38 resultados para lactate threshold

em Deakin Research Online - Australia


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The accumulated oxygen deficit (AOD) method assumes a linear VO<sub>2</sub>-power relationship for exercise intensities increasing from below the lactate threshold (BLT) to above the lactate threshold (ALT). Factors that were likely to effect the linearity of the VO<sub>2</sub>-power regression and the precision of the estimated total energy demand (ETED) were investigated. These included the slow component of VO<sub>2</sub> kinetics (SC), a forced resting y-intercept and exercise intensities BLT and ALT. Criteria for linearity and precision included the Pearson correlation coefficient (PCC) of the VO<sub>2</sub>-power relationship, the length of the 95% confidence interval (95% CI) of the ETED and the standard error of the predicted value (SEP), respectively. Eight trained male and one trained female triathlete completed the required cycling tests to establish the AOD when pedalling at 80 rev/min. The influence of the SC on the linear extrapolation of the ETED was reduced by measuring VO<sub>2</sub> after three min of exercise. Measuring VO<sub>2</sub> at this time provided a new linear extrapolation method consisting of ten regression points spread evenly from BLT and ALT. This method produced an ETED with increased precision compared to using regression equations developed from intensities BLT with no forced y-intercept value; (95%CI (L), 0.70±0.26 versus 1.85±1.10, P<0.01; SEP(L/Watt), 0.07±0.02 versus 0.28±0.17; P<0.01). Including a forced y-intercept value with five regression points either BLT or ALT increased the precision of estimating the total energy demand to the same level as when using 10 regression points, (5 points BLT + y-intercept versus 5 points ALT + y-intercept versus 10 points; 95%CI(l), 0.61±0.32, 0.87±0.40, 0.70±0.26; SEP(L/Watt), 0.07±0.03, 0.08±0.04, 0.07±0.02; p>0.05). The VO<sub>2</sub>-power regression can be designed using a reduced number of regression points... ABSTRACT FROM AUTHOR

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The aim of the present study was to determine the influence of pedal rate on the precision and quantification of the accumulated oxygen deficit (AOD). Eight trained male triathletes completed a lactate threshold test, VO2 peak test, 10 x 3 min submaximal exercise bouts and a high-intensity exercise bout, all performed at 80 and 120 rev/min. For both pedal rates the intensities for the sub-maximal and high-intensity tests were relative to the lactate threshold and VO2 peak work rates. The VO2-power regressions were calculated using 5 intensities from above the lactate threshold combined with a y intercept value with VO2 measured after 3 min of exercise. For the 120 compared to the 80 rev/min tests, the lactate threshold work rate (255±13 versus 276±47 Watts) (p<0.01) and VO2 peak work rate (352±17 versus 382±20, Watts) (p<0.05) were lower at 120 rev/m. Conversely, the VO2 peak and the VO2 measured during the exhaustive exercise were the same for both pedal rates (p>0.05). Using linear regression modelling the slope of the VO2-power regression (0.0112 versus 0.010 L/Watt) (p<0.01), the estimated total energy demand (ETED) (5.13±0.75 versus 4.89±0.88 L/min) and the AOD (4.27±0.94 versus 3.66±1.25 L) (p<0.05) were greater at 120 rev/m. However, the 95% confidence interval for the ETED and the standard error of the predicted value were the same for both pedal rates (p>0.05). Our results demonstrate that pedal rate effects the size but not the precision of the calculated AOD and should therefore be considered when developing an AOD protocol.

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The effects of carbohydrate or water ingestion on metabolism were investigated in seven male subjects during two running and two cycling trials lasting 60 min at individual lactate threshold using indirect calorimetry, U-14C-labeled tracer-derived measures of the rates of oxidation of plasma glucose, and direct determination of mixed muscle glycogen content from the vastus lateralis before and after exercise. Subjects ingested 8 ml/kg body mass of either a 6.4% carbohydrate-electrolyte solution (CHO) or water 10 min before exercise and an additional 2 ml/kg body mass of the same fluid after 20 and 40 min of exercise. Plasma glucose oxidation was greater with CHO than with water during both running (65 ± 20 vs. 42 ± 16 g/h; P < 0.01) and cycling (57 ± 16 vs. 35 ± 12 g/h; P < 0.01). Accordingly, the contribution from plasma glucose oxidation to total carbohydrate oxidation was greater during both running (33 ± 4 vs. 23 ± 3%; P < 0.01) and cycling (36 ± 5 vs. 22 ± 3%; P < 0.01) with CHO ingestion. However, muscle glycogen utilization was not reduced by the ingestion of CHO compared with water during either running (112 ± 32 vs. 141 ± 34 mmol/kg dry mass) or cycling (227 ± 36 vs. 216 ± 39 mmol/kg dry mass). We conclude that, compared with water, 1) the ingestion of carbohydrate during running and cycling enhanced the contribution of plasma glucose oxidation to total carbohydrate oxidation but 2) did not attenuate mixed muscle glycogen utilization during 1 h of continuous submaximal exercise at individual lactate threshold.

