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Fatiguing expiratory muscle work in otherwise resting humans elicits an increase in sympathetic motor outflow; whether limb blood flow ([Formula: see text]) and leg vascular resistance (LVR) are affected remains unknown. We found that fatiguing expiratory resistive loaded breathing (ERL) did not affect group mean [Formula: see text] or LVR. However, within-breath oscillations in [Formula: see text] may reflect a sympathetically mediated vasoconstriction that was counteracted by transient increases in [Formula: see text] due to the mechanical effects of high intra-abdominal pressure during ERL.

Background Epidemiological studies have indicated an inverse association between citrus fruit consumption and cardiovascular disease (CVD) risk. There is, however, a paucity of data concerning effects of blood orange juice (BOJ) intake on endothelial function and cardiovascular risk biomarkers. Objectives We examined short-term effects of BOJ on endothelial function, blood pressure, lipid profile, and inflammatory markers in healthy participants of European origin who were overweight or obese. Methods In a randomized, controlled, single-blind, crossover trial, 15 men and women (age: 28.7 ± 6.5 y; BMI: 28.3 ± 3.1 kg/m2) consumed BOJ or a sugar-matched control drink (CD) (200 mL twice daily) for 2 wk with a washout period of 1 wk. Endothelial function, measured as flow-mediated dilation (FMD) (primary outcome), and the secondary outcomes blood pressure, anthropometric measures, lipid profile, inflammatory markers, markers of vasodilation and vasoconstriction, and urinary flavanone metabolites were evaluated prior to and at the end of each treatment period following an overnight fast. Changes between treatments over time were assessed using repeated-measures ANOVA. Results The results demonstrate a significant increase in FMD following BOJ consumption (pre: 8.15% ± 2.92%; post: 10.2% ± 3.31%; P = 0.002) compared with CD (pre: 8.11% ± 2.52%; post: 7.77% ± 2.43%; time × treatment interaction: P = 0.001). Concurrent significant increases in urinary hesperetin-3'-glucuronide and hesperetin-7-glucuronide were observed following BOJ supplementation only (time × treatment interaction: P ≤ 0.01). Baseline blood pressure, lipid profile, high-sensitivity C-reactive protein, and endothelin-1 were generally within healthy ranges and unaffected by the intervention. Conclusions A 2-wk consumption of BOJ exerted favorable effects on endothelial function in healthy women and men who were overweight or obese, which is likely mediated by the combined actions of anthocyanin and flavanone metabolites on mechanisms that contribute to enhancing NO bioavailability. This trial was registered at clinicaltrials.gov as NCT03611114.

The mechanism(s) of exercise intolerance at V˙O2max remain poorly understood. In health, standard ramp-incremental (RI) exercise is limited by fatigue-induced reductions in maximum voluntary cycling power. Whether neuromuscular fatigue also limits exercise when the RI rate is slow and RI peak power at intolerance is lower than standard RI exercise, is unknown.In twelve healthy participants, maximal voluntary cycling power was measured during a short (~6 s) isokinetic effort at 80 rpm (Piso) at baseline and, using an instantaneous switch from cadence-independent to isokinetic cycling, immediately at the limit of RI exercise with RI rates of 50, 25, and 10 W·min-1 (RI-50, RI-25, and RI-10). Breath-by-breath pulmonary gas exchange was measured throughout.Baseline Piso was not different among RI rates (analysis of variance; P0.05). Tolerable duration increased with decreasing RI rate (RI-50, 411 ± 58 s vs RI-25, 732 ± 93 s vs RI-10, 1531 ± 288 s; P0.05). At intolerance, V˙O2peak was not different among RI rates (analysis of variance; P0.05), but RI peak power decreased with RI rate (RI-50, 361 ± 48 W vs RI-25, 323 ± 39 W vs RI-10, 275 ± 38 W; P0.05). Piso at intolerance was 346 ± 43 W, 353 ± 45 W, and 392 ± 69 W for RI-50, RI-25, and RI-10, respectively (P0.05 for RI-10 vs RI-50 and RI-25). At intolerance, in RI-50 and RI-25, Piso was not different from RI peak power (P0.05), thus there was no "power reserve." In RI-10, Piso was greater than RI peak power at intolerance (P0.001), that is, there was a "power reserve."In RI-50 and RI-25, the absence of a power reserve suggests the neuromuscular fatigue-induced reduction in Piso coincided with V˙O2max and limited the exercise. In RI-10, the power reserve suggests neuromuscular fatigue was insufficient to limit the exercise, and additional mechanisms contributed to intolerance at V˙O2max.

