OBJECTIVE:To investigate the effects of exercise on activation of mitogen-activated protein kinase (MAPK) signaling proteins in horses.ANIMALS:6 young trained Standardbred geldings.PROCEDURE:Horses performed a 20-minute bout of exercise on a treadmill at 80% of maximal heart rate. Muscle biopsy specimens were obtained from the vastus lateralis and pectoralis descendens muscles before and after exercise. Amount of expression and intracellular location of phosphospecific MAPK pathway intermediates were determined by use of western blotting and immunofluorescence staining.RESULTS:Exercise resulted in a significant increase in phosphorylation of p38 pathway intermediates, c-Jun NH2 terminal kinase (JNK), and heat shock protein 27 (HSP27) in the vastus lateralis muscle, whereas no significant changes were found in phosphorylation of extracellular regulated kinase. In the pectoralis descendens muscle, phosphorylation of p38 and HSP27 was significantly increased after exercise. Immunohistochemical analysis revealed fiber-type- specific locations of phosphorylated JNK in type 2a/b intermediate and 2b fibers and phosphorylated p38 in type 1 fibers. Phosphorylated HSP27 was strongly increased after exercise in type 1 and 2a fibers.CONCLUSIONS AND CLINICAL RELEVANCE:The p38 pathway and JNK are activated in the vastus lateralis muscle after a single 20-minute bout of submaximal exercise in trained horses. Phosphorylation of HSP27 as detected in the study reported here is most likely induced through the p38 signaling pathway.

The purpose of the study was to investigate whether severe fatigue, possibly leading to overreaching, could be diagnosed at an early stage by a combination of parameters. Seven well-trained mate subjects (age [mean SD]: 25.3 +/- 4.7yr; body mass: 76 +/- 6.6kg; VO2 max: 61.1 +/- 7ml(.)kg(-1.)min(-1)) increased their training load by doubling their training volume and increasing the intensity by 15% over a period of two weeks. Before and after this intensified training period subjects underwent a series of tests including a maximal incremental cycle ergometer test (Wmax) with continuous ventilatory measurements and blood lactate values, time trial, basal blood parameter tests (red and white blood profile), hormones [growth hormone (GH), insulin-like growth factor 1(IGF-1), adreno-corticotropic hormone (ACTH), cortisol], neuro-endocrine stress test [short insulin tolerance test (SITT), combined anterior pituitary test (CAPT) and exercise], a shortened Profile of Mood State (POMS), the estimated rate of perceived exertion (RPE) and a cognitive reaction time test. The intensified training period resulted in a significant increase of the training load (p < 0.01), training monotony (p < 0.01) and training strain (p < 0.01). The RPE during training increased significantly (p < 0.01) during the intensified training period. Total mood score obtained from the POMS tended to in-crease (p = 0.06), reflecting an increase in worse mood state. A novel finding was that reaction times increased significantly, indicating that overreaching might adversely affect speed of information processing by the brain, especially for the most difficult conditions. After the intensified training period, neither changes in exercise-induced plasma hormone values, nor SITT values were observed. During the CAPT only cortisol showed a significant decrease after the intensified training period. Hemoglobin showed a significant decrease after the intensified training period whereas hematocrit, red blood cell count (RBC) and MCV tended to decrease. The intensified training had no effect on physical performance (Wmax or time trial), maximal blood lactate, maximal heart rate and white blood cell profile. The most sensitive parameters for detecting overreaching are reaction time performance (indicative for cognitive brain functioning), RPE and to a lesser extend the shortened POMS. This strongly suggests, that central fatigue precedes peripheral fatigue. All other systems,including the neuro-endocrine, are more robust and react most likely at a later stage in exhaustive training periods.

