Maximal Dynamic Exercise Research Articles

The effect of tDCS on improving physical performance and attenuating effort perception during maximal dynamic exercise in non-athletes

ObjectivesThis study aimed to test the effects of transcranial direct current stimulation (tDCS), using different electrode positioning and montages, on physical performance in maximum incremental tests of healthy non-athlete subjects. DesignA double-blinded, crossover, sham-controlled study. MethodFifteen subjects (aged 25.8 ± 5 years, nine women) received one of five different tDCS protocols: (i) anodal tDCS on the primary motor cortex (M1) (a-tDCS/M1), (ii) anodal tDCS on the left temporal cortex (T3) (a-tDCS/T3), (iii) cathodal tDCS on M1 (c-tDCS/M1), (iv) cathodal on T3 (c-tDCS/T3), or (v) sham tDCS. The protocols were assigned in a random order in separate sessions. After tDCS, the volunteers performed the maximal incremental exercise test (MIT) on a cycle ergometer in each session. The following measures were used to evaluate physical performance (primary outcome) during MIT: time to exhaustion (TE), maximum power (MAX-P), and Borg Rating of Perceived Exertion (RPE) scale. In addition, as a secondary outcome measure, we assessed the lower-limb corticospinal excitability and electrical muscular activity. ResultstDCS applied over T3 or M1 did not influence electrical muscular activity or increase physical performance during MIT in healthy non-athlete subjects. However, our data confirmed that a-tDCS on the M1 increases lower-limb cortical excitability. ConclusionsOur results suggest that tDCS is not effective in improving performance during maximal dynamic exercise in non-athletes. However, we confirmed that the a-tDCS M1 protocol used in this study might increase cortical excitability in the lower limb motor cortex.

Short-term effects of maximal dynamic exercise on flow-mediated dilation in professional female soccer players.

Endothelial function assessment may provide important insights into the cardiovascular function and long-term effects of exercise training. Many studies have investigated the possible negative effects on cardiovascular function due to extreme athletic performance, leading to undesirable effects. The purposes of this study were to investigate the acute effects of maximal intensity exercise on endothelium-dependent vasodilation, and to understand the patterns of flow-mediated dilation (FMD) change following maximal exercise in elite female athletes with a high-volume training history. Twenty-six elite female soccer players (mean age, 22±4 years; BMI, 21±2 kg/m2; VO<inf>2max</inf>, 41±4 mL/kg/min) were evaluated. Brachial artery FMD was determined using high-resolution ultrasound at rest, and after 15 and 60 min of maximal cardiopulmonary exercise (CPX) testing on a treadmill. Flow velocity was measured at baseline and during reactive hyperemia at the same periods. Rest FMD was 12.4±5.5%. Peak diameter in response to reactive hyperemia was augmented after 15 min of CPX (3.5±0.4 vs. 3.6±0.4 mm, P<0.05), returning to resting values after 60 min. However, %FMD did not change among time periods. There were two characteristic patterns of FMD response following CPX. Compared to FMD at rest, half of the subjects responded with an increased FMD following maximum exercise (10.5±6.1 vs. 17.8±7.5%, P<0.05). The other subjects demonstrated a reduced FMD response following maximum exercise (14.2±4.3 vs. 10.9±3.2%, P<0.01). These results indicate that elite female soccer players presented robust brachial artery FMD at rest, with a heterogeneous FMD response to acute exercise with a 50% FMD improvement rate.

Influence of hyperoxic recovery on cardiopulmonary and muscle oxygenation following maximal dynamic exercise in healthy adults

Influence of hyperoxic recovery on cardiopulmonary and muscle oxygenation following maximal dynamic exercise in healthy adults

A high-salt meal does not augment blood pressure responses during maximal exercise.