ObjectivesThis study aimed to characterise the exercise performed in UK cardiac rehabilitation (CR) and explore relationships between exercise dose and changes in physiological variables.DesignObservational cohort study.SettingOutpatient community-based CR in Leeds, UK. Rehabilitation sessions were provided twice per week for 6 weeks.ParticipantsSixty patients (45 male/15 female 33–86 years) were recruited following referral to local outpatient CR.Outcome measuresThe primary outcome was heart rate achieved during exercise sessions. Secondary outcomes were measured before and after CR and included incremental shuttle walk test (ISWT) distance and speed, blood pressure, brachial artery flow-mediated dilatation, carotid arterial stiffness and accelerometer-derived habitual physical activity behaviours.ResultsThe mean % of heart rate reserve patients exercised at was low and variable at the start of CR (42%±16 %) and did not progress by the middle (48%±17 %) or end (48%±16 %) of the programme. ISWT performance increased following CR (440±150 m vs 633±217 m, p0.05).ConclusionPatients in a UK CR cohort exercise at intensities that are variable but generally low. The exercise dose achieved using this CR format appears inadequate to impact markers of health. Attending CR had no effect on physical activity behaviours. Strategies to increase the dose of exercise patients achieve during CR and influence habitual physical activity behaviours may enhance the effectiveness of UK CR.

Background The role of omega-3 polyunsaturated fatty acids (n-3PUFA), and the potential impact of n-3PUFA supplementation, in the treatment and management of type 1 diabetes (T1D) remains unclear and controversial. Therefore, this study aimed to examine the efficacy of daily high-dose-bolus n-3PUFA supplementation on vascular health, glycaemic control, and metabolic parameters in subjects with T1D. Methods Twenty-seven adults with T1D were recruited to a 6-month randomised, double-blind, placebo-controlled trial. Subjects received either 3.3 g/day of encapsulated n-3PUFA or encapsulated 3.0 g/day corn oil placebo (PLA) for 6-months, with follow-up at 9-months after 3-month washout. Erythrocyte fatty acid composition was determined via gas chromatography. Endpoints included inflammation-associated endothelial biomarkers (vascular cell adhesion molecule-1 [VCAM-1], intercellular adhesion molecule-1 [ICAM-1], E-selectin, P-selectin, pentraxin-3, vascular endothelial growth factor [VEGF]), and their mediator tumor necrosis factor alpha [TNFα] analysed via immunoassay, vascular structure (carotid intima-media thickness [CIMT]) and function (brachial artery flow mediated dilation [FMD]) determined via ultrasound technique, blood pressure, glycosylated haemoglobin (HbA1c), fasting plasma glucose (FPG), and postprandial metabolism. Results Twenty subjects completed the trial in full. In the n-3PUFA group, the mean ± SD baseline n-3PUFA index of 4.93 ± 0.94% increased to 7.67 ± 1.86% (P P P P > 0.05). Conclusions This study indicates that daily high-dose-bolus of n-3PUFA supplementation for 6-months does not improve vascular health, glucose homeostasis, or metabolic parameters in subjects with T1D. The findings from this preliminary RCT do not support the use of therapeutic n-3PUFA supplementation in the treatment and management of T1D and its associated complications. Trial Registration ISRCTN, ISRCTN40811115. Registered 27 June 2017, http://www.isrctn.com/ISRCTN40811115.

Endothelial cell phenotype and endothelial function are regulated by hemodynamic forces, particularly wall shear stress (WSS). During a single bout of exercise, the specific exercise protocol can affect in-exercise WSS patterns and, consequently, endothelial function. MicroRNAs might provide a biomarker of in-exercise WSS pattern to indicate whether a specific exercise bout will have a positive effect on endothelial function. We evaluated the effect of acute interval (IT) and continuous (CON) in-exercise WSS patterns upon postexercise endothelial function and circulating microRNA (miR)-21 expression. Methods and results: 13 participants performed CON and 3 different IT exercise protocols matched for duration and intensity on separate days. Oxygen uptake, heart rate, and brachial artery blood flow were recorded throughout the exercise. Brachial artery flow-mediated dilation (FMD) was performed pre-exercise and 15 min postexercise. Plasma samples were acquired pre-exercise and 6 h postexercise to determine miR-21 expression. In-exercise shear rate (SR) patterns (a surrogate of WSS) differed according to the CON or IT work-rate profile. In-exercise anterograde SR was greater in CON than IT exercise ( P < 0.05), but retrograde SR was equivalent between exercise protocols ( P > 0.05). Oscillatory shear index was higher during IT versus CON exercise ( P < 0.05). Postexercise FMD increased (pre: 7.08% ± 2.95%, post: 10.54% ± 4.24%, P < 0.05), whereas miR-21 expression was unchanged (pre: 12.0% ± 20.7% cel-miR-39, post: 11.1 ± 19.3% cel-miR-39, P > 0.05) with no effect of exercise protocol ( P > 0.05). Conclusions: CON and IT exercise induced different SR patterns but equivalent improvements in acute endothelial function. The absence of change in miR-21 expression suggests that miR-21 is not a suitable biomarker of exercise-induced SR. NEW & NOTEWORTHY Interval exercise has the potential to negatively impact vascular adaptations because of repeated oscillations in vascular shear. To our knowledge, we are the first to continuously assess exercise-induced shear throughout different acute exercise protocols and examine its relationship with acute endothelial function and a circulating biomarker of shear (miR-21). These experiments provide clear data indicating enhancement of the acute vascular response from differing interval exercise protocols, with the study also providing detailed vascular and shear responses for future reference.