The present study was designed to determine postexercise muscle protein synthesis and whole body protein balance following the combined ingestion of carbohydrate with or without protein and/or free leucine. Eight male subjects were randomly assigned to three trials in which they consumed drinks containing either carbohydrate (CHO), carbohydrate and protein (CHO+PRO), or carbohydrate, protein, and free leucine (CHO+PRO+Leu) following 45 min of resistance exercise. A primed, continuous infusion of L-[ring-13C6]phenylalanine was applied, with blood samples and muscle biopsies collected to assess fractional synthetic rate (FSR) in the vastus lateralis muscle as well as whole body protein turnover during 6 h of postexercise recovery. Plasma insulin response was higher in the CHO+PRO+Leu compared with the CHO and CHO+PRO trials (+240 +/- 19% and +77 +/- 11%, respectively, P < 0.05). Whole body protein breakdown rates were lower, and whole body protein synthesis rates were higher, in the CHO+PRO and CHO+PRO+Leu trials compared with the CHO trial (P < 0.05). Addition of leucine in the CHO+PRO+Leu trial resulted in a lower protein oxidation rate compared with the CHO+PRO trial. Protein balance was negative during recovery in the CHO trial but positive in the CHO+PRO and CHO+PRO+Leu trials. In the CHO+PRO+Leu trial, whole body net protein balance was significantly greater compared with values observed in the CHO+PRO and CHO trials (P < 0.05). Mixed muscle FSR, measured over a 6-h period of postexercise recovery, was significantly greater in the CHO+PRO+Leu trial compared with the CHO trial (0.095 +/- 0.006 vs. 0.061 +/- 0.008%/h, respectively, P < 0.05), with intermediate values observed in the CHO+PRO trial (0.0820 +/- 0.0104%/h). We conclude that coingestion of protein and leucine stimulates muscle protein synthesis and optimizes whole body protein balance compared with the intake of carbohydrate only.

Objective-To determine the effects of short-term IV administration of hydrocortisone or equine growth hormone (eGH) or long-term IM administration of eGH to horses on tissue sensitivity to exogenous insulin.Animals-5, Standardbreds and 4 Dutch Warmblood horses.Procedure-The euglycemic-hyperinsulinemic clamp technique was used to examine sensitivity of peripheral tissues to exogenous insulin 24 hours after administration of a single dose of hydrocortisone (0.06 mg/kg), eGH (20 mu g/kg), or saline (0.9% NaCl) solution and after long-term administration (11 to 15 days) of eGH to horses. The amounts of metabolized glucose (M) and plasma insulin concentration (1) were determined.Results-Values for M and the M-to-1 ratio were significantly higher 24 hours after administration of a single dose of hydrocortisone than after single-dose administration of eGH or saline solution. After long-term administration of eGH, basal I concentration was increased and the mean M-to-1 ratio was 22% lower, compared with values for horses treated with saline solution.Conclusions and Clinical Relevance-Increases in M and the M-to-l ratio after a single dose of hydrocortisone imply that short-term hydrocortisone treatment increases glucose use by, and insulin sensitivity of, peripheral tissues. Assuming a single dose of hydrocortisone improves sensitivity of peripheral tissues to insulin, it may be an interesting candidate for use in reducing insulin resistance in peripheral tissues of horses with several disease states. In contrast, long-term administration of eGH decreased tissue sensitivity to exogenous insulin associated with hyperinsulinemia. Therefore, increased concentrations of growth hormone may contribute to insulin resistance in horses with various disease states.

OBJECTIVE:It has been suggested that adiponectin regulates plasma free fatty acid (FFA) clearance by stimulating FFA uptake and/or oxidation in muscle. We aimed to determine changes in plasma adiponectin concentration and adiponectin receptor 1 and 2 mRNA expression in skeletal muscle during and after prolonged exercise under normal, fasting conditions (high FFA trial; HFA) and following pharmacological inhibition of adipose tissue lipolysis (low FFA trial; LFA). Furthermore, we aimed to detect and locate adiponectin in skeletal muscle tissue.METHODS:Ten subjects performed two exercise trials (120 min at 50% VO(2max)). Indirect calorimetry was used to determine total fat oxidation rate. Plasma samples were collected at rest, during exercise and during post-exercise recovery to determine adiponectin, FFA and glycerol concentrations. Muscle biopsies were taken to determine adiponectin protein and adiponectin receptor 1 and 2 mRNA expression and to localise intramyocellular adiponectin.RESULTS:Basal plasma adiponectin concentrations averaged 6.57+/-0.7 and 6.63+/-0.8 mg/l in the HFA and LFA trials respectively, and did not change significantly during or after exercise. In the LFA trial, plasma FFA concentrations and total fat oxidation rates were substantially reduced. However, plasma adiponectin and muscle adiponectin receptor 1 and 2 mRNA expression did not differ between trials. Immunohistochemical staining of muscle cross-sections showed the presence of adiponectin in the sarcolemma of individual muscle fibres and within the interfibrillar arterioles.CONCLUSION:Plasma adiponectin concentrations and adiponectin receptor 1 and 2 mRNA expression in muscle are not acutely regulated by changes in adipose tissue lipolysis and/or plasma FFA concentrations. Adiponectin is abundantly expressed in muscle, and, for the first time, it has been shown to be present in/on the sarcolemma of individual muscle fibres.

