 51 ± 43 mm²) but decreased in the non-trained arm (∆ = -53 ± 50 mm²) in UNI. CSA_Flexor decreased in both arms in Detrain and at a similar rate to the non-trained arm in UNI. Conclusion: UNI attenuated the effects of detraining in the weaker arm as shown by the improvement in 1-RM strength. However, the cross-education of strength did not attenuate the decline in muscle size in the contralateral arm.