Background:Physical activity is important for maintaining independence and quality of life in older people living in care homes. Little is known about patterns of physical activity or sedentary behavior in this population.Methods:Thirty-three care home residents (82.6 ± 9.2 years) wore an ActiGraph GTX3 accelerometer for seven days, which provided minutes of sedentary behavior and low, light, and moderate-to-vigorous physical activity. Participants undertook the Mini-Mental State Examination and care staff reported activities of daily living (Barthel index) and functional ambulation classification (FAC) for each participant.Results:Participants spent on average 79% of their day sedentary, 14% in low, 6% in light, and 1% in moderate-to-vigorous physical activity. Activity levels did not significantly differ between days or hours of the day (P > .05).Conclusion:Levels of physical activity were very low and time being sedentary was high. This study can inform physical activity and sedentary behavior interventions for care homes’ residents.

Scaling left ventricular (LV) mass and other cardiac dimensions to account for individual body size is important. The traditional method of simple ratio scaling using, for example, body surface area (BSA) assumes a linear and proportional relationship and accurate measurement of both LV mass and BSA. These assumptions can be questioned; hence, we examined the appropriateness of methods and different indices using highly accurate magnetic resonance imaging scans. Cardiac and whole-body scans were performed in 172 young, healthy, male subjects (age range, 17-28 years) to assess LV mass, volume, linear dimensions, lean body mass and fat mass. Height, body mass and BSA were determined anthropometrically. Relationships were examined for linearity and closeness of fit using log-log least-squares linear regression to determine the slope exponent b (where 1.0 indicates linearity). The relationship between LV mass and lean body mass (b=.90+/-.15; r(2)=.66) was linear and geometrically consistent. This was also the case for LV end-diastolic volume (b=.70), although the confidence intervals were broader (+/-0.32) and the r(2) (.31) smaller. The relationships between LV mass, volume and other variables were generally not linear or geometrically consistent. LV linear dimensions did not demonstrate any linear relationships, and in particular, those with BSA were extremely poor (r(2)=.02-.09). In summary, the traditional scaling of LV measurements to BSA does not remove the influence of body size and other techniques should be considered. Lean body mass was the most appropriate variable for simple indexing of LV mass. No body size variable had a linear and proportional relationship with LV linear dimensions, and the use of simple ratio scaling for these is seriously questioned.

Traditional continuous aerobic exercise training attenuates age-related increases of arterial stiffness, however, training studies have not determined whether metabolic stress impacts these favourable effects. Twenty untrained healthy participants (n = 11 heavy metabolic stress interval training, n = 9 moderate metabolic stress interval training) completed 6 weeks of moderate or heavy intensity interval training matched for total work and exercise duration. Carotid artery stiffness, blood pressure contour analysis, and linear and non-linear heart rate variability were assessed before and following training. Overall, carotid arterial stiffness was reduced (p 0.05). This study demonstrates the effectiveness of interval training at improving arterial stiffness and autonomic function, however, the metabolic stress was not a mediator of this effect. In addition, these changes were also independent of improvements in aerobic capacity, which were only induced by training that involved a high metabolic stress.

Introduction It is well established that endurance exercise results in cardiac adaptation including eccentric hypertrophy of the left ventricle which can complicate the differential diagnosis of the athletic heart from some cardiac pathologies that may pre-dispose to sudden cardiac death. The impact of physiological conditioning on RV structure and function, and a similar diagnostic challenge with arrhythmogenic right ventricular cardiomyopathy (ARVC), has received less attention. A recent guideline paper from the American Society of Echocardiography (ASE) has provided a range for normal RV dimensions and functional deformation. These guidelines suggest the RV inflow (RVI) should be 36 mm or 21 mm/m 2 is a major criterion for the diagnosis of ARVC and furthermore longitudinal RV deformation has been shown to be impaired in these patients. In view of this, the aims of this study are twofold: To provide a range of absolute values for RV dimensions in 102 endurance athletes as well as providing a range of data indexed for body surface area (BSA). To provide normal athlete data for indices of RV strain (ɛ) and strain rate (SR). Methods and Results One hundred and two (102) endurance athletes (86 males and 16 females) with a broad age range (mean ± SD age (range)=36 ± 11 (21–71) years) volunteered and were consecutively enrolled in the study. All subjects were either endurance runners or cyclists and were scanned at peak condition. Echocardiography provided measurements of RVI, RV length, RVOT and RV diastolic area (RVDarea). A 2D strain technique was utilised to provide indices of RVɛ and systolic and diastolic SR. The values for RVI ranged from 30 to 55 mm with 57% of the population having values greater than the normal range. Proximal RVOT ranged from 26 to 49 mm with 40% of the population above the normal range. 28% of the population had RVOT values greater than the proposed “major criteria” for ARVC. RV length ranged from 70 to 110 mm and RVDarea from 13 to 38 cm 2 with values falling above ASE cut-offs in 69% and 59% of the population, respectively. When indexed (ratio scaling) for BSA proximal RVOT ranged from 13 to 25 mm/m 2 with 6% of the population meeting the major criteria for ARVC. Peak RVɛ ranged from −18 to −41% and peak RV SRS′ from −0.75 to −2.65 l/s, consistent with normal ranges proposed by the ASE. RV diastolic deformation indices displayed marked individual variability with a dominant SRE′ (mean ± SD=2.0±0.61 l/s) and smaller SRA′ (1.25±0.56 l/s). Conclusion RV dimensions in endurance athletes are higher than those proposed as “normal” and likewise may be consistent with the criteria for ARVC. Despite this enlargement, RV function in endurance athletes is preserved and therefore the role of RV strain imaging may provide additional diagnostic value in differentiating physiological from pathological adaptation.

