29 resultados para ergometer

em Deakin Research Online - Australia


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The aim of this study was to evaluate the influence of pacing on performance, oxygen uptake (V̇O2), oxygen deficit and blood lactate accumulation during a 6-minute cycle ergometer test. Six recreational cyclists completed three 6-minute cycling tests using fast-start, even-pacing and slow-fast pacing conditions. Cycle ergometer performance was measured as the mean power output produced for each cycling test. Energy system contribution during each cycling trial was estimated using a modified accumulated oxygen deficit (AOD) method. Blood lactate concentration was analysed from blood sampled using a catheter in a forearm vein prior to exercise, at 2 minutes, 4 minutes and 6 minutes during exercise, and at 2 minutes, 5 minutes and 10 minutes post-exercise. There was no significant difference between the pacing conditions for mean power output (P=0.09), peak V̇O2 (P=0.92), total V̇O2 (P=0.76), AOD (P=0.91), the time-course of V̇O2 (P=0.22) or blood lactate accumulation (P=0.07). There was, however, a significant difference between the three pacing conditions in the oxygen deficit measured over time (P=0.02). These changes in the time-course of oxygen deficit during cycling trials did not, however, significantly affect the mean power output produced by each pacing condition.

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PURPOSE: To compare a novel sprint test on a cycle ergometer with a countermovement-jump (CMJ) test for monitoring neuromuscular fatigue after Australian rules football match play. METHODS: Twelve elite under-18 Australian rules football players (mean ± SD age 17.5 ± 0.6 y, stature 184.7 ± 8.8 cm, body mass 75.3 ± 7.8 kg) from an Australian Football League club's Academy program performed a short sprint test on a cycle ergometer along with a single CMJ test 1 h prematch and 1, 24, and 48 h postmatch. The cycle-ergometer sprint test involved a standardized warm-up, a maximal 6-s sprint, a 1-min active recovery, and a 2nd maximal 6-s sprint, with the highest power output of the 2 sprints recorded as peak power (PP). RESULTS: There were small to moderate differences between postmatch changes in cycle-ergometer PP and CMJ PP at 1 (ES = 0.49), 24 (ES = -0.85), and 48 h postmatch (ES = 0.44). There was a substantial reduction in cycle-ergometer PP at 24 h postmatch (ES = -0.40) compared with 1 h prematch. CONCLUSIONS: The cycle-ergometer sprint test described in this study offers a novel method of neuromuscular-fatigue monitoring in team-sport athletes and specifically quantifies the concentric component of the fatigue-induced decrement of force production in muscle, which may be overlooked by a CMJ test.

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We have estimated the reliability of performance in a commonly employed exercise test consisting of repeated sprints on a cycle ergometer. Eight recreationally active young men completed a practice trial and three more trials at 3- to 6-day intervals. Each trial consisted of two bouts of 30-s maximal-effort cycling on an electromagnetically braked cycle ergometer; the bouts were separated by 4 min of rest. The typical (standard) errors of measurement for peak and mean power between trials 2 to 4 were 2.5 and 1.7% respectively for the first bout and 1.9 and 1.8% for the second bout. These errors are substantially less than those in previous reliability studies of single 30-s sprint tests, probably because of differences in quality of ergometer. The typical errors for the difference between bouts (i.e., fatigue) for peak power and mean power were 3.0 and 2.5%, respectively. Typical errors for the average of the two bouts were 1.6 and 1.2% for peak and mean power respectively, which are small enough to give adequate precision for moderate treatment effects in studies with modest sample sizes.

