Influence of estrogen on markers of muscle tissue damage following eccentric exercise.

This study tested the hypothesis that estrogen levels of women influences the development of a muscle-tissue damage (creatine kinase, CK) marker and delayed onset muscle soreness (DOMS) following eccentric exercise. Seventeen oral contraceptive (OC) users and ten eumenorrheic (EU) subjects completed a 30-min downhill running bout at approximately 60% VO2max. The OC completed the exercise during the mid-luteal phase (day 22.9 +/- 1.5; high estrogen) while the EU did their exercise in the mid-follicular phase (day 9.6 +/- 4.4; low estrogen) of the menstrual cycle, respectively. The CK activity and DOMS were assessed pre-exercise, immediately post-, 24, 48 and 72 h post-exercise. ANOVA results indicated that there was a significant increase in CK activity in response to the downhill run (p < 0.001), and the interaction of group x time was significantly different (p < 0.01). The OC group had lower CK at 72 h post-exercise than did the EU group. Pre-exercise estrogen levels correlated with the overall mean CK (r = -0.43, p < 0.05) and 72 h (r = -0.38, p < 0.05) responses, respectively. Exercise caused an increase in DOMS in both groups (p < 0.001); but, no significant interaction was observed. These findings suggest that elevated estrogen levels have a protective effect on muscle tissue following eccentric exercise. The mechanism of this protective effect is unclear but may be related to the anti-oxidant characteristics and membrane stability properties associated with estrogen and its derivatives.     

Influence of Estrogen on Markers of Muscle Tissue Damage Following Eccentric Exercise

This study tested the hypothesis that estrogen levels of women influences the development of a muscle-tissue damage (creatine kinase, CK) marker and delayed onset muscle soreness (DOMS) following eccentric exercise. Seventeen oral contraceptive (OC) users and ten eumenorrheic (EU) subjects completed a 30-min downhill run at 60% VO_2max. The OC completed the exercise during the midluteal phase (day 22.9 ± 1.5; high estrogen) while the EU did their exercise in the midfollicular phase (day 9.6 ± 4.4; low estrogen) of the menstrual cycle, respectively. The CK activity and DOMS were assessed preexercise, immediately postexcercise, 24, 48, and 72 h postexercise. ANOVA results indicated that there was a significant increase in CK activity in response to the downhill run (p< 0.001), and the interaction of group x time was significantly different (p< 0.01). The OC group had lower CK at 72 h postexercise than did the EU group. Preexercise estrogen levels correlated with the overall mean CK (r= –0.43. p< 0.05) and 72 h (r= –0.38, p < 0.05) responses, respectively. Exercise caused an increase in DOMS in both groups (p< 0.001); but, no significant interaction was observed. These findings suggest that elevated estrogen levels have a protective effect on muscle tissue following eccentric exercise. The mechanism of this protective effect is unclear, but it may be related to the antioxidant characteristics and membrane stability properties associated with estrogen and its derivatives.     

Effects of menstrual cycle and physical training on heat loss responses during dynamic exercise at moderate intensity in a temperate environment

We evaluated the effects of the menstrual cycle and physical training on heat loss (sweating and cutaneous vasodilation) responses during moderate exercise in a temperate environment. Ten untrained (group U) and seven endurance-trained (group T) women (maximal O2 uptake of 36.7+/-1.1 vs. 49.4+/-1.7 ml.kg-1.min-1, respectively; P<0.05) performed a cycling exercise at 50% maximal O2 uptake for 30 min during both the midfollicular and midluteal menstrual phase in a temperate environment (ambient temperature of 25 degrees C, relative humidity of 45%). In group U, plasma levels of estrone, estradiol, and progesterone at rest and esophageal temperature (Tes) during exercise were significantly higher during the midluteal than during the midfollicular phase (P<0.05). Sweating rate and cutaneous blood flow (measured via laser-Doppler flowmetry) on the chest, back, forearm, and thigh were lower during the midluteal than during the midfollicular phase during exercise. Tes threshold for heat loss responses was significantly higher and sensitivity of the heat loss responses was significantly lower in the midluteal than in the midfollicular phase, regardless of body site. These effects of the menstrual cycle in group U were not observed in group T. The sweating rate and cutaneous blood flow were significantly higher in group T than in group U, regardless of menstrual phase or body site. Tes threshold for heat loss responses was significantly lower and sensitivity of heat loss responses was significantly greater in group T than in group U in the midluteal phase; however, sensitivity of the sweating response was significantly greater in the midfollicular phase. These results suggest that heat loss responses in group U were inhibited in the midluteal phase compared with in the midfollicular phase. Menstrual cycle had no remarkable effects in group T. Physical training improved heat loss responses, which was more marked in the midluteal than in the midfollicular phase.     