The mechanism for slow pulmonary O2uptake (V̇o2) kinetics in patients with chronic heart failure (CHF) is unclear but may be due to limitations in the intramuscular control of O2utilization or O2delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O2delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed V̇o2kinetics during exercise in CHF. Fifteen men with CHF (New York Heart Association I–III) due to left ventricular systolic dysfunction performed two 6-min moderate-intensity exercise transitions ( bouts 1 and 2, separated by 6 min of rest) from rest to 90% of lactate threshold on a cycle ergometer. V̇o2was measured using a turbine and a mass spectrometer, and muscle tissue oxygenation index (TOI) was determined by near-infrared spectroscopy. Prior exercise increased resting TOI by 5.3 ± 2.4% ( P = 0.001), attenuated the deoxygenation overshoot (−3.9 ± 3.6 vs. −2.0 ± 1.4%, P = 0.011), and speeded the V̇o2time constant (τV̇o2; 49 ± 19 vs. 41 ± 16 s, P = 0.003). Resting TOI was correlated to τV̇o2before ( R2= 0.51, P = 0.014) and after ( R2= 0.36, P = 0.051) warm-up exercise. However, the mean response time of TOI was speeded between bouts in half of the patients (26 ± 8 vs. 20 ± 8 s) and slowed in the remainder (32 ± 11 vs. 44 ± 16 s), the latter group having worse New York Heart Association scores ( P = 0.042) and slower V̇o2kinetics ( P = 0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds V̇o2kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits V̇o2kinetics during moderate exercise.

Objective— Circulating progenitor cells (CPC) have emerged as potential mediators of vascular repair. In experimental models, CPC mobilization is critically dependent on nitric oxide (NO). South Asian ethnicity is associated with reduced CPC. We assessed CPC mobilization in response to exercise in Asian men and examined the role of NO in CPC mobilization per se. Methods and Results— In 15 healthy, white European men and 15 matched South Asian men, CPC mobilization was assessed during moderate-intensity exercise. Brachial artery flow-mediated vasodilatation was used to assess NO bioavailability. To determine the role of NO in CPC mobilization, identical exercise studies were performed during intravenous separate infusions of saline, the NO synthase inhibitor l -NMMA, and norepinephrine. Flow-mediated vasodilatation (5.8%±0.4% vs 7.9%±0.5%; P =0.002) and CPC mobilization (CD34 + /KDR + 53.2% vs 85.4%; P =0.001; CD133 + /CD34 + /KDR + 48.4% vs 73.9%; P =0.05; and CD34 + /CD45 − 49.3% vs 78.4; P =0.006) was blunted in the South Asian group. CPC mobilization correlated with flow-mediated vasodilatation and l -NMMA significantly reduced exercise-induced CPC mobilization (CD34 + /KDR + −3.3% vs 68.4%; CD133 + /CD34 + /KDR + 0.7% vs 71.4%; and CD34 + /CD45 − −30.5% vs 77.8%; all P Conclusion— In humans, NO is critical for CPC mobilization in response to exercise. Reduced NO bioavailability may contribute to imbalance between vascular damage and repair mechanisms in South Asian men.

This study investigated the contribution of muscle architecture to the differences in the torque-velocity and power-velocity relationships between older (OM n = 9, aged 69-82 years) and younger men (YM n = 15, aged 19-35 years). Plantarflexors' (PF) maximal isometric and concentric torques were recorded at 0.87, 1.75, 2.62, 3.49 and 4.36 rad s(-1). Physiological cross-sectional area (PCSA) was calculated as the ratio of muscle volume (determined by magnetic resonance imaging) to muscle fascicle length (Lf, measured by ultrasonography). GM PCSA and Lf of the OM were, respectively, 14.3% (P < 0.05) and 19.3% (P < 0.05) smaller than of the YM. In the OM, GM maximum isometric torque and maximum contraction velocity (Vmax), estimated from Hill's equation were, respectively, 48.5 and 38.2% lower (P < 0.001) than in the YM. At all contraction velocities, the OM produced less torque than the YM (46.3% of YM at 0.87 rad s(-1) to 14.7% at 4.36 rad s(-1), P < 0.001). Peak power (PP) of the OM was 80% lower than that of the YM and normalisation of PP to muscle volume only reduced this difference by 10%. Normalisation of torque to PCSA reduced, but did not eliminate, differences in torque between YM and OM (9.6%) and differences in torque/PCSA increased with contraction velocity (P < 0.05). After normalisation of velocity to Lf, the difference in Vmax between the OM and the YM was reduced to 15.9%. Thus, although muscle architecture contributes significantly to the differences in the torque- and power-velocity properties of OM and YM, other contractile factors, intrinsic to the muscle, seem to play a role. It is noteworthy that the deficit in PP between OM and YM is far greater than that of muscle torque, even after normalisation of PP to muscle volume. This finding likely plays an important role in the loss of mobility in old age.

