Phlebotomy eliminates the maximal cardiac output response to six weeks of exercise training.

With this study we tested the hypothesis that 6 wk of endurance training increases maximal cardiac output (Qmax) relatively more by elevating blood volume (BV) than by inducing structural and functional changes within the heart. Nine healthy but untrained volunteers (Vo2max 47 ± 5 ml·min(-1)·kg(-1)) underwent supervised training (60 min; 4 times weekly at 65% Vo2max for 6 wk), and Qmax was determined by inert gas rebreathing during cycle ergometer exercise before and after the training period. After the training period, blood volume (determined in duplicates by CO rebreathing) was reestablished to pretraining values by phlebotomy and Qmax was quantified again. Resting echography revealed no structural heart adaptations as a consequence of the training intervention. After the training period, plasma volume (PV), red blood cell volume (RBCV), and BV increased (P < 0.05) by 147 ± 168 (5 ± 5%), 235 ± 64 (10 ± 3%), and 382 ± 204 ml (7 ± 4%), respectively. Vo2max was augmented (P < 0.05) by 10 ± 7% after the training period and decreased (P < 0.05) by 8 ± 7% with phlebotomy. Concomitantly, Qmax was increased (P < 0.05) from 18.9 ± 2.1 to 20.4 ± 2.3 l/min (9 ± 6%) as a consequence of the training intervention, and after normalization of BV by phlebotomy Qmax returned to pretraining values (18.1 ± 2.5 l/min; 12 ± 5% reversal). Thus the exercise training-induced increase in BV is the main mechanism increasing Qmax after 6 wk of endurance training in previously untrained subjects.

The effects of a 6-hour ultra-endurance run on postexercise parasympathetic reactivation responses.

BACKGROUND: Alterations in cardiac autonomic control reflecting depressed parasympathetic activity have been previously reported after ultra-endurance events at rest and during dynamic tasks assessing cardiac autonomic responsiveness. This study investigated the impact of a 6-hour ultra-endurance run on parasympathetic reactivation indices, using an exercise-recovery transition approach. METHODS: Nine trained runners (VO2max 67±12 mL/kg/min) completed a 6-hour run (EXP) whilst other six runners (VO2max 66±10 mL/kg/min) served as a control (CON). Before (PRE) and after the run/control period (POST) participants completed standard cardiac autonomic activity assessments. Postexercise parasympathetic reactivation was assessed by means of heart rate recovery (HRR) and vagal-related time-domain HRV indices. RESULTS: HR was increased at rest (P<0.001, ES=3.53), during exercise (P<0.05, ES=0.38) and recovery (all P<0.001, ES from 0.91 to 1.46) at POST in EXP and not in CON (all P>0.05). At POST vagal-related HRV indices were significantly decreased at rest (P<0.001, ES from -2.38 to -3.54) and during postexercise recovery (all P<0.001, ES from -0.97 to -1.58) only in EXP. HRR at 30 and 60 s were markedly reduced at POST in EXP both when expressed in bpm and normalized for the exercising HR (all P<0.001, ES from -1.21 to -1.74). CONCLUSIONS: A 6-hour run markedly impacted upon postexercise parasympathetic reactivation responses causing a decrease in HRR and HRV recovery indices. For the first time, this study attested blunted postexercise parasympathetic reactivation responses following an acute bout of ultra-endurance exercise.

Effects of 2 Different Protocols of Repeated-Sprint Training in Hypoxia in Elite Female Rugby Sevens Players During an Altitude Training Camp.