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The present study examined the validity and reliability of measuring the expression of various genes in human skeletal muscle using quantitative real-time RT-PCR on a GeneAmp 5700 sequence detection system with SYBR Green 1 chemistry. In addition, the validity of using some of these genes as endogenous controls (i.e., housekeeping genes) when human skeletal muscle was exposed to elevated total creatine levels and exercise was also examined. For all except 28S, linear relationships between the logarithm of the starting RNA concentrations and the cycle threshold (CT) values were established for ß-actin, ß2-microglobulin (ß2M), cyclophilin (CYC), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). We found a linear response between CT values and the logarithm of a given amount of starting cDNA for all the genes tested. The overall intra-assay coefficient of variance for these genes was 1.3% and 21% for raw CT values and the linear value of 2-CT, respectively. Interassay variability was 2.3% for raw CT values and 34% for the linear value of 2-CT. We also examined the expression of various housekeeping genes in human skeletal muscle at days 0, 1, and 5 following oral supplementation with either creatine or a placebo employing a double-blind crossover study design. Treatments were separated by a 5-wk washout period. Immediately following each muscle sampling, subjects performed two 30-s all-out bouts on a cycle ergometer. Creatine supplementation increased (P < 0.05) muscle total creatine content above placebo levels; however, there were no changes (P > 0.05) in CT values across the supplementation periods for any of the genes. Nevertheless, 95% confidence intervals showed that GAPDH was variable, whereas ß-actin, ß2M, and CYC were the least varying genes. Normalization of the data to these housekeeping genes revealed variable behavior for ß2M with more stable expressions for both ß-actin and CYC. We conclude that, using real-time RT-PCR, ß-actin or CYC may be used as housekeeping genes to study gene expression in human muscle in experiments employing short-term creatine supplementation combined with high-intensity exercise.

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To investigate the effect of exercise on protein kinase C (PKC) activity and localization in human skeletal muscle, eight healthy men performed cycle  ergometer exercise for 40 min at 76±1% the peak pulmonary O2 uptake (VO2peak), with muscle samples obtained at rest and after 5 and 40 min of exercise. PKC expression, phosphorylation and activities were examined by immunoblotting and in vitro kinase assays of fractionated and whole tissue preparations. In response to exercise, total PKC activity was slightly higher at 40 min in an enriched membrane fraction, and using a pSer-PKC-substrate motif antibody it was revealed that exercise increased the serine phosphorylation of a ∼50 kDa protein. There were no changes in conventional PKC (cPKC) or PKCθ activities; however, atypical PKC (aPKC) activity was ∼70% higher at 5 and 40 min, and aPKC expression and Thr410/403 phosphorylation were unaltered by exercise. There were no effects of exercise on the abundance of PKCα, PKCδ, PKCθ and aPKC within cytosolic or enriched membrane fractions of skeletal muscle. These data indicate that aPKC, but not cPKC or PKCθ, are activated by exercise in contracting muscle suggesting a potential role for aPKC in the regulation of skeletal muscle function and metabolism during exercise in humans.

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The authors addressed the hypothesis that economy in motor coordination is a learning phenomenon realized by both reduced energy cost for a given workload and more external work at the same prepractice metabolic and attentional energy expenditure. "Self-optimization" of movement parameters has been proposed to reflect learned motor adaptations that minimize energy costs. Twelve men aged 22.3 [+ or -] 3.9 years practiced a 90[degrees] relative phase, upper limb, independent ergometer cycling task at 60 rpm, followed by a transfer test of unpracticed (45 and 75 rpm) and self-paced cadences. Performance in all conditions was initially unstable, inaccurate, and relatively high in both metabolic and attentional energy costs. With practice, coordinative stability increased, more work was performed for the same metabolic and attentional costs, and the same work was done at a reduced energy cost. Self-paced cycling was initially below the metabolically optimal, but following practice at 60 rpm was closer to optimal cadence. Given the many behavioral options of the motor system in meeting a variety of everyday movement task goals, optimal metabolic and attentional energy criteria may provide a solution to the problem of selecting the most adaptive coordination and control parameters.

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Nine endurance-trained men exercised on a cycle ergometer at ~68% peak O2 uptake to the point of volitional fatigue [232 ± 14 (SE) min] while ingesting an 8% carbohydrate solution to determine how high glucose disposal could increase under physiological conditions. Plasma glucose kinetics were measured using a primed, continuous infusion of [6,6-2H]glucose and the appearance of ingested glucose, assessed from [3-3H]glucose that had been added to the carbohydrate drink. Plasma glucose was increased (P < 0.05) after 30 min of exercise but thereafter remained at the preexercise level. Glucose appearance rate (Ra) increased throughout exercise, reaching its peak value of 118 ± 7 µmol · kg-1 · min-1 at fatigue, whereas gut Ra increased continuously during exercise, peaking at 105 ± 10 µmol · kg-1 · min-1 at the point of fatigue. In contrast, liver glucose output never rose above resting levels at any time during exercise. Glucose disposal (Rd) increased throughout exercise, reaching a peak value of 118 ± 7 µmol · kg-1 · min-1 at fatigue. If we assume 95% oxidation of glucose Rd, estimated exogenous glucose oxidation at fatigue was 1.36 ± 0.08 g/min. The results of this study demonstrate that glucose uptake increases continuously during prolonged, strenuous exercise when carbohydrate is ingested and does not appear to limit exercise performance.