OBJECTIVE:To investigate whether protein kinase C (PKC) isoforms are expressed in equine skeletal muscle and determine their distribution in various types of fibers by use of immunofluorescence microscopy.ANIMALS:5 healthy adult Dutch Warmblood horses.PROCEDURE:In each horse, 2 biopsy specimens were obtained from the vastus lateralis muscle. Cryosections of equine muscle were stained with PKC isoform (alpha, beta1, beta2, delta, epsilon, or zeta)-specific polyclonal antibodies and examined by use of a fluorescence microscope. Homogenized muscle samples were evaluated via western blot analysis.RESULTS:The PKC alpha, beta1, beta2, delta, epsilon, and zeta isoforms were localized within the fibers of equine skeletal muscle. In addition, PKC alpha and beta2 were detected near or in the plasma membrane of muscle cells. For some PKC isoforms, distribution was specific for fiber type. Staining of cell membranes for PKC alpha was observed predominantly in fibers that reacted positively with myosin heavy chain (MHC)-IIa; PKC delta and epsilon staining were more pronounced in MHC-I-positive fibers. In contrast, MHC-I negative fibers contained more PKC zeta than MHC-I-positive fibers. Distribution of PKC beta1 was equal among the different fiber types.CONCLUSIONS AND CLINICAL RELEVANCE:Results indicated that PKC isoforms are expressed in equine skeletal muscle in a fiber type-specific manner. Therefore, the involvement of PKC isoforms in signal transduction in equine skeletal muscle might be dependent on fiber type.

Objectives: To investigate the effects of two different regimens of androgenic-anabolic steroid (AAS) administration on serum lipid and lipoproteins, and recovery of these variables after drug cessation, as indicators of the risk for cardiovascular disease in healthy male strength athletes.Methods: In a non-blinded study ( study 1) serum lipoproteins and lipids were assessed in 19 subjects who self administered AASs for eight or 14 weeks, and in 16 non-using volunteers. In a randomised double blind, placebo controlled design, the effects of intramuscular administration of nandrolone decanoate ( 200 mg/week) for eight weeks on the same variables in 16 bodybuilders were studied ( study 2). Fasting serum concentrations of total cholesterol, triglycerides, HDL-cholesterol (HDL-C), HDL2-cholesterol (HDL2-C), HDL3-cholesterol (HDL3-C), apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B), and lipoprotein ( a) ( Lp(a)) were determined.Results: In study 1 AAS administration led to decreases in serum concentrations of HDL-C ( from 1.08 (0.30) to 0.43 (0.22) mmol/l), HDL2-C ( from 0.21 (0.18) to 0.05 (0.03) mmol/l), HDL3-C (from 0.87 (0.24) to 0.40 (0.20) mmol/l, and Apo-A1 ( from 1.41 (0.27) to 0.71 (0.34) g/l), whereas Apo-B increased from 0.96 (0.13) to 1.32 (0.28) g/l. Serum Lp( a) declined from 189 ( 315) to 32 ( 63) U/l. Total cholesterol and triglycerides did not change significantly. Alterations after eight and 14 weeks of AAS administration were comparable. No changes occurred in the controls. Six weeks after AAS cessation, serum HDL-C, HDL2-C, Apo-A1, Apo-B, and Lp( a) had still not returned to baseline concentrations. Administration of AAS for 14 weeks was associated with slower recovery to pretreatment concentrations than administration for eight weeks. In study 2, nandrolone decanoate did not influence serum triglycerides, total cholesterol, HDL-C, HDL2-C, HDL3-C, Apo-A1, and Apo-B concentrations after four and eight weeks of intervention, nor six weeks after withdrawal. However, Lp( a) concentrations decreased significantly from 103 (68) to 65 (44) U/l in the nandrolone decanoate group, and in the placebo group a smaller reduction from 245 (245) to 201 (194) U/l was observed. Six weeks after the intervention period, Lp( a) concentrations had returned to baseline values in both groups.Conclusions: Self administration of several AASs simultaneously for eight or 14 weeks produces comparable profound unfavourable effects on lipids and lipoproteins, leading to an increased atherogenic lipid profile, despite a beneficial effect on Lp( a) concentration. The changes persist after AAS withdrawal, and normalisation depends on the duration of the drug abuse. Eight weeks of administration of nandrolone decanoate does not affect lipid and lipoprotein concentrations, although it may selectively reduce Lp( a) concentrations. The effect of this on atherogenesis remains to be established.