OBJECTIVES: Repeated-sprint training in hypoxia (RSH) is an effective way of improving physical performance compared with similar training in normoxia. RSH efficiency relies on hypoxia severity, but also on the oxidative-glycolytic balance determined by both sprint duration and exercise-to-rest ratio. This study investigated the effect of 2 types of RSH sessions during a classic altitude camp in world-class female rugby sevens players. METHODS: Sixteen players performed 5 RSH sessions on a cycle ergometer (simulated altitude: 3000 m above sea level [asl]) during a 3-week natural altitude camp (1850 m asl). Players were assigned to 2 different protocols with either a high (RSH1:3, sprint duration: 8-10 s; exercise-to-rest ratios: 1:2-1:3; n = 7) or a low exercise-to-rest ratio (RSH1:5, sprint duration: 5-15 s; exercise-to-rest ratios: 1:2-1:5; n = 9). Repeated-sprint performances (maximal and mean power outputs [PPOmax, and PPOmean]) were measured before and after the intervention, along with physiological responses. RESULTS: PPOmax (962 [100] to 1020 [143] W, P = .008, Cohen d = 0.47) and PPOmean (733 [71] to 773 [91] W, P = .008, d = 0.50) increased from before to after. A significant interaction effect (P = .048, d = 0.50) was observed for PPOmean, with a larger increase observed in RSH1:3 (P = .003). No interaction effects were observed (P > .05) for the other variables. CONCLUSION: A classic altitude camp with 5 RSH sessions superimposed on rugby-sevens-specific training led to an improved repeated-sprint performance, suggesting that RSH effects are not blunted by prolonged hypoxic exposure. Interestingly, using a higher exercise-to-rest ratio during RSH appears to be more effective than when applying a lower exercise-to-rest ratio.

Physiological Implication of Slope Gradient during Incremental Running Test.

Uphill running induces a higher physiological demand than level conditions. Although many studies have investigated this locomotion from a psychological point of view, there is no clear position on the effects of the slope on the physiological variables during an incremental running test performed on a slope condition. The existing studies have heterogeneous designs with different populations or slopes and have reported unclear results. Some studies observed an increase in oxygen consumption, whereas it remained unaffected in others. The aim of this study is to investigate the effect of a slope on the oxygen consumption, breathing frequency, ventilation and heart rate during an incremental test performed on 0, 15, 25 and 40% gradient slopes by specialist trail runners. The values are compared at the first and second ventilatory threshold and exhaustion. A one-way repeated measures ANOVA, with a Bonferroni post-hoc analysis, was used to determine the effects of a slope gradient (0, 15, 25 and 40%) on the physiological variables. Our study shows that all the variables are not affected in same way by the slopes during the incremental test. The heart rate and breathing frequency did not differ from the level condition and all the slope gradients at the ventilatory thresholds or exhaustion. At the same time, the ventilation and oxygen consumption increased concomitantly with the slope (p < 0.001) in all positions. The post-hoc analysis highlighted that the ventilation significantly increased between each successive gradient (0 to 15%, 15% to 25% and 25% to 40%), while the oxygen consumption stopped increasing at the 25% gradient. Our results show that the 25 and 40% gradient slopes allow the specialist trail runners to reach the highest oxygen consumption level.

Specific Incremental Test for Aerobic Fitness in Trail Running: IncremenTrail.

Trail running (TR) is performed in a natural environment, including various ranges of slopes where maximal oxygen consumption is a major contributor to performance. The aim of this study is to investigate the validity of tests performed in uphill conditions named the "IncremenTrail" (IncT), based on the incremental ascending speed (AS) to evaluate trail runners' cardiorespiratory parameters. IncT protocol included a constant gradient slope set at 25% during the whole test; the starting speed was 500 m·h-1 (25% slope and 2.06 km·h-1) and increased by 100 m·h-1 every minute (0.41 km·h-1). Twenty trail runner specialists performed the IncT and a supramaximal exercise bout to exhaustion with intensity set at 105% of maximal AS (Tlim). Oxygen consumption, breathing frequency, ventilation, respiratory exchange ratio (RER), and heart rate were continuously recorded during the exercises. The blood lactate concentration and rate of perceived exertion were collected at the end of the exercises. During the IncT test, 16 athletes (80%) reached a plateau of maximal oxygen uptake (65.5 ± 7.6 mL·kg-1·min-1), 19 athletes (95%) reached RER values over 1.10 (1.12 ± 0.02) and all the athletes achieved blood lactate concentration over 8.0 mmol·L-1 (17.1 ± 3.5 mmol·L-1) and a maximal heart rate ≥90% of the theoretical maximum (185 ± 11 bpm). Maximal values were not significantly different between IncT and Tlim. In addition, ventilatory thresholds could be determined for all runners with an associated AS. IncT provided a suitable protocol to evaluate trail runners' cardiorespiratory limitations and allowed us to obtain specific intensities based on the ascending speed useful for training purposes in specific conditions.