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Most research on creatine has focused on short-term creatine loading and its effect on high-intensity performance capacity. Some studies have investigated the effect of prolonged creatine use during strength training. However, studies on the effects of prolonged creatine supplementation are lacking. In the present study, we have assessed the effects of both creatine loading and prolonged supplementation on muscle creatine content, body composition, muscle and whole-body oxidative capacity, substrate utilization during submaximal exercise, and on repeated supramaximal sprint, as well as endurance-type time-trial performance on a cycle ergometer. Twenty subjects ingested creatine or a placebo during a 5-day loading period (20g·day-1) after which supplementation was continued for up to 6 weeks (2g·day-1). Creatine loading increased muscle free creatine, creatine phosphate (CrP) and total creatine content (P<0.05). The subsequent use of a 2g·day-1 maintenance dose, as suggested by an American College of Sports Medicine Roundtable, resulted in a decline in both the elevated CrP and total creatine content and maintenance of the free creatine concentration. Both short- and long-term creatine supplementation improved performance during repeated supramaximal sprints on a cycle ergometer. However, whole-body and muscle oxidative capacity, substrate utilization and time-trial performance were not affected. The increase in body mass following creatine loading was maintained after 6 weeks of continued supplementation and accounted for by a corresponding increase in fat-free mass. This study provides definite evidence that prolonged creatine supplementation in humans does not increase muscle or whole-body oxidative capacity and, as such, does not influence substrate utilization or performance during endurance cycling exercise. In addition, our findings suggest that prolonged creatine ingestion induces an increase in fat-free mass.

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The influence of allopurinol on urinary purine loss was examined in 7 active male subjects (age 24.9 ± 3.0 years, weight 82.8 ± 8.3 kg, V˙o2peak 48.1 ± 6.9 mL · kg−1 · min−1). These subjects performed, in random order, a trial with 5 days of prior ingestion of a placebo or allopurinol. Each trial consisted of eight 10-second sprints on an air-braked cycle ergometer and was separated by at least a week. A rest period of 50 seconds separated each repeated sprint. Forearm venous plasma inosine, hypoxanthine (Hx) and uric acid concentrations were measured at rest and during 120 minutes of recovery from exercise. Urinary inosine, Hx, xanthine, and uric acid excretion were also measured before and for 24 hours after exercise. During the first 120 minutes of recovery, plasma Hx concentrations, as well as the urinary Hx and xanthine excretion rates, were higher (P < .05) with allopurinol compared with the placebo trial. In contrast, plasma uric acid concentration and urinary uric acid excretion rates were lower (P < .05) with allopurinol. The total urinary excretion of purines (inosine + Hx + xanthine + uric acid) above basal levels was higher in the allopurinol trial compared with placebo. These results indicate that the total urinary purine excretion after intermittent sprint exercise was enhanced with allopurinol treatment. Furthermore, the composition of urinary purines was markedly affected by this drug.

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Background
To determine whether the provision of higher levels of compulsory school physical activity is associated with higher physical activity and fitness levels and less overweight in childhood and 20 years later.

Methods
As part of the 1985 Australian Schools Health and Fitness Survey, 109 schools reported how much compulsory physical education (PE) and school sport they provided and were classified as low (<110 and <150 minutes/week for primary and secondary schools, respectively), medium (110–149 and 150–189 minutes/week for primary and secondary schools, respectively) or high (≥150 and ≥190 minutes/week for primary and secondary schools, respectively) compulsory physical activity schools by tertile cutpoints. 6,412 children reported frequency and duration of school (PE and sport) and non-school (commuting and non-organised exercise) physical activity and had height and weight measured; overweight was defined using body mass index (BMI) (m/kg2) cutpoints. 9, 12 and 15 year-olds (n = 2,595) completed a cycle ergometer fitness test (physical working capacity at heart rate 170, PWC170). At follow-up in 2004–5, 2,346 participants kept a pedometer record, completed the International Physical Activity Questionnaire and/or a PWC170 fitness test; and had height and weight measured (overweight = BMI≥25 m/kg2).