Sarcopenia and muscle weakness are well-known consequences of aging. The aim of the present study was to ascertain whether a decrease in fascicle force (Ff) could be accounted for entirely by muscle atrophy. In vivo physiological cross-sectional area (PCSA) and specific force (Ff/PCSA) of the lateral head of the gastrocnemius (GL) muscle were assessed in a group of elderly men [EM, aged 73.8 yr (SD 3.5), height 173.4 cm (SD 4.4), weight 78.4 kg (SD 8.3); means (SD)] and for comparison in a group of young men [YM, aged 25.3 yr (SD 4.4), height 176.4 cm (SD 7.7), weight 79.1 kg (SD 11.9)]. GL muscle volume (Vol) and Achilles tendon moment arm length were evaluated using magnetic resonance imaging. Pennation angle and fiber fascicle length (Lf) were measured using B-mode ultrasonography during isometric maximum voluntary contraction of the plantar flexors. PCSA was estimated as Vol/Lf. GL Ff was calculated by dividing Achilles tendon force by the cosine of θ, during the interpolation of a supramaximal doublet, and accounting for antagonist activation level (assessed using EMG), Achilles tendon moment arm length, and the relative PCSA of the GL within the plantar flexor group. Voluntary activation of the plantar flexors was lower in the EM than in the YM (86 vs. 98%, respectively, P < 0.05). Compared with the YM, plantar flexor maximal voluntary contraction torque and Ff of the EM were lower by 47 and 40%, respectively ( P < 0.01). Both Vol and PCSA were smaller in the EM by 28% ( P < 0.01) and 16% ( P < 0.05), respectively. Also, pennation angle was 12% smaller in the EM, whereas there was no significant difference in Lf between the YM and EM. After accounting for differences in agonists and antagonists activation, the Ff/PCSA of the EM was 30% lower than that of the YM ( P < 0.01). These findings demonstrate that the loss of muscle strength with aging may be explained not only by a reduction in voluntary drive to the muscle, but mostly by a decrease in intrinsic muscle force. This phenomenon may possibly be due to a reduction in single-fiber specific tension.

1. Muscle strength of the adductor pollicis (AP) was studied throughout the menstrual cycle to determine whether any variation in force is similar to the known cyclical changes in ovarian hormones. Three groups of young women were studied: trained regularly menstruating athletes (trained), untrained regularly menstruating (untrained) and trained oral contraceptive pill users (OCU). In addition a group of untrained young men was studied as controls. 2. Maximum voluntary force (MVF) of AP was measured over a maximum period of 6 months. Ovulation was detected by luteinizing hormone measurements or change in basal body temperature. There was a significant increase in MVF (about 10%) during the follicular phase of the menstrual cycle when oestrogen levels are rising, in both the trained and untrained groups. This was followed by a similar in MVF around the time of ovulation. Neither the OCU nor the male subjects showed cyclical changes in MVF.

Physiological variables must often be scaled for body size differences to permit meaningful comparisons between groups. Using multivariate allometric scaling (MAS), this study aimed to compare the anaerobic performance of adult males and females in 12 pairs matched for physical activity status. Peak power output (PPO) was assessed via a 30-s supramaximal cycle ergometer test. Fat-free mass (FFM) and thigh muscle and bone cross-sectional area (CSA) were determined anthropometrically and served as indicators of active musculature. The MAS revealed power functions of the form PPO = a∙genderc∙FFMb (or CSAb). Common b exponents of 0.1 were identified for both FFM and CSA (negative allometry). Sex differences were found in absolute PPO (1,252 vs. 681 W, p 0.1 and CSA0.1 entered as cavariates) did not eliminate the sex difference (adjusted means 1,243 vs. 690 W, p

To determine the intraobserver reproducibility of peak and temporal values for myocardial strain (ɛ) and strain rate (SR) using a speckle tracking technique in the left ventricle (LV), right ventricle (RV), and left atrium (LA).Myocardial speckle tracking echocardiograms of the LV, RV, and LA were obtained on 20 healthy adults to provide indices of longitudinal, radial, circumferential ɛ, and SR as well as LV rotation and twist. Each participant had two separate acquisitions approximately 30 minutes apart. No systematic bias was present in ɛ data. LV ɛ across all planes provided "good" to "very good" intraclass correlation coefficient (ICC) values (0.714-0.807), however radial ɛ was inferior in terms of coefficients of variation (CoV) (19%). SR data were more variable than ɛ with LV radial SR performing least favorably. RV and LA ɛ demonstrated excellent reproducibility (ICCs of 0.834, 0.959, and CoVs of 7% and 6%, respectively). RV and LA SR were again more variable but generally acceptable ICC0.6 and CoV15%. Peak basal and apical rotation demonstrated quite high variability while derived torsion had low variability and excellent agreement (ICC = 0.940, CoV = 10%). Time-to-peak values demonstrated acceptable agreement with the exception of systolic SR from all chambers.Good reproducibility was obtained for peak ɛ indices although radial ɛ performs less favorably. Intraobserver variation of peak ɛ appears superior to values obtained for peak SR. Time-to-peak values demonstrate very good intraobserver reproducibility across all planes of contraction with exception of (time-to-peak) systolic strain rate (SRS).