Effects of hydration state and resistance exercise on markers of muscle damage

It is well established that resistance exercise can damage muscle tissue, but the combined effects of hypohydration and resistance exercise on muscle damage are unclear. Two common circulating markers of muscle damage, myoglobin (Mb) and creatine kinase (CK) may be attenuated by fluid ingestion post-exercise. The purpose of this study was to examine the combined effect of resistance exercise and hydration state on muscle damage. Seven healthy resistance-trained males (age = 23 +/- 4 years; body mass = 87.8 +/- 6.8 kg; body fat = 11.5 +/- 5.2%) completed 3 identical resistance exercise bouts (6 sets of up to 10 repetitions of the back squat) in different hydration states: euhydrated (HY0), hypohydrated approximately 2.5% body mass (HY2.5), and hypohydrated approximately 5.0% body mass (HY5). Subjects achieved desired hydration states via controlled water deprivation, exercise-heat stress, and fluid intake. Both Mb and CK were measured during euhydrated rest (PRE). Mb was also measured immediately post-exercise, 1 hour (+1H) and 2 hours (+2H) post-exercise; CK was measured at 24 and 48 hours post-exercise. Body mass decreased 0.2 +/- 0.4%, 2.4 +/- 0.4%, and 4.8 +/- 0.4% during HY0, HY2.5, and HY5, respectively. Mb concentrations increased significantly (effect size >or=1, p < 0.05) from PRE (2.6 +/- 1.1, 3.5 +/- 2.8, and 3.2 +/- 1.6 nmol x L(-1)) to +1H (5.3 +/- 3.4, 6.8 +/- 3.2, and 7.6 +/- 2.8 nmol x L(-1)), and +2H (5.5 +/- 3.8, 6.2 +/- 3.0, and 7.2 +/- 3.0 nmol x L(-1)) for HY0, HY2.5, and HY5, respectively, but were not significantly different between trials. CK concentrations remained within the normal resting range at all time points. Thus, hypohydration did not enhance muscle damage following the resistance exercise challenge. Despite these results, athletes are encouraged to commence exercise in a euhydrated state to maximize endogenous hormonal, mechanical, and metabolic benefits.     

Impact of a Single Bout of Aerobic Exercise on Regional Brain Perfusion and Activation Responses in Healthy Young Adults

Purpose

Despite the generally accepted view that aerobic exercise can have positive effects on brain health, few studies have measured brain responses to exercise over a short time span. The purpose of this study was to examine the impact within one hour of a single bout of exercise on brain perfusion and neuronal activation.

Methods

Healthy adults (n = 16; age range: 20–35 yrs) were scanned using Magnetic Resonance Imaging (MRI) before and after 20 minutes of exercise at 70% of their age-predicted maximal heart rate. Pseudo-continuous arterial spin labeling (pcASL) was used to measure absolute cerebral blood flow (CBF) prior to exercise (pre) and at 10 min (post-10) and 40 min (post-40) post-exercise. Blood oxygenation level dependent (BOLD) functional MRI (fMRI) was performed pre and post-exercise to characterize activation differences related to a go/no-go reaction time task.

Results

Compared to pre-exercise levels, grey matter CBF was 11% (±9%) lower at post-10 (P<0.0004) and not different at post-40 (P = 0.12), while global WM CBF was increased at both time points post-exercise (P<0.0006). Regionally, the hippocampus and insula showed a decrease in perfusion in ROI-analysis at post-10 (P<0.005, FDR corrected), whereas voxel-wise analysis identified elevated perfusion in the left medial postcentral gyrus at post-40 compared to pre (p_corrected = 0.05). BOLD activations were consistent between sessions, however, the left parietal operculum showed reduced BOLD activation after exercise.

