STIM1 should therefore be considered for patients with tubular aggregate myopathies involving either muscle weakness or myalgia as the first and predominant clinical sign.
We found that COL1A1 (minor) T-allele carriers ( rs1800012 ) and (major) T-allele homozygotes ( rs2249492 ) were generally weaker ( P ≤ 0.019); and (minor) A-allele carriers of COL2A1 ( P = 0.002) and (major) T-allele carriers of COL5A1 ( P = 0.004) SNPs reported greater muscle soreness, all compared with their respective major ( rs1800012 ; rs2070739 ) and minor ( rs2249492 ; rs12722 ) allele homozygote counterparts.
A patient with mitochondrial trifunctional protein deficiency due to the mutations in the HADHB gene showed recurrent myalgia since early childhood and was diagnosed in adolescence.
Muscle aches/pain are strongly associated with decreased CRP and IL-8 levels and increased IL-6 levels suggesting the need for further investigation of the biological pathways contributing to pain in PLWH.
Creatine kinase (CK), interleukin-6 (IL-6), salivary cortisol, rating of muscle pain, pressure pain threshold (PPT), and mood states were evaluated before (Pre-ex), immediately (Post-ex0), 2 h (Post-ex2h) and 4 h (Post-ex4h) after exercise.
Muscle strength (MVC), muscle damage (CK), oxidative stress (GPx), inflammation (IL6) and volunteer-reported muscle soreness intensity were assessed pre and post exercise.
Countermovement vertical jump (CMJ) performance, perceived muscle soreness, sit-and-reach flexibility, plasma creatine kinase (CK), lactate dehydrogenase (LDH), and myoglobin (Mb) concentrations were quantified immediately before and after and 45 minutes, 24 and 48 hours after repeated-sprint running protocols.
At the end of the race, jump height reduction (-11±12% vs. -25±19%; P=0.03), serum myoglobin concentration (186.1±93.6 vs. 564.1±370.7 µg·mL-1; P<0.01) and self-reported muscle pain (3.0 ±2.3 vs. 5.5 ±1.0 A.U.; P<0.01) were lower in half-marathoners vs. marathoners.
On days 0, 2, and 4, nerve growth factor was injected into the right forearm to induce progressively developing muscle soreness and mechanical hyperalgesia.
Using repeated intramuscular injection of nerve growth factor to induce the development of sustained muscle pain (lasting weeks), 30 healthy individuals were randomized to receive 5 consecutive daily treatments of active or sham left DLPFC rTMS, starting before the first nerve growth factor injection on day 0.
We previously demonstrated that nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) were upregulated after lengthening contractions (LC) in exercised muscle through B2 bradykinin receptor activation and cyclooxygenase (COX)-2 upregulation, respectively, and that these trophic factors sensitized nociceptors resulting in mechanical hyperalgesia (delayed-onset muscle soreness, DOMS).
Intramuscular injection of Nerve Growth Factor (NGF) may influence the responsiveness of active chemo-sensitive channels affecting muscle pain sensitivity.
Enrichment juices maintained basal levels of blood markers of muscle damage, such as lactate dehydrogenase and myoglobin, and showed a significant maintenance of force during the exercise and a significant decrease in the rating of perceived exertion and muscle soreness after exercise.
To test whether PAF can provide information about pain sensitivity occurring over clinically relevant timescales (i.e., weeks), EEG was recorded before and while participants experienced a long-lasting pain model, repeated intramuscular injection of nerve growth factor (NGF), that produces progressively developing muscle pain for up to 21 days.
Changes in maximal voluntary isometric contraction strength (MVC) and muscle soreness, plasma creatine kinase (CK) activity and myoglobin concentration after 80% EC were compared between groups by a mixed-factor ANOVA.
At baseline, 24 and 48 h, creatine kinase, lactate dehydrogenase, interleukin-6 and -10, tumor necrosis factor alpha, and muscle soreness were assessed.
Mutations in the extracellular domain of the 55-kD tumor-necrosis factor (TNF) receptor (TNFRSF1A), a key regulator of inflammation, define a periodic-fever syndrome, TRAPS (TNF receptor-associated periodic syndrome [MIM 142680]), which is characterized by attacks of fever, sterile peritonitis, arthralgia, myalgia, skin rash, and/or conjunctivitis; some patients also develop systemic amyloidosis.
In addition, exercise increased the endocannabinoid anandamide levels and cannabinoid CB<sub>2</sub> receptors expression whereas it reduced Iba1 (microglial marker) protein expression as well as pro-inflammatory cytokines (TNF-α and IL-1β) in the spinal cord of mice with inflammatory muscle pain.