Augmented blood pressure (BP) responses during exercise are predictive of future cardiovascular disease. High dietary sodium (Na+) increases BP responses during static exercise. It remains unclear if high dietary Na+ augments BP responses during dynamic exercise. The purpose of this study was to test the hypothesis that an acute high-Na+ meal would augment BP responses during dynamic exercise. Twenty adults (10 male/10 female; age, 26 ± 5 years; BP, 105 ± 10/57 ± 6 mm Hg) were given a high-Na+ meal (HSM; 1495 mg Na+) and a low-Na+ meal (LSM; 138 mg Na+) separated by at least 1 week, in random order. Serum Na+ and plasma osmolality were measured. Eighty minutes following the meal, participants completed a graded-maximal exercise protocol on a cycle ergometer. Heart rate, beat-by-beat BP, cardiac output, total peripheral resistance, and manual BP were measured at rest and during exercise. Both serum Na+ (HSM: Δ1.6 ± 2.0 vs LSM: Δ1.1 ± 1.8 mmol/L, P = 0.0002) and plasma osmolality (HSM: Δ3.0 ± 4.5 vs LSM: Δ2.0 ± 4.2 mOsm/(kg·H2O), P = 0.01) were higher following the HSM. However, the HSM did not augment BP during peak exercise (systolic BP: HSM: 170 ± 23 vs LSM: 171 ± 21 mm Hg, P = 0.81). These findings suggest that an acute high-salt meal does not augment BP responses during dynamic exercise in adults. Novelty The high-salt meal increased serum sodium and plasma osmolality compared with the low-salt meal. The high-salt meal did not augment blood pressure responses during maximal dynamic exercise. This is important as augmented blood pressure responses during exercise put individuals at greater risk for development of cardiovascular disease.

Blood pressure response to maximal dynamic exercise testing in an athletic population.

Exaggerated blood pressure (BP) response to exercise testing has been linked to left ventricular hypertrophy and myocardial fibrosis in competitive athletes. Due to frequent training, athletes are particularly exposed to high BP levels, but data on the magnitude and distribution of BP response to exercise in athletic populations is scarce. Cycle ergometry was performed in 2419 healthy competitive adolescent, professional and master athletes (age 26 ± 12 years, range 9-74, 27% women, 84 disciplines) for preparticipation screening. Fulfilling both subjective and at least two out of three objective exhaustion criteria (maximal heart rate >85% predicted, lactate ≥7 mmol/l, rate of perceived exertion ≥17) was required. Echocardiography was also performed. Maximal workload was 305 ± 59 W (mean ± SD) in men and 218 ± 40 in women. SBP increased significantly (men, Δ80 ± 20; women, Δ67 ± 16 mmHg; P < 0.001) to 204 ± 22 (men) and 180 ± 17 mmHg (women). DBP changed minimally (men: Δ0 ± 9, women: Δ2 ± 8 mmHg). The upper normative limit of SBP in men was 247 [95% CI 245-249; women: 214 (212-216) mmHg]. ESC guidelines of upper limits of maximal SBP were exceeded in 43% in men (>210 mmHg) and 28% in women (>190 mmHg). SBP response was more pronounced in endurance athletes, whereas DBP was slightly higher in strength athletes. Among cardiac dimensions, the strongest association for maximal SBP was found for left ventricular mass (r = 0.489; P < 0.001). SBP response to exercise testing is markedly exaggerated particularly in male endurance athletes. The prognostic significance of these findings regarding long-term cardiovascular alterations requires further clarification.

Time-course Of Changes In Maximal Force And Rate Of Force Development After A Plyometric Training Session