Conclusion

This study provides preliminary evidence of regionalized brain effects associated with a single bout of aerobic exercise. The observed acute cerebrovascular responses may provide some insight into the brain’s ability to change in relation to chronic interventions.     

17 β-hydroxysteroid dehydrogenase in monkey endometrium during the menstrual cycle and at the time of implantation

In order to further identify physiological similarities between 17β-hydroxysteroid dehydrogenase (HSD) in human and monkey endometrium, and to evaluate the role of estradiol-17β (E₂) oxidation to estrone (E₁) during periimplantation events, 30 rhesus monkeys were studied at different intervals of the nonfertile menstrual cycle (days 8, 12, 15, 18 and 24). Also, five pregnant monkeys provided endometrial tissue on day 24 of the fertile menstrual cycle, near the expected time of implantation. HSD activity in endometrium was low at midfollicular phase (day 8), increased to maximal levels (8-fold) during the periovulatory span (days 12 and 15),and was intermediate in mid to late luteal phase (days 18 and 24) in non-fertile menstrual cycles. In the absence of ovulation, HSD was low throughout. These enzyme data fit with a pattern of daily peripheral serum levels of E₂ and progesterone (P) and suggest that when the normal sequence of P follows elevated estrogens in late follicular phase, HSD activity is markedly enhanced in the early luteal phase. However, HSD activity in endometrium did not increase more in the fertile menstrual cycle, despite further elevations of serum P during rescue of the corpus luteum.     

Whey protein supplementation accelerates satellite cell proliferation during recovery from eccentric exercise

Human skeletal muscle satellite cells (SCs) are essential for muscle regeneration and remodeling processes in healthy and clinical conditions involving muscle breakdown. However, the potential influence of protein supplementation on post-exercise SC regulation in human skeletal muscle has not been well investigated. In a comparative human study, we investigated the effect of hydrolyzed whey protein supplementation following eccentric exercise on fiber type-specific SC accumulation. Twenty-four young healthy subjects received either hydrolyzed whey protein + carbohydrate (whey, n = 12) or iso-caloric carbohydrate (placebo, n = 12) during post-exercise recovery from 150 maximal unilateral eccentric contractions. Prior to and 24, 48 and 168 h post-exercise, muscle biopsies were obtained from the exercise leg and analyzed for fiber type-specific SC content. Maximal voluntary contraction (MVC) and serum creatine kinase (CK) were evaluated as indices of recovery from muscle damage. In type II fiber-associated SCs, the whey group increased SCs/fiber from 0.05 [0.02; 0.07] to 0.09 [0.06; 0.12] (p < 0.05) and 0.11 [0.06; 0.16] (p < 0.001) at 24 and 48 h, respectively, and exhibited a difference from the placebo group (p < 0.05) at 48 h. The whey group increased SCs/myonuclei from 4?% [2; 5] to 10?% [4; 16] (p?p < 0.001) and muscle soreness and CK increased (p < 0.001), irrespective of supplementation. In conclusion, whey protein supplementation may accelerate SC proliferation as part of the regeneration or remodeling process after high-intensity eccentric exercise.     

Indices of skeletal muscle damage and connective tissue breakdown following eccentric muscle contractions

 Indirect indices of exercise-induced human skeletal muscle damage and connective tissue breakdown were studied following a single bout of voluntary eccentric muscle contractions. Subjects (six female, two male), mean (SD) age 22 (2) years performed a bout of 50 maximum voluntary eccentric contractions of the knee extensors of a single leg. The eccentric exercise protocol induced muscle soreness (P < 0.05 Wilcoxon test), chronic force loss, and a decline in the 20:100 Hz percutaneous electrical myostimulation force ratio [P < 0.01, repeated measures analysis of variance (ANOVA)]. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities were elevated (P < 0.01, repeated measures ANOVA) following the bout. The mean (SD) CK and LDH levels recorded 3 days post-exercise were 2815 (4144) IU · l^–1 and 375 (198) IU · l^–1, respectively. Serum alkaline phosphatase activity showed no changes throughout the study, and a non-significant increase (P = 0.058, repeated measures ANOVA) in pyridinoline was recorded following the bout. Urinary hydroxyproline (HP) and hydroxylysine (HL) excretion, expressed in terms of creatinine (Cr) concentration, increased after exercise (P < 0.05 and P < 0.01, respectively, repeated measures ANOVA). An increased HP:Cr was recorded 2 days post-exercise and HL:Cr was increased above baseline on days 2, 5, and 9 post-exercise. This indirect evidence of exercise-induced muscle damage suggests that myofibre disruption was caused by the eccentric muscle contractions. Elevated urine concentrations of indirect indices of collagen breakdown following eccentric muscle contractions suggests an increased breakdown of connective tissue, possibly due to a localised inflammatory response. Accepted: 9 October 1996     