Fractal correlation properties of heart rate variability as a biomarker of endurance exercise fatigue in ultramarathon runners.

Although heart rate variability (HRV) indexes have been helpful for monitoring the fatigued state while resting, little data indicate that there is comparable potential during exercise. Since an index of HRV based on fractal correlation properties, alpha 1 of detrended fluctuation analysis (DFA a1) displays overall organismic demands, alteration during exertion may provide insight into physiologic changes accompanying fatigue. Two weeks after collecting baseline demographic and gas exchange data, 11 experienced ultramarathon runners were divided into two groups. Seven runners performed a simulated ultramarathon for 6 h (Fatigue group, FG) and four runners performed daily activity over a similar period (Control group, CG). Before (Pre) and after (Post) the ultramarathon or daily activity, DFA a1, heart rate (HR), running economy (RE) and countermovement jumps (CMJ) were measured while running on a treadmill at 3 m/s. In Pre versus Post comparisons, data showed a decline with large effect size in DFA a1 post intervention only for FG (Pre: 0.71, Post: 0.32; d = 1.34), with minor differences and small effect sizes in HR (d = 0.02) and RE (d = 0.21). CG showed only minor differences with small effect sizes in DFA a1 (d = 0.19), HR (d = 0.15), and RE (d = 0.31). CMJ vertical peak force showed fatigue-induced decreases with large effect size in FG (d = 0.82) compared to CG (d = 0.02). At the completion of an ultramarathon, DFA a1 decreased with large effect size while running at low intensity compared to pre-race values. DFA a1 may offer an opportunity for real-time tracking of physiologic status in terms of monitoring for fatigue and possibly as an early warning signal of systemic perturbation.

Effect of a Fatiguing Ultratrail on the Graded Energetically Optimal Stride Frequency.

PURPOSE: To study the consequences of a fatiguing ultratrail run of 6 hours on self-optimizing capability during uphill and downhill (DR) running. METHODS: The authors collected temporal stride kinematics and metabolic data in 8 (experimental group) male runners before and after the ultratrail run and in 6 (control group) male ultramarathon runners who did not run but stayed awake and performed normal, daily physical activities avoiding strenuous exercises over the 6-hour period. For each subject, preferred and optimal stride frequencies were measured, where stride frequency was systematically varied above and below the preferred one (±4% and ±8%) while running 3 conditions on level, 5% uphill, or 5% DR in a randomized order. RESULTS: Preferred and optimal stride frequencies across grade, group, and time showed no significant differences (P ≥ .184). Metabolic cost and the energetically optimum metabolic cost showed a grade × group × time interaction (P ≥ .011), with an ∼11% increase in the 2 variables only during the DR bouts (P ≥ .037). CONCLUSIONS: Despite maintaining similar dynamics of stride frequency adjustments during the DR bout, the experimental group was not able to optimize its gait. This suggests that the DR section of ultratrail runs can introduce a perturbing factor in the runners' optimization process, highlighting the need for incorporating DR bouts in the training programs of ultratrail runners to minimize the deleterious effects of DR on the energetically optimal gait.

Energetically optimal stride frequency is maintained with fatigue in trained ultramarathon runners.