Exercise-induced left ventricular hypertrophy is well documented, but whether this occurs merely in line with concomitant increases in lean body mass is unclear. PURPOSE: Our aim was to model the extent of left ventricular hypertrophy associated with increased lean body mass attributable to an exercise training program. METHODS: Cardiac and whole-body magnetic resonance imaging was performed before and after a 10-wk intensive British Army basic training program in a sample of 116 healthy Caucasian males (aged 17-28 yr). The within-subjects repeated-measures allometric relationship between lean body mass and left ventricular mass was modeled to allow the proper normalization of changes in left ventricular mass for attendant changes in lean body mass. To linearize the general allometric model (Y = aX b), data were log-transformed before analysis; the resulting effects were therefore expressed as percent changes. We quantified the probability that the true population increase in normalized left ventricular mass was greater than a predefined minimum important difference of 0.2 SD, assigning a probabilistic descriptive anchor for magnitude-based inference. RESULTS: The absolute increase in left ventricular mass was 4.8% (90% confidence interval = 3.5%-6%), whereas lean body mass increased by 2.6% (2.1%-3.0%). The change in left ventricular mass adjusted for the change in lean body mass was 3.5% (1.9%-5.1%), equivalent to an increase of 0.25 SD (0.14-0.37). The probability that this effect size was greater than or equal to our predefined minimum important change of 0.2 SD was 0.78-likely to be important. CONCLUSIONS: After correction for allometric growth rates, left ventricular hypertrophy and lean body mass changes do not occur at the same magnitude in response to chronic exercise. Copyright © 2011 by the American College of Sports Medicine.

Background— Running an ultramarathon has been shown to have a transient negative effect on right ventricular (RV) and left ventricular (LV) function. Additionally, recent findings suggested that ultraendurance athletes may be more at risk of developing a RV cardiomyopathy. The standard echocardiographic assessment of RV function is problematic; however, the introduction of ultrasonic speckle tracking technology has the potential to yield a comprehensive evaluation of RV longitudinal function, providing new insights into this phenomenon. Thus, the primary aim of this exploratory study was to evaluate comprehensively RV structure and function after a 161-km ultramarathon and establish whether changes in the RV are associated with alterations in LV function. Methods and Results— Myocardial speckle tracking echocardiograms of the RV and LV were obtained before and immediately after a 161-km ultramarathon in 16 healthy adults. Standard echocardiography was used to determine RV size and function and LV eccentricity index. Speckle tracking was used to determine the temporal evaluation of indices of RV and LV function. RV size was significantly increased postrace (RV outflow, 32 to 35 mm, P =0.002; RV inflow, 42 to 45 mm, P =0.027) with an increase in LV eccentricity index (1.03 to 1.13, P =0.006). RV strain (ε) was significantly reduced postrace (−27% to −24%, P =0.004), but there was no change in the rates of ε. Peak ε in all planes of LV motion were reduced postrace (longitudinal, −18.3 to −16.3%, P =0.012; circumferential, −20.2% to −15.7%, P =0.001; radial, 53.4% to 40.3%, P =0.009). Changes in RV size and function correlated with diastolic strain rates in the LV. Conclusions— This exploratory study demonstrates RV dilatation and reduction in function after an ultramarathon. Further research is warranted to elucidate the mechanisms responsible for these findings. It is not clear what clinical impact might result from consecutive bouts of postexercise RV dysfunction.

Two-dimensional (2D) strain imaging from speckle tracking is a Doppler independent technique allowing assessment of left ventricular (LV) strain (ɛ); systolic strain rate (SRs') and early diastolic strain rate (SRe') in the radial and circumferential planes. We set out to investigate whether (i) these parameters facilitated assessment of dyssynchronous contraction and (ii) these measures could predict response to cardiac resynchronization therapy (CRT).Forty-one patients with severe, symptomatic heart failure on optimal medical therapy were recruited. Thirty-two healthy subjects were used as controls. Time to peak ɛ, SRs', and SRe' of 6 LV segments were measured in the parasternal short axis prior to and 6 weeks post CRT implantation. Time delays between segments were then calculated and ANOVA assessed for prediction of response, classified as reduction in LV end systolic volume of15%. 2D strain demonstrated significantly more dyssynchronous contraction in the heart failure population at baseline compared to healthy controls. Significant reduction in dyssynchrony was seen in ɛ and SRs' following CRT, largely confined to those with evidence of remodeling. The time delay between peak circumferential SRs' of opposing walls was the best predictor of reverse remodeling.2D strain imaging appears to be a useful measure to predict response to CRT. The time to peak circumferential SR is a new predictor of response.