Taurine supplementation decreases oxidative stress in skeletal muscle after eccentric exercise

Infrequent exercise, typically involving eccentric actions, has been shown to cause oxidative stress and to damage muscle tissue. High taurine levels are present in skeletal muscle and may play a role in cellular defences against free radical‐mediated damage. This study investigates the effects of taurine supplementation on oxidative stress biomarkers after eccentric exercise (EE). Twenty‐four male rats were divided into the following groups (n = 6): control; EE; EE plus taurine (EE + Taurine); EE plus saline (EE + Saline). Taurine was administered as a 1‐ml 300 mg kg^?1 per body weight (BW) day^?1 solution in water by gavage, for 15 consecutive days. Starting on the 14th day of supplementation, the animals were submitted to one 90‐min downhill run session and constant velocity of 1·0 km h^?1. Forty‐eight hours after the exercise session, the animals were killed and the quadriceps muscles were surgically removed. Production of superoxide anion, creatine kinase (CK) levels, lipoperoxidation, carbonylation, total thiol content and antioxidant enzyme were analysed. Taurine supplementation was found to decrease superoxide radical production, CK, lipoperoxidation and carbonylation levels and increased total thiol content in skeletal muscle, but it did not affect antioxidant enzyme activity after EE. The present study suggests that taurine affects skeletal muscle contraction by decreasing oxidative stress, in association with decreased superoxide radical production. Copyright © 2010 John Wiley & Sons, Ltd.     

Effect of maximal-intensity exercise on systemic nitro-oxidative stress in men and women

Objectives: The aim of this study was to test the hypotheses: (1) there is a negative correlation between protein and lipid oxidative damage following maximal-intensity exercise, and oxygen uptake and work intensity (%VO_2max) at the respiratory compensation point (RCP) in women and men; (2) nitro-oxidative stress following maximal-intensity exercise results from the intensification of anaerobic processes and muscle fibre micro-damage.

Methods: Study participants comprised 20 women (21.34±1.57 years) and 20 men (21.97±1.41 years) who performed a treadmill incremental test (IT); VO_2max: 45.08?±?0.91 and 57.38?±?1.22?mL?kg^?1?min^?1 for women and men, respectively. The oxidized low-density lipoprotein (ox-LDL), 3-nitrotyrosine (3-NT) concentration and creatine kinase (CK) as well as lactate dehydrogenase (LDH) activity were measured in the blood serum, and total antioxidative capacity (TAC) and lactate concentration (Lac) were determined in blood plasma before and after IT.

Results: After the IT, increases in ox-LDL, 3-NT, CK, and LDH were seen in both groups (P?P?P?Conclusions: The gain of ox-LDL and 3-NT following maximal-intensity exercise is independent of VO_2max, oxygen consumption and exercise intensity at RCP. This increase of ox-LDL and 3-NT is indicative of similar lipid and protein damage in women and men. A significant increase in TAC in women following maximal-intensity exercise is the result of muscle fibre micro-injuries.     

Acute and remote biochemical and physiological effects of exhaustive weightlifting exercise

The goal of the work was a study of exhaustive weightlifting exercise effect on prolonged changes in physiological and biochemical variables characterized functional status of skeletal muscles. An exercise gave rise to significant blood lactate concentration increase that was indicative of an anaerobic metabolism to be a predominant mechanism of muscle contraction energy supply. A reduction of m. rectus femoris EMG activity (amplitude and frequency), tonus of tension and an increase in tonus of relaxation were found immediately after exercise. Both EMG amplitude and frequency were increased 1 day post-exercise. However, after 3 days of recovery, EMG amplitude and frequency were decreased again and, in parallel, blood serum creatine kinase (CK) activity was significantly increased. After 9 recovery days, all measured variables with the exception of CK were normalized. A significant reverse correlation was found between blood serum lactate concentration and m. rectus femoris EMG activity at the same time points. Blood serum CK activity and m. rectus femoris EMG and tonus variables were observed to be significantly reversely correlated on the 3rd post-exercise day. Presented data demonstrate that exhaustive exercise-induced muscle injury resulted in phase alterations in electrical activity and tonus which correlated with lactate concentration and CK activity in blood serum.     

