Effect of high intensity interval training on 2,3-diphosphoglycerate at rest and after maximal exercise

The purpose of this study was to examine the effect of intense interval training on erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels at rest and after maximal exercise. Eight normal men, mean +/- SE = 24.2 +/- 4.3 years, trained 4 days X week-1 for a period of 8 weeks. Each training session consisted of eight maximal 30-s rides on a cycle ergometer, with 4 min active rest between rides . Prior to and after training the subjects performed a maximal 45-s ride on an isokinetic cycle ergometer at 90 rev X min-1 and a graded leg exercise test ( GLET ) to exhaustion on a cycle ergometer. Blood samples were obtained from an antecubital vein before, during and after the GLET only. Training elicited significant increases in the amount of work done during the 45-s ride (P less than 0.05), and also in maximal oxygen uptake (VO2 max: Pre = 4.01 +/- 0.13; Post = 4.29 +/- 0.07 1 X min-1; P less than 0.05) during exercise and total recovery VO2 (Pre = 19.14 +/- 0.09; Post = 21.45 +/- 0.10 1 X 30 min-1; P less than 0.05) after the GLET . After training blood lactate was higher, base excess lower and pH lower during and following the GLET (P less than 0.05 for all variables).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of cycling exercise on lumbopelvic control performance in elite female cyclists

Objectives:The purpose of the present study is to assess the effects of an intense cycling training session on the stability of the lumbopelvic-hip complex through two dynamic exercise tests - the single-leg-deadlift (SLD) and a variation of the bird-modified dog (BD), via the OCTOcore application.Methods:Thirty-one elite female road cyclists were self-evaluated with their own smartphones, before and immediately after finishing their training sessions. Right, left and composite were measured for each exercise test.Results:There was a significant time effect on performance for both the SLB and BD tests (p<0.05; η²=0.137), and the SLD and BD tests were increased with respect to the pre-test at 15% and 17%, respectively.Conclusion:An intense cycling training session produced significant alterations in lumbopelvic behavior in the elite female cyclists. The OCTOcore application demonstrated that it was a sensitive tool in detecting these changes and it could easily be used by the cyclists themselves.     

Effects of endurance exercise training on markers of cholesterol absorption and synthesis

Abnormal cholesterol metabolism, including low intestinal cholesterol absorption and elevated synthesis, is prevalent in diabetes, obesity, hyperlipidemia, and the metabolic syndrome. Diet-induced weight loss improves cholesterol absorption in these populations, but it is not known if endurance exercise training also improves cholesterol homeostasis. To examine this, we measured circulating levels of campesterol, sitosterol, and lathosterol in 65 sedentary subjects (average age 59 years; with at least one metabolic syndrome risk factor) before and after 6 months of endurance exercise training. Campesterol and sitosterol are plant sterols that correlate with intestinal cholesterol absorption, while lathosterol is a marker of whole body cholesterol synthesis. Following the intervention, plant sterol levels were increased by 10% (p<0.05), but there was no change in plasma lathosterol. In addition, total and LDL-cholesterol were reduced by 0.16 mmol and 0.10 mmol, respectively (p<0.05), while HDL-C levels increased by 0.09 mmol (p<0.05). Furthermore, the change in plant sterols was positively correlated with the change in VO2max (r=0.310, p=0.004), independent of other metabolic syndrome risk factors. These data indicate that exercise training reduces plasma cholesterol despite increasing cholesterol absorption in subjects with metabolic syndrome risk factors.     

Effect of exercise intensity and duration on postexercise metabolism

Data are reported on the net recovery O2 consumption (VO2) for nine male subjects (mean age 21.9 yr, VO2max 63.0 ml.kg-1.min-1, body fat 10.6%) used in a 3 (independent variables: intensities of 30, 50, and 70% VO2max) x 3 (independent variables: durations of 20, 50, and 80 min) repeated measures design (P less than or equal to 0.05). The 8-h mean excess postexercise O2 consumptions (EPOCs) for the 20-, 50-, and 80-min bouts, respectively, were 1.01, 1.43, and 1.04 liters at 30% VO2max (6.8 km/h); 3.14, 5.19, and 6.10 liters at 50% VO2max (9.5 km/h); and 5.68, 10.04, and 14.59 liters at 70% VO2max (13.4 km/h). The mean net total O2 costs (NTOC = net exercise VO2 + EPOC) for the 20-, 50-, and 80-min bouts, respectively, were 20.48, 53.20, and 84.23 liters at 30% VO2max; 38.95, 100.46, and 160.59 liters at 50% VO2max; and 58.30, 147.48, and 237.17 liters at 70% VO2max. The nine EPOCs ranged only from 1.0 to 8.9% of the NTOC (mean 4.8%) of the exercise. These data, therefore, indicate that in well-trained subjects the 8-h EPOC per se comprises a very small percentage of the NTOC of exercise.     

