Allopurinol partially prevents disuse muscle atrophy in mice and humans.

Disuse muscle wasting will likely affect everyone in his or her lifetime in response to pathologies such as joint immobilization, inactivity or bed rest. There are no good therapies to treat it. We previously found that allopurinol, a drug widely used to treat gout, protects muscle damage after exhaustive exercise and results in functional gains in old individuals. Thus, we decided to test its effect in the prevention of soleus muscle atrophy after two weeks of hindlimb unloading in mice, and lower leg immobilization following ankle sprain in humans (EudraCT: 2011-003541-17). Our results show that allopurinol partially protects against muscle atrophy in both mice and humans. The protective effect of allopurinol is similar to that of resistance exercise which is the best-known way to prevent muscle mass loss in disuse human models. We report that allopurinol protects against the loss of muscle mass by inhibiting the expression of ubiquitin ligases. Our results suggest that the ubiquitin-proteasome pathway is an appropriate therapeutic target to inhibit muscle wasting and emphasizes the role of allopurinol as a non-hormonal intervention to treat disuse muscle atrophy.

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy.

In the literature, the terms physical inactivity and immobilization are largely used as synonyms. The present review emphasizes the need to establish a clear distinction between these two situations. Physical inactivity is a behavior characterized by a lack of physical activity, whereas immobilization is a deprivation of movement for medical purpose. In agreement with these definitions, appropriate models exist to study either physical inactivity or immobilization, leading thereby to distinct conclusions. In this review, we examine the involvement of oxidative stress in skeletal muscle insulin resistance and atrophy induced by, respectively, physical inactivity and immobilization. A large body of evidence demonstrates that immobilization-induced atrophy depends on the chronic overproduction of reactive oxygen and nitrogen species (RONS). On the other hand, the involvement of RONS in physical inactivity-induced insulin resistance has not been investigated. This observation outlines the need to elucidate the mechanism by which physical inactivity promotes insulin resistance.

The calcineurin antagonist RCAN1-4 is induced by exhaustive exercise in rat skeletal muscle.

The aim of this work was to study the regulation of the calcineurin antagonist regulator of calcineurin 1 (RCAN1) in rat skeletal muscles after exhaustive physical exercise, which is a physiological modulator of oxidative stress. Three skeletal muscles, namely extensor digitorum longus (EDL), gastrocnemius, and soleus, were investigated. Exhaustive exercise increased RCAN1-4 protein levels in EDL and gastrocnemius, but not in soleus. Protein oxidation as an index of oxidative stress was increased in EDL and gastrocnemius, but remained unchanged in soleus. However, lipid peroxidation was increased in all three muscles. CuZnSOD and catalase protein levels were increased at 3 h postexercise in soleus, whereas they remained unchanged in EDL and gastrocnemius. Calcineurin enzymatic activity declined in EDL and gastrocnemius but not in soleus, and its protein expression was decreased in all three muscles. The level of PGC1-α protein remained unchanged, whereas the protein expression of the transcription factor NFATc4 was decreased in all three muscles. Adiponectin expression was increased in all three muscles. RCAN1-4 expression in EDL and gastrocnemius muscles was augmented by the oxidative stress generated from exhaustive exercise. We propose that increased RCAN1-4 expression and the signal transduction pathways it regulates represent important components of the physiological adaptation to exercise-induced oxidative stress.

Dietary α-lactalbumin supplementation alleviates normocaloric western diet-induced glucose intolerance in Göttingen minipigs.

OBJECTIVE: The pandemic of obesity in Western countries is mainly due to the high-fat, high-energy diet prevailing there. Obesity-associated metabolic disorders are the consequence of fat mass increase leading to altered adipokine secretion, hyperlipemia, oxidant stress, low-grade inflammation, and eventually glucose intolerance. Yet not all people consuming a Western diet become obese, and the question is raised whether these people are also at risk of developing metabolic disorders. METHODS: Glucose tolerance, lipid profile, and oxidant and inflammation status were investigated longitudinally in lean Göttingen minipigs receiving for 16 weeks either a normal diet (ND), a Western diet (WD), or a Western diet supplemented with a whey protein isolate (WPI) rich in α-lactalbumin known to improve glucose tolerance. ND and WD were supplied isoenergetically. RESULTS: Lean minipigs fed WD displayed glucose intolerance and altered lipid profile after 6 weeks of diet but no inflammation or oxidative stress. Supplementation with WPI alleviated glucose intolerance by improving insulin secretion, but not lipid profile. CONCLUSIONS: Western diet consumption is deleterious for glucose tolerance even in the absence of fat mass accretion, and dyslipemia is a major determinant for this metabolic dysfunction. Stimulating insulin secretion with a WPI is an effective strategy to improve glucose tolerance.

