Effects of wrist position on eccentric exercise-induced muscle damage of the elbow flexors.

We tested the hypothesis that the magnitude of changes in indirect muscle damage markers would be greater after maximal elbow flexor eccentric exercise in the supinated (shorter biceps brachii) than neutral wrist (longer) position, and the difference in the magnitude would be associated with greater elongation over contractions for the supinated than neutral position, rather than the initial muscle length. Ten untrained men (21-39 years) performed two bouts of 10 sets of 6 maximal isokinetic eccentric contractions of the elbow flexors in the supinated position for one arm and neutral position for the other arm separated by 2 weeks in a randomized order. Biceps brachii myotendinous junction (MTJ) movements during eccentric contractions were recorded by B-mode ultrasonography, and the displacement from the start to end of each contraction was quantified. Peak torque (supinated: 367.8 ± 112.5 Nm, neutral: 381.5 ± 120.4 Nm) and total work (1816 ± 539 J, 1865 ± 673 J) produced during eccentric contractions were similar between conditions. The average MTJ displacement increased (P < .05) from the 1st set (8.0 ± 2.0 mm) to 10th set (15.8 ± 1.9 mm) for the supinated condition, but no such increase was found in the neutral condition (1st set: 5.1 ± 1.0 mm, 10th set: 5.0 ± 0.8 mm). Changes in indirect muscle damage markers (maximal voluntary isometric contraction torque, range of motion, serum creatine kinase activity, and muscle soreness) after exercise were greater (P < .05) for the supinated than neutral condition. These results suggest that the greater muscle damage marker changes for the supinated than neutral wrist position was associated with the greater muscle lengthening (strain).

Strain differences in the attenuation of bone accrual in a young growing mouse model of insulin resistance.

Skeletal fractures are considered a chronic complication of type 2 diabetes mellitus (T2DM), but the etiology of compromised bone quality that develops over time remains uncertain. This study investigated the concurrent alterations in metabolic and skeletal changes in two mouse strains, a responsive (C57BL/6) and a relatively resistant (C3H/HeJ) strain, to high-fat diet-induced glucose intolerance. Four-week-old male C57BL/6 and C3H/HeJ mice were randomized to a control (Con = 10 % kcal fat) or high-fat (HF = 60 % kcal fat) diet for 2, 8, or 16 weeks. Metabolic changes, including blood glucose, plasma insulin and leptin, and glucose tolerance were monitored over time in conjunction with alterations in bone structure and turn over. Elevated fasting glucose occurred in both the C57BL/6 and C3H/HeJ strains on the HF diet at 2 and 8 weeks, but only in the C57BL/6 strain at 16 weeks. Both strains on the HF diet demonstrated impaired glucose tolerance at each time point. The C57BL/6 mice on the HF diet exhibited lower whole-body bone mineral density (BMD) by 8 and 16 weeks, but the C3H/HeJ strain had no evidence of bone loss until 16 weeks. Analyses of bone microarchitecture revealed that trabecular bone accrual in the distal femur metaphysis was attenuated in the C57BL/6 mice on the HF diet at 8 and 16 weeks. In contrast, the C3H/HeJ mice were protected from the deleterious effects of the HF diet on trabecular bone. Alterations in gene expression from the femur revealed that several toll-like receptor (TLR)-4 targets (Atf4, Socs3, and Tlr4) were regulated by the HF diet in the C57BL/6 strain, but not in the C3H/HeJ strain. Structural changes observed only in the C57BL/6 mice were accompanied with a decrease in osteoblastogenesis after 8 and 16 weeks on the HF diet, suggesting a TLR-4-mediated mechanism in the suppression of bone formation. Both the C57BL/6 and C3H/HeJ mice demonstrated an increase in osteoclastogenesis after 8 weeks on the HF diet; however, bone turnover was decreased in the C57BL/6 with prolonged hyperglycemia. Further investigation is needed to understand how hyperglycemia and hyperinsulinemia suppress bone turnover in the context of T2DM and the role of TLR-4 in this response.

Effects of air-pulsed cryotherapy on neuromuscular recovery subsequent to exercise-induced muscle damage.