Serum creatine kinase activity following repeated bouts of isometric exercise with different muscle groups

The purpose of this study was to examine the relationship between the muscle mass involved in exercise and post-exercise serum creatine kinase (CK) elevation. Twelve untrained college-aged men completed three isometric exercises: one arm flexion (OAF), two arm flexion (TAF) and one leg knee extension (OLE). These exercises were balanced over subjects and days and separated by two week intervals. Each exercise consisted of 40 maximal isometric concentrations lasting for 10 s with a 20 s rest between contractions. Relative increases in serum CK for OAF, TAF, and OLE were 181 +/- 70% (SD), 222 +/- 69% and 297 +/- 67%, respectively. An ANOVA using a latin square design for analysis of carry over effects showed that these CK increases were not significantly different (p greater than 0.05). However, the increase in serum CK following the first exercise (379 +/- 90%), regardless of what it was (OAF, TAF, or OLE), was significantly greater (p less than 0.05) than those following bouts 2 and 3 (155 +/- 29%; 167 +/- 54%). Regression analysis indicated that post-exercise serum CK elevation was not related to the amount of muscle mass involved in the exercise (r = 0.30, p greater than 0.05) nor to muscle tension developed (r = 0.28, p greater than 0.05). We conclude that post-exercise serum CK elevation is not necessarily related to the muscle mass involved in the exercise. Because each exercise involved the use of different muscle groups, factors outside the exercising muscle may contribute to post-exercise serum enzyme activity.     

Improved Inflammatory Balance of Human Skeletal Muscle during Exercise after Supplementations of the Ginseng-Based Steroid Rg1

The purpose of the study was to determine the effect of ginseng-based steroid Rg1 on TNF-alpha and IL-10 gene expression in human skeletal muscle against exercise challenge, as well as on its ergogenic outcomes. Randomized double-blind placebo-controlled crossover trials were performed, separated by a 4-week washout. Healthy young men were randomized into two groups and received capsule containing either 5 mg of Rg1 or Placebo one night and one hour before exercise. Muscle biopsies were conducted at baseline, immediately and 3 h after a standardized 60-min cycle ergometer exercise. While treatment differences in glycogen depletion rate of biopsied quadriceps muscle during exercise did not reach statistical significance, Rg1 supplementations enhanced post-exercise glycogen replenishment and increased citrate synthase activity in the skeletal muscle 3 h after exercise, concurrent with improved meal tolerance during recovery (P<0.05). Rg1 suppressed the exercise-induced increases in thiobarbituric acids reactive substance (TBARS) and reversed the increased TNF-alpha and decreased IL-10 mRNA of quadriceps muscle against the exercise challenge. PGC-1 alpha and GLUT4 mRNAs of exercised muscle were not affected by Rg1. Maximal aerobic capacity (VO_2max) was not changed by Rg1. However, cycling time to exhaustion at 80% VO_2max increased significantly by ~20% (P<0.05). Conclusion: Our result suggests that Rg1 is an ergogenic component of ginseng, which can minimize unwanted lipid peroxidation of exercised human skeletal muscle, and attenuate pro-inflammatory shift under exercise challenge.     

Exercise-induced oxidative stress in humans: cause and consequences

The observation that muscular exercise is associated with oxidative stress in humans was first reported over 30 years ago. Since this initial report, numerous studies have confirmed that prolonged or high-intensity exercise results in oxidative damage to macromolecules in both blood and skeletal muscle. Although the primary tissue(s) responsible for reactive oxygen species (ROS) production during exercise remains a topic of debate, compelling evidence indicates that muscular activity promotes oxidant production in contracting skeletal muscle fibers. Mitochondria, NADPH oxidase, PLA₂-dependent processes, and xanthine oxidase have all been postulated to contribute to contraction-induced ROS production in muscle but the primary site of contraction-induced ROS production in muscle fibers remains unclear. Nonetheless, contraction-induced ROS generation has been shown to play an important physiological function in the regulation of both muscle force production and contraction-induced adaptive responses of muscle fibers to exercise training. Although knowledge in the field of exercise and oxidative stress has grown markedly during the past 30 years, this area continues to expand and there is much more to be learned about the role of ROS as signaling molecules in skeletal muscle.     