Plyometric exercise causes reductions in muscular performance that may persist for several days. However, there may be differences in the magnitude and the duration of changes in maximal force and muscle power. PURPOSE: To evaluate the effects of a single session of plyometric training on the time-course of changes in maximal force and rate of force development (RFD) measured during maximal isometric and dynamic exercise METHODS: Seven moderately trained university students (4 males and 3 females, age: 20.0±0.7 yrs, height: 174±3 cm, body mass: 70±5 kg) performed a plyometric training session consisting of 3 sets of 10 repetitions of 7 jumping exercises: drop, scissor, box, stride crossover and depth jumps and steps and single leg hops on the track (total volume: 210 jumps), with 1 min recovery between sets and 3 min between exercises. Maximal isometric leg press strength and RFD (knee angle set at 90o) and countermovement jump (CMJ) height and RFD were measured using a force platform, before, 30 min after and 24, 48, 72, and 144 h after the plyometric training session. Data were analyzed using one-way ANOVA with repeated measures and Tukey’s post-hoc test. RESULTS: Maximal isometric force was decreased by 26±9% (from 3541±456 to 2436±256 N, p<0.05) only 30 min post-training and returned to baseline after 24 h. However, RFD during isometric exercise was decreased to a greater extent 30 min after (-38±9%, p<0.01), remained lower than baseline 24 h later (-16±8%, p<0.05) and returned to baseline 48 h after training. The reduction in CMJ height was larger 48 h after training (-7.2±2.5 %, p<0.05) and remained below baseline for 72 h after training (-5.2±2.5 %, p<0.05). RFD during the CMJ exhibited a decrease that was larger 48 h after training (-30±9 %, p<0.01) and persisted until the 72 h time-point. CONCLUSION: These data show that a single training session with a high volume of plyometric jumping exercises reduces maximal isometric force only temporarily, while the decrease in RFD is larger and persisting, especially during dynamic muscle contractions.

Hemodynamic mechanisms of the attenuated blood pressure response to mental stress after a single bout of maximal dynamic exercise in healthy subjects

To determine the hemodynamic mechanisms responsible for the attenuated blood pressure response to mental stress after exercise, 26 healthy sedentary individuals (age 29 ± 8 years) underwent the Stroop color-word test before and 60 min after a bout of maximal dynamic exercise on a treadmill. A subgroup (N = 11) underwent a time-control experiment without exercise. Blood pressure was continuously and noninvasively recorded by infrared finger photoplethysmography. Stroke volume was derived from pressure signals, and cardiac output and peripheral vascular resistance were calculated. Perceived mental stress scores were comparable between mental stress tests both in the exercise (P = 0.96) and control (P = 0.24) experiments. After exercise, the systolic blood pressure response to mental stress was attenuated (pre: 10 ± 13 vs post: 6 ± 7 mmHg; P < 0.01) along with lower values of systolic blood pressure (pre: 129 ± 3 vs post: 125 ± 3 mmHg; P < 0.05), stroke volume (pre: 89.4 ± 3.5 vs post: 76.8 ± 3.8 mL; P < 0.05), and cardiac output (pre: 7.00 ± 0.30 vs post: 6.51 ± 0.36 L/min; P < 0.05). Except for heart rate, the hemodynamic responses and the mean values during the two mental stress tests in the control experiment were similar (P > 0.05). In conclusion, a single bout of maximal dynamic exercise attenuates the blood pressure response to mental stress in healthy subjects, along with lower stroke volume and cardiac output, denoting an acute modulatory action of exercise on the central hemodynamic response to mental stress.

Impact of endothelial nitric oxide synthase gene polymorphisms on hemodynamic after a bout of maximal dynamic exercise

Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene (NOS3) have been associated with lower eNOS expression and activation, which can lead to impairment in eNOS related traits. Thus, we investigated the individual (genotype analysis) and combined (haplotype analysis) impact of three polymorphisms in the NOS3 (−786T&gt;C, 4b4a and 894G&gt;T) on hemodynamic variables. Sedentary, non‐obese, healthy subjects were enrolled [n = 93, age 31 ± 9 years (mean ± SD)]. Genotypes were determined by PCR‐RFLP and haplotypes were inferred by a Bayesian based algorithm. Heart rate (ECG) and blood pressure (BP; finger photoplethismography) were continuously measured during 10 min in the supine position before [baseline (BL)], 10, 60 and 120 min after a maximal cardiopulmonary exercise test. Stroke volume was estimated by the Model Flow method. Then, cardiac output (CO) and total peripheral resistance (TPR) were calculated. There was no difference between subjects in genotype analysis. However, subjects with haplotype containing the polymorphisms −786T&gt;C and 4b4a had higher systolic BP at 10, 60 and 120 min after exercise than subjects with wild haplotype (P &lt; 0.05), which occurred due to higher CO (P &lt; 0.05), while TPR was similar between groups (P &gt; 0.05). In conclusion, NOS3 haplotype containing the polymorphisms −786T&gt;C and 4b4a was associated with impaired hemodynamic response after a bout of maximal dynamic exercise.

