Mind the Gap: Comparison of External Load and Load Variation Between a Reserve Team in a 1-Game Week Microcycle and Its First Team in a 2-Game Week Microcycle Within an Elite Professional Soccer Club.

ABSTRACT: Carpels, T, Scobie, N, Macfarlane, NG, and Kemi, OJ. Mind the gap: comparison of external load and load variation between a reserve team in a 1-game week microcycle and its first team in a 2-game week microcycle within an elite professional soccer club. J Strength Cond Res 38(5): e235-e242, 2024-The aim of this study was to quantify and compare weekly external load and within-week load variation of reserve team players (RES) in a 1-game week microcycle to first team players (FT) in a 2-game week microcycle within the same professional soccer club. External load data were collected between 2017 and 2020 for the following parameters: duration, total distance (TD), total high-speed distance (THSD; >19.8 km·h -1 ), high-speed distance (HSD; 19.8-25.2 km·h -1 ), sprint distance (SD; >25.2 km·h -1 ), number of sprints (number of efforts >25.2 km·h -1 ), number of high-speed efforts (number of HS efforts >19.8 km·h -1 ), meters per minute (m·min -1 ), and high-speed meters per minute (HS m·min -1 ). First team players were subcategorized into starters (ST) and nonstarters (NST). Intergroup differences in cumulative weekly load and weekly load patterns were statistically analyzed, whereas training monotony (TM) was quantified to assess intragroup, within-week, load variation. Reserve team players showed similar weekly loads to ST, apart from significant differences ( p < 0.005) in duration (8%), TD (21%), and HS efforts (16%). Similar to ST, RES showed greater values than NST ( p < 0.0005) for duration (10%), TD (9%), THSD (30%), HSD (26%), SD (45%), sprints (40%), and HS efforts (22%). Weekly patterns in RES were different from ST and NST ( p < 0.05). Training monotony was highest for NST for all parameters, apart from the number of sprints. Reserve team players need to be prepared to cope with cumulative weekly loads and the lack of recovery between games that ST face. However, when RES become NST, effective loading strategies need to be designed within the limits of 2-game week microcycles to ensure continuous development.

Inherited physical capacity: Widening divergence from young to adult to old.

Cardiorespiratory performance segregates into rat strains of inherited low- and high-capacity runners (LCRs and HCRs); during adulthood, this segregation remains stable, but widens in senescence and is followed by segregated function, health, and mortality. However, this segregation has not been investigated prior to adulthood. We, therefore, assessed cardiorespiratory performance and cardiac cell (cardiomyocyte) structure-function in 1- and 4-month-old LCRs and HCRs. Maximal oxygen uptake was 23% less in LCRs at 1-month compared to HCRs at 1-month, and 72% less at 4 months. Cardiomyocyte contractility was 37-56% decreased, and Ca2+ release was 34-62% decreased, in 1- and 4-month LCRs versus HCRs. This occurred because HCRs had improved contractility and Ca2+ release during maturation, whereas LCRs did not. In quiescent cardiomyocytes, LCRs displayed 180% and 297% more Ca2+ sparks and 91% and 38% more Ca2+ waves at 1 and 4 months versus HCRs. Cell sizes were not different between LCRs and HCRs, but LCRs showed reduced transverse-tubules versus HCRs, though no discrepant transverse-tubule generation occurred during maturation. In conclusion, LCRs show reduced scores for aerobic capacity and cardiomyocyte structure-function compared to HCRs and there is a widening divergence between LCRs and HCRs during juvenile to near-adult maturation.

Graduate prospects explain undergraduate program standing in university league sports science tables.

UK university undergraduate programs are compared by independent subject-specific rankings (Complete, Guardian, and Times), based on data from the National Student Survey, Higher Education Statistics Agency, Universities and Colleges Admissions Service, Research Excellence Framework, and the universities. The sports and exercise science program at the University of Glasgow has steadily risen to currently rank as the top UK program. This investigation aimed to identify the underlying factors that explain this. Therefore, we obtained underlying scores for entry standard, student satisfaction, research foundation, graduate prospects, staff-to-student ratio, expenditure/student, continuation, program support to students, and teaching quality from the ranking providers for years 2010-2024, and statistically modeled which factors significantly affected the rankings. We found that entry standards and graduate prospects strongly correlated significantly with ranking results. Principal component analysis indicated that a model of graduate prospects and entry standards explained 66.2% of the variance in ranking results. Multiple linear regression with all underlying factors included in the model indicated they explained 78% (R2 = 0.78) of the total variance, while stepwise elimination of insignificant factors identified graduate prospects as the sole factor that significantly affected outcome by explaining 71% (R2 = 0.71) of the variance. Therefore, the primary predictor of ranking success in UK university league tables for sports science is graduates' professional success (graduate prospects).NEW & NOTEWORTHY University rankings are used by applicants and stakeholders to judge programs, including undergraduate studies. In the rankings, undergraduate UK programs are compared and contrasted against each other based on how they score for criteria that affect student life and future prospects. Here, we determined the relative influence of those criteria and found that graduate prospects, how students professionally benefit from their study after graduation, is the factor that matters most for the ranking results.

Electrically stimulated in vitro heart cell mimic of acute exercise reveals novel immediate cellular responses to exercise: Reduced contractility and metabolism, but maintained calcium cycling and increased myofilament calcium sensitivity.

