Isotonic Injections Research Articles

Effects of experimentally induced muscle pain on endurance performance: A proof-of-concept study assessing neurophysiological and perceptual responses.

Pain arising from exercise potentiates fatigue and impairs the performance of endurance exercise. We assessed neurophysiological and perceptual responses to endurance exercise performed under experimentally induced muscle pain by a model that separates muscle pain from muscle fatigue. After a series of pilot studies investigating different hypertonic saline volumes, 17 healthy males performed a preliminary VO2PEAK test before performing a familiarization of the cycling time-to-exhaustion exercise (80% of the peak power output in the VO2PEAK test). Participants, performed a baseline exercise session before the sessions with hypertonic and isotonic saline injections in the vastus lateralis of both legs, in a crossover and counterbalanced design. Neurophysiological and perceptual responses such as electroencephalography (EEG) in frontal, prefrontal, parietal, and motor cortex, electromyography (EMG) of the vastus lateralis and biceps femoris muscles, ratings of perceived exertion (RPE), pain sensation, and affective valence were measured at rest and during exercise. The hypertonic injection reduced the resting EEG alpha-beta ratio in the frontal and prefrontal cortex. When compared to exercise performed after the isotonic injection (430.5±152.6 s), hypertonic injection shortened the time-to-exhaustion (357.5±173.0 s), reduced the EMG of the assessed muscles, and increased the muscle co-contraction during exercise. The hypertonic injection also reduced the EEG alpha-beta ratio in the prefrontal and parietal cortex, increased RPE and pain sensation, and reduced affective valence during exercise. This proof-of-concept study showed that hypertonic injection-induced muscle pain reduced endurance performance, promoting centrally mediated alterations in motor command and cortical activation, as well as an interplay of perceptual responses.

Experimental muscle pain of the vastus medialis reduces knee joint extensor torque and alters quadriceps muscle contributions as revealed through musculoskeletal modeling

BackgroundVoluntary activation deficit of the quadriceps muscle group is a common symptom in populations with knee joint injury. Musculoskeletal modeling and simulations can improve our understanding of pathological conditions; however, they are mathematically complex which can limit their clinical application. A practical subject-specific modeling framework is introduced to evaluate knee extensor inhibition and muscle force contributions to isometric knee joint torques in healthy adults with and without experimentally induced quadriceps muscle pain. MethodsA randomized cross-over placebo controlled study design was used. Subject-specific maximum knee joint extension torque and quadriceps electromyographic data from 13 uninjured young adults were combined in a modeling framework to determine optimal muscle strength scaling parameters and ideal torque. Strength deficit ratios (experimental torque/ideal torque) and individual muscle contribution to experimental torque was computed before and after intramuscular hypertonic (pain inducing) and isotonic (sham) saline was injected to the vastus medialis. FindingsDecreased experimental knee extension torque (−8%) and vastus medialis electromyography (−26%) amplitude pre- to post- hypertonic injection was observed. Correspondingly, significant decreases in the knee extensor strength deficit ratio (−18%) and percent contribution of vastus medialis to experimental torque (−24%) was observed pre- to post- hypertonic injection. No differences were observed with isotonic injections, confirming the validity of the model. InterpretationOur practical method to estimate strength ratios can be easily implemented within a musculoskeletal modeling framework to improve the validity of model estimates. This, in turn, can increase our understanding of the relationship between neuromuscular deficits and functional outcomes in patient populations.

Experimental calf muscle pain attenuates the postural stability during quiet stance and perturbation

Background The purpose of this study was to evaluate how acute pain changes the postural control and stability during quiet standing and after unexpected perturbations. Methods Nine subjects stood as quiet as possible on a movable force platform that recorded the centre of pressure position and provided unexpected floor perturbations, before, during and after experimental calf muscle pain. Bilateral surface electromyography from the tibialis anterior and medial gastrocnemius muscles was recorded. The foot pressure distributions were measured using pressure insoles. Intramuscular injections of hypertonic saline were administrated (right leg) to induce acute pain in the tibialis anterior and/or medial gastrocnemius muscles, and an isotonic injection was used as control. Findings Simultaneous pain in tibialis anterior and medial gastrocnemius altered the postural control. During quiet standing: higher medial-lateral centre of pressure speed and increased total sway displacement ( P < 0.05), weight moved to the non-painful side, ( P < 0.05) and plantar centre of pressure of the left foot was shifted towards the heel’s direction ( P < 0.05). During forward perturbation: higher mean displacement in the medial-lateral direction ( P < 0.05). After the perturbation: larger sway area ( P < 0.05). Pain only in the medial gastrocnemius muscle increased medial-lateral centre of pressure speed ( P < 0.05) during the quiet standing. Pain only in the tibialis anterior muscle increased peak pressure on the contralateral foot ( P < 0.05). Interpretation These findings suggest that large acute painful areas on the calf muscles impair the postural control and potentially increase the risk factors for falls. Further strategies aiming to reduce pain in patients may lead to improvement in balance.

Experimental muscle pain decreases the frequency threshold of electrically elicited muscle cramps

This study in humans tested the hypothesis that nociceptive muscle afferent input facilitates the occurrence of muscle cramps. In 13 healthy adults, muscle cramps were experimentally induced in the foot by stimulating the tibialis posterior nerve at the ankle with 2-s bursts of stimuli separated by 30 s, with stimulation frequency increasing by 2-Hz increments from 10 Hz until the cramp appeared. The minimum stimulation frequency that induced the cramp was defined "cramp frequency threshold". In 2 days, elicitation of the cramp was performed in the two-feet with and without (baseline condition) injection of hypertonic (painful condition) or isotonic (control condition) saline into the deep midportion of the flexor hallucis brevis muscle, from where surface EMG signals were recorded. The cramp frequency threshold was lower for the painful condition with respect to its baseline (mean +/- SE, hypertonic saline: 25.7 +/- 2.1 Hz, corresponding baseline: 31.2 +/- 2.8 Hz; P < 0.01) while there was no difference between the threshold with isotonic injection with respect to baseline. EMG average rectified value and power spectral frequency were higher during the cramp than immediately before the stimulation that elicited the cramp (pre-cramp: 13.9 +/- 1.6 muV and 75.4 +/- 3.8 Hz, respectively; post-cramp: 19.9 +/- 3.2 muV and 101.6 +/- 6.0 Hz; P < 0.05). The results suggest that nociceptive muscle afferent activity induced by injection of hypertonic saline facilitates the generation of electrically elicited muscle cramps.

Caffeine-induced taste aversion and mimetic responses

Novel tastes preceded a range of caffeine doses (10–80 mg/kg) in a taste aversion training trial. One week later rats which had doses of 30 mg or higher showed strong aversions as measured by a single bottle consumption test. The 10 and 20 mg dose produced the most hyperactivity and apparently enhanced intake of the taste paired with caffeine. During the training trial, rats receiving the 80 mg dose exhibited copious gapes and chin-rubs, mimetic responses to noxious tastes. Gapes also occurred in these subjects during the aversion test. Consumption was more sensitive than mimetic responding as a measure of the aversive effects of caffeine. Only the 80 mg dose produced neophobia. Tests with isotonic injections indicated that tonicity was not the source of the aversions.