Recent evidence suggests that intramyocellular lipid (IMCL) accretion is associated with obesity and the development of insulin resistance and/or type 2 diabetes. However, trained endurance athletes are markedly insulin sensitive, despite an elevated mixed muscle lipid content. In an effort to explain this metabolic paradox, we compared muscle fiber type-specific IMCL storage between populations known to have elevated IMCL deposits. Immunofluorescence microscopy was performed on muscle biopsies obtained from eight highly trained endurance athletes, eight type 2 diabetes patients, and eight overweight, sedentary men after an overnight fast. Mixed muscle lipid content was substantially greater in the endurance athletes (4.0 +/- 0.4% area lipid stained) compared with the diabetes patients and the overweight men (2.3 +/- 0.4 and 2.2 +/- 0.5%, respectively). More than 40% of the greater mixed muscle lipid content was attributed to a higher proportion type I muscle fibers (62 +/- 8 vs. 38 +/- 3 and 33 +/- 7%, respectively), which contained 2.8 +/- 0.3-fold more lipid than the type II fibers. The remaining difference was explained by a significantly greater IMCL content in the type I muscle fibers of the trained athletes. Differences in IMCL content between groups or fiber types were accounted for by differences in lipid droplet density, not lipid droplet size. IMCL distribution showed an exponential increase in lipid content from the central region toward the sarcolemma, which was similar between groups and fiber types. In conclusion, IMCL contents can be substantially greater in trained endurance athletes compared with overweight and/or type 2 diabetes patients. Because structural characteristics and intramyocellular distribution of lipid aggregates seem to be similar between groups, we conclude that elevated IMCL deposits are unlikely to be directly responsible for inducing insulin resistance.

Comparisons of visual perception, response-selection, and response-execution performance were made between Type 2 diabetes mellitus patients and a matched nondiabetic control group. 10 well-controlled male patients with Type 2 diabetes without diabetic complications ( M age 58 yr.) and an age and IQ-matched nondiabetic control group consisting of 13 male healthy volunteers ( M age 57 yr.) were included. Significant differences were round only between the two groups on response-selection performance, which concerns the selection and preparation of an appropriate motor action.

Both stable isotope methodology and fluorescence microscopy were applied to define the use of intramuscular triglyceride (IMTG) stores as a substrate source during exercise on a whole‐body as well as on a fibre type‐specific intramyocellular level in trained male cyclists. Following an overnight fast, eight subjects were studied at rest, during 120 min of moderate intensity exercise (60 % maximal oxygen uptake capacity (V̇O2,max)) and 120 min of post‐exercise recovery. Continuous infusions of [U‐13C]palmitate and [6,6‐2H2]glucose were administered at rest and during subsequent exercise to quantify whole‐body plasma free fatty acid (FFA) and glucose oxidation rates and the contribution of other fat sources (sum of muscle‐ plus lipoprotein‐derived TG) and muscle glycogen to total energy expenditure. Fibre type‐specific intramyocellular lipid content was determined in muscle biopsy samples collected before, immediately after and 2 h after exercise. At rest, fat oxidation provided 66 ± 5 % of total energy expenditure, with FFA and other fat sources contributing 48 ± 6 and 17 ± 3 %, respectively. FFA oxidation rates increased during exercise, and correlated well with the change in plasma FFA concentrations. Both the use of other fat sources and muscle glycogen declined with the duration of exercise, whereas plasma glucose production and utilisation increased (P < 0.001). On average, FFA, other fat sources, plasma glucose and muscle glycogen contributed 28 ± 3, 15 ± 2, 12 ± 1 and 45 ± 4 % to total energy expenditure during exercise, respectively. Fluorescence microscopy revealed a 62 ± 7 % net decline in muscle lipid content following exercise in the type I fibres only, with no subsequent change during recovery. We conclude that IMTG stores form an important substrate source during moderate intensity exercise in endurance‐trained male athletes following an overnight fast, with the oxidation rate of muscle‐ plus lipoprotein‐derived TG being decreased with the duration of exercise.