Serum and urinary markers of skeletal muscle tissue damage after weight lifting exercise

The purpose of this study was to determine whether high intensity weight lifting exercise produces elevations of urinary 3-methylhistidine (3-MH), serum creatine kinase activity (CK), and serum myoglobin concentration (MY), and whether trained weight lifters differed in such responses when compared to a group of untrained subjects. Ten experienced male weight lifters (EWL) and seven untrained male subjects (IWL) performed three sets of six weight lifting exercises at 70%-80% of 1 RM. All subjects consumed a meat-free diet. The 3-MH:creatinine (3-MH:CR) values decreased 24 h and 48 h following exercise (P less than 0.05). The 12-h and 24-h postexercise CK response and the 12-h postexercise MY response increased for both EWL and IWL (P less than 0.05). However, EWL had a lower 24-h postexercise CK response and lower 12-h and 24-h postexercise MY responses compared to IWL (P less than 0.05). Within 48 h following weight lifting exercise, skeletal muscle protein degradation (as assessed by 3-MH:CR values) decreased regardless of prior training experience whereas skeletal muscle tissue damage (as assessed by CK and MY responses) increased. However, prior weight lifting training appeared to diminish the extent of muscle tissue damage.     

急性运动对大鼠骨骼肌中丙二醛和血清肌酸激酶的影响

研究一次急性力竭运动对大鼠骨骼肌红肌、白肌中脂质过氧化水平的影响及血清酶的变化情况。发现运动组大鼠红肌中丙二醛（ＭＤＡ）含量和碱性磷酸酶（ＡＫＰ）活性比安静组显著升高;白肌中ＭＤＡ含量、超氧化物歧化酶（ＳＯＤ）活性和ＡＫＰ活性有升高的趋势;血清肌酸激酶（ＣＫ）活性运动组比安静组有显著升高;但肌肉中ＭＤＡ含量与血清ＣＫ活性之间无显著相关。因此,ＭＤＡ增多可能并不是血清ＣＫ活性升高的主要原因。     

The relationship of creatine kinase variability with body composition and muscle damage markers following eccentric muscle contractions

[Purpose]

The purpose of the study was to investigate the relationship between CK variability and body composition and muscle damage markers following eccentric exercise.

[Methods]

Total 119 healthy male subjects were recruited to perform 50 eccentric contractions consisted of 2 sets of 25 contractions. Then, blood creatine kinase (CK) activity was analyzed to divide into three groups based on their CK activity levels. Maximum isometric strength (MIS), muscle soreness (SOR) and body composition data were obtained before and after exercise.

[Results]

The results showed that high CK responders had a significant decrease in MIS (p<0.001) and greater SOR (p<0.01) following eccentric exercise compared to low CK responders. Percent body fat was also higher in high responders compared to low responders (p=0.014). Peak CK activity was significantly correlated with MIS and SOR but no correlation with % body fat, muscle mass, and body mass index.

[Conclusion]

CK variability following eccentric exercise is closely related to MIS and SOR and % body fat may be a potent factor for CK variability.     

Eccentric exercise facilitates mesenchymal stem cell appearance in skeletal muscle