Results
At baseline and follow-up, median total physical activity, fitness and BMI were similar in participants who attended low, medium and high physical activity schools, and those attending high physical activity schools reported only modestly higher school physical activity. There was no difference in the prevalence of high total physical activity and fitness levels in childhood or adulthood across compulsory school physical activity categories. The prevalence of overweight in childhood and adulthood was similar across low, medium and high compulsory physical activity schools.

Conclusion
The amount of compulsory physical activity reported by schools was not associated with total physical activity, fitness or overweight in childhood or in adulthood. Policies promoting amounts of compulsory school physical activity in this range may not be sufficient to increase physical activity and fitness or reduce the prevalence of obesity in children.

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BACKGROUND
Implementation of a structured physical exercise program can improve glycemic control in patients with type 2 diabetes mellitus.

OBJECTIVE
To evaluate the efficacy of aerobic exercise and resistance training (either alone or in combination) in the management of type 2 diabetes mellitus.

DESIGN AND INTERVENTION
DARE (Diabetes Aerobic and Resistance Exercise) was a 26-week, single-center, parallel-group, randomized, controlled trial of patients with type 2 diabetes mellitus of >6 months' duration. Participants were aged 39-70 years with a baseline [HbA.sub.1c] level 6.6-9.9%. Exclusion criteria included current insulin therapy, regular exercise regime and blood pressure >160/95 mmHg. All participants underwent a 4-week run-in period that comprised 12 sessions of combined aerobic exercise and resistance training; participants who attended [greater than or equal to] 10 sessions were eligible to enter the study. Eligible participants were randomly allocated to one of four groups: aerobic exercise alone; resistance training alone; combined aerobic exercise and resistance training; and no intervention (control group). Exercise was performed three times weekly. The aerobic exercise group progressed from 15-20 min on a treadmill or bicycle ergometer per session at 60% of the maximum heart rate to 45 min per session at 75% of the maximum heart rate. The resistance training group performed 7 different exercises on weight machines per 45 min session, and progressed to 2-3 sets of each exercise at the maximum weight that could be lifted 7-9 times. The combined exercise group performed the full aerobic exercise program plus the full resistance training program. Participants in the control group reverted to their pre-study exercise levels.

OUTCOME MEASURES
The primary outcome measure was the change in [HbA.sub.1c] from baseline. Secondary outcome measures included changes in blood pressure, lipid profile, and body composition.

RESULTS
A total of 251 participants were eligible for intervention. The median session attendance was 80% (aerobic exercise), 85% (resistance training) and 86% (combined exercise). When compared with the control group, the HbA1c levels were reduced by 0.50% in the aerobic exercise group (P = 0.007) and by 0.38% in the resistance training group (P = 0.038). The combined exercise group had an additional reduction of 0.46% when compared with the aerobic exercise group (P = 0.014) and of 0.59% when compared with the resistance training group (P = 0.001). Decreases in [HbA.sub.1c] levels were greatest for participants with a baseline [HbA.sub.1c] level = 7.5% (P <0.001). For participants with a baseline level [HbA.sub.1c] <7.5%, significant improvements in glycemic control were observed in the combined exercise group only (P = 0.002). Changes in blood pressure and lipid profiles did not differ between the groups. By contrast, participation in a structured exercise program improved body composition.

CONCLUSION
Although aerobic exercise or resistance training alone improved glycemic control, additional improvements were observed with the combined exercise regimen.