OBJECTIVES: At a given running speed, humans naturally endeavor to achieve an optimal stride frequency that minimizes metabolic cost. Research has suggested that runners select this near optimal stride frequency in some process of self-optimization even during fatiguing tasks up to 1-h of high-intensity running. Here, we studied whether runners demonstrate a similar self-optimizing capability after an ultramarathon of 6 h. DESIGN: Controlled pre-post study. METHOD: We collected temporal stride kinematics and metabolic data in nine (experimental group) male runners before and after 6 h of running and in six (control group) male ultramarathon runners who did not run, but stayed awake and performed normal, daily physical activities avoiding strenuous exercises over the 6-h period. For each participant, preferred and optimal stride frequencies were measured, where stride frequency was systematically varied above and below PSF (±4% and ±8%). RESULTS: Preferred and optimal stride frequencies across time and group showed no significant differences (p ≥ 0.276). Furthermore, neither the overall relationship between metabolic cost and stride frequency, nor the energetically optimal stride frequency changed substantially after several hours of running. CONCLUSIONS: Similar dynamics of stride frequency adjustments in the experimental group occurred as those found in a non-fatigued state. This suggests that after an ultramarathon of 6 h, runners were still able to optimize their gait, and automatically adjust it in order to converge on the energetically optimal gait.

Heart mechanics at high altitude: 6 days on the top of Europe.

AIMS: The aim of this study was to analyse the underlying mechanisms of left and right ventricular (LV and RV) functional alterations during several days in high-altitude hypoxia. METHODS AND RESULTS: Resting evaluations of LV and RV function and mechanics were assessed by Speckle Tracking Echocardiography on 11 subjects at sea level (SLPRE), 3 ± 2 h after helicopter transport to high altitude (D0), at day 2 (D2), day 4 (D4) and day 6 (D6) at 4350 m and 5 ± 2 h after return to sea level (SLPOST). Subjects experienced acute mountain sickness (AMS) during the first days at 4350 m. LV systolic function, RV systolic and diastolic function, LV and RV strains and LV synchrony were unchanged at high altitude. Peak twist was increased at D0, continued to increase until D6 (SLPRE: 9.0 ± 5.1deg; D6: 13.0 ± 4.0deg, P < 0.05), but was normalized at SLPOST. Early filling decreased at high altitude with a nadir at D2 (SLPRE: 78 ± 13 cm s-1; D2: 66 ± 11 cm s-1, P < 0.05). LV filling pressures index was decreased at high altitude with the minimum value obtained at D2 and remained reduced at SLPOST. Untwisting, an important factor of LV filling, was not decreased but was delayed at 4350 m. CONCLUSIONS: High-altitude exposure impaired LV diastolic function with the greatest effect observed at D2, concomitantly with the occurrence of AMS. The LV early filling impairments resulted from an increased RV afterload, a decrease in LV filling pressure and a delayed LV untwist. However, the increased LV twist probably acted as a compensatory mechanism to maintain cardiac performance during high-altitude hypoxia.

Pulmonary Vascular Function and Aerobic Exercise Capacity at Moderate Altitude.

PURPOSE: There has been suggestion that a greater "pulmonary vascular reserve" defined by a low pulmonary vascular resistance (PVR) and a high lung diffusing capacity (DL) allow for a superior aerobic exercise capacity. How pulmonary vascular reserve might affect exercise capacity at moderate altitude is not known. METHODS: Thirty-eight healthy subjects underwent an exercise stress echocardiography of the pulmonary circulation, combined with measurements of DL for nitric oxide (NO) and carbon monoxide (CO) and a cardiopulmonary exercise test at sea level and at an altitude of 2250 m. RESULTS: At rest, moderate altitude decreased arterial oxygen content (CaO2) from 19.1 ± 1.6 to 18.4 ± 1.7 mL·dL, P < 0.001, and slightly increased PVR, DLNO, and DLCO. Exercise at moderate altitude was associated with decreases in maximum O2 uptake (V˙O2max), from 51 ± 9 to 43 ± 8 mL·kg⋅min, P < 0.001, and CaO2 to 16.5 ± 1.7 mL·dL, P < 0.001, but no different cardiac output, PVR, and pulmonary vascular distensibility. DLNO was inversely correlated to the ventilatory equivalent of CO2 (V˙E/V˙CO2) at sea level and at moderate altitude. Independent determinants of V˙O2max as determined by a multivariable analysis were the slope of mean pulmonary artery pressure-cardiac output relationship, resting stroke volume, and resting DLNO at sea level as well as at moderate altitude. The magnitude of the decrease in V˙O2max at moderate altitude was independently predicted by more pronounced exercise-induced decrease in CaO2 at moderate altitude. CONCLUSION: Aerobic exercise capacity is similarly modulated by pulmonary vascular reserve at moderate altitude and at sea level. Decreased aerobic exercise capacity at moderate altitude is mainly explained by exercise-induced decrease in arterial oxygenation.