The data of the present case demonstrate that the abuse of androgenic anabolic steroids (AAS) may lead to serious health effects. Although most clinical attention is usually directed towards peripheral side effects, the most serious central side effect, hypothalamic-pituitary-dysfunction, is often overlooked in severe cases. Although this latter central side-effect usually recovers spontaneously when AAS intake is discontinued, the present case shows that spontaneous recovery does not always take place. We suggest that hypothalamic-pituitary dysfunction should always be considered in the differential diagnosis in athletes seen with typical presentation of anabolic steroid use. In order to regain normal hypothalamic-pituitary function, supraphysiological doses of 200 microg LH-RH should be considered when the physiological challenge test with LH-RH (50 microg) fails to show an acceptable response.

Recently, we observed that impairments exist in skeletal muscle free fatty acid (FFA) utilization during exercise in obese subjects with Type II diabetes. The main objective of the present study was to investigate whether plasma FFA oxidation is impaired during exercise in non-obese Type II diabetic patients. Stable isotope tracers of palmitate and glucose were infused for 2 h at rest and 1h of bicycle exercise at 40% peak oxygen consumption ( V*O(2)max) in volunteers with Type II diabetes and a healthy control group. At rest, plasma FFA oxidation was not significantly different between subjects with Type II diabetes and control subjects (2.13+/-0.51 versus 1.93+/-0.54 micromol.kg(-1).min(-1) respectively). During exercise, Type II diabetic patients and control subjects had similar rates of total fat [Type II diabetes, 9.62+/-1.84 micromol.kg(-1).min(-1); control, 12.08+/-4.59 micromol.kg(-1).min(-1); not significant (NS)] and glucose oxidation (Type II diabetes, 44.24+/-10.36 micromol.kg(-1).min(-1); control, 57.37+/-14.54 micromol.kg(-1).min(-1); NS). No aberrations were present in plasma FFA uptake [rate of disappearance ( Rd ); Type II diabetes, 11.78+/-4.82; control, 10.84+/-3.39; NS] and oxidation rates (Type II diabetes 8.10+/-1.44; control 8.00+/-3.12, NS) in Type II diabetic patients; triacylglycerol-derived fatty acid oxidation was 2.6-fold lower in Type II diabetic patients than in control subjects, but this difference was not statistically significant. Muscle glycogen oxidation was lower in diabetes patients than in control subjects (Type II diabetes, 25.16+/-13.82 micromol.kg(-1).min(-1); control, 42.04+/-10.58 micromol.kg(-1).min(-1); P <0.05) and plasma glucose contributed more to energy expenditure in Type II diabetes (26+/-3% in diabetic versus 15+/-2% in control, P <0.05). We conclude that plasma FFA oxidation is not impaired during exercise in non-obese Type II diabetic patients. The data confirm that Type II diabetes is a heterogeneous disease, and that the adaptation at the substrate level differs between obese and non-obese patients and may contribute to differences in the final appearance of the various phenotypes.

The purpose of this study was to monitor general and individual changes in hematological variables during long-term endurance training, detraining and altitude training in elite Olympic distance triathletes. Over a period of three years, a total of 102 blood samples were collected in eleven (7-male and 4 female) elite Olympic distance triathletes (mean +/- SD; age = 26.4 +/- 5.1 yr; VO(2) max = 67.9 +/- 6.6 ml/min/kg) for determination of hemoglobin (Hb), hematocrit (Hct), red blood cell count (RBC), Mean corpuscular hemoglobin (MCH), Mean corpuscular hemoglobin content (MCHC), Mean corpuscular volume (MCV) and plasma ferritin. The data were pooled and divided into three periods; off-season, training season and race season. Blood samples obtained before and after altitude training were analyzed separately. Of all measured variables only RBC showed a significant decrease (p < 0.05) during the race season compared to the training season. Hematological values below the lower limit of the normal range were found in 46 % of the athletes during the off-season. This percentage increased from 55 % during the training season to 72 % of the athletes during the race season. Hemoglobin and ferritin values were most frequently below the normal range. There was a weak correlation between Hb levels and VO(2) max obtained during maximal cycling (r = 0.084) and running (r = 0.137) tests. Unlike training at 1500 m and 1850 m, training at an altitude of 2600 m for three weeks showed significant increases in Hb (+ 10 %; p < 0.05), Hct (+ 11 %; p < 0.05) and MCV (+ 5 %; p < 0.05). Long-term endurance training does not largely alter hematological status. However, regular screening of hematological variables is desirable as many athletes have values near or below the lower limit of the normal range. The data obtained from altitude training suggest that a minimum altitude (>2000 m) is necessary to alter hematological status.