Fermented soy permeate reduces cytokine level and oxidative stress in streptozotocin-induced diabetic rats.

Oxidative stress and inflammation are involved in the development of type 1 diabetes and its complications. Because two compounds found in soy, that is, isoflavones and alpha-galactooligosaccharides, have been shown to exert antioxidant and anti-inflammatory effects, this study aimed to assess the effects of a dietary supplement containing these two active compounds, the fermented soy permeate (FSP). We hypothesized that FSP would be able to reduce in vivo oxidative stress and inflammation in streptozotocin (STZ)-induced type 1 diabetic rats. Thirty male Wistar rats were divided into the control placebo, diabetic placebo, and diabetic FSP-supplemented groups. They received daily, by oral gavage, water (placebo groups) or diluted FSP (0.1 g/day; FSP-supplemented group). After 3 weeks, glycemic regulation (glycemia and fructosamine level); the plasma level of carboxymethyllysine (CML), a marker of systemic oxidative stress in diabetes; and the plasma levels of inflammatory markers (CRP, IL-1ß, IL-6, and uric acid) were evaluated. Markers of oxidative damage (isoprostanes and GSH/GSSG), antioxidant enzymatic activity (SOD and GPX), and Mn-SOD content were determined in skeletal muscle (gastrocnemius). Diabetic placebo rats exhibited higher CML levels, lower SOD and GPX activities, and decreased Mn-SOD contents. FSP supplementation in diabetic animals normalized the CML and antioxidant enzymatic activity levels and tended to increase Mn-SOD expression. The markers of inflammation whose levels were increased in the diabetic placebo group were markedly decreased by FSP (IL-1ß: -75%, IL-6: -46%, and uric acid: -17%), except for CRP. Our results demonstrate that FSP exhibited antioxidant and anti-inflammatory properties in vivo in STZ-induced diabetic rats.

Exercise training combined with antioxidant supplementation prevents the antiproliferative activity of their single treatment in prostate cancer through inhibition of redox adaptation.

In preclinical models, exercise training (ET) or pomegranate juice (PJ) prevents prostate cancer progression. Here, we hypothesized that physical exercise combined with antioxidants could induce synergistic effects through oxidative stress modulation. Forty male Copenhagen rats with prostate tumors were divided into four groups: control, PJ, ET, and PJ+ET. Rats from the PJ group consumed 750 µl of PJ daily, rats from the ET group ran on a treadmill 5 days per week, and PJ+ET rats received the combined treatment. Each week, tumor growth was evaluated. After 4 weeks of treatment, the rats were euthanized and blood, muscles, and tumors were collected. Tumor Ki67, extracellular signal-regulated kinase (ERK) activation, Bcl-2 expression, and enzymatic and nonenzymatic antioxidant defenses, as well as oxidative stress markers (oxidized base, lipid peroxidation, protein carbonylation), were measured. PJ or ET significantly decreased prostate tumor proliferation (Ki67 staining, p<0.05) through the modulation of ERK phosphorylation, whereas the combination of treatments did not limit cancer progression. PJ significantly reduced Bcl-2 expression in tumors (p<0.05) and the combination of PJ and ET prevented this effect. PJ or ET increased enzymatic antioxidant defenses in muscle, PJ increased nonenzymatic antioxidant defenses in plasma and whole blood. In addition, PJ reduced TBARS and 8-oxodGuo levels in tumors as well as ET (p<0.05), whereas protein carbonyl levels were not affected by these two strategies. Paradoxically, association of PJ+ET did not increase antioxidant defenses and no reduction in oxidative stress markers was induced. Loading cancer cells with antioxidants blunts the positive effects of ET and interferes with important reactive oxygen species-mediated physiological processes such as antioxidant adaptations.