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1. This series of studies was undertaken to examine the adrenergic regulation of carbohydrate metabolism during exercise. Recreationally active males were tested during moderate to intense exercise on a stationary cycle ergometer. Venous and arterial plasma obtained from indwelling catheters was analysed for hormonal and metabolite responses, and hepatic glucose production and glucose uptake were measured using the tracer-dilution method with stable isotopes. Muscle samples were obtained by the needle biopsy technique to examine muscle glycogen utilisation and the flux of related muscle metabolites using enzymatic, fluorometric and radioisotopic techniques. 2. During moderate exercise adrenaline infusion induced a marked hyperglycemia and this was due to reduced glucose uptake rather than enhanced hepatic glucose production. The reduction in glucose uptake was most likely mediated by a decrease in glucose phosphorylation, as indicated by the accumulation of glucose 6-phosphate with adrenaline infusion. 3. The hyperglycemic response to intense exercise was prevented by the administration of α- and β-adrenergic antagonists. Adrenergic blockade was without effect on hepatic glucose production whereas glucose uptake was enhanced when compared with control subjects. These data support the notion that adrenergic mechanisms are more important in restraining glucose uptake than enhancing hepatic glucose production during intense exercise. Other glucoregulatory factors are responsible for the increase in glucose production during intense exercise. 4. Elevated plasma adrenaline levels during moderate exercise in untrained men increases skeletal muscle glycogen breakdown and PDH activation which results

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Physical inactivity is a leading factor associated with cardiovascular disease and a major contributor to the global burden of disease in developed countries. Subjective mood states associated with acute exercise are likely to influence future exercise adherence and warrant further investigation. The present study examined the effects of a single bout of vigorous exercise on mood and anxiety between individuals with substantially different exercise participation histories. Mood and anxiety were assessed one day before an exercise test (baseline), 5 minutes before (pre-test) and again 10 and 25 minutes post-exercise. Participants were 31 university students (16 males, 15 females; Age M = 20), with 16 participants reporting a history of regular exercise with the remaining 15 reporting to not exercise regularly. Each participant completed an incremental exercise test on a Monark cycle ergometer to volitional exhaustion. Regular exercisers reported significant post-exercise improvements in mood and reductions in state anxiety. By contrast, non-regular exercisers reported an initial decline in post-exercise mood and increased anxiety, followed by an improvement in mood and reduction in anxiety back to pre-exercise levels. Our findings suggest that previous exercise participation mediates affective responses to acute bouts of vigorous exercise. We suggest that to maximise positive mood changes following exercise, practitioners should carefully consider the individual's exercise participation history before prescribing new regimes.

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Aims To examine the oxygen (O2) kinetics during early recovery from peak exercise in patients with Type 2 diabetes and to examine whether oxygen O2 recovery is associated with fasting glucose and HbA1c in this population.

Methods Eighty-nine participants (52 men) aged 51.8 ± 7.1 years (mean ± sd) were divided into three groups: normal weight (BMI ≤ 25.0 kg/m2), overweight/obese without diabetes (BMI ≥ 26 kg/m2) and overweight/obese with Type 2 diabetes. Participants were assessed for their aerobic power (VO2peak) on a cycle ergometer, provided a fasting blood sample and underwent a series of anthropometric measurements. Early recovery period was measured for 60 s from cessation of exercise and expressed as percentage of VO2peak (higher percentage represents slower recovery).

Results No significant differences were observed for age between the three study groups. Both the overweight/obese groups without diabetes and with Type 2 diabetes had higher BMI than the normal weight group, with no significant differences between overweight/obese participants without diabetes and those with diabetes. Participants with Type 2 diabetes had lower VO2peak than overweight/obese participants without diabetes and normal weight individuals (19.6 ± 4.8, 22.6 ± 5.4 and 25.7 ± 5.3 ml kg−1 min−1, respectively, P < 0.004 for overall trends). Participants with Type 2 diabetes also had slower recovery in oxygen O2 kinetics after exercise, compared with both normal weight and overweight/obese individuals without diabetes (56.5 ± 7.7, 49.2 ± 7.2, 47.7 ± 7.4%, P < 0.004 for overall trends). Multiple regression analysis revealed that percentage of oxygen O2 recovery was a stronger predictor than VO2peak, BMI or age for fasting glucose and HbA1c.

Conclusions Patients with Type 2 diabetes have lower VO2peak and prolonged oxygen O2 recovery from peak exercise. However, only prolonged oxygen O2 recovery was associated with fasting glucose and HbA1c.