Background Standard marathon running can result in a depression of left ventricular (LV) diastolic function during early recovery. Left atrial (LA) mechanics are integral in maintaining an early diastolic pressure gradient as well as being responsive to changes in LV diastolic function, and therefore the detailed assessment of LA mechanics may provide further insight. The aim of this study was to determine the impact of prolonged strenuous exercise on mechanics of the left atrium and the association with changes in LV diastolic function. Methods Myocardial speckle-tracking echocardiograms of the left atrium and left ventricle were obtained prior to, immediately after, and 6 hours after the completion of a marathon (42.2 km) in 17 healthy adult men. Speckle tracking was used to determine peak atrial deformation, early diastolic deformation rate, and contractile function, including atrial activation time. LA volumes throughout the cardiac cycle were also assessed to provide reservoir, conduit, and booster pump volumes. Diastolic assessment of the left ventricle included peak early diastolic strain rate, late diastolic strain rate, and standard indices. Temporal assessment of LV “twist” and “untwist” was also evaluated. Results All 17 subjects completed the marathon (mean finishing time, 209 ± 19 minutes; range, 173-241 minutes). Although contractile function was significantly increased, there was a reduction in early diastolic deformation rate that was correlated with reduced atrial deformation. Atrial activation time was significantly increased after the race. All LV indices of diastolic function were reduced in early diastole, whereas late diastolic function was increased after the race. LV torsion was significantly reduced at end-systole and significantly elevated in the isovolumic period and early diastole, after the race. All indices returned toward baseline at 6 hours after exercise. Conclusions This study demonstrates transient changes in LV diastolic relaxation following prolonged exercise that appear to have a direct impact on subsequent LA deformation. The impact of reduced LA preload on these findings and the delay in LA activation time requires further exploration.

The aim of the present investigation was to determine whether muscle force per physiological cross sectional area (PCSA) of the lateral gastrocnemius (GL) of elderly males increased following a 12-month physical training programme. Eleven elderly males were assigned to a 12-month training programme (TRN mean age 72.7 +/- 3.3 years, mean +/- SD) and eight elderly males were allocated to a control group (CTRL, 73.9 +/- 4.0 years) who maintained their habitual physical activity levels. In vivo measurements of muscle architecture, muscle volume (VOL), achilles tendon moment arm length and plantarflexor torque were used to estimate GL PCSA (VOL/fascicle length) and specific force (GL fascicle force/GL PCSA). Maximal GL fascicle force was calculated accounting for agonist muscle activation and antagonist co-activation. Following training GL fascicle force increased by 31% (P0.01), which was not entirely accounted for by a 17% increase in PCSA (from 27.2 +/- 5.9 to 31.8 +/- 6.2 cm(2), P0.05). Specific force increased significantly from 8.9 +/- 1.9 to 11.2 +/- 3.0 N cm(-2) (P0.05). Pennation angle, but not fascicle length, increased by 12% with training (P0.05). The CTRL group showed no change in muscle size, strength or architecture over the 12-month period. In conclusion, with the level of agonist and antagonist muscle activity accounted for a 12-month strength training programme resulted in an increase in both PCSA and specific force in elderly males.

This study investigated whether loss of power with aging is fully accounted for by a decrease in muscle volume. Triceps surae power and volume (VOL) were measured in 18 older (OM: 69-82 years) and 12 younger men (YM: 19-35 years). Isokinetic peak torque was measured to determine torque-velocity and power-velocity relationships. Both peak power observed (PP(obs)) and peak power estimated from Hill's equation (PP(est)) were markedly reduced in the OM (PP(obs) was 45% and PP(est) was 43% of those of the YM). VOL was 81% of that of the YM (p

This study investigated the influence of tendon elongation (TE) on postcontraction doublet (PCD) torque in the assessment of activation in the plantar flexors of nine elderly men (EM, age 73.7 ± 3.6 yr) and nine young men (YM, age 24.7 ± 4.7 yr). Plantar flexion maximal voluntary contractions (MVC) and activation were assessed at ankle joint angles of −20° (dorsiflexion), 0°, and 20° (plantar flexion). Across the ankle joint angles tested, compared with YM, the EM had a 36–49% lower plantar flexion MVC ( P < 0.01), TE was greater by 25–31% ( P < 0.01), and electromechanical delay was 65–108% greater ( P < 0.01). Activation (PCD torque to interpolated doublet torque) was 15% lower in EM compared with YM at −20° ( P < 0.05), but no different at 0 and 20°. In the EM, PCD torque relative to MVC torque was significantly lower at 20° compared with 0° ( P < 0.05). Electromechanical delay was positively correlated with TE ( R2 = 0.489, P < 0.01). In conclusion, this investigation demonstrates that, although a negative association exists between TE and PCD torque, the consequence of a greater TE on the estimation of activation in EM is negligible. This is due to a greater influence of ankle joint angle on the occlusion of a superimposed doublet, which counteracts the lesser influence of joint angle on TE and PCD torque. However, a greater TE in EM was found to significantly increase electromechanical delay, which is expected to influence the time needed for postural readjustments.