Impaired hemodynamic response to mental stress in subjects with prehypertension is improved after a single bout of maximal dynamic exercise

INTRODUCTION:High blood pressure during mental stress in subjects with prehypertension is associated with blunted vasodilation in skeletal muscles, which might be improved by an acute bout of exercise.OBJECTIVE:To investigate the hemodynamic responses to mental stress before and after a bout of exercise in subjects with prehypertension.METHOD:Eighteen subjects with prehypertension and 16 with normotension underwent a mental stress test before and after a maximal cardiopulmonary exercise test on a treadmill. Blood pressure was measured by auscultation, and forearm blood flow was measured by venous occlusion plethysmography; from these measurements, the vascular conductance was calculated.RESULTS:Subjects with prehypertension had a higher mean blood pressure during mental stress (prehypertension 112±2 vs. normotension 101±3 mm Hg, p<0.05), and their vascular conductance did not increase (baseline 0.025±0.004 vs. mental stress 0.022±0.003 a.u., p>0.05). After the exercise bout, the mean blood pressure during mental stress was lower in subjects with prehypertension (before exercise 112±2 vs. after exercise 107±2 mm Hg, p<0.05), and vascular conductance increased (baseline 0.011±0.001 vs. mental stress 0.024±0.004 a.u., p<0.05).CONCLUSION:Subjects with prehypertension had elevated blood pressure and a blunted vasodilator response during mental stress, but their blood pressure was attenuated and their vasodilator response was normalized after a single bout of maximal dynamic exercise.

The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humans

The mechanism underlying the plateau or relative decrease in cerebral blood flow (CBF) during maximal incremental dynamic exercise remains unclear. We hypothesized that cerebral perfusion is limited during high-intensity dynamic exercise due to a redistribution of carotid artery blood flow. To identify the distribution of blood flow among the arteries supplying the head and brain, we evaluated common carotid artery (CCA), internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA) blood flow during dynamic exercise using Doppler ultrasound. Ten subjects performed graded cycling exercise in a semi-supine position at 40, 60 and 80% of peak oxygen uptake (VO2 peak) for 5 min at each workload. The ICA blood flow increased by 23.0 ± 4.6% (mean ± SE) from rest to exercise at 60% (VO2 peak). However, at 80% (VO2 peak), ICA blood flow returned towards near resting levels (9.6 ± 4.7% vs. rest). In contrast, ECA, CCA and VA blood flow increased proportionally with workload. The change in ICA blood flow during graded exercise was correlated with end-tidal partial pressure of CO2 (r = 0.72). The change in ICA blood flow from 60% (VO2 peak) to 80% (VO2 peak) was negatively correlated with the change in ECA blood flow (r = −0.77). Moreover, there was a significant correlation between forehead cutaneous vascular conductance and ECA blood flow during exercise (r = 0.79). These results suggest that during high-intensity dynamic exercise the plateau or decrease in ICA blood flow is partly due to a large increase in ECA blood flow, which is selectively increased to prioritize thermoregulation.

Caffeine improves neuromuscular function during maximal dynamic exercise

In this study we tested the hypothesis that caffeine supplementation improves neuromuscular function, which has both nutritional and clinical relevance. Fourteen male subjects (mean ± SD: 23.8 ± 2.8 years) volunteered in a double-blind, repeated-measures study with placebo (PLA) or caffeine (CAFF) (6 mg kg(-1)). Maximal voluntary isometric contractions (MVCs), evoked maximal twitch, and maximal isokinetic contractions during elbow flexion were assessed. Mechanical and electromyographic (EMG) signals from the biceps brachii muscle were recorded, and muscle fiber conduction velocity (CV) was calculated to evaluate changes in the muscle force-velocity relationship and muscle fiber recruitment. The torque-angular velocity curve was enhanced after CAFF supplementation. This was supported by a concomitant increase of CV values (8.7% higher in CAFF). Caffeine improves muscle performance during short-duration maximal dynamic contractions. The concomitant improvement of mean fiber CV supports the hypothesis of an effect of caffeine on motor unit recruitment.

