Moderate intensity continuous versus high intensity interval training: Metabolic responses of slow and fast skeletal muscles in rat.

The healthy benefits of regular physical exercise are mainly mediated by the stimulation of oxidative and antioxidant capacities in skeletal muscle. Our understanding of the cellular and molecular responses involved in these processes remain often uncomplete particularly regarding muscle typology. The main aim of the present study was to compare the effects of two types of exercise training protocol: a moderate-intensity continuous training (MICT) and a high-intensity interval training (HIIT) on metabolic processes in two muscles with different typologies: soleus and extensor digitorum longus (EDL). Training effects in male Wistar rats were studied from whole organism level (maximal aerobic speed, morphometric and systemic parameters) to muscle level (transcripts, protein contents and enzymatic activities involved in antioxidant defences, aerobic and anaerobic metabolisms). Wistar rats were randomly divided into three groups: untrained (UNTR), n = 7; MICT, n = 8; and HIIT, n = 8. Rats of the MICT and HIIT groups ran five times a week for six weeks at moderate and high intensity, respectively. HIIT improved more than MICT the endurance performance (a trend to increased maximal aerobic speed, p = 0.07) and oxidative capacities in both muscles, as determined through protein and transcript assays (AMPK-PGC-1α signalling pathway, antioxidant defences, mitochondrial functioning and dynamics). Whatever the training protocol, the genes involved in these processes were largely more significantly upregulated in soleus (slow-twitch fibres) than in EDL (fast-twitch fibres). Solely on the basis of the transcript changes, we conclude that the training protocols tested here lead to specific muscular responses.

Effect of personalized moderate exercise training on Wistar rats fed with a fructose enriched water.

BACKGROUND: Metabolic Syndrom has become a public health problem. It mainly results from the increased consumption of fat and sugar. In this context, the benefits of personalized moderate exercise training were investigated on a metabolic syndrome male wistar rat model food with fructose drinking water (20-25% w/v). Different markers including body weight, metabolic measurements, blood biochemistry related to metabolic syndrome complications have been evaluated. METHODS: Male Wistar rats were randomly allocated to 4 groups: control (sedentary (C, n = 8) and exercise trained (Ex, n = 8)), fructose fed (sedentary (FF, n = 8) and exercise trained fructose fed rats (ExFF, n = 10)). ExFF and Ex rats were trained at moderate intensity during the last 6 weeks of the 12 weeks-long protocol of fructose enriched water. Metabolic control was determined by measuring body weight, fasting blood glucose, HOMA 2-IR, HIRI, MISI, leptin, adiponectin, triglyceridemia and hepatic dysfunction. RESULTS: After 12 weeks of fructose enriched diet, rats displayed on elevated fasting glycaemia and insulin resistance. A reduced food intake, as well as increased body weight, total calorie intake and heart weight were also observed in FF group. Concerning biochemical markers, theoretical creatinine clearance, TG levels and ASAT/ALAT ratio were also affected, without hepatic steatosis. Six weeks of 300 min/week of moderate exercise training have significantly improved overweight, fasting glycaemia, HOMA 2-IR, MISI without modify HIRI. Exercise also decreased the plasma levels of leptin, adiponectin and the ratio leptin/adiponectin. Regarding liver function and dyslipidemia, the results were less clear as the effects of exercise and fructose-enriched water interact together, and, sometimes counteract each other. CONCLUSION: Our results indicated that positive health effects were achieved through a personalized moderate training of 300 min per week (1 h/day and 5 days/week) for 6 weeks. Therefore, regular practice of aerobic physical exercise is an essential triggering factor to attenuate MetS disorders induced by excessive fructose consumption.

Metabolic Syndrome and Hypertension Resulting from Fructose Enriched Diet in Wistar Rats.

Increased sugar consumption, especially fructose, is strongly related to the development of type 2 diabetes (T2D) and metabolic syndrome. The aim of this study was to evaluate long term effects of fructose supplementation on Wistar rats. Three-week-old male rats were randomly divided into 2 groups: control (C; n = 14) and fructose fed (FF; n = 18), with a fructose enriched drink (20-25% w/v fructose in water) for 21 weeks. Systolic blood pressure, fasting glycemia, and bodyweight were regularly measured. Glucose tolerance was evaluated three times using an oral glucose tolerance test. Insulin levels were measured concomitantly and insulin resistance markers were evaluated (HOMA 2-IR, Insulin Sensitivity Index for glycemia (ISI-gly)). Lipids profile was evaluated on plasma. This fructose supplementation resulted in the early induction of hypertension without renal failure (stable theoretical creatinine clearance) and in the progressive development of fasting hyperglycemia and insulin resistance (higher HOMA 2-IR, lower ISI-gly) without modification of glucose tolerance. FF rats presented dyslipidemia (higher plasma triglycerides) and early sign of liver malfunction (higher liver weight). Although abdominal fat weight was increased in FF rats, no significant overweight was found. In Wistar rats, 21 weeks of fructose supplementation induced a metabolic syndrome (hypertension, insulin resistance, and dyslipidemia) but not T2D.