Cardiac cellular responses to acute exercise remain undescribed. We present a model for mimicking acute aerobic endurance exercise to freshly isolated cardiomyocytes by evoking exercise-like contractions over prolonged periods of time with trains of electrical twitch stimulations. We then investigated immediate contractile, Ca2+ , and metabolic responses to acute exercise in perfused freshly isolated left ventricular rat cardiomyocytes, after a matrix-design optimized protocol and induced a mimic for acute aerobic endurance exercise by trains of prolonged field twitch stimulations. Acute exercise decreased cardiomyocyte fractional shortening 50%-80% (p < .01). This was not explained by changes to intracellular Ca2+ handling (p > .05); rather, we observed a weak insignificant Ca2+ transient increase (p = .11), while myofilament Ca2+ sensitivity increased 20%-70% (p < .05). Acidic pH 6.8 decreased fractional shortening 20%-70% (p < .05) because of 20%-30% decreased Ca2+ transients (p < .05), but no difference occurred between control and acute exercise (p > .05). Addition of 1 or 10 mM La- increased fractional shortening in control (1 mM La- : no difference, p > .05; 10 mM La- : 20%-30%, p < .05) and acute exercise (1 mM La- : 40%-90%, p < .01; 10 mM La- : 50%-100%, p < .01) and rendered acute exercise indifferent from control (p > .05). Intrinsic autofluorescence showed a resting NADstate of 0.59 ± 0.04 and FADstate of 0.17 ± 0.03, while acute exercise decreased NADH/FAD ratio 8% (p < .01), indicating intracellular oxidation. In conclusion, we show a novel approach for studying immediate acute cardiomyocyte responses to aerobic endurance exercise. We find that acute exercise in cardiomyocytes decreases contraction, but Ca2+ handling and myofilament Ca2+ sensitivity compensate for this, while acidosis and reduced energy substrate and mitochondrial ATP generation explain this.

When one says yes and the other says no; does calcineurin participate in physiologic cardiac hypertrophy?

Developing engaging activities that build skills for understanding and appreciating research is important for undergraduate and postgraduate science students. Comparing and contrasting opposing research studies does this, and more: it also appropriately for these cohorts challenges higher level cognitive processing. Here, we present and discuss one such scenario, that of calcineurin in the heart and its response to exercise training. This scenario is further accentuated by the existence of only two studies. The background is that regular aerobic endurance exercise training stimulates the heart to physiologically adapt to chronically increase its ability to produce a greater cardiac output to meet the increased demand for oxygenated blood in working muscles, and this happens by two main mechanisms: 1) increased cardiac contractile function and 2) physiologic hypertrophy. The major underlying mechanisms have been delineated over the last decades, but one aspect has not been resolved: the potential role of calcineurin in modulating physiologic hypertrophy. This is partly because the existing research has provided opposing and contrasting findings, one line showing that exercise training does activate cardiac calcineurin in conjunction with myocardial hypertrophy, but another line showing that exercise training does not activate cardiac calcineurin even if myocardial hypertrophy is blatantly occurring. Here, we review and present the current evidence in the field and discuss reasons for this controversy. We present real-life examples from physiology research and discuss how this may enhance student engagement and participation, widen the scope of learning, and thereby also further facilitate higher level cognitive processing.

Youth-to-Senior Transition in Elite European Club Soccer.

The priority for soccer academies is to develop youth players that graduate and transfer directly to their senior squads. The aim of this study was to assess the effectiveness of this direct youth-to-senior pathway by examining the extent to which club-trained players (CTPs) are currently involved in elite male European soccer. Relevant demographic longitudinal studies between 2009 and 2020 conducted by the International Centre for Sports Studies Football Observatory were analysed. The main findings were that the proportion of CTPs in senior squads has decreased from 23% to 17% over this time period, while the proportion of expatriates (EXPs) has increased from 35% to 42%. Moreover, clubs resorted more frequently to making new signings (NS, i.e. association-trained players (ATPs) and/or EXPs), with squad proportion increasing from 37% to 44%, while only launching one debutant (DBT, i.e. CTP with no previous senior experience) on average per season. Similar trends are observed in the evolution of playing time: while the fielding of CTPs remained constant (15%), EXPs and NS are fielded increasingly more (49% and 36%, respectively), despite a positive relationship between CTP match fielding and league ranking, with a Spearman Rank correlation r = 0.712 (95% confidence interval [0.381-0.881]), p < 0.01. In conclusion, young talents are still provided opportunities; however, these are limited and increasingly less frequent at their parent clubs. This potentially suggests a dysfunctional direct youth-to-senior development pathway.

Blackcurrant extract does not affect the speed-duration relationship during high-intensity running.

Anthocyanin-rich blackcurrant extract (BC) has been shown to ergogenically aid high-intensity exercise. Capacity for such exercise is evaluated by the hyperbolic speed-tolerable duration (S-Dtol) relationship. Therefore, in double-blinded and cross-over randomised controlled trials, 15 males underwent treadmill running incremental exercise testing and were assessed for S-Dtol, quantified by critical speed (CS) and D' (distance), and assessments of time to exhaustion performance to empirically test the limits of the S-Dtol relationship, after daily supplementation of 300 mg/d BC (105 mg/d anthocyanin) or placebo. Supplementation with BC did not change CS (placebo 12.1 ± 1.0 km/h vs BC 11.9 ± 1.0 km/h, p > .05) or D' (placebo 918.6 ± 223.2 m vs BC 965.2 ± 231.2 m, p > .05), although further analysis indicated D' increased in 60% of subject (p = .08), indicating a trend toward cohorts potentially benefiting from BC supplementation. BC supplementation did not change time to exhaustion at or above CS, maximal oxygen uptake (VO2max), lactate threshold (LT), submaximal running economy (CR), or substrate utilisation during exercise (all p > .05). In conclusion, we could not detect any beneficial effect of BC supplementation during high-intensity running exercise, including the determining factors S-Dtol relationship, VO2