Polymorphisms in the endothelial nitric oxide gene are associated with lower vascular reactivity after a maximal dynamic exercise

Our aim was to investigate the influence of three polymorphisms in the endothelial nitric oxide (eNOS) gene (−786T>C, intron 4b4a and 894G>T), on the vascular reactivity (VR) to an ischemic stimulus. We evaluated 106 healthy, sedentary, non-obese women (31 ± 9 years). Genotypes were determined by PCR-RFLP and haplotypes inferred based on the Bayesian method. VR was considered the change in forearm vascular conductance [blood flow (plethysmography) divided by mean blood pressure (auscultation); ml/100ml.min.100mmHg] provoked by 5 min of ischemia before, 10 and 60 min after a maximal cardiopulmonary exercise test (CPET). VR increased 10 min after the CPET in the entire sample (p<0.001 vs. baseline). Subjects with polymorphic alleles at position −786 and intron 4 had a trend for lower VR 10 min after the CPET versus wild type counterparts (−786CC: 7.7 ± 1.5 vs. −786TT: 10.1 ± 0.6, p = 0.06; 4b4a/4a4a: 8.5 ± 5.9 vs. 4b4b: 10.0 ± 0.5, p = 0.06). In addition, a haplotype with polymorphic alleles at positions −786 and 894 (−786C/4b/894T; 8.9 ± 0.7) and another with polymorphic allele in intron 4 (−786T/4a/894G; 7.5 ± 1.3) had lower VR 10 min after the CPET versus a haplotype with wild type alleles (−786T/4b/894G; 10.1 ± 0.4, p = 0.02 and 0.05, respectively). Thus, these results suggest that the −786T>C, intron 4b4a and 894G>T polymorphisms are associated with lower VR after a maximal dynamic exercise. Support: CAPES, CNPq and FAPERJ.

894G&gt;T polymorphism of endothelial nitric oxide synthase impairs hemodynamic responses to mental stress

Our aim was to evaluate the effect of the 894G&gt;T polymorphism on the hemodynamic responses to mental stress performed before and after exercise. Subjects without (wild type, WT; n=16) or with (polymorphic type, PT; n=19) the polymorphism underwent a mental stress challenge before and after a bout of maximal dynamic exercise on a treadmill. Blood pressure and forearm blood flow were measured during mental stress. Before exercise, systolic blood pressure (SBP) response during mental stress was higher in the PT group (ΔWT: 8.0±2.0% vs. ΔPT: 12.5±1.8%, P=0.01), while the increase in forearm vascular conductance (FVC) was similar between the groups (ΔWT 90.8±26.4% vs. ΔPT: 86.3±24.1%, P=0.44). After exercise, the SBP at baseline and during mental stress was lower than before exercise in the whole group (P&lt;0.05), but the pressure response during mental stress was still higher in the PT group (ΔWT: 5.8±1.5% vs. ΔPT: 10.2±1.4%, P=0.01). The increase in FVC was inhibited only in the PT group (Δbefore exercise 86.3±24.1% vs. Δafter exercise: 41.5±12.6%, P=0.04). In conclusion, subjects with the 894G&gt;T polymorphism presented higher blood pressure response to mental stress, both before and after exercise along with blunted FVC increase after exercise. These results suggest that the 894G&gt;T polymorphism is associated with altered hemodynamic responses to mental stress with potential clinical implications. Support: CNPq, FAPERJ, FINEP.

