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Biomedical subjects

Mark A Tarnopolsky

Publications and source records attributed to Mark A Tarnopolsky.

At least 19 recordsLinked to original sources
PubMed2007

Beneficial effects of creatine, CoQ10, and lipoic acid in mitochondrial disorders.

Mitochondrial disorders share common cellular consequences: (1) decreased ATP production; (2) increased reliance on alternative anaerobic energy sources; and (3) increased production of reactive oxygen species. The purpose of the present study was to determine the effect of a combination therapy (creatine monohydrate, coenzyme Q(10), and lipoic acid to target the above-mentioned cellular consequences) on several outcome variables using a randomized, double-blind, placebo-controlled, crossover study design in patients with mitochondrial cytopathies. Three patients had mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), four had mitochondrial DNA deletions (three patients with chronic progressive external ophthalmoplegia and one with Kearns-Sayre syndrome), and nine had a variety of other mitochondrial diseases not falling into the two former groups. The combination therapy resulted in lower resting plasma lactate and urinary 8-isoprostanes, as well as attenuation of the decline in peak ankle dorsiflexion strength in all patient groups, whereas higher fat-free mass was observed only in the MELAS group. Together, these results suggest that combination therapies targeting multiple final common pathways of mitochondrial dysfunction favorably influence surrogate markers of cellular energy dysfunction. Future studies with larger sample sizes in relatively homogeneous groups will be required to determine whether such combination therapies influence function and quality of life.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

Influence of endurance exercise training and sex on intramyocellular lipid and mitochondrial ultrastructure, substrate use, and mitochondrial enzyme activity.

Impaired mitochondrial function and structure and intramyocellular lipid (IMCL) accumulation have been associated with obesity and Type 2 diabetes. We examined whether endurance exercise training and sex influenced IMCL and mitochondrial morphology using electron microscopy, whole-body substrate use, and mitochondrial enzyme activity. Untrained men (n = 5) and women (n = 7) were tested before and after 7 wk of endurance exercise training. Testing included 90 min of cycle ergometry at 60% Vo(2 peak) with preexercise muscle biopsies analyzed for IMCL and mitochondrial size/area using electron microscopy and short-chain beta-hydroxyacyl-CoA dehydrogenase (SCHAD) and citrate synthase (CS) enzyme activity. Training increased the mean lipid area density (P = 0.090), the number of IMCL droplets (P = 0.055), the number of IMCL droplets in contact with mitochondria (P = 0.010), the total mitochondrial area (P < 0.001), and the size of individual mitochondrial fragments (P = 0.006). Women had higher mean lipid area density (P = 0.030) and number of IMCL droplets (P = 0.002) before and after training, but higher individual IMCL area only before training (P = 0.013), compared with men. Women oxidized more fat (P = 0.027) and less carbohydrate (P = 0.032) throughout the study. Training increased Vo(2 peak) (P < 0.001), %fat oxidation (P = 0.018), SCHAD activity (P = 0.003), and CS activity (P = 0.042). In summary, endurance exercise training increased IMCL area density due to an increase in the number of lipid droplets, whereas the increase in total mitochondrial area was due to an increase in the size of individual mitochondrial fragments. In addition, women have higher IMCL content compared with men due mainly to a greater number of individual droplets. Finally, endurance exercise training increased the proportion of IMCL in physical contact with mitochondria.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2006

Hypertrophy with unilateral resistance exercise occurs without increases in endogenous anabolic hormone concentration.

We aimed to gain insight into the role that the transitory increases in anabolic hormones play in muscle hypertrophy with unilateral resistance training. Ten healthy young male subjects (21.8 +/- 0.4 years, 1.78 +/- 0.04 m, 75.6 +/- 2.9 kg; mean +/- SE) engaged in unilateral resistance training for 8 week (3 days/week). Exercises were knee extension and leg press performed at 80-90% of the subject's single repetition maximum (1RM). Blood samples were collected in the acute period before and after the first training bout and following the last training bout and analyzed for total testosterone, free-testosterone, luteinizing hormone, sex hormone binding globulin, growth hormone, cortisol, and insulin-like growth factor-1. Thigh muscle cross sectional area (CSA) and muscle fibre CSA by biopsy (vastus lateralis) were measured pre- and post-training. Acutely, no changes in systemic hormone concentrations were observed in the 90 min period following exercise and there was no influence of training on these results. Training-induced increases were observed in type IIx and IIa muscle fibre CSA of 22 +/- 3 and 13 +/- 2% (both P < 0.001). No changes were observed in fibre CSA in the untrained leg (all P > 0.5). Whole muscle CSA increased by 5.4 +/- 0.9% in the trained leg (P < 0.001) and remained unchanged in the untrained leg (P = 0.76). Isotonic 1RM increased in the trained leg for leg press and for knee extension (P < 0.001). No changes were seen in the untrained leg. In conclusion, unilateral training induced local muscle hypertrophy only in the exercised limb, which occurred in the absence of changes in systemic hormones that ostensibly play a role in muscle hypertrophy.