Exercise-Induced Hypoxaemia Developed at Sea-Level Influences Responses to Exercise at Moderate Altitude.

PURPOSE: The aim of this study was to investigate the impact of exercise-induced hypoxaemia (EIH) developed at sea-level on exercise responses at moderate acute altitude. METHODS: Twenty three subjects divided in three groups of individuals: highly trained with EIH (n = 7); highly trained without EIH (n = 8) and untrained participants (n = 8) performed two maximal incremental tests at sea-level and at 2,150 m. Haemoglobin O2 saturation (SpO2), heart rate, oxygen uptake (VO2) and several ventilatory parameters were measured continuously during the tests. RESULTS: EIH athletes had a drop in SpO2 from 99 ± 0.8% to 91 ± 1.2% from rest to maximal exercise at sea-level, while the other groups did not exhibit a similar decrease. EIH athletes had a greater decrease in VO2max at altitude compared to non-EIH and untrained groups (-22 ± 7.9%, -16 ± 5.3% and -13 ± 9.4%, respectively). At altitude, non-EIH athletes had a similar drop in SpO2 as EIH athletes (13 ± 0.8%) but greater than untrained participants (6 ± 1.0%). EIH athletes showed greater decrease in maximal heart rate than non-EIH athletes at altitude (8 ± 3.3 bpm and 5 ± 2.9 bpm, respectively). CONCLUSION: EIH athletes demonstrated specific cardiorespiratory response to exercise at moderate altitude compared to non-EIH athletes with a higher decrease in VO2max certainly due to the lower ventilator and HRmax responses. Thus EIH phenomenon developed at sea-level negatively impact performance and cardiorespiratory responses at acute moderate altitude despite no potentiated O2 desaturation.

Endurance training minimizes age-related changes of left ventricular twist-untwist mechanics.

BACKGROUND: The aim of this study was to test the effect of endurance training on the age-related changes of left ventricular (LV) twist-untwist mechanics. Aging has been shown to induce a decline of diastolic function and more recently an impairment of twist-untwist mechanics, which constitutes an important factor for early diastolic suction and filling. On the other hand, endurance training has been shown to improve cardiac function. METHODS: Speckle-tracking echocardiography was performed in 106 endurance-trained male athletes and 75 controls (age range 18-70 years), divided into three groups according to age. RESULTS: From the younger to older age groups, progressive increases in LV apical rotation and twist angle and a decrease in LV untwisting rate during isovolumic relaxation time were observed. Athletes had lower systolic twist angles (P < .01) but higher untwist/twist ratios and LV untwisting rate during isovolumic relaxation time compared with controls, with the largest difference between senior groups (51 ± 24% vs 42 ± 22% in the young and 42 ± 29% vs 24 ± 25% in seniors, P < .001, respectively). The normal timing of untwisting rate occurring before radial displacement was preserved in athletes with increasing age, whereas it was blunted in controls. CONCLUSIONS: Endurance training does not prevent but minimizes changes in LV twist-untwist mechanics from young subjects to seniors. Athletes showed smaller increases of twist angle with age and smaller declines of LV untwisting rate during isovolumic relaxation time and untwist/twist ratio compared with controls. This training-improved preservation of LV twist-untwist mechanics is likely to play a key role for systolic-diastolic coupling and diastolic filling, particularly during exercise.

Time course of asymptomatic interstitial pulmonary oedema at high altitude.