Effect of a moderate intensity exercise training protocol on the metabolism of macrophages and lymphocytes of tumour-bearing rats

It is commonly accepted that moderate intensity exercise is beneficial to the immune system. We tested the influence of a moderate intensity training protocol (8 weeks) upon immune system function in Wistar tumour-bearing (TB) rats. The metabolism of glucose and glutamine in lymphocytes and macrophages was assessed, together with some functional parameters (hydrogen peroxide production and lymphocyte proliferative response). These substrates were chosen since they represent the most important energetic and synthetic metabolites for these cellular types. The training protocol caused a decrease of 17.4 per cent in the production of H(2)O(2) by macrophages, as well as a decrease in glucose consumption (25 per cent) and lactate production (47.1 per cent), and an increase in the production of labelled CO(2) from the oxidation of [U-(14)C]-glucose, in TB rats. The training protocol was also able to induce changes in the maximal activity of some key enzymes in the metabolism of glucose and glutamine, a reduction of hexokinase (68.8 per cent) activity and an increase in the activity of citrate synthase (10.1 per cent) in TB rats. The training protocol increased the proliferative response of lymphocytes cultivated in the absence of mitogens (75 per cent), of those cultivated in the presence of ConA (38.2 per cent) and in the presence of LPS (45.0 per cent). These cells also showed an increase in the maximal activity of some key enzymes of the glycolytic and glutaminolytic pathways. Our data demonstrated that the training protocol was able to induce an increase in aerobic utilisation of both substrates in lymphocytes and macrophages. The training protocol was also able to prevent several changes in glucose and glutamine metabolism that are normally present in sedentary TB rats. These changes in immune cell metabolism induced by the training protocol were able to increase TB rat survival.     

不同强度运动训练对心肌凋亡途径微小RNA及其靶蛋白的影响

目的：考察不同负荷运动训练对小鼠心肌凋亡相关miR-1,miR-21和靶蛋白的影响,探讨运动干预心肌凋亡的可能机制。方法：选取21只C57BL/6小鼠,随机分为3组（n=7）：安静组（SE组）、训练1组（ET1组）、训练2组（ET2）。SE组不进行训练,ET1组完成8周递增负荷游泳训练,5天/周,1次/天,第1周30 min/count,每周增加10 min,第7、8周时间维持在90 min;ET2组在ET1组方案基础上增加负荷,前5周与ET1相同,后3周每天训练2次。TUNEL检测考察心肌凋亡水平,Western blot和RT-PCR分别测定蛋白和miRs的变化。结果：ET1组游泳训练对小鼠心肌凋亡影响不明显,miR-1表达无显著变化,但其靶蛋白Bcl-2表达显著增高（P<0.01）,miR-21及其靶蛋白PDCD4表达均无显著变化。ET2组游泳训练显著降低心肌凋亡水平及miR-1表达（P<0.01）、提高Bcl-2表达（P<0.05）;同时显著提高miR-21表达（P<0.05）,但对PDCD4表达无明显影响。结论：ET1组训练对心肌凋亡干预不明显,ET2组运动训练可降低心肌凋亡水平,miR-1及靶蛋白Bcl-2变化可能是机制之一,PDCD4对运动训练不敏感,miR-21可能与其它靶蛋白参与运动干预心肌凋亡的分子机制。     

Effect of exercise intensity on mild rhythmic-handgrip-exercise-induced functional sympatholysis

This study attempts to clarify whether intensity of exercise influences functional sympatholysis during mild rhythmic handgrip exercise (RHG). We measured muscle oxygenation in both exercising and non-exercising muscle in the same arm in 11 subjects using near infrared spectroscopy (NIRS), heart rate, and blood pressure. We used the total labile signal to assess the relative muscle oxygenation by occlusion for 6 min. Subjects performed RHG (20 times/min) for 6 min at 10%, 20%, and 30% of maximal voluntary contraction (MVC) at random. We used a non-hypotensive lower body negative pressure (LBNP) of 220 mmHg for 2 min to elicit reproducible enhancement in muscle sympathetic nerve activity (MSNA) at rest and during RHG. LBNP caused decreases of 16.4% and 17.7% of the level of muscle oxygenation at rest (pre) in exercising (forearm) and non-exercising (upper arm) muscle respectively. Muscle oxygenation in non-exercising muscle with the application of LBNP during RHG did not change significantly at each intensity. In contrast, the decrease in muscle oxygenation in exercising muscle attenuated progressively as exercise intensity increased (10% MVC 8.8+/-2.8%, 20% MVC 7.1+/-2.0%, 30% MVC 4.6+/-3.0%), when LBNP was applied during RHG. The attenuation of the decrease in muscle oxygenation due to LBNP during RHG at 10%, 20%, and 30% was significantly different from that at rest (p<0.01). These findings indicate that functional sympatholysis during mild RHG might be attributed to exercise intensity.     

Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training

It is welldocumented that endurance exercise training results in a bluntednorepinephrine (NE) response to exercise of a given absolute exerciseintensity. However, it is not clear what effect traininghas on the catecholamine response to exercise of the same relativeintensity because previous studies have provided conflicting results.The purpose of the present study was, therefore, to determine thecatecholamine response to exercise of the same relative exerciseintensity before and after endurance exercise training. Six women andthree men [age 28 ± 8 (SD) yr] performed 10 wk oftraining. Maximal O₂ uptake(O_{2 max}) wasdetermined during treadmill exercise. Fifteen-minute treadmill exercisebouts were performed at 60, 65, 70, 75, 80, and 85% ofO_{2 max} before andafter training.O_{2 max} was increasedby 20% (from 39.2 ± 7.7 to 46.9 ± 8.1 ml · kg¹ · min¹;P < 0.05) in response to training.Plasma NE concentrations were higher(P < 0.05) during exercise at thesame relative intensity after, compared with before, training at65-85% ofO_{2 max.}Differences between heart rates and plasma epinephrine concentrationsafter, compared with before, training were not statisticallysignificant. These results provide evidence that the NE response toexercise is dependent on the absolute as well as the relative intensity of the exercise.     

Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet

These studies investigated the effects of 2 weeks of either a high-fat (HIGH-FAT: 70% fat, 7% CHO) or a high-carbohydrate (HIGH-CHO: 74% CHO, 12% fat) diet on exercise performance in trained cyclists (n = 5) during consecutive periods of cycle exercise including a Wingate test of muscle power, cycle exercise to exhaustion at 85% of peak power output [90% maximal oxygen uptake ( O_2max), high-intensity exercise (HIE)] and 50% of peak power output [60% O_2max, moderate intensity exercise (MIE)]. Exercise time to exhaustion during HIE was not significantly different between trials: nor were the rates of muscle glycogen utilization during HIE different between trials, although starting muscle glycogen content was lower [68.1 (SEM 3.9) vs 120.6 (SEM 3.8) mmol · kg ^–1 wet mass, P < 0.01] after the HIGH-FAT diet. Despite a lower muscle glycogen content at the onset of MIE [32 (SEM 7) vs 73 (SEM 6) mmol · kg ^–1 wet mass, HIGH-FAT vs HIGH-CHO, P < 0.01], exercise time to exhaustion during subsequent MIE was significantly longer after the HIGH-FAT diet [79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, HIGH-FAT vs HIGH-CHO, P<0.01]. Enhanced endurance during MIE after the HIGH-FAT diet was associated with a lower respiratory exchange ratio [0.87 (SEM 0.03) vs 0.92 (SEM 0.02), P<0.05], and a decreased rate of carbohydrate oxidation [1.41 (SEM 0.70) vs 2.23 (SEM 0.40) g CHO · min^–1, P<0.05]. These results would suggest that 2 weeks of adaptation to a high-fat diet would result in an enhanced resistance to fatigue and a significant sparing of endogenous carbohydrate during low to moderate intensity exercise in a relatively glycogen-depleted state and unimpaired performance during high intensity exercise.     

Effect of exercise timing on postprandial lipemia and HDL cholesterol subfractions

The purpose ofthe study was to examine the effect of exercise timing on postprandiallipemia responses. Subjects were 21 recreationally trained men (ages 27 ± 1.7 yr). Each subject performed four trials:1) Control (fat meal only),2) Post (exercise 1 h after a fat meal), 3) 1 h-Pre(exercise 1 h before a fat meal), and4) 12 h-Pre (exercise 12 h before afat meal). In each trial, subjects had a standard fat meal to inducepostprandial hypertriglyceridemia. Blood samples were taken at 0 h(immediately before the fat meal) and at 2, 4, 6, 8, and 24 h after themeal. In the exercise trials, each subject exercised at 60% of maximalO₂ consumption for 1 h. Theresults indicated that triglyceride area under the curve scores inpremeal-exercise trials were lower (P < 0.05) than those in Post and Control. At 24 h, total high-densitylipoprotein (HDL)-cholesterol in the premeal-exercise trials was higher(P < 0.05) than that at 0 h, whereastotal HDL-cholesterol was not changed in Control and Post. At 24 h, HDLsubtype 2-cholesterol was higher (P < 0.05) in the premeal-exercise trials than in Control, which did not differ from Post. These results suggest that exercising before a fatmeal may have a beneficial effect on the triglyceride response and HDLmetabolism, which may blunt atherosclerotic process induced by the fatmeal.