Effect of the 894G&gt;T polymorphism of the endothelial nitric oxide synthase on vascular reactivity following maximal dynamic exercise

Considering that the role of nitric oxide as a vasodilator is increased after an acute bout of exercise and that the 894G>T polymorphism of the endothelial nitric oxide synthase seems to reduce the nitric oxide release in response to shear stress, the present study investigated the 894G>T polymorphism in relation to vascular reactivity following maximal dynamic exercise. We studied 110 healthy volunteers (wild-type group 45.5% and polymorphic group 54.5%). The protocol included vascular reactivity assessment at baseline and during reactive hyperemia, before, 10, 60 and 120 min after a maximal cardiopulmonary exercise test. Genomic DNA was extracted from blood samples to determine the 894G>T polymorphism. There were no differences between the wild-type and polymorphic groups concerning anthropometric, metabolic and hemodynamic characteristics. Blood flow, before maximal exercise, was similar between the wild-type and the polymorphic groups. The polymorphic group presented lower vascular reactivity regardless of time (P = 0.019 for group main effect), and posthoc analysis revealed that polymorphic patients had lower values than wild-type only at the 120 min measurement (P = 0.002). Concerning within-group analysis, vascular reactivity increased at 10 min after exercise (P = 0.029) returning to baseline at 120 min (P = 0.005) in the polymorphic group. Patients with the 894G>T polymorphism had lower vascular reactivity after a single bout of exercise.

EMG Wavelet Analysis of Quadriceps Muscle during Repeated Knee Extension Movement

Wavelet transform is a time-frequency analysis method that quantifies temporal changes of the frequency content of nonstationary signals without losing resolution in time or frequency. It may be used to analyze surface EMG (sEMG) signals under dynamic conditions. However, this method is difficult to apply clinically because it generates large quantity of data in a very short time, and the change in muscle fiber length and diameter during dynamic contraction induces a large variability of the data at various wavelet domains and joint positions. This study aimed to determine a wavelet domain and a joint range that has the lowest variance and highest sensitivity to document the shift of the frequency intensity that relates to the decline of dynamic muscle power. Eleven active young males were tested for maximal isokinetic knee extension and flexion exercise for 50 repetitions at 180 degrees x s and at a range of 100 degrees-0 degrees x sEMG measurement of vastus medialis (VM), vastus lateralis (VL), and rectus femoris (RF) were recorded during the exercise. Wavelet transform was used to filter the sEMG data into 11 wavelet domains. The movement was divided into five 20 degrees-angle range groups. On the basis of the statistical analysis, the most significant and consistent trend of decrease in sEMG intensity power under maximal dynamic exercise for VM, VL, and RF was identified at the angle range of 40 degrees -20 degrees in wavelet domain 4. We concluded that the shift in intensity within this angle range and wavelet domain might be used to document fatigue of the quadriceps during dynamic maximal knee extension exercise.