In elderly males muscle plantar flexor maximal voluntary contraction (MVC) torque normalised to muscle volume (MVC/VOL) is reduced compared to young males as a result of incomplete muscle activation in the elderly. The aim of the present study was to determine the influence of a 12-month resistance training programme on muscle volume, strength, MVC/VOL, agonist activation and antagonist coactivation of the plantarfexors in elderly males. Thirteen elderly males aged 70 years and over (range 70-82 years), completed a 12-month whole body resistance-training programme (TRN), training three times a week. Another eight males (range 18-30 years), who maintained their habitual physical activity for the same 12-month period as the TRN group acted as controls (CTRL). Isometric plantarflexor maximal voluntary contraction (MVC) torque increased in the TRN group by 20% (P < 0.01), from 113.1 +/- 22.0 Nm to 141.5 +/- 19.2 Nm. Triceps surae volume (TS VOL) assessed using MRI, increased by 12%, from 796.3 +/- 78.9 cm(3) to 916.8 +/- 144.4 cm(3) . PF activation, measured using supramaximal double twitch interpolation, increased from 83.6+/-11.0% pre training, to 92.1 +/- 7.6% post training (P < 0.05). Dorsiflexion MVC and antagonist coactivation (assessed using surface electromyography) did not change with training. Plantarflexor MVC torque normalized for triceps surae muscle volume (MVC/VOL) was 142.6 +/- 32.4 kN m(-2) before training and 157.0 +/- 27.9 kN m(-2) after training (a non-significant increase of 8%). No significant change in any measurement was observed in the CTRL group. This study has shown that the gain in muscle strength in response to long-term (12-month) training in older men is mostly accounted for by an increased muscle volume and activation.

Previous studies have reported a decrease in muscle torque per cross-sectional area in old age. This investigation aimed at determining the influence of agonists muscle activation and antagonists co-activation on the specific torque of the plantarflexors (PF) in recreationally active elderly males (EM) and, for comparison, in young men (YM). Twenty-one EM, aged 70-82 years, and 14 YM, aged 19-35 years, performed isometric maximum voluntary contractions (MVC). Activation was assessed by comparing the amplitude of interpolated supramaximal twitch doublets at MVC, with post-tetanic doublet peak torque. Co-activation of the tibialis anterior (TA) was evaluated as the ratio of TA-integrated EMG (IEMG) activity during PF MVC compared to TA IEMG during maximal voluntary dorsiflexion. Triceps surae muscle volume (VOL) was assessed using magnetic resonance imaging (MRI), and PF peak torque was normalised to VOL (PT/VOL) since the later approximates physiological cross-sectional area (CSA) more closely than anatomical CSA. Also, physical activity level, assessed by accelerometry, was significantly lower (21%) in the elderly males. In comparison to the YM group, a greater difference in PT (39%) than VOL (19%) was found in the EM group. PT/VOL and activation capacity were respectively lower by 25% and 21% in EM compared to YM, whereas co-activation was not significantly different. In EM PT/VOL correlated with activation (R(2)=0.31, P

Buckley JG, Jones SF, Birch KM. Oxygen consumption during ambulation: comparison of using a prosthesis fitted with and without a tele-torsion device. Arch Phys Med Rehabil 2002;83:576-81. Objective: To determine the energy expenditure and sub- jective comfort rating of walking in transtibial amputee patients using their prosthesis fitted either with or without a tele-torsion device (TT Pylon). Design: Randomized, before-after trial. Setting: Gait laboratory. Participants: Six men, moderately active, with unilateral transtibial amputation (mean age, 39.5 9.9y). Intervention: Subjects walked on a motorized treadmill using their prosthesis fitted either with (ProsWith) or without (ProsWith- out) a TT Pylon. Trials were repeated with subjects walking at speeds 100%, 130%, and 160% of their "normal" pace. Main Outcome Measures: The energy expended (VO2) and subjective comfort rating during each walking trial. Results: VO2 during walking with the prosthesis fitted with the TT Pylon was 5.4% and 9.1% lower than when using the prosthesis without the TT Pylon, at the speeds 130% and 160% of normal, respectively. Findings at the speed 160% greater than normal were significant (P.05). Two of the subjects perceived no difference in prosthetic comfort between Pros- With and ProsWithout. The other 4 subjects preferred the TT Pylon at all speeds. Conclusion: Use of a TT Pylon can significantly reduce the

The purpose of this study was to construct an isometric lift dynamometer and relate isometric lifting strength to dynamic measures of muscular fitness, leg and back strength and muscular power output. Thirty-one male subjects, aged 19-24 years, performed a standing broad jump (for distance), a vertical jump (for flight time), 3 maximal pulls (for peak power) on a rowing ergometer and maximal isometric leg and back extensions on a conventional dynamometer. The results of these tests were correlated with the maximum isometric lifting strength (MILS) obtained on the lift dynamometer using cluster correlation and multiple regression. Significant correlations (p0.001) were found between isometric lifting strength and back strength (BS) (r = 0.59), and leg strength (LS) (r = 0.74). A significant correlation was also noted between isometric lifting strength and both standing broad jump (SBJ) (r = 0.58, p0.001) and power output (PO) (r = 0.38, (p0.05). Multiple regression analysis was used to predict lifting performance from a battery of standard fitness tests. The prediction equation for maximal isometric lifting strength included the terms LS, BS, SBJ and PO (r = 0.80). The relation between isometric lifting strength and other muscular fitness variables suggest that the method used provides an acceptable measure of strength and an indication of the involvement of back and leg musculature in squat lifting.