Inactivity-induced oxidative stress: a central role in age-related sarcopenia?

Ageing causes a progressive decline in skeletal muscle mass that may lead to decreased strength and functionality. The term sarcopenia is especially used to characterise this geriatric syndrome. Numerous conditions and behaviours are considered to accelerate the progression of sarcopenia such as chronic diseases, malnutrition and physical inactivity. As people in modern countries are more and more sedentary, the impact of physical inactivity on the prevalence of sarcopenia might be more and more important in the future. In this review, we discuss how reactive oxygen species (ROS) could mediate the effects of lifelong inactivity in the onset and progression of age-related sarcopenia. Although the cellular mechanisms responsible for muscle ROS production are not necessarily the same, both inactivity and ageing are indeed known to increase basal ROS concentrations in skeletal muscle. New data and literature review are provided showing that chronic ROS overproduction induced by physical inactivity may exacerbate the activation of some redox-sensitive signalling pathways involved in age-related sarcopenia. We also address the scientific evidences implicating the role of ROS overproduction in the precocious failure of aged muscles to activate intracellular signalling responses to contractions.

De novo ceramides synthesis is not involved in skeletal muscle atrophy induced by short-term mechanical unloading.

Patients admitted to the intensive care unit commonly develop skeletal muscle weakness that can exacerbate illness and complicate their recovery. Beyond the primary disease or aging, weakness is promoted by a variety of prolonged hospitalization-associated conditions. These include altered nutritional status, pharmacologic side effects, physical inactivity, and prolonged bed rest. The two latter conditions (i.e. inactivity and bed rest) are the most ubiquitous, affecting all patients during a prolonged hospitalization. In both cases, skeletal muscle utilization is decreased with a concomitant reduction in fatty acid oxidation. Subsequent fatty acids accumulation converted to ceramides could be a cellular mechanism leading to muscle wasting. Indeed these sphingolipids act as second messengers in several of molecular signaling pathways involved in muscle atrophy. Consequently, the aim of this work is to determine the effects of immobilization on muscle ceramides accumulation, and identify the role of these ectopic lipids in molecular mechanisms involved in skeletal muscle atrophy. For this purpose, male Wistar rats were treated with an inhibitor of de novo synthesis of ceramides (i.e. myriocin) and subjected to hindlimb unloading for 7 days. We found that hindlimb unloading induced skeletal muscle atrophy, in part through proteolysis (i.e. decrease in AKT activation, increase in MuRF1 and polyubiquinated proteins content) and apoptosis activations (i.e. increase in Bax/Bcl-2 ratio and cleaved caspase-3). Myriocin treatment did not prevent skeletal muscle atrophy and concomitant induction of apoptosis and proteolysis. Data concerning muscle ceramides content are being analyzed. Together, these results suggest that de novo synthesis of ceramides is not involved in muscle atrophy induced by a short period of hindlimb unloading.

A fermented soy permeate improves the skeletal muscle glucose level without restoring the glycogen content in streptozotocin-induced diabetic rats.

Exercise is essential into the therapeutic management of diabetic patients, but their level of exercise tolerance is lowered due to alterations of glucose metabolism. As soy isoflavones have been shown to improve glucose metabolism, this study aimed to assess the effects of a dietary supplement containing soy isoflavones and alpha-galactooligosaccharides on muscular glucose, glycogen synthase (GSase), and glycogen content in a type 1 diabetic animal model. The dietary supplement tested was a patented compound, Fermented Soy Permeate (FSP), developed by the French Company Sojasun Technologies. Forty male Wistar rats were randomly assigned to control or diabetic groups (streptozotocin, 45 mg/kg). Each group was then divided into placebo or FSP-supplemented groups. Both groups received by oral gavage, respectively, water or diluted FSP (0.1 g/day), daily for a period of 3 weeks. At the end of the protocol, glycemia was noticed after a 24-h fasting period. Glucose, total GSase, and the glycogen content were determined in the skeletal muscle (gastrocnemius). Diabetic animals showed a higher blood glucose concentration, but a lower glucose and glycogen muscle content than controls. Three weeks of FSP consumption allowed to restore the muscle glucose concentration, but failed to reduce glycemia and to normalize the glycogen content in diabetic rats. Furthermore, the glycogen content was increased in FSP-supplemented controls compared to placebo controls. Our results demonstrated that diabetic rats exhibited a depleted muscle glycogen content (-25%). FSP-supplementation normalized the muscle glucose level without restoring the glycogen content in diabetic rats. However, it succeeded to increase it in the control group (+20%).