Rebuttal from Dr. Ekblom

POINT-COUNTERPOINTRebuttal from Dr. EkblomPublished Online:01 Jan 2009https://doi.org/10.1152/japplphysiol.90844.2008cMoreSectionsPDF (40 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat The reason for not adding late references is that there are no new experiments or support for CGM in the discussion regarding limitation of V̇o2max, only variants on the same theme and discussions about exercise fatigue. The reader can see very easily that our opponents try to escape the fact that while V̇o2max is unchanged, the heart is doing more work in the “120%” than the “105%” situation (3). The heart is not allowed to do so, according the CGM (7), since already at 105% there should be “a wide range of biological signals monitored to ensure that exercise always terminates before loss of homeostasis.” The motor units may have worked submaximally in the 105% but evidently higher in the A+Lspurt, 120 and 140% situation, but CGM predicts a reduction in motor unit activation (7).To convince the reader, Noakes and Marino move from “power” to “amount of work” to disprove findings in our second study. But that is very risky and wrong. If a 350-W maximal two-leg work rate is divided on 100 W for arms and 250 W for legs, work time is doubled, but V̇o2max is the same (1). The A+L exercise doubles aerobic and anaerobic yields compared with that with legs only. As long as work rate is high enough, total work is not a factor for the limitation of V̇o2max.In their article above Noakes and Marino use the Zhou et al. study (10), criticized by us (4), which fits their hypothesis but avoid those that disprove it (2). I believe that SV is limited by the pericardium. Experiments on dogs and pigs clearly show that Q̇ during maximal exercise increases by cutting the pericardium (6, 9). In parallel, V̇o2max increases but aBP is unchanged during maximal exercise after pericardioectomy. It is obvious that aBP is well regulated even after pericardioectomy, which means that the peripheral resistance can be changed in accordance with the availability of V̇o2max during maximal exercise and not the opposite—that the periphery determines cardiac output during maximal dynamic exercise.All experimental facts speak in favor of the concept that the blood flow output from the heart is the critical point in the Fick equation (V̇o2max) during maximal exercise. Our (3) and other (5) experiments show that the heart is not near “loss of homeostasis” during normal maximal dynamic exercise as suggested in CGM.REFERENCES1 Åstrand PO, Saltin B. Maximal oxygen uptake and heart rate in various types of muscular activity. J Appl Physiol 16: 977–981, 1961.Link | ISI | Google Scholar2 Boutcher SH, McLaren PF, Cotton Y, Boutcher Y. Stroke volume response to incremental submaximal exercise in aerobically trained active and sedentary men. Can J Appl Physiol 28: 12–26, 2003.Crossref | Google Scholar3 Elfegoun-Brink T, Kaijser L, Gustafsson T, Ekblom B. Maximal oxygen uptake is not limited by a Central Nervous System Governor. J Appl Physiol 102: 781–786, 2007.Link | ISI | Google Scholar4 Ekblom B, EkblomÖ . Stroke volume and the endurance athlete. Scand J Med Sci Sports 16: 70–71, 2006.Crossref | ISI | Google Scholar5 Gubbström L, Berglund B, Kaijser L. Myocardial blood flow and lactate metabolism at rest and during exercise with reduced arterial oxygen content. Acta Physiol Scand 142: 467–474, 1991.Crossref | PubMed | Google Scholar6 Hammond HK, White FC, Bhargava V, Shabetai R. Heart size and maximal cardiac output are limited by the pericardium. Am J Physiol Heart Circ Physiol 263: 1675–1681, 1992.Link | ISI | Google Scholar7 Noakes TD. Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance. Scand J Med Sci Sports 10: 123–145, 2000.Crossref | PubMed | ISI | Google Scholar8 Noakes TD, Marino FE. Point: Maximal oxygen uptake is limited by a central nervous system governor. J Appl Physiol; doi:10.1152/japplphysiol.90844.2008.Link | ISI | Google Scholar9 Stray-Gundersen J, Musch TA, Haidet CG, Swain DP, Ordway GA, Mitchell JH. The effect of pericardioectomi on maximal oxygen uptake and maximal cardiac output in untrained dogs. Circ Res 58: 523–530, 1986.Crossref | PubMed | ISI | Google Scholar10 Zhou B, Conlee RK, Jensen R, Fellingham GW, George JD, Fisher AG. Stroke volume does not plateau during graded exercise in elite male distance runners. Med Sci Sports Exerc 33: 1849–1854, 2001.Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 106Issue 1January 2009Pages 341-342 Copyright & PermissionsCopyright © 2009 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.90844.2008cHistory Published online 1 January 2009 Published in print 1 January 2009 Metrics

Modificações Agudas dos Níveis Séricos de Creatina Quinase em Adultos Jovens Submetidos ao Trabalho de Flexionamento Estático e de Força Máxima

Strength and flexibility are common components of a training program and their maximal values are obtained through specific tests. However, little information about the damage effect of these training procedures in a skeletal muscle is known. The aim was to verify a serum CK changes 24h after a sub maximal stretching routine and after the static flexibility and maximal strength tests. The sample was composed by 14 subjects (man and women, 28±6 yr.) physical education students. The volunteers were divided in a control group (CG) and experimental group (EG) that was submitted in a stretching routine (EG-ST), in a maximal flexibility static test (EG-FLEX) and in 1-RM test (EG--1-RM), with one week interval among tests. The anthropometrics characteristics were obtained by digital scale with stadiometer (Filizola, Sao Paulo, Brasil, 2002). The blood samples were obtained using the IFCC method with reference values 26-155 U/L. The DeLorme and Watkins technique was used to access maximal maximal strength through bench press and leg press. The maximal flexibility test consisted in three 20 seconds sets until the point of maximal discomfort. The stretching was done in normal movement amplitude during 6 seconds. The basal and post 24h CK values in CG and EG (ST; Flex and 1RM) were respectively 195,0 ± 129,5vs. 202,1 ± 124,2; 213,3 ± 133,2 vs.174,7 ± 115,8; 213,3 ± 133,2 vs.226,6 ± 126,7 e 213,3 ± 133,2 vs.275,9 ± 157,2. It was only observed a significant difference (p = 0,02) in the pre and post values inGE-1RM. In conclusion, only maximal strength dynamic exercise was capable to cause skeletal muscle damage.

