128 resultados para high-intensity exercise


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Light-intensity physical activity (LIPA) accounts for much of adults' waking hours (≈40%) and substantially contributes to overall daily energy expenditure. Encompassing activity behaviours of low intensity (standing with little movement) through to those with a higher intensity (slow walking), LIPA is ubiquitous, yet little is known about how associations with health may vary depending on its intensity. We examined the associations of objectively assessed LIPA, categorized as either low- or high- LIPA, and MVPA, with cardiometabolic risk biomarkers.

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The purpose of this study was to identify the validity of an upper-body mounted accelerometer to measure peak acceleration during high-intensity treadmill running. A twelve camera motion analysis (MA) system was used as the criterion measure with markers placed on and close to the accelerometer. Ten peak impacts per participant were compared (n = 390). All accelerometer values were significantly different between the MA unit and T6 reflective marker’s acceleration data. Smoothing accelerometer data at 8 and 6 Hz provides an acceptable indirect measure of peak impact acceleration performed during high-intensity running. Consequently, smoothing algorithms should be incorporated into the commercially available software that the devices are supplied with.

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Background: Remote telemonitoring holds great potential to augment management of patients with coronary heart disease (CHD) and atrial fibrillation (AF) by enabling regular physiological monitoring during physical activity. Remote physiological monitoring may improve home and community exercise-based cardiac rehabilitation (exCR) programs and could improve assessment of the impact and management of pharmacological interventions for heart rate control in individuals with AF.

Objective: Our aim was to evaluate the measurement validity and data transmission reliability of a remote telemonitoring system comprising a wireless multi-parameter physiological sensor, custom mobile app, and middleware platform, among individuals in sinus rhythm and AF.

Methods: Participants in sinus rhythm and with AF undertook simulated daily activities, low, moderate, and/or high intensity exercise. Remote monitoring system heart rate and respiratory rate were compared to reference measures (12-lead ECG and indirect calorimeter). Wireless data transmission loss was calculated between the sensor, mobile app, and remote Internet server.

Results: Median heart rate (-0.30 to 1.10 b∙min-1) and respiratory rate (-1.25 to 0.39 br∙min-1) measurement biases were small, yet statistically significant (all P≤.003) due to the large number of observations. Measurement reliability was generally excellent (rho=.87-.97, all P<.001; intraclass correlation coefficient [ICC]=.94-.98, all P<.001; coefficient of variation [CV]=2.24-7.94%), although respiratory rate measurement reliability was poor among AF participants (rho=.43, P<.001; ICC=.55, P<.001; CV=16.61%). Data loss was minimal (<5%) when all system components were active; however, instability of the network hosting the remote data capture server resulted in data loss at the remote Internet server during some trials.

Conclusions: System validity was sufficient for remote monitoring of heart and respiratory rates across a range of exercise intensities. Remote exercise monitoring has potential to augment current exCR and heart rate control management approaches by enabling the provision of individually tailored care to individuals outside traditional clinical environments.

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Purpose: Increased risk of arrhythmic events occurs at certain times during the circadian cycle with the highest risk being in the second and fourth quarter of the day. Exercise improves treatment outcome in individuals with cardiovascular disease. How different exercise protocols affect the circadian rhythm and the associated decrease in adverse cardiovascular risk over the circadian cycle has not been shown. Methods: Fifty sedentary male participants were randomized into an 8-week high volume and moderate volume training and a control group. Heart rate was recorded using Polar Electronics and investigated with Cosinor analysis and by Poincaré plot derived features of SD1, SD2 and the complex correlation measure (CCM) at 1-h intervals over the 24-h period. Results: Moderate exercise significantly increased vagal modulation and the temporal dynamics of the heart rate in the second quarter of the circadian cycle (p = 0.004 and p = 0.007 respectively). High volume exercise had a similar effect on vagal output (p = 0.003) and temporal dynamics (p = 0.003). Cosinor analysis confirms that the circadian heart rate displays a shift in the acrophage following moderate and high volume exercise from before waking (1st quarter) to after waking (2nd quarter of day). Conclusions: Our results suggest that exercise shifts vagal influence and increases temporal dynamics of the heart rate to the 2nd quarter of the day and suggest that this may be the underlying physiological change leading to a decrease in adverse arrhythmic events during this otherwise high-risk period.

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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 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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Purpose: Given the widespread use of water immersion during recovery from exercise, we aimed to investigate the effect of contrast water immersion on recovery of sprint cycling performance, HR and, blood lactate.

Methods: Two groups completed high-intensity sprint exercise before and after a 30-min randomized recovery. The Wingate group (n = 8) performed 3 x 30-s Wingate tests (4-min rest periods). The repeated intermittent sprint group (n = 8) cycled for alternating 30-s periods at 40% of predetermined maximum power and 120% maximum power, until exhaustion. Both groups completed three trials using a different recovery treatment for each trial (balanced randomized application). Recovery treatments were passive rest, 1:1 contrast water immersion (2.5 min of cold (8-C) to 2.5 min of hot (40-C)), and 1:4 contrast water immersion (1 min of cold to 4 min of hot). Blood lactate and HR were recorded throughout, and peak power and total work for pre- and postrecovery Wingate performance and exercise time and total work for repeated sprinting were recorded.