Inhibition of xanthine oxidase by allopurinol prevents skeletal muscle atrophy: role of p38 MAPKinase and E3 ubiquitin ligases.

Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in rats, and its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinase, and the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, the Muscle atrophy F-Box (MAFbx; also known as atrogin-1) and Muscle RING (Really Interesting New Gene) Finger-1 (MuRF-1). We found that hindlimb unloading induced a significant increase in XO activity and in the protein expression of the antioxidant enzymes CuZnSOD and Catalase in skeletal muscle. The most relevant new fact reported in this paper is that inhibition of XO with allopurinol, a drug widely used in clinical practice, prevents soleus muscle atrophy by ~20% after hindlimb unloading. This was associated with the inhibition of the p38 MAPK-MAFbx pathway. Our data suggest that XO was involved in the loss of muscle mass via the activation of the p38MAPK-MAFbx pathway in unloaded muscle atrophy. Thus, allopurinol may have clinical benefits to combat skeletal muscle atrophy in bedridden, astronauts, sarcopenic, and cachexic patients.

Age associated low mitochondrial biogenesis may be explained by lack of response of PGC-1α to exercise training.

Low mitochondriogenesis is critical to explain loss of muscle function in aging and in the development of frailty. The aim of this work was to explain the mechanism by which mitochondriogenesis is decreased in aging and to determine to which extent it may be prevented by exercise training. We used aged rats and compared them with peroxisome proliferator-activated receptor-γ coactivator-1α deleted mice (PGC-1α KO). PGC-1α KO mice showed a significant decrease in the mitochondriogenic pathway in muscle. In aged rats, we found a loss of exercise-induced expression of PGC-1α, nuclear respiratory factor-1 (NRF-1), and of cytochrome C. Thus muscle mitochondriogenesis, which is activated by exercise training in young animals, is not in aged or PGC-1α KO ones. Other stimuli to increase PGC-1α synthesis apart from exercise training, namely cold induction or thyroid hormone treatment, were effective in young rats but not in aged ones. To sum up, the low mitochondrial biogenesis associated with aging may be due to the lack of response of PGC-1α to different stimuli. Aged rats behave as PGC-1α KO mice. Results reported here highlight the role of PGC-1α in the loss of mitochondriogenesis associated with aging and point to this important transcriptional coactivator as a target for pharmacological interventions to prevent age-associated sarcopenia.

Combined insulin treatment and intense exercise training improved basal cardiac function and Ca(2+)-cycling proteins expression in type 1 diabetic rats.

This study investigated the effects of 8 weeks of intense exercise training combined with insulin treatment on the Ca(2+)-cycling protein complex expression and their functional consequences on cardiac function in type 1 diabetic rat hearts. Diabetic Wistar rats were randomly assigned into the following groups: received no treatment, insulin-treated diabetic, trained diabetic, and trained insulin-treated diabetic. A control group was also included. Insulin treatment and (or) treadmill intense exercise training were conducted over 8 weeks. Basal cardiac function was evaluated by Langendorff technique. Cardiac expression of the main Ca(2+)-cycling proteins (RyR2, FKBP 12.6, SERCA2, PLB, NCX1) was assessed by Western blot. Diabetes altered basal cardiac function (±dP/dt) and decrease the expression of the main Ca(2+)-cycling proteins expression: RyR2, SERCA2, and NCX1 (p < 0.05). Whereas combined treatment was not able to normalize -dP/dt, it succeeded to normalize +dP/dt of diabetic rats (p < 0.05). Moreover, both insulin and intense exercise training, applied solely, increased the expression of the Ca(2+)-cycling proteins: RyR2, SERCA2, PLB. and NCX1 (p < 0.05). But this effect was higher when the 2 treatments were combined. These data are the first to show that combined insulin treatment and intense exercise training during diabetes synergistically act on the expression of the main Ca(2+)-cycling proteins, providing insights into mechanisms by which the dual treatment during diabetes improves cardiac function.