Recently, a role for uncoupling protein-3 (UCP3) in carbohydrate metabolism and in type 2 diabetes has been suggested. Mice overexpressing UCP3 in skeletal muscle showed reduced fasting plasma glucose levels, improved glucose tolerance after an oral glucose load, and reduced fasting plasma insulin levels. However, data regarding the expression of UCP3 in patients with type 2 diabetes is inconsistent, and so far, there have been no reports of UCP3 protein content. Here we compared, for the first time, the protein levels of UCP3 in vastus lateralis muscle in 14 male type 2 diabetic patients (age 49.8 +/-2.1 years; BMI 27.2 +/-1.2 kg/m(2); mean +/- SE) with 16 male control subjects (age 48.0 +/-1.9 years; BMI 23.4 +/-0.6 kg/m(2)). We found that UCP3 protein levels were twice as low in patients with type 2 diabetes compared with control subjects (117 +/- 16 vs. 58 +/- 12 AU; P=0.007). There was no correlation between UCP3 content and BMI. In conclusion, UCP3 content is lower in type 2 diabetic patients compared with healthy control subjects. These results are consistent with a role for UCP3 in glucose homeostasis and suggest a role for UCP3 in type 2 diabetes.

The aim of the study was to validate a new, fast metabolic measurement system (the Oxycon-Pro) during low and high exercise intensities against the Douglas bag method. For this purpose twelve highly trained subjects performed an incremental cycle ergometer test. In the third minute of each exercise step simultaneous measurements of the Douglas bag and the Oxycon-Pro were performed. No significant differences between the Oxycon-Pro and the Douglas bag measurements for minute ventilation (VE), oxygen uptake (VO2) and carbon dioxide expiration (VCO2) were found. Bland and Altman analysis of validity demonstrated minimal bias and low standard deviations. In conclusion, the results show that the Oxycon-Pro is a valid apparatus for determination of minute ventilation (VE), oxygen uptake (VO2) and carbon dioxide expiration (VCO2) during low as well as during maximal exercise intensities. Unlike with the Douglas bag method, this fast metabolic measurement system can be used for accurate and quick determination of ventilatory variables during exercise.

Physical activity has a beneficial effect on insulin sensitivity in normal as well as insulin resistant populations. A distinction should be made between the acute effects of exercise and genuine training effects. Up to two hours after exercise, glucose uptake is in part elevated due to insulin independent mechanisms, probably involving a contraction-induced increase in the amount of GLUT4 associated with the plasma membrane and T-tubules. However, a single bout of exercise can increase insulin sensitivity for at least 16 h post exercise in healthy as well as NIDDM subjects. Recent studies have accordingly shown that acute exercise also enhances insulin stimulated GLUT4 translocation. Increases in muscle GLUT4 protein content contribute to this effect, and in addition it has been hypothesized that the depletion of muscle glycogen stores with exercise plays a role herein. Physical training potentiates the effect of exercise on insulin sensitivity through multiple adaptations in glucose transport and metabolism. In addition, training may elicit favourable changes in lipid metabolism and can bring about improvements in the regulation of hepatic glucose output, which is especially relevant to NIDDM. It is concluded that physical training can be considered to play an important, if not essential role in the treatment and prevention of insulin insensitivity.