Adult↗
PubMed2006

Carnosine, taurine and enzyme activities of human skeletal muscle fibres from elderly subjects with osteoarthritis and young moderately active subjects.

Ageing is associated with a reduction in muscle carnosine (beta-alanyl-L-histidine), but there are no data on the changes specifically in type I and type II muscle fibres. Given the higher carnosine content of type II fibers, changes observed in whole muscle may be secondary to a shift in fibre composition. Carnosine, beta-alanine, histidine, taurine, and citrate synthase (CS) and glycogen phosphorylase (Phos), were measured in pools of single muscle fibres from freeze-dried muscle biopsies of vastus lateralis of nine elderly sedentary subjects (65-80 years) with osteoarthritis of the knee and undergoing total knee replacement, and nine young moderately active healthy subjects (20-35 years). Fibres were characterised as type I or II by myosin ATPase activity. Carnosine was 53.2% lower in type II fibres of older subjects resulting in an estimated 7% (and most probably still higher) decline in intracellular physico-chemical buffering capacity. Younger subjects showed higher CS activities in type I and higher Phos activities in type II fibres. These differences were less apparent in elderly subjects. Possible causes for the change in the carnosine content are reduced physical activity, reduced meat intake, or the result of progressive denervation.

Adult↗
PubMed2006

Short-term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance.

Brief, intense exercise training may induce metabolic and performance adaptations comparable to traditional endurance training. However, no study has directly compared these diverse training strategies in a standardized manner. We therefore examined changes in exercise capacity and molecular and cellular adaptations in skeletal muscle after low volume sprint-interval training (SIT) and high volume endurance training (ET). Sixteen active men (21 +/- 1 years, ) were assigned to a SIT or ET group (n = 8 each) and performed six training sessions over 14 days. Each session consisted of either four to six repeats of 30 s 'all out' cycling at approximately 250% with 4 min recovery (SIT) or 90-120 min continuous cycling at approximately 65% (ET). Training time commitment over 2 weeks was approximately 2.5 h for SIT and approximately 10.5 h for ET, and total training volume was approximately 90% lower for SIT versus ET ( approximately 630 versus approximately 6500 kJ). Training decreased the time required to complete 50 and 750 kJ cycling time trials, with no difference between groups (main effects, P </= 0.05). Biopsy samples obtained before and after training revealed similar increases in muscle oxidative capacity, as reflected by the maximal activity of cytochrome c oxidase (COX) and COX subunits II and IV protein content (main effects, P </= 0.05), but COX II and IV mRNAs were unchanged. Training-induced increases in muscle buffering capacity and glycogen content were also similar between groups (main effects, P </= 0.05). Given the large difference in training volume, these data demonstrate that SIT is a time-efficient strategy to induce rapid adaptations in skeletal muscle and exercise performance that are comparable to ET in young active men.

Adaptation, Physiological↗
PubMed2006

Menstrual cycle phase and sex influence muscle glycogen utilization and glucose turnover during moderate-intensity endurance exercise.