The time course of asymptomatic pulmonary oedema during high-altitude exposure and its potential relationship with changes in cardiac function remain to clarify. Eleven volunteers were rapidly exposed to 4350m during a 4-day period. Each subject received clinical examination and thoracic ultrasonography to assess ultrasound lung comets (USLC) on day 1, 2 and 3 after arrival. Echocardiography was performed on day 2 and 4 at 4350m. All subjects had a significant increase in the number of USLC on day 1 (n=8±3), day 2 (n=7±4) and day 3 (n=3±2) compared to sea level (n=1±1) (P<0.01). Although left ventricle diastolic function and systolic tricuspid regurgitation gradient were significantly different at altitude compared to sea level, they did not correlate with the number of USLC (P>0.05). Asymptomatic pulmonary oedema seems to be transiently present in fast-ascending recreational climbers. The lack of correlation between the number of USLC and indices of cardiac changes suggest that non-cardiogenic mechanisms may underlie this transient increase in lung water.

Specific left ventricular twist-untwist mechanics during exercise in children.

BACKGROUND: In adults, left ventricular (LV) systolic twist is an important factor that determines LV filling, both at rest and during exercise. In children, lower LV twist has been demonstrated at rest, but its adaptation during exercise and its functional consequences on LV filling are unknown. METHODS: Using speckle-tracking echocardiography, LV twist-untwist mechanics were studied in 25 children (aged 10-12 years) and 20 young adults (aged 18-44 years) at rest and during three exercise workloads performed at 20%, 30%, and 40% of their maximal aerobic power. RESULTS: At rest, LV twist was lower in children, because of a higher temporal dispersion of peak rotation between base and apex. During exercise, the increase of basal rotation was blunted in children compared with adults (-6.7 ± 2.7° vs -9.0 ± 2.0° at 40% of maximal aerobic power, P < .05). Consequently, LV twist increased to a lesser extent (13.0 ± 5.0° vs 15.8 ± 4.5° at 40% of maximal aerobic power, P < .05). The increase in LV untwisting rates during exercise was also lower in children, leading to a lower percentage of untwisting during early diastole (8 ± 8% vs 29 ± 20% at 40% of maximal aerobic power, P < .001). Consequently, during early diastole, the normal timing of diastolic events observed in young adults, with untwist occurring before radial displacement, was blunted in children. Nevertheless, children exhibited normal LV filling due to higher diastolic radial and longitudinal strain rates. CONCLUSIONS: Twist-untwist mechanics may evolve with advancing age. In children, early diastolic LV untwisting appears to be less important than in adults. Their better LV intrinsic myocardial relaxation may ensure adequate LV filling during exercise without dependence on the additional effect of suction resulting from LV energy recoil.

Exercise response in hypertrophic cardiomyopathy: blunted left ventricular deformational and twisting reserve with altered systolic-diastolic coupling.

BACKGROUND: Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. METHODS AND RESULTS: Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (-15.7±5.0% versus -19.4±2.6%, P<0.001) and radial (38.1±11.3% versus 44.7±14.4%, P<0.05) strains but higher circumferential strain (-21.9±4.0% versus -18.8±2.3%, P<0.05) and twist (15.7±3.6° versus 9.3±2.6°, P<0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to -18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (-119.0±31.5°/s versus -137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P<0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (ß=-0.0807, P<0.001) but not in HCM patients (ß=-0.0051, P=0.68). CONCLUSIONS: HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.

ß-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger.

Prolonged strenuous exercise (PSE) induces transient left ventricular (LV) dysfunction. Previous studies suggest that ß-adrenergic pathway desensitization could be involved in this phenomenon, but it remains to be confirmed. Moreover, other underlying mechanisms involving oxidative stress have been recently proposed. The present study aimed to evaluate the involvement of both the ß-adrenergic pathway and NADPH oxidase (Nox) enzyme-induced oxidative stress in myocardial dysfunction in rats following PSE. Rats were divided into 4 groups: controls (Ctrl), 4-h exercised on treadmill (PSE), and 2 groups in which Nox enzyme was inhibited with apocynin treatment (Ctrl APO and PSE APO, respectively). We evaluated cardiac function in vivo and ex vivo during basal conditions and isoproterenol stress. GSH/GSSG ratio, cardiac troponin I (cTnI) release, and lipid peroxidation (MDA) were evaluated. PSE induced a decrease in LV developed pressure, intrinsic myocardial contractility, and relaxation associated with an increase in plasma cTnI release. Our in vivo and ex vivo results demonstrated no differences in myocardial response to isoproterenol and of effective dose 50 between control and PSE rats. Interestingly, the LV dysfunction was reversed by apocynin treatment. Moreover, apocynin prevented cellular oxidation [GSH/GSSG ratio: PSE APO rats vs. PSE rats in arbitrary units (au): 1.98 ± 0.07 vs. 1.35 ± 0.10; P < 0.001]. However, no differences in MDA were observed between groups. These data suggest that myocardial dysfunction observed after PSE was not due to ß-adrenergic receptor desensitization but could be due to a signaling oxidative stress from the Nox enzyme.