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This study examined the effect of glycerol ingestion on fluid homeostasis, thermoregulation, and metabolism during rest and exercise. Six endurance-trained men ingested either 1 g glycerol in 20 ml H2O.kg-1 body weight (bw) (GLY) or 20 ml H2O.kg-1bw (CON) in a randomized double-blind fashion, 120 min prior to undertaking 90 min of steady state cycle exercise (SS) at 98 % of lactate threshold in dry heat (35 degrees C, 30 % RH), with ingestion of CHO-electrolyte beverage (6 % CHO) at 15-min intervals. A 15-min cycle, where performance was quantified in kJ, followed (PC). Pre-exercise urine volume was lower in GLY than CON (1119 ± 97 vs. 1503 ± 146 ml· 120 min-1; p < .05). Heart rate was lower (p < .05) throughout SS in GLY, while forearm blood flow was higher (17.1 ± 1.5 vs. 13.7 ± 3.0 ml.100 g tissue·min-1; p < .05) and rectal  temperature lower (38.7 ± 0.1 vs. 39.1 ± 0.1 ° C; p < .05) in GLY late in SS. Despite these changes, skin and muscle temperatures and circulating catecholamines were not different between trials. Accordingly, no differences were observed in muscle glycogenolysis, lactate accumulation, adenine nucleotide, and phosphocreatine degradation or inosine 5'-monophosphate accumulation when comparing GLY with CON. Of note, the work performed during PC was 5 % greater in GLY (252 ± 10 vs. 240 ± 9 kJ; p < .05). These results demonstrate that glycerol, when ingested with a bolus of water 2 hours prior to exercise, results in fluid retention, which is capable of reducing cardiovascular strain and enhancing thermoregulation. Furthermore, this practice increases exercise performance in the heat by mechanisms other than alterations in muscle metabolism.

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The aim of this study was to compare the oxygen uptake (VO^sub 2^) slow component (SC) during level and uphill running in endurance runners, and to identify associations between the SC and the following aerobic fitness indicators: peak VO^sub 2^, running speed associated with the peak VO^sub 2^ (Vpeak), running speed at the lactic threshold and the VO^sub 2^ fraction elicited at the lactic threshold. Fourteen male endurance-trained runners underwent several 6-min bouts of level (LTR) and 10.5% uphill treadmill running. VO^sub 2^ SC was calculated as the difference between mean VO^sub 2^ during the 6th and the 3rd minutes. The highest mean values for the SC were 181.9±240.2 mL*min^sup -1^ for level running at ~94% peak VO^sub 2^ and 105.4±154.6 mL*min^sup -1^ for uphill running at ~90% peak VO^sub 2^. The SC observed during the last bout of the LTR correlated with peak VO^sub 2^ and with Vpeak (-0.71 and -0.76, P<0.05, respectively). The results show that for endurance-trained runners the magnitude of the SC is not affected by the treadmill gradient and that within a homogeneous sample of endurance-trained runners the SC does not correlate with indicators of aerobic fitness.

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Background : The Angiotensin Converting Enzyme (ACE) gene may influence the risk of heart disease and the response to various forms of exercise training may be at least partly dependent on the ACE genotype. We aimed to determine the effect of ACE genotype on the response to moderate intensity circuit resistance training in chronic heart failure (CHF) patients.

Methods :
The relationship between ACE genotype and the response to 11 weeks of resistance exercise training was determined in 37 CHF patients (New York Heart Association Functional Class = 2.3 ± 0.5; left ventricular ejection fraction 28 ± 7%; age 64 ± 12 years; 32:5 male:female) who were randomised to either resistance exercise (n = 19) or inactive control group (n = 18). Outcome measures included VO2peak power output and muscle strength and endurance. ACE genotype was determined using standard methods.

Results :
At baseline, patients who were homozygous for the I allele had higher VO2peak (p = 0.02) and peak power (p = 0.003) compared to patients who were homozygous for the D allele. Patients with the D allele, who were randomised to resistance training, compared to non-exercising controls, had greater peak power increases (ID p < 0.001; DD p < 0.001) when compared with patients homozygous for the I allele, who did not improve. No significant genotype-dependent changes were observed in VO2peak, muscle strength, muscle endurance or lactate threshold.