Results: Recovery of Wingate peak power was 8% greater after 1:4 contrast water immersion than after passive rest, whereas both contrast water immersion ratios provided a greater recovery of exercise time (È10%) and total work (È14%) for repeated sprinting than for passive rest. Blood lactate was similar between trials. Compared with passive rest, HR initially declined more slowly during contrast water immersion but increased with each transition to a cold immersion phase.

Conclusions: These data support contrast water immersion being effective in maintaining performance during a short-term recovery from sprint exercise. This effect needs further investigation but is likely explained by cardiovascular mechanisms, shown here by an elevation in HR upon each cold immersion.

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Achieving an appropriate balance between training and competition stresses and recovery is important in maximising the performance of athletes. A wide range of recovery modalities are now used as integral parts of the training programmes of elite athletes to help attain this balance. This review examined the evidence available as to the efficacy of these recovery modalities in enhancing between-training session recovery in elite athletes. Recovery modalities have largely been investigated with regard to their ability to enhance the rate of blood lactate removal following high-intensity exercise or to reduce the severity and duration of exercise-induced muscle injury and delayed onset muscle soreness (DOMS). Neither of these reflects the circumstances of between-training session recovery in elite athletes. After high-intensity exercise, rest alone will return blood lactate to baseline levels well within the normal time period between the training sessions of athletes. The majority of studies examining exercise-induced muscle injury and DOMS have used untrained subjects undertaking large amounts of unfamiliar eccentric exercise. This model is unlikely to closely reflect the circumstances of elite athletes. Even without considering the above limitations, there is no substantial scientific evidence to support the use of the recovery modalities reviewed to enhance the between-training session recovery of elite athletes. Modalities reviewed were massage, active recovery, cryotherapy, contrast temperature water immersion therapy, hyperbaric oxygen therapy, nonsteroidal anti-inflammatory drugs, compression garments, stretching, electromyostimulation and combination modalities. Experimental models designed to reflect the circumstances of elite athletes are needed to further investigate the efficacy of various recovery modalities for elite athletes. Other potentially important factors associated with recovery, such as the rate of post-exercise glycogen synthesis and the role of inflammation in the recovery and adaptation process, also need to be considered in this future assessment.

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Unlike exercising mammals, migratory birds fuel very high intensity exercise (e.g., flight) with fatty acids delivered from the adipose tissue to the working muscles by the circulatory system. Given the primary importance of fatty acids for fueling intense exercise, we discuss the likely limiting steps in lipid transport and oxidation for exercising birds and the ecological factors that affect the quality and quantity of fat stored in wild birds. Most stored lipids in migratory birds are comprised of three fatty acids (16:0, 18:1 and 18:2) even though migratory birds have diverse food habits. Diet selection and selective metabolism of lipids play important roles in determining the fatty acid composition of birds which, in turn, affects energetic performance during intense exercise. As such, migratory birds offer an intriguing model for studying the implications of lipid metabolism and obesity on exercise performance. We conclude with a discussion of the energetic costs of migratory flight and stopover in birds, and its implications for bird migration strategies.

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PURPOSE: This study investigated the efficacy of an intermittent critical power model, termed the "work-balance" (W'BAL) model, during high-intensity exercise in hypoxia. METHODS: Eleven trained, male cyclists (mean ± SD; age 27 ± 6.6 yr, V[Combining Dot Above]O2peak 4.79 ± 0.56 L.min) completed a maximal ramp test and a 3 min "all-out" test to determine critical power (CP) and work performed above CP (W'). On another day an intermittent exercise test to task failure was performed. All procedures were performed in normoxia (NORM) and hypoxia (HYPO; FiO2 ≈ 0.155) in a single-blind, randomized and counter-balanced experimental design. The W'BAL model was used to calculate the minimum W' (W'BALmin) achieved during the intermittent test. W'BALmin in HYPO was also calculated using CP + W' derived in NORM (N+H). RESULTS: In HYPO there was an 18% decrease in V[Combining Dot Above]O2peak (4.79 ± 0.56 vs 3.93 ± 0.47 L.min ; P<0.001) and a 9% decrease in CP (347 ± 45 vs 316 ± 46 W; P<0.001). No significant change for W' occurred (13.4 ± 3.9 vs 13.7 ± 4.9 kJ; P=0.69; NORM vs HYPO). The change in V[Combining Dot Above]O2peak was significantly correlated with the change in CP (r = 0.72; P=0.01). There was no difference between NORM and HYPO for W'BALmin (1.1 ± 0.9 kJ vs 1.2 ± 0.6 kJ). The N+H analysis grossly overestimated W'BALmin (7.8 ± 3.4 kJ) compared with HYPO (P<0.001). CONCLUSION: The W'BAL model produced similar results in hypoxia and normoxia, but only when model parameters were determined under the same environmental conditions as the performance task. Application of the W'BAL model at altitude requires a modification of the model, or that CP and W' are measured at altitude.