Effects of exercise training combined with insulin treatment on cardiac NOS1 signaling pathways in type 1 diabetic rats.

This study examined the effects of a dual treatment combining insulin treatment and exercise training on basal cardiac function and signaling pathways involving ß3-AR, NOS1, and RyR2 in type 1 diabetic rats. Male Wistar rats were assigned into a diabetic group receiving no treatment (D), an insulin-treated diabetic (Ins), a trained diabetic (TD), and a trained insulin-treated diabetic (TIns) group. Control group (C) was included in order to confirm the deleterious effects of diabetes. Insulin treatment and/or treadmill exercise training were conducted for 8 weeks. Basal cardiac function was evaluated by Langendorff technique. Cardiac protein expression of ß3-AR, NOS1, and RyR2 was assessed using Western blots. Diabetes induced a decrease of both basal diastolic and systolic (±dP/dt) cardiac function (P < 0.05). Moreover, diabetes was associated with an increase of ß3-AR and NOS1 and a decrease of RyR2 expression (P < 0.05). Although combined treatment was not able to normalize -dP/dt, it succeeded to normalize +dP/dt of diabetic rats. Combined treatment led to an overexpression of RyR2. Effects of this combined treatment on +dP/dt and RyR2 were greater than the effects of insulin and exercise training, applied solely. Treatments, applied solely or in combination, resulted in a complete normalization of ß3-AR and in a down-regulation of NOS1 because this protein expression in all treated diabetic rats became lower than control values (P < 0.01). Our study shows that unlike single treatments, dual treatment combining insulin treatment and exercise training was able to normalize basal systolic function of diabetic rats by a specific regulation of ß3-AR-NOS1-RyR2 signaling pathways.

Inverse relationship between percentage body weight change and finishing time in 643 forty-two-kilometre marathon runners.

OBJECTIVE: The purpose of this study was to determine the relationship between athletic performance and the change in body weight (BW) during a 42 km marathon in a large cohort of runners. METHODS: The study took place during the 2009 Mont Saint-Michel Marathon (France). 643 marathon finishers (560 males and 83 females) were studied. The change in BW during the race was calculated from measurements of each runner's BW immediately before and after the race. RESULTS: BW loss was 2.3 ± 2.2% (mean±SEM) (p<0.01). BW loss was -3.1 ± 1.9% for runners finishing the marathon in less than 3 h; -2.5 ± 2.1% for runners finishing between 3 and 4 h; and -1.8 ± 2.4% for runners who required more than 4 h to complete the marathon. The degree of BW loss was linearly related to 42 km race finishing time (p<0.0000001). Neither age nor gender influenced BW loss during the race. CONCLUSIONS: BW loss during the marathon was inversely related to race finishing time in 643 marathon runners and was >3% in runners completing the race in less than 3 h. These data are not compatible with laboratory-derived data suggesting that BW loss greater than 2% during exercise impairs athletic performance. They match an extensive body of evidence showing that the most successful athletes in marathon and ultra-marathon running and triathlon events are frequently those who lose substantially more than 3-4% BW during competition.

Intense exercise training induces adaptation in expression and responsiveness of cardiac ß-adrenoceptors in diabetic rats.