In several studies, artery wall properties have been shown to differ between men and women. It has been hypothesized that these differences may result from hormonal influences but, in a previous study, we were unable to detect any influence of the menstrual cycle on artery wall properties. Therefore, we investigated the differences in artery wall properties, if any, between the menstrual cycle and the use of a third-generation oral contraceptive for 3 months. We investigated the right common carotid (CCA) and femoral (CFA) arteries of normotensive young (18–25-y-old) women volunteers (n = 14). The arterial cross-sectional distensibility and compliance coefficients were determined by means of a specially designed ultrasonic wall-tracking device and automatic brachial artery cuff blood-pressure measurements. The menstrual cycles and the cycles during oral contraceptive use (30 μg ethinylestradiol and 75 μg gestodene) were monitored by ultrasonographic evaluation and the assessment of plasma levels of 17β-oestradiol and progesterone. The distensibility and cross-sectional compliance coefficients of both the CCA and CFA did not differ significantly between the menstrual cycle and the use of oral contraceptives, despite different ovarian hormone levels. Brachial arterial blood pressure was also not affected. We conclude that 3 months use of a third-generation oral contraceptive does not influence the wall properties of peripheral arteries and cannot explain the observed difference between genders. The absence of a rise in blood pressure and the low androgenic profile of this specific oral contraceptive may have contributed to our findings.

Plasma total homocysteine (tHcy) has been identified as an independent risk factor for cardiovascular diseases (CVD). The difference in tHcy between the sexes has most often been related to the sex hormones, but also to a higher muscle mass in men. The purpose of this study was to assess the effects of acute exercise, brief exhaustive training, and menstrual cycle phase on circulating plasma tHcy concentrations. Fifteen untrained eumenorrheic women (mean age [+/-SD]: 18.7+/-0.4 yr, body fat: 25.8+/-3.4%, VO2max: 43.8+/-2.3 ml x kg(-1) x min(-1)) volunteered for the present study, which covered two menstrual cycles. During the second cycle the subjects participated in two exhaustive 5-day training programs on a cycle ergometer: one in the follicular (FPh) and one in the luteal phase (LPh). Pre- and posttraining plasma tHcy and total estrogen (E) responses were determined in blood samples obtained immediately before, during and immediately after incremental exercise to exhaustion. tHcy levels showed a large between-subject variation, but differences between FPh and LPh levels were consistent (P=0.063). Mean tHcy levels at rest were 9.44+/-1.65 micromol/L and 8.93+/-1.71 micromol/L during the FPh and LPh, respectively. Brief exhaustive training did not elicit any changes in plasma tHcy concentrations, although posttraining LPh E levels were lower (P<0.01). Overall, the differences between FPh and LPh values for tHcy and E were attenuated by training. Acute exercise increased plasma tHcy concentrations (P<0.001). At exhaustion, tHcy levels increased by 17% and 16% during the FPh and LPh, respectively. This was also significantly above tHcy levels at submaximal exercise (P=0.044). After a short period of training tHcy levels did not increase as much during acute exercise as they did before training; however, the increments were still significant (P=0.048). In conclusion, acute exercise in women produces significant increases in plasma tHcy concentrations, whereas brief exhaustive training does not significantly alter plasma tHcy levels. Our findings also suggest that plasma tHcy concentrations are menstrual cycle phase-dependent and that there is a close association between estrogen status and tHcy levels.

To study the occurrence and contributing factors of transient hypoglycemia after pre-exercise ingestion of glucose after a 4-hour fast, 19 well-trained cyclists ingested 50 grams of glucose dissolved in water around noon after having a normal breakfast. The ingestion of the glucose solution was followed by 30 minutes rest after which the subjects cycled for 40 minutes at 60% of the predetermined maximal power output. Every 10 minutes blood was sampled for determination of glucose, catecholamines, and insulin concentrations. In 6 subjects (hypo-group) plasma glucose levels dropped transiently below 3.0 mmol/l, while in the other 13 subjects (non-hypo group) plasma glucose level remained above this level. Although at the onset of exercise the plasma glucose levels were lower in the hypo-group, insulin levels were similar in both groups, suggesting a higher insulin sensitivity in the hypo-group. During exercise, norepinephrine was lower in the hypo-group, indicating a lower sympathetic activity in the hypo-group. The lowest plasma glucose levels in both groups were observed after 20 minutes of exercise, after which plasma glucose concentration returned to normal levels. It is concluded that pre-exercise carbohydrate ingestion after a 4-hour fast is sufficient to induce a transient hypoglycemia. The data suggest that the occurrence of hypoglycemia is determined by a combination of a high insulin sensitivity, a small amount of ingested glucose, and a low sympathetic activity.