Numerous studies from our and other laboratories have shown that women have a lower respiratory exchange ratio (RER) during exercise than equally trained men, indicating a greater reliance on fat oxidation. Differences in estrogen concentration between men and women likely play a role in this sex difference. Differing estrogen and progesterone concentrations during the follicular (FP) and luteal (LP) phases of the female menstrual cycle suggest that fuel use may also vary between phases. The purpose of the current study was to determine the effect of menstrual cycle phase and sex upon glucose turnover and muscle glycogen utilization during endurance exercise. Healthy, recreationally active young women (n = 13) and men (n = 11) underwent a primed constant infusion of [6,6-2H]glucose with muscle biopsies taken before and after a 90-min cycling bout at 65% peak O2 consumption. LP women had lower glucose rate of appearance (Ra, P = 0.03), rate of disappearance (Rd, P = 0.03), and metabolic clearance rate (MCR, P = 0.04) at 90 min of exercise and lower proglycogen (P = 0.04), macroglycogen (P = 0.04), and total glycogen (P = 0.02) utilization during exercise compared with FP women. Men had a higher RER (P = 0.02), glucose Ra (P = 0.03), Rd (P = 0.03), and MCR (P = 0.01) during exercise compared with FP women, and men had a higher RER at 75 and 90 min of exercise (P = 0.04), glucose Ra (P = 0.01), Rd (P = 0.01), and MCR (P = 0.001) and a greater PG utilization (P = 0.05) compared with LP women. We conclude that sex, and to a lesser extent menstrual cycle, influence glucose turnover and glycogen utilization during moderate-intensity endurance exercise.

Adult↗
PubMed2006

Sex-based effects on the distribution of NK cell subsets in response to exercise and carbohydrate intake in adolescents.

Carbohydrate (CHO) supplementation and female sex independently influence the natural killer (NK) cell response to acute exercise. Consequently, this study sought to elucidate sex-based differences in the distribution of NK cell subsets (i.e., CD56dim and CD56bright) in response to exercise and CHO intake. Twenty-two healthy 14-yr-old girls (n = 11) and boys (n = 11) cycled for 60 min at 70% maximal oxygen consumption while drinking 6% CHO (CT) or flavored water (WT). Blood was collected at rest, during exercise (30 and 60 min), and during recovery (30 and 60 min) to identify CD3- CD56dim and CD3- CD56bright NK cells. The activation marker CD69 was also determined on CD3- CD56+ cells. CD56dim responses, expressed as proportions or cell counts, were greater (P < or = 0.01) in girls by 67 and 105%, respectively. CD56bright cell counts (P = 0.006), but not CD56bright proportions (P = 0.89), were greater in girls by 82%. Both CD56dim and CD56bright subset responses, expressed as proportions or cell counts, were lower (P < or = 0.01) in CT vs. WT by 33-36%. The CD56bright-to-CD56dim ratio decreased at 30 min of exercise but increased during recovery (P < 0.001), with no effect of sex or CHO. Regardless of trial, CD3- CD56+ cells expressed approximately 18% higher levels of CD69 during recovery in girls but not boys (P = 0.03), despite similar proportions and counts of CD69+ cells. These results demonstrate sex-based differences in the distribution of NK cell subsets and activation status in response to exercise, but not CHO intake, and further support the need to control for sex in exercise immunology studies.

Adolescent↗
PubMed2006

Nutritional therapy improves function and complements corticosteroid intervention in mdx mice.

Corticosteroid therapy for Duchenne muscular dystrophy is effective but associated with long-term side effects. To determine the potential therapeutic benefit from four nutritional compounds (creatine monohydrate, conjugated linoleic acid, alpha-lipoic acid, and beta-hydroxy-beta-methylbutyrate) alone, in combination, and with corticosteroids (prednisolone), we evaluated the effects on several variables in exercising mdx mice. Outcome measures included grip strength, rotarod performance, serum creatine kinase levels, muscle metabolites, internalized myonuclei, and retroperitoneal fat pad weight. In isolation, each nutritional treatment showed some benefit, with the combination therapy showing the most consistent benefits. Prednisolone and the combination therapy together provided the most consistent evidence of efficacy; increased peak grip strength (P < 0.05), decreased grip strength fatigue (P < 0.05), decreased number of internalized myonuclei (P < 0.01), and smaller retroperitoneal fat pad stores (P < 0.001). This study provided evidence for therapeutic benefit from a four-compound combination therapy alone, and in conjunction with corticosteroids in the mdx model of DMD.

Animals↗
PubMed2006

Oxidative stress and antioxidant enzyme upregulation in SOD1-G93A mouse skeletal muscle.