BACKGROUND: Informations about the effects of intense exercise training on diabetes-induced myocardial dysfunctions are lacking. We have examined the effects of intense exercise training on the cardiac function of diabetic rats, especially focusing on the Langendorff ß-adrenergic responsiveness and on the ß-adrenoceptors protein expression. METHODS: Control or Streptozotocin induced-diabetic male Wistar rats were randomly assigned to sedentary or trained groups. The training program consisted of 8 weeks running on a treadmill (10° incline, up to 25 m/min, 60 min/day) and was considered to be intense for diabetic rats. RESULTS: This intense exercise training amplified the in vivo diabetes-induced bradycardia. It had no effect on Langendorff basal cardiac contraction and relaxation performances in control and diabetic rats. In diabetic rats, it accentuated the Langendorff reduced responsiveness to ß-adrenergic stimulation. It did not blunt the diabetes-induced decrease of ß1-adrenoceptors protein expression, displayed a significant decrease in the ß2-adrenoceptors protein expression and normalized the ß3-adrenoceptors protein expression. CONCLUSIONS: Intense exercise training accentuated the decrease in the myocardial responsiveness to ß-adrenergic stimulation induced by diabetes. This defect stems principally from the ß2-adrenoceptors protein expression reduction. Thus, these results demonstrate that intense exercise training induces specific effects on the ß-adrenergic system in diabetes.

A comparison between ventilation and heart rate as indicator of oxygen uptake during different intensities of exercise.

The aim of this study is to compare the relation between ventilation (VE) and oxygen uptake (VO2) [VO2=ƒ(VE)] and between heart rate (HR) and VO2 [VO2=ƒ(HR)]. Each one of the subjects performed three types of activities of different intensities (walking without load, walking with load and intermittent work). VO2, VE, and HR were measured continuously by using indirect calorimetry and an electrocardiogram. Linear regressions and coefficients of determination (r(2)) were calculated to compare the relation VO2 =ƒ(VE) and VO2 =ƒ(HR) for two different regroupings: by session duration (r(2) session) and by subject (r(2) subject). Results showed that r(2) session of the relation VO2 =ƒ(VE) were significantly higher than those of the relation VO2 =ƒ(HR) for steady state activities (walking with or without load during 3 or 6 min, p < 0.01) and for activities without oxygen consumption steady state (walking with or without load during 1 min, p < 0.01 and intermittent work, p < 0.05). VE is more strongly correlated with VO2 than with HR. This is a very promising approach to develop a new method to estimate energy expenditure. Key pointsVentilation is more strongly correlated with oxygen uptake than heart rate during physical activities of different intensities.This study shows the interest to looking for ventilation to estimate energy expenditure.This study is a promising approach to develop a new method to estimate energy expenditureAn interesting perspective could be to develop a light and portable device to measure ventilation based on the coupling of four magnetometers.

Early advancing age alters plasma glucose and glucoregulatory hormones in response to supramaximal exercise.

After the age of 60, the decrease in physical activity and the increase in fat mass (FM) are two essential factors contributing to the alteration of glucose, insulin, and catecholamines responses induced by exercise. To discard these two factors, we compared the glucoregulatory responses in three different groups of men between the ages 21 and 34, and matched pairs: trained groups (T34 and T21) were matched for training level; T21 and U21 (U for untrained) were matched for age; T34 and U21 were matched for FM. The glucoregulatory responses were determined by venous plasma concentrations of glucose ([GLU]), insulin ([INS]), and catecholamines (adrenaline: [A], noradrenaline: [NA]) before and after a Wingate test. [GLU], [INS], and [A] did not differ between T21 and U21, indicating that high-level training had no effects on these parameters. On the other hand, T34 compared to T21 and U21, had higher GLU associated with lower INS post-exercise concentrations. Moreover, [A(max)] was significantly lower in this group. Consequently, T34 only exhibited a significant alteration in glucose and glucoregulatory responses after a Wingate test, which could not be explained by the usual decrease in physical activity and/or the increase in FM. Therefore, aging alone seems to be one main factor of this deterioration.

Catecholamines and the effects of exercise, training and gender.