Kinetics of left ventricular strains and torsion during incremental exercise in healthy subjects: the key role of torsional mechanics for systolic-diastolic coupling.

BACKGROUND: The dynamics of systolic and diastolic strains and torsional mechanics of the left ventricle (LV) and their relation to diastolic filling never have been evaluated at various exercise intensities. METHODS AND RESULTS: Speckle tracking echocardiography was performed in 20 healthy sedentary subjects at rest and during a progressive submaximal exercise test at 20%, 30%, and 40% of maximal aerobic power. LV twist increased progressively with exercise intensity (10.5 ± 3.2 to 15.8 ± 4.5°; P<0.001), whereas longitudinal strain remained unchanged after the first workload, underlining the key role of torsional reserve in systolic-diastolic coupling during exercise. The increase in diastolic untwisting (-88.7 ± 34.2 to -182.9 ± 53.5 deg · s(-1); P<0.01) was correlated to enhanced systolic twist (R=0.61; P<0.001), and its magnitude of increase was significantly higher compared to diastolic longitudinal and circumferential strain rates (119 ± 64% versus 65 ± 44% and 57 ± 24%, respectively), emphasizing its contribution to diastolic filling. The timing of peak untwisting and the chronology of diastolic mechanical events were unchanged during effort. Untwisting was driven mainly by apical rotation and determined mitral opening and isovolumic relaxation time (R=0.47 and 0.61, respectively; P<0.001), whereas basal rotation and longitudinal and circumferential diastolic strain rates were major determinants of increased early diastolic filling (R=0.64, 0.79, and 0.81, respectively; P<0.001). CONCLUSIONS: The use of speckle tracking echocardiography gives new insights into physiological adaptive LV mechanics during incremental exercise in healthy subjects, underlining the key role of torsional mechanics. It might be useful to better understand the mechanisms of diastolic dysfunction and exercise intolerance in various pathological conditions.

Alteration in left ventricular strains and torsional mechanics after ultralong duration exercise in athletes.

BACKGROUND: Numerous studies have reported evidence of cardiac injury associated with transient left ventricular (LV) systolic and diastolic dysfunction after prolonged and strenuous exercise. We used 2D ultrasound speckle tracking imaging to evaluate the effect of an ultralong-duration exercise on LV regional strains and torsion. We speculated that systolic dysfunction after exercise is associated with depressed LV strains and torsion, and diastolic dysfunction results from decreased and delayed untwisting, a key factor of LV suction and early filling. METHODS AND RESULTS: Twenty-three triathletes underwent conventional and speckle tracking imaging echocardiography at rest before and immediately after an ultralong distance triathlon. Measurements included LV longitudinal, circumferential and radial strains, LV rotations, and LV torsion. After the race, LV systolic dysfunction was characterized by a decrease in LV longitudinal, radial, and circumferential strains, especially for apical radial strains (44.6+/-15.1% versus 31.1+/-13.8%, P<0.001). Peak torsion was slightly decreased (8.3+/-5.1 degrees versus 6.4+/-3.9 degrees , respectively, P=0.09) and significantly delayed (91+/-18% versus 128+/-31% of systolic duration, P<0.001) beside end-ejection. Peak untwisting was also depressed and delayed beside isovolumic relaxation. CONCLUSIONS: This study documented major alterations in cardiac strains and torsion after an ultralong distance triathlon. LV systolic strains were depressed but not delayed, whereas twisting was decreased and delayed. This altered pattern hampered the rapid untwisting during isovolumic relaxation phase, reducing LV diastolic suction and early filling.