BACKGROUND: Localized cooling has been proposed as an effective strategy to limit the deleterious effects of exercise-induced muscle damage on neuromuscular function. However, the literature reports conflicting results. PURPOSE: This randomized controlled trial aimed to determine the effects of a new treatment, localized air-pulsed cryotherapy (-30°C), on the recovery time-course of neuromuscular function following a strenuous eccentric exercise. STUDY DESIGN: Controlled laboratory study. METHODS: A total of 24 participants were included in either a control group (CONT) or a cryotherapy group (CRYO). Immediately after 3 sets of 20 maximal isokinetic eccentric contractions of elbow flexors, and then 1, 2, and 3 days after exercise, the CRYO group received a cryotherapy treatment (3 × 4 minutes at -30°C separated by 1 minute). The day before and 1, 2, 3, 7, and 14 days after exercise, several parameters were quantified: maximal isometric torque and its associated maximal electromyographic activity recorded by a 64-channel electrode, delayed-onset muscle soreness (DOMS), biceps brachii transverse relaxation time (T2) measured using magnetic resonance imaging, creatine kinase activity, interleukin-6, and C-reactive protein. RESULTS: Maximal isometric torque decreased similarly for the CONT (-33% ± 4%) and CRYO groups (-31% ± 6%). No intergroup differences were found for DOMS, electromyographic activity, creatine kinase activity, and T2 level averaged across the whole biceps brachii. C-reactive protein significantly increased for CONT (+93% at 72 hours, P < .05) but not for CRYO. Spatial analysis showed that cryotherapy delayed the significant increase of T2 and the decrease of electromyographic activity level for CRYO compared with CONT (between day 1 and day 3) in the medio-distal part of the biceps brachii. CONCLUSION: Although some indicators of muscle damage after severe eccentric exercise were delayed (ie, local formation of edema and decrease of muscle activity) by repeated air-pulsed cryotherapy, we provide evidence that this cooling procedure failed to improve long-term recovery of muscle performance. CLINICAL RELEVANCE: Four applications of air-pulsed cryotherapy in the 3 days after a strenuous eccentric exercise are ineffective overall in promoting long-term muscle recovery. Further studies taking into account the amount of exercise-induced muscle damage would allow investigators to make stronger conclusions regarding the inefficiency of this recovery modality.

Effects of estrogen on gastrocnemius muscle strain injury and regeneration in female rats.

AIM: To study the effects of estrogen on muscle damage and regeneration after acute passive gastrocnemius muscle strain injury in female Sprague-Dawley rats. METHODS: Rats were divided into 5 groups: ovariectomized, strained and treated with low-dosage estradiol (20 microg/d) (E(low)), treated with high-dosage estradiol (200 microg/d) (E(high)), treated with oil placebo (Oil), strained with no ovariectomy (Strain), and sham operated with no strain and no ovariectomy (Con). Muscle damage index [plasma creatine kinase (CK)], antioxidant indexes [glutathione (GSH), Vitamin E (Vit E), total antioxidant capability (TAC)], and muscle regeneration index (desmin) were investigated at 7 d. RESULTS: The plasma CK activity increased but GSH, Vit E, and TAC levels decreased after muscle strain injury (Strain vs Con P<0.05). Plasma CK activity was the greatest while GSH, Vit E, and TAC were the lowest in the Oil group among the five groups (P<0.01). Plasma CK in the E(high) and Strain groups was lower than that in the E(low) group. Plasma GSH, Vit E, and TAC were higher in the E(high) and Strain groups compared with the E(low) group (P<0.05). The expression of desmin in the E(high) and Strain groups was higher than that in the E(low) group (P<0.01) while that in the Oil group was the lowest in all the five groups (P<0.01). CONCLUSION: Endogenous estrogen in normal female rats or exogenous estrogen in ovariectomized rats could improve antioxidant capability in vivo, so that reduced muscle damage and accelerated muscle regeneration post gastronemius muscle strain injury.

Effects of head and extracranial injuries on serum protein S100B levels in trauma patients.

BACKGROUND: Serum protein S100B determinations have been recently suggested as markers of traumatic brain injury. However, little is known about the effects of extracranial injuries on S100B levels in trauma patients. METHODS: We studied 224 patients with head trauma (54 of whom also had extracranial injuries), 155 patients with various types of extracranial injuries, and 8 healthy pilots exposed to high Gz forces. The head trauma patients had either no brain injury (n = 35), mild brain injury (n = 165), or moderate to severe brain injury (n = 24). The extracranial injuries were divided into small and large injuries. Serum protein S100B levels were determined from samples taken within 6 hours after the trauma event. RESULTS: The head trauma patients had a significantly higher median S100B (0.17 microg/L) than the patients with extracranial injuries (0.07 microg/L) (p < 0.001). Serum S100B levels also correlated with the severity of brain injury (p < 0.001), the highest values occurring in the patients with moderate to severe brain injury (1.27 microg/L). However, large extracranial injuries also elevated S100B levels (0.35 microg/L), whereas small extracranial injuries in the absence of head trauma did not significantly affect S100B levels (0.07 microg/L). Above the cutoff level of 0.13 microg/L, there were 61% of the head trauma patients and 26% of those with extracranial injuries (Pearson chi test, p < 0.001). However, only 4% of the patients with purely extracranial injuries had a concentration of S100B above the cutoff level of 0.50 microg/L, whereas the head trauma patients with moderate to severe brain injury exceeded this cutoff in 67% of the cases. Exposure to high Gz forces did not influence serum S100B levels in healthy individuals. CONCLUSION: We conclude that serum S100B is a sensitive marker of brain injury, which correlates with the severity of the injury. Large extracranial injuries also elevate S100B levels. However, S100B has a high negative predictive power, and the finding of a normal S100B value shortly after trauma should thus exclude significant brain injury with a high accuracy.