Eccentric, or lengthening, contractions result in injury and subsequently stimulate the activation and proliferation of satellite stem cells which are important for skeletal muscle regeneration. The discovery of alternative myogenic progenitors in skeletal muscle raises the question as to whether stem cells other than satellite cells accumulate in muscle in response to exercise and contribute to post-exercise repair and/or growth. In this study, stem cell antigen-1 (Sca-1) positive, non-hematopoetic (CD45^-) cells were evaluated in wild type (WT) and α7 integrin transgenic (α7Tg) mouse muscle, which is resistant to injury yet liable to strain, 24 hr following a single bout of eccentric exercise. Sca-1⁺CD45⁻ stem cells were increased 2-fold in WT muscle post-exercise. The α7 integrin regulated the presence of Sca-1⁺ cells, with expansion occurring in α7Tg muscle and minimal cells present in muscle lacking the α7 integrin. Sca-1⁺CD45⁻ cells isolated from α7Tg muscle following exercise were characterized as mesenchymal-like stem cells (mMSCs), predominantly pericytes. In vitro multiaxial strain upregulated mMSC stem cells markers in the presence of laminin, but not gelatin, identifying a potential mechanistic basis for the accumulation of these cells in muscle following exercise. Transplantation of DiI-labeled mMSCs into WT muscle increased Pax7⁺ cells and facilitated formation of eMHC⁺DiI⁻ fibers. This study provides the first demonstration that mMSCs rapidly appear in skeletal muscle in an α7 integrin dependent manner post-exercise, revealing an early event that may be necessary for effective repair and/or growth following exercise. The results from this study also support a role for the α7 integrin and/or mMSCs in molecular- and cellular-based therapeutic strategies that can effectively combat disuse muscle atrophy.     

SOD2 gene polymorphism and muscle damage markers in elite athletes

Abstract

Exercise-induced oxidative stress is a state that primarily occurs in athletes involved in high-intensity sports when pro-oxidants overwhelm the antioxidant defense system to oxidize proteins, lipids, and nucleic acids. During exercise, oxidative stress is linked to muscle metabolism and muscle damage, because exercise increases free radical production. The T allele of the Ala16Val (rs4880 C/T) polymorphism in the mitochondrial superoxide dismutase 2 (SOD2) gene has been reported to reduce SOD2 efficiency against oxidative stress. In the present study we tested the hypothesis that the SOD2 TT genotype would be underrepresented in elite athletes involved in high-intensity sports and associated with increased values of muscle and liver damage biomarkers. The study involved 2664 Caucasian (2262 Russian and 402 Polish) athletes. SOD2 genotype and allele frequencies were compared to 917 controls. Muscle and liver damage markers [creatine kinase (CK), creatinine, alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP)] were examined in serum from 1444 Russian athletes. The frequency of the SOD2 TT genotype (18.6%) was significantly lower in power/strength athletes (n = 524) compared to controls (25.0%, p = 0.0076) or athletes involved in low-intensity sports (n = 180; 33.9%, p < 0.0001). Furthermore, the SOD2 T allele was significantly associated with increased activity of CK (females: p = 0.0144) and creatinine level (females: p = 0.0276; males: p = 0.0135) in athletes. Our data show that the SOD2 TT genotype might be unfavorable for high-intensity athletic events.     

Creatine kinase activity of urinary bladder and skeletal muscle from control and streptozotocin-diabetic rats

The urinary bladder depends on intracellular ATP for the support of a number of essential intracellular processes including contraction. The concentration of ATP is maintained constant primarily via the rapid transfer of a phosphate from creatine phosphate (CP) to ADP catalyzed by the enzyme creatine kinase (CK). Since muscular pathologies associated with diabetes are in part related to intracellular alterations in metabolism, we have characterized the CK activity in both skeletal muscle and urinary bladder from control and streptozotocin-diabetic rats.The following is a summary of the results: 1) Bladder tissue from control rats showed linear kinetics with a V_max = 390 nmoles/mg protein/min, and a K_m = 275 µM. 2) Urinary bladder tissue isolated from diabetic rats displayed biphasic kinetics with V_max = 65 and 324 nmoles/mg protein/min, and K_m's = 10 µM and 190 µM respectively. 3) Skeletal muscle isolated from control rats showed linear kinetics with an approximate V_max of 800 nmoles/mg protein/min and a K_m of 280 µM CP. 4) Homogenates of skeletal muscle from diabetic rats showed complex kinetics not separable into distict component forms. 5) The K_m for ADP for both skeletal muscle and bladder was approximately 10 µM.These studies demonstrate that whereas bladders isolated from both control and diabetic rats possess a low-affinity isomer(s) of CK with similar maximum enzymatic activity, there is a high affinity isomer present within the urinary bladder muscle of diabetic rats that is not present in bladder tissue isolated from control rats. Skeletal muscle isolated from both diabetic and control rats exhibited a maximal activity 2 to 3 times higher than that of the bladder.