Amyotrophic lateral sclerosis (ALS) is caused by motor neuron loss in the spinal cord, but the mechanisms responsible are not known. Ubiquitous transgenic overexpression of copper/zinc superoxide dismutase (SOD1) mutations causing familial ALS (SOD1mut) leads to an ALS phenotype in mice; however, restricted expression of SOD1mut in neurons alone is not sufficient to cause this phenotype, suggesting that non-neuronal SOD1mut expression is also required for disease manifestation. Recently, several investigators have suggested that SOD1mut -mediated oxidative stress in skeletal muscle may contribute to ALS pathogenesis. The purpose of this study was to examine oxidative stress and antioxidant enzyme adaptation in 95-day-old SOD1-G93A skeletal muscle. We observed significant elevations in both malondialdehyde (22% and 31% in red and white gastrocnemius, respectively) and protein carbonyls (53% in red gastrocnemius) in SOD1-G93A mice. Copper/zinc SOD activity was higher in red and white SOD1-G93A gastrocnemius (7- and 10-fold, respectively), as was manganese SOD (4- and 5-fold, respectively) and catalase (2- and 2.5-fold, respectively). Taken together, our data demonstrate oxidative stress and compensatory antioxidant enzyme upregulation in SOD1-G93A skeletal muscle.

Animals↗
PubMed2006

Sporadic rippling muscle disease unmasked by simvastatin.

We report a 53-year-old-man who developed rippling muscle disease (RMD) 2 months after starting simvastatin therapy for hypercholesterolemia. He experienced stiffness, myalgias, and classic rippling, which was confirmed on clinical examination. Discontinuation of the statin improved his symptoms. Simvastatin therapy was resumed and resulted in a prompt and severe return of his symptoms. Approximately 1 year after symptom onset he developed mild seropositive oculobulbar myasthenia gravis, which spontaneously remitted after 5 months. We postulate that an immune-mediated disruption of caveolar function was exacerbated by statin exposure. We are unaware of any previous cases of statin-mediated unmasking of RMD.

Anticholesteremic Agents↗
PubMed2006

Transient caloric restriction in early adulthood hastens disease endpoint in male, but not female, Cu/Zn-SOD mutant G93A mice.

Long-term caloric restriction (CR) prolongs the lifespan in healthy insects, rodents, and nonhuman primates. We previously reported that long-term CR improves motor performance but hastens clinical onset of disease in an animal model of amyotrophic lateral sclerosis (G93A mice). G93A mice overexpress the mutant human Cu/Zn-SOD gene and show progressive lower motor neuron weakness and increased oxidative stress. To study short-term (15 days) CR in the same animal model, we investigated the effect of transient caloric restriction (TCR) on paw grip endurance, clinical onset, disease progression (time from clinical onset to endpoint), and lifespan. Starting at age 40 days, 32 separately caged G93A mice were randomly divided into two groups: ad libitum (AL, n = 17; 10 females, 7 males) and TCR (n = 15; 6 females, 9 males) with a diet equal to 60% of AL. When the TCR mice lost 30% of their weight they were offered food AL until endpoint, otherwise all TCR mice were provided food AL from age 55 days until endpoint (i.e., range of TCR = 13-15 days). Paw grip endurance started to decrease significantly at age 96 days compared with baseline values for all the groups. TCR males reached clinical onset 5 days sooner than TCR females. Disease progression was 8 days faster in TCR mice than AL mice and 6 days faster in male mice than female mice. The probability of survival was significantly different between the groups, with the TCR males having a faster rate of reaching endpoint than TCR females, AL males, and AL females. We conclude that TCR hastens clinical onset of disease and shortens the lifespan in male, but not female, G93A mice. Moreover, TCR hastens progress of disease but has no effect on paw grip endurance. The female sex is protective against the detrimental effects of short-term CR in G93A mice. Assuming we can extrapolate these results to humans, short-term CR should be avoided in patients with amyotrophic lateral sclerosis, especially men.

Amyotrophic Lateral Sclerosis↗
PubMed2006

The effect of body weight-supported treadmill training on muscle morphology in an individual with chronic, motor-complete spinal cord injury: A case study.