     

Plasma metabolic profile in COPD patients: effects of exercise and endurance training

The study examines plasma metabolic profiles of patients with chronic obstructive pulmonary disease (COPD) to prove whether the disease influences metabolism at rest and after endurance training. This is based on the hypothesis that metabolome levels should reflect impaired skeletal muscle bioenergetics in COPD. The study aims to test this hypothesis by evaluating plasma metabolic profiles in COPD patients before and after 8?weeks of endurance exercise training. We studied blood samples from 18 COPD patients and 12 healthy subjects. Pre- and post-training blood plasma samples at rest and after constant-work rate exercise (CWRE) at 70% of pre-training Watts peak were analyzed by ¹H-nuclear magnetic resonance spectroscopy to assess metabolite profiles. The two groups presented training-induced physiological changes in the VO₂ peak and in blood lactate levels (P?<?0.01 each). Before training, the two groups also showed differences in metabolic profiles at rest (P?<?0.05). Levels of valine (r?=?0.51, P?<?0.01), alanine (r?=?0.45, P?<?0.05) and isoleucine (r?=?0.51, P?<?0.01) were positively associated with body composition (Fat Free Mass Index). While training showed a significant impact on the metabolic profile in healthy subjects (P?<?0.001), with changes in levels of amino acids, creatine, succinate, pyruvate, glucose and lactate (P?<?0.05 each), no equivalent training-induced effects were seen in COPD patients in whom only lactate decreased (P?<?0.05). This study shows that plasma metabolic profiling contributes to the phenotypic characterization of COPD patients.     

Effect of exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoA carboxylase

Rasmussen, B. B., and W. W. Winder. Effectof exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoAcarboxylase. J. Appl. Physiol. 83(4):1104-1109, 1997.Malonyl-CoA is synthesized by acetyl-CoAcarboxylase (ACC) and is an inhibitor of fatty acid oxidation. Exerciseinduces a decline in skeletal muscle malonyl-CoA, which is accompaniedby inactivation of ACC and increased activity of AMP-activated proteinkinase (AMPK). This study was designed to determine the effect ofexercise intensity on the enzyme kinetics of ACC, malonyl-CoA levels,and AMPK activity in skeletal muscle. Male Sprague-Dawley rats werekilled (pentobarbital sodium anesthesia) at rest or after 5 min ofexercise (10, 20, 30, or 40 m/min at 5% grade). The fast-twitch redand white regions of the quadriceps muscle were excised and frozen inliquid nitrogen. A progressive decrease in red quadriceps ACC maximalvelocity (from 28.6 ± 1.5 to 14.3 ± 0.7 nmol · g¹ · min¹,P < 0.05), an increase in activationconstant for citrate, and a decrease in malonyl-CoA (from 1.9 ± 0.2 to 0.9 ± 0.1 nmol/g, P < 0.05) were seen with theincrease in exercise intensity from rest to 40 m/min. AMPK activityincreased more than twofold. White quadriceps ACC activity decreasedonly during intense exercise. We conclude that the extent of ACCinactivation during short-term exercise is dependent on exerciseintensity.

     

Influence of high-intensity interval training on adaptations in well-trained cyclists

The purpose of the present study was to examine the influence of 3 different high-intensity interval training regimens on the first and second ventilatory thresholds (VT(1) and VT(2)), anaerobic capacity (ANC), and plasma volume (PV) in well-trained endurance cyclists. Before and after 2 and 4 weeks of training, 38 well-trained cyclists (Vo(2)peak = 64.5 +/- 5.2 ml.kg(-1).min(-1)) performed (a) a progressive cycle test to measure Vo(2)peak, peak power output (PPO), VT(1), and VT(2); (b) a time to exhaustion test (T(max)) at their Vo(2)peak power output (P(max)); and (c) a 40-km time-trial (TT(40)). Subjects were assigned to 1 of 4 training groups (group 1: n = 8, 8 x 60% T(max) at P(max), 1:2 work-recovery ratio; group 2: n = 9, 8 x 60% T(max) at P(max), recovery at 65% maximum heart rate; group 3: n = 10, 12 x 30 seconds at 175% PPO, 4.5-minute recovery; control group: n = 11). The TT(40) performance, Vo(2)peak, VT(1), VT(2), and ANC were all significantly increased in groups 1, 2, and 3 (p < 0.05) but not in the control group. However, PV did not change in response to the 4-week training program. Changes in TT(40) performance were modestly related to the changes in Vo(2)peak, VT(1), VT(2), and ANC (r = 0.41, 0.34, 0.42, and 0.40, respectively; all p < 0.05). In conclusion, the improvements in TT(40) performance were related to significant increases in Vo(2)peak, VT(1), VT(2), and ANC but were not accompanied by significant changes in PV. Thus, peripheral adaptations rather than central adaptations are likely responsible for the improved performances witnessed in well-trained endurance athletes following various forms of high-intensity interval training programs.