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The effect of exercise intensity on skeletal muscle AMP-activated protein kinase (AMPK) signaling and substrate metabolism was examined in eight men cycling for 20 min at each of three sequential intensities: low (40 ± 2% Vo2 peak), medium (59 ± 1% Vo2 peak), and high (79 ± 1% Vo2 peak). Muscle free AMP/ATP ratio only increased at the two higher exercise intensities (P < 0.05). AMPK a1 (1.5-fold) and AMPK a2 (5-fold) activities increased from low to medium intensity, with AMPK a2 activity increasing further from medium to high intensity. The upstream AMPK kinase activity was substantial at rest and only increased 50% with exercise, indicating that, initially, signaling through AMPK did not require AMPK kinase posttranslational modification. Acetyl-CoA carboxylase (ACC)-ßphosphorylation was sensitive to exercise, increasing threefold from rest to low intensity, whereas neuronal NO synthase (nNOS)µphosphorylation was only observed at the higher exercise intensities. Glucose disappearance (tracer) did not increase from rest to low intensity, but increased sequentially from low to medium to high intensity. Calculated fat oxidation increased from rest to low intensity in parallel with ACCß phosphorylation, then declined during high intensity. These results indicate that ACCß phosphorylation is especially sensitive to exercise and tightly coupled to AMPK signaling and that AMPK activation does not depend on AMPK kinase activation during exercise.

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To investigate the in vivo effects of resistance exercise on translational control in human skeletal muscle, we determined the phosphorylation of AMP-activated kinase (AMPK), eukaryotic initiation factor 4E-binding protein (4E-BP1), p70/p85-S6 protein kinase (S6K1), and ribosomal S6 protein (S6). Furthermore, we investigated whether changes in the phosphorylation of S6K1 are muscle fiber type specific. Eight male subjects performed a single high-intensity resistance exercise session. Muscle biopsies were collected before and immediately after exercise and after 30 and 120 min of postexercise recovery. The phosphorylation statuses of AMPK, 4E-BP1, S6K1, and S6 were determined by Western blotting with phospho-specific and pan antibodies. To determine fiber type-specific changes in the phosphorylation status of S6K1, immunofluorescence microscopy was applied. AMPK phosphorylation was increased approximately threefold immediately after resistance exercise, whereas 4E-BP1 phosphorylation was reduced to 27 ± 6% of preexercise values. Phosphorylation of S6K1 at Thr421/Ser424 was increased 2- to 2.5-fold during recovery but did not induce a significant change in S6 phosphorylation. Phosphorylation of S6K1 was more pronounced in the type II vs. type I muscle fibers. Before exercise, phosphorylated S6K1 was predominantly located in the nuclei. After 2 h of postexercise recovery, phospho-S6K1 was primarily located in the cytosol of type II muscle fibers. We conclude that resistance exercise effectively increases the phosphorylation of S6K1 on Thr421/Ser424, which is not associated with a substantial increase in S6 phosphorylation in a fasted state.

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The Na+-K+-ATPase enzyme is vital in skeletal muscle function. We investigated the effects of acute high-intensity interval exercise, before and following high-intensity training (HIT), on muscle Na+-K+-ATPase maximal activity, content, and isoform mRNA expression and protein abundance. Twelve endurance-trained athletes were tested at baseline, pretrain, and after 3 wk of HIT (posttrain), which comprised seven sessions of 8 x 5-min interval cycling at 80% peak power output. Vastus lateralis muscle was biopsied at rest (baseline) and both at rest and immediately postexercise during the first (pretrain) and seventh (posttrain) training sessions. Muscle was analyzed for Na+-K+-ATPase maximal activity (3-O-MFPase), content ([3H]ouabain binding), isoform mRNA expression (RT-PCR), and protein abundance (Western blotting). All baseline-to-pretrain measures were stable. Pretrain, acute exercise decreased 3-O-MFPase activity [12.7% (SD 5.1), P < 0.05], increased α1, α2, and α3 mRNA expression (1.4-, 2.8-, and 3.4-fold, respectively, P < 0.05) with unchanged ß-isoform mRNA or protein abundance of any isoform. In resting muscle, HIT increased (P < 0.05) 3-O-MFPase activity by 5.5% (SD 2.9), and α3 and ß3 mRNA expression by 3.0- and 0.5-fold, respectively, with unchanged Na+-K+-ATPase content or isoform protein abundance. Posttrain, the acute exercise induced decline in 3-O-MFPase activity and increase in α1 and α3 mRNA each persisted (P < 0.05); the postexercise 3-O-MFPase activity was also higher after HIT (P < 0.05). Thus HIT augmented Na+-K+-ATPase maximal activity despite unchanged total content and isoform protein abundance. Elevated Na+-K+-ATPase activity postexercise may contribute to reduced fatigue after training. The Na+-K+-ATPase mRNA response to interval exercise of increased α - but not ß-mRNA was largely preserved posttrain, suggesting a functional role of α mRNA upregulation.