OBJECTIVE: The purpose of this pilot study was to examine the effects of 4 months of thrice-weekly body weight-supported treadmill training (BWSTT) on skeletal muscle morphology in a woman (age 27 y) with chronic, motor-complete (ASIA B) spinal cord injury (SCI). METHODS: The participant performed passive thrice-weekly BWSTT for 4 months (48 total sessions) with manual assistance from therapists. Muscle biopsies of the vastus lateralis were taken prior to the beginning of the training program as well as following the completion of 4 months of training. Histochemical analysis was utilized to evaluate changes in muscle fiber size and type following training. RESULTS: At baseline, vastus lateralis muscle biopsies showed evidence of fiber atrophy and fiber type redistribution typical of persons with SCI, with mean fiber areas (and % distributions) of type I, type IIa and type IIx fibers being 3474 microm2 (1.3%), 3146 microm2 (30.8%) and 1284 microm2 (68.0%), respectively. Following training, there were increases in treadmill walking speed (pre: 1.0km/h; post: 2.5km/h) and distance walked/session (pre: 500m; post: 1875m). Vastus lateralis mean fiber area increased by 27.1% and type I fiber % distribution increased to 24.6%, whereas type IIa and type IIx fiber % distributions both decreased following training. CONCLUSION: These data indicate that 4 months of thrice-weekly BWSTT improved muscle morphology in an individual with chronic, motor-complete SCI.

Adult↗
PubMed2006

The effect of aging on anaerobic and aerobic enzyme activities in human skeletal muscle.

The effect of aging on metabolic enzyme activity remains controversial, possibly due to physical activity differences. We examined the effect of aging on the enzyme activity for anaerobic and aerobic pathways in nonweight-bearing human skeletal muscle from relatively sedentary males. The muscle obliquus internus abdominis was analyzed for anaerobic (creatine kinase, adenylate kinase, and lactate dehydrogenase) and aerobic (2-oxoglutarate dehydrogenase and carnitine palmitoyltransferase) enzyme activities in two groups: middle-aged (29-54 years) and older (61-74 years) adults. All enzyme activities were lower in older versus middle-aged adults when results were expressed as muscle wet weight (p <.05). When activity was expressed relative to the protein content, only lactate dehydrogenase remained significantly lower in older versus middle-aged adults (p <.001). In conclusion, some of the reduction in muscle performance in older adults may be due to lower activity of the anaerobic and aerobic enzymes as well as protein content, not solely due to a decrease in physical activity.

Abdominal Muscles↗
PubMed2006

What can metabolic myopathies teach us about exercise physiology?

Exercise physiologists are interested in metabolic myopathies because they demonstrate how knocking out a component of a specific biochemical pathway can alter cellular metabolism. McArdle's disease (myophosphorylase deficiency) has often been studied in exercise physiology to demonstrate the influence of removing the major anaerobic energy supply to skeletal muscle. Studies of patients with McArdle's disease have shown the increased reliance on blood-borne fuels, the importance of glycogen to maximal aerobic capacity, and the use of nutritional strategies to bypass metabolic defects. Myoadenylate deaminase deficiency is the most common metabolic enzyme deficiency in human skeletal muscle. It is usually compensated for endogenously and does not have a major influence on high-energy power output. Nutritional interventions such as carbohydrate loading and carbohydrate supplementation during exercise are essential components of therapy for patients with fatty acid oxidation defects. Cases of mitochondrial myopathies illustrate the importance of peripheral oxygen extraction for maximal aerobic capacity and show how both exercise and nutritional interventions can partially compensate for these mutations. In summary, metabolic myopathies provide important insights into regulatory and nutritional aspects of the major biochemical pathways of intermediary metabolism in human skeletal muscle.

Azasteroids↗
PubMed2006

Immunological changes in response to exercise: influence of age, puberty, and gender.

PURPOSE: This study tested the hypothesis that exercise-induced perturbation and recovery of the immune system would vary with age, puberty, and gender in healthy children and adolescents. METHODS: Twelve-year-old girls (YG; N = 14) and boys (YB; N = 20), and 14-yr-old girls (OG; N = 11) and boys (OB; N = 13) cycled for 60 min at 70% VO2max. Blood was collected before, at 30 and 60 min of exercise, and at 30 and 60 min of recovery to measure total leukocytes, leukocyte and lymphocyte subsets, and cytokines. Age and pubertal (Tanner stage) effects within genders and gender effects within age and pubertal groups were determined. RESULTS: Exercise-induced increases in lymphocytes, CD3-CD16+CD56+ counts, and IL-6 were approximately 83, 90, and 390% greater in OG versus YG (P < 0.05). Recovery leukocytosis and neutrophilia were approximately 56 and 35% greater in OB versus YB (P < 0.05). Pubertal stage did not have a statistically significant influence on responses in girls, but the lowest pubertal stage consistently showed smaller changes in lymphocytes and CD3-CD16+CD56+ counts. Recovery neutrophilia was approximately 120% greater in postpubertal boys versus prepubertal or pubertal boys (P < 0.05). Responses of lymphocytes and CD3-CD16+CD56+ counts, respectively, were approximately 120 and 82% greater in OG versus OB (P < 0.05), with no differences between YG and YB. Exercise-induced increases in total leukocytes, lymphocytes, and CD3-CD16+CD56+ counts were at least 35% greater in girls versus boys of similar pubertal status (P < 0.05). Regardless of age, puberty, or gender, IL-8 levels were significantly higher during recovery versus rest (P < 0.05). CONCLUSION: These results highlight the need to control for age, puberty, and gender when interpreting immunologic responses to exercise in a pediatric population.