Acute and Chronic Impact of Dynamic Exercise on Arterial Stiffness in Older Hypertensives

Arterial stiffness increases with ageing and hypertension. Regular physical activity has been recommended as an important management component of hypertension. The purpose of this study was to examine the acute impact of maximal dynamic exercise and the effect of 20 weeks of aerobic exercise on arterial stiffness of the carotid and brachial arteries in older hypertensives. Nine previously sedentary and treated older hypertensives (2 men and 7 women, age 68.2 ± 5.4 yrs) performed maximal treadmill exercise to volitional fatigue while arterial stiffness indices (arterial distensibility and β stiffness index) were measured prior to, immediately (about 10 min) following, and 24 h following maximal exercise. These measurements were repeated following 20 weeks of moderate intensity aerobic exercise training. Maximal exercise had no impact on arterial stiffness indices immediately and 24 h following exercise intervention. Following 20 weeks of training, arterial stiffness indices remained unchanged at rest and following maximal exercise. These data show that, in older hypertensives, 1) acute maximal dynamic exercise had no impact on arterial stiffness of the carotid and brachial arteries, and 2) 20 weeks of moderate intensity aerobic exercise training failed to modify arterial stiffness.

Structural and functional determinants of human muscle power

Measurements of human power need to be interpreted in relation to the movement frequency, since that will determine the velocity of contraction of the active muscle and hence the power available according to the power-velocity relationship. Techniques are described which enable movement frequency to be kept constant during human exercise under different conditions. Combined with microdissection and analysis of muscle fibre fragments from needle biopsies obtained pre- and postexercise we have been able 'to take the muscle apart', having measured the power output, including the effect of fatigue, under conditions of constant movement frequency. We have shown that fatigue may be the consequence of a metabolic challenge to a relatively small population of fast fatigue-sensitive fibres, as indicated by [ATP] depletion to approximately 30% of resting values in those fibres expressing myosin heavy chain isoform IIX after just 10 s of maximal dynamic exercise. Since these same fibres will have a high maximal velocity of contraction, they also make a disproportionate contribution to power output in relation to their number, especially at faster movement rates. The microdissection technique can also be used to measure phosphocreatine concentration ([PCr]), which is an exquisitely sensitive indicator of muscle fibre activity; thus, in just seven brief maximal contractions [PCr] is depleted to levels < 50% of rest in all muscle fibre types. The technique has been applied to study exercise at different intensities, and to compare recruitment in lengthening, shortening and isometric contractions, thus yielding new information on patterns of recruitment, energy turnover and efficiency.

Exercise function and biochemical properties of β-adrenergic receptors of canine heart

We tested the hypothesis that the biochemical properties of cardiac beta-adrenergic receptors (βAR), as determined by standard in vitro methods, limit physiological responsiveness of dogs to PAR stimulation during peak exercise. Accordingly, we measured oxygen consumption, left ventricular dP/dt at 40 mmHg developed pressure, heart rate, and cardiac output during maximal dynamic exercise in 13 adult mongrel dogs. These studies were followed by biochemical analysis of PAR in membrane homogenates of left ventricle from the same animals using saturation binding and agonist competition curves for [125I] cyanopindolol. There was a substantial range in both biochemical and physiological variables within this population of normal dogs. However, there were no significant correlations between biochemical descriptors of cardiac PAR and any physiological variables measured during exercise. These results suggest that receptor-effector coupling and maximal cardiac performance during intense sympathetic stimulation of peak exercise are limited by factors other than the biochemical properties of cardiac PAR.