Stress hormones, adrenaline (epinephrine) and noradrenaline (norepinephrine), are responsible for many adaptations both at rest and during exercise. Since their discovery, thousands of studies have focused on these two catecholamines and their importance in many adaptive processes to different stressors such as exercise, hypoglycaemia, hypoxia and heat exposure, and these studies are now well acknowledged. In fact, since adrenaline and noradrenaline are the main hormones whose concentrations increase markedly during exercise, many researchers have worked on the effect of exercise on these amines and reported 1.5 to >20 times basal concentrations depending on exercise characteristics (e.g. duration and intensity). Similarly, several studies have shown that adrenaline and noradrenaline are involved in cardiovascular and respiratory adjustments and in substrate mobilization and utilization. Thus, many studies have focused on physical training and gender effects on catecholamine response to exercise in an effort to verify if significant differences in catecholamine responses to exercise could be partly responsible for the different performances observed between trained and untrained subjects and/or men and women. In fact, previous studies conducted in men have used different types of exercise to compare trained and untrained subjects in response to exercise at the same absolute or relative intensity. Their results were conflicting for a while. As research progressed, parameters such as age, nutritional and emotional state have been found to influence catecholamine concentrations. As a result, most of the recent studies have taken into account all these parameters. Those studies also used very well trained subjects and/or more intense exercise, which is known to have a greater effect on catecholamine response so that differences between trained and untrained subjects are more likely to appear. Most findings then reported a higher adrenaline response to exercise in endurance-trained compared with untrained subjects in response to intense exercise at the same relative intensity as all-out exercise. This phenomenon is referred to as the 'sports adrenal medulla'. This higher capacity to secrete adrenaline was observed both in response to physical exercise and to other stimuli such as hypoglycaemia and hypoxia. For some authors, this phenomenon can partly explain the higher physical performance observed in trained compared with untrained subjects. More recently, these findings have also been reported in anaerobic-trained subjects in response to supramaximal exercise. In women, studies remain scarce; the results are more conflicting than in men and the physical training type (aerobic or anaerobic) effects on catecholamine response remain to be specified. Conversely, the works undertaken in animals are more unanimous and suggest that physical training can increase the capacity to secrete adrenaline via an increase of the adrenal gland volume and adrenaline content.

Exercise training and cardiovascular risk factors in type 1 diabetic adolescent girls.

Sixteen postmenarcheal Type 1 diabetic adolescent girls were randomized into training (involving aerobic and strength exercises) and nontraining groups. Body composition (skinfold thickness), aerobic fitness (PWC170), plasma lipids, serum apolipoproteins, lipoprotein(a), leptin, and adiponectin were assessed before and after the 6-month period. After the 6-month period, fat mass and leptin increased significantly in the nontraining group but not in the training group. Conversely, in the latter group, fat-free mass increased (P < .01). Moreover, PWC170 improved and apolipoproteinB:apolipoproteinA-1 ratio decreased with physical training (P < .05). Thus, physical training reduces cardiovascular risks and the increase of insulin resistance risk factors in diabetic adolescent girls.

Nutritional and plasmatic antioxidant vitamins status of ultra endurance athletes.

OBJECTIVE: The "Marathon des Sables" (MDS) is a competition known to induce oxidative stress. Antioxidant vitamins prevent exercise-induced oxidative damages. The purpose of this study was to evaluate daily intake and plasma level of the main antioxidant vitamins (alpha-tocopherol, vitamin C, beta-carotene and retinol) in 19 male athletes who participated in this competition. METHODS: Data collected before the beginning of the competition included daily dietary intake using a 7-day food record and plasma biochemical measurements (alpha-tocopherol, vitamin C, beta-carotene and retinol). RESULTS: First, total energy intake was obviously lower than the energetic intake usually observed in well-trained endurance athletes. Second, antioxidant vitamins intake was also insufficient. Indeed, the intake was lower than the French Dietary Reference Intakes (DRI) for this population in 18 subjects for vitamin E and 6 subjects for vitamin C, beta-carotene and Retinol Equivalent. As a significant relationship was found between total energy intake and the intake of vitamin E (r = 0.73; p < 0.001) and vitamin C (r = 0.78; p < 0.001), the low total energy intake contributed partially to the insufficient antioxidant vitamins intake. The dietary questionnaire analysis also revealed a low intake of vegetable oils, fruits and vegetables. However, plasma concentrations of these antioxidant vitamins were similar to the literature data observed in athletes. CONCLUSION: This study evidenced obvious insufficient energy intake in ultra endurance athletes associated with a low antioxidant vitamin intake.