Conclusion :
ACE genotype may have a role in exercise tolerance in CHF and could also influence the effectiveness of resistance training in this condition.

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We compared the effects of concurrent exercise, incorporating either high-intensity interval training (HIT) or moderate-intensity continuous training (MICT), on mechanistic target of rapamycin complex 1 (mTORC1) signaling and microRNA expression in skeletal muscle, relative to resistance exercise (RE) alone. Eight males (mean ± SD: age, 27 ± 4 yr; V̇o2 peak , 45.7 ± 9 ml·kg(-1)·min(-1)) performed three experimental trials in a randomized order: 1) RE (8 × 5 leg press repetitions at 80% 1-repetition maximum) performed alone and RE preceded by either 2) HIT cycling [10 × 2 min at 120% lactate threshold (LT); HIT + RE] or 3) work-matched MICT cycling (30 min at 80% LT; MICT + RE). Vastus lateralis muscle biopsies were obtained immediately before RE, either without (REST) or with (POST) preceding endurance exercise and +1 h (RE + 1 h) and +3 h (RE + 3 h) after RE. Prior HIT and MICT similarly reduced muscle glycogen content and increased ACC(Ser79) and p70S6K(Thr389) phosphorylation before subsequent RE (i.e., at POST). Compared with MICT, HIT induced greater mTOR(Ser2448) and rps6(Ser235/236) phosphorylation at POST. RE-induced increases in p70S6K and rps6 phosphorylation were not influenced by prior HIT or MICT; however, mTOR phosphorylation was reduced at RE + 1 h for MICT + RE vs. both HIT + RE and RE. Expression of miR-133a, miR-378, and miR-486 was reduced at RE + 1 h for HIT + RE vs. both MICT + RE and RE. Postexercise mTORC1 signaling following RE is therefore not compromised by prior HIT or MICT, and concurrent exercise incorporating HIT, but not MICT, reduces postexercise expression of miRNAs implicated in skeletal muscle adaptation to RE.

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Over-representation of indigenous persons in the criminal justice system has changed little since the Royal Commission into Aboriginal Deaths in Custody (RCIADIC) - claim by the Victorian Department of Justice that a key recommendation of RCIADIC had been implemented, namely that imprisonment should be a sentence of last resort for indigenous offenders - how to ensure that imprisonment is a sanction of last resort when indigenous prisoners present for sentence.

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Detection thresholds and psychophysical curves were established for caffeine, quinine-HCl (QHCl), and propylthiouracil (PROP) in a sample of 33 subjects (28 female mean age 24 ± 4). The mean detection threshold (±standard error) for caffeine, QHCl, and PROP was 1.2 ± 0.12, 0.0083 ± 0.001, and 0.088 ± 0.07 mM, respectively. Pearson product–moment analysis revealed no significant correlations between detection thresholds of the compounds. Psychophysical curves were constructed for each bitter compound over 6 concentrations. There were significant correlations between incremental points of the individual psychophysical curves for QHCl and PROP. Regarding caffeine, there was a specific concentration (6 mM) below and above which the incremental steps in bitterness were correlated. Between compounds, analysis of psychophysical curves revealed no correlations with PROP, but there were significant correlations between the bitterness of caffeine and QHCl at higher concentrations on the psychophysical curve (P < 0.05). Correlation analysis of detection threshold and suprathreshold intensity within a compound revealed a significant correlation between PROP threshold and suprathreshold intensity (r = 0.46–0.4, P < 0.05), a significant negative correlation for QHCl (r = –0.33 to –0.4, P < 0.05), and no correlation for caffeine. The results suggest a complex relationship between chemical concentration, detection threshold, and suprathreshold intensity.

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This paper investigates the behaviour of US stock prices using an unrestricted two-regime threshold autoregressive (TAR) model with an autoregressive unit root. The TAR model is applied to monthly stock price (NYSE Common Stocks) data for the US for the period 1964:06 to 2003:04. Amongst our main results, we find that the US stock price is a nonlinear series that is characterized by a unit root process, consistent with the efficient market hypothesis.

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The goal of this paper is to examine evidence for co-integration between nominal exchange rates for Canada, the UK, Japan, Germany, Italy and France (G6) vis-à-vis the US dollar, and the relative price ratios using monthly data over the period 1973:01 to 1997:04. Motivated by the fact that exchange rate adjustment may be asymmetric, we allowed for asymmetric adjustment in exchange rates by using the threshold autoregressive model and the momentum threshold autoregressive model. We do not find any evidence of a co-integrating relationship; hence, we fail to establish long-run purchasing power parity.