Progressive Induction of Type 2 Diabetes: Effects of a Reality-Like Fructose Enriched Diet in Young Wistar Rats.

PURPOSE: The aim of this study was to characterize short and medium-lasting effects of fructose supplementation on young Wistar rats. The diet was similar to actual human consumption. METHODS: Three week old male rats were randomly divided into 2 groups: control (C; n = 16), fructose fed (FF; n = 16) with a fructose enriched drink for 6 or 12 weeks. Bodyweight, fasting glycemia and systolic blood pressure were monitored. Glucose tolerance was evaluated using an oral glucose tolerance test. Insulinemia was measured concomitantly and enable us to calculate insulin resistance markers (HOMA-IR, Insulin Sensitivity Index for glycemia: ISI-gly). Blood chemistry analyses were performed. RESULTS: After six weeks of fructose supplementation, rats were not overweight but presented increased fasting glycemia, reduced glucose tolerance, and lower insulin sensitivity compared to control group. Systolic blood pressure and heart weight were also increased without any change in renal function (theoretical creatinine clearance). After twelve weeks of fructose supplementation, FF rats had increased bodyweight and presented insulin resistance (higher HOMA-IR, lower ISI-gly). Rats also presented higher heart volume and lower ASAT/ALAT ratio (presumed liver lesion). Surprisingly, the Total Cholesterol/Triglycerides ratio was increased only after six weeks of fructose supplementation, predicting a higher LDL presence and thus a higher risk of developing cardiovascular disease. This risk was no longer present after twelve weeks of a fructose enriched diet. CONCLUSION: On young Wistar rats, six weeks of fructose supplementation is sufficient to induce signs of metabolic syndrome. After twelve weeks of fructose enriched diet, rats are insulin resistant. This model enabled us to study longitudinally the early development of type 2 diabetes.

Effect of exercise training on oxidative stress and mitochondrial function in rat heart and gastrocnemius muscle.

OBJECTIVE: This study aimed to explore the effect of endurance training on oxidative parameters and mitochondrial function in gastrocnemius and heart muscle. METHODS: Male Wistar rats were trained by running for 6 weeks. In vitro measurements of the rates of hydroxyl radical ((•)OH) production, oxygen consumption (in either the absence, basal rate (V0), or the presence, maximal rate (Vmax), of adenosine diphosphate), and adenosine triphosphate (ATP) production were made simultaneously in permeabilized fibers. The mitochondrial function was explored after exposure or non-exposure to an in vitro generator system of reactive oxygen species (ROS). RESULTS: Vmax was not affected by training, but V0 decreased. In conditions of maximal mitochondrial functioning, an increase in ATP rate and a decrease in (•)OH production occurred simultaneously. In vitro ROS exposure disturbed mitochondrial function, but training modified the vulnerability of Vmax and ATP rate to ROS in different ways. DISCUSSION: We hypothesize that the part of Vmax devoted to proton leakage was decreased in trained rats, consequently improving ATP synthesis. The data suggest that, after training, there is more efficient use of electrons in respiratory chain energy production, rather than a greater ROS scavenging capacity.

Effect of tetrahydrobiopterin and exercise training on endothelium-dependent vasorelaxation in SHR.

We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10(-5) M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02). Training alone improved EDV in both WKY (p = 0.01) and SHR (p = 0.0001). Moreover, EDV was not different in trained SHR than in trained WKY (p = 0.934). Pretreatment of rings with L-NAME (50 µM) cancelled the difference in ACh-induced relaxation between all groups, suggesting that NO pathway is involved in these differences. The presence of 10(-5) M BH4 in the organ bath significantly improved EDV for sedentary SHR (p = 0.030) but not WKY group (p = 0.815). Exercise training turned the beneficial effect of BH4 on SHR to impairment of ACh-induced vasorelaxation in both SHR-Tr (p = 0.01) and WKY-Tr groups (p = 0.04). These results suggest that beneficial effect of exercise training on endothelial function is due partly to a BH4-dependent mechanism in established hypertension.

Effect of tetrahydrobiopterin and exercise training on endothelium-dependent vasorelaxation in SHR

We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10−5 M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02). Training alone improved EDV in both WKY (p = 0.01) and SHR (p = 0.0001). Moreover, EDV was not different in trained SHR than in trained WKY (p = 0.934). Pretreatment of rings with L-NAME (50 ìM) cancelled the difference in ACh-induced relaxation between all groups, suggesting that NO pathway is involved in these differences. The presence of 10−5 M BH4 in the organ bath significantly improved EDV for sedentary SHR (p = 0.030) but not WKY group (p = 0.815). Exercise training turned the beneficial effect of BH4 on SHR to impairment of ACh-induced vasorelaxation in both SHR-Tr (p = 0.01) and WKY-Tr groups (p = 0.04). These results suggest that beneficial effect of exercise training on endothelial function is due partly to a BH4-dependent mechanism in established hypertension (AU)