Adolescent↗
PubMed2006

Puberty effects on NK cell responses to exercise and carbohydrate intake in boys.

UNLABELLED: Previous research has demonstrated that younger versus older animals and humans experience smaller perturbations in natural killer (NK) cells in response to physiological stress. PURPOSE: To determine whether the smaller perturbations in NK cells induced by strenuous exercise and carbohydrate (CHO) intake, previously reported in children, are influenced by puberty. METHODS: Twenty 12-yr-old boys, distinguished as prepubertal (Tanner (T) 1, N = 7), early pubertal (T2, N = 7), or pubertal (T3-5, N = 6), cycled for 60 min at 70% VO(2max) while drinking 6% CHO (CT) or flavored water (WT). Blood was collected at rest and during (30 and 60 min) and following (30 and 60 min) exercise to identify NK cells as CD3(-)CD56(dim) or CD3(-)CD56(dim). CD69 expression on CD3(-)CD56(+) cells was also determined. RESULTS: A puberty x CHO x exercise interaction was found for the proportion, but not number, of CD56(dim) cells (P = 0.06). CD56(dim) cell counts were lower in CT versus WT (P < 0.001). Responses of CD56(bright) proportions (P = 0.007) and counts (P = 0.03) depended on pubertal status, but not CHO. The CD56(bright):CD56(dim) ratio remained stable during exercise, but during recovery was higher in T1 and T3-5 versus T2 (P = 0.08) and in CT versus WT (P = 0.04). During recovery, CD3(-)CD56(+) cells expressed higher levels of CD69 (P = 0.01), with no change in the proportion of CD69(+) cells. CONCLUSION: These results confirm the influence of puberty on the distribution of NK cell subsets in response to exercise and CHO intake. Increased CD69 expression suggests that NK cells increase activation status during recovery from physiological stress.

Antigens, CD↗
PubMed2005

No effect of short-term 17beta-estradiol supplementation in healthy men on systemic inflammatory responses to exercise.

Sex-based differences in inflammatory responses to exercise may be mediated by estrogen through increased muscle membrane stability and/or inhibited cytokine production. In this study, in vivo effects of estrogen on systemic inflammation-related responses to exercise were assessed in healthy men. In a double-blind, placebo-controlled, crossover design, 11 men cycled for 90 min at 65% Vo2 max after 8 days of 17beta-estradiol supplementation (ES; 2 mg/day) or placebo (PL; glucose polymer). After a 2-wk washout, exercise was repeated after 8 days on the alternate treatment. Blood was collected pre- and postexercise to determine IL-6, soluble intercellular adhesion molecule-1 (sICAM-1), neutrophil counts, and cortisol. Preexercise serum was assayed for sex hormones. ES increased estradiol (133+/-71 to 840+/-633 pmol/l, P=0.005) and reduced testosterone (19.9+/-3.7 to 16.1+/-3.9 nmol/l, P=0.007). Exercise increased cortisol (P=0.02), IL-6 (P<0.001) and neutrophil counts (P<0.001) with no influence on sICAM-1 (P=0.34) and no effect of ES on these changes. Postexercise IL-6 and neutrophil counts were correlated (r=0.58, P=0.005); postexercise IL-6 and cortisol (r=0.18, P=0.43) and postexercise cortisol and neutrophil counts (r=0.06, P=0.78) were not. Postexercise sICAM-1 was not correlated with the above variables (P>or=0.79). In conclusion, 8 days of ES in healthy men did not influence systemic inflammation-related responses to acute exercise. Future studies should investigate 17beta-estradiol effects on IL-6 production and neutrophil infiltration within skeletal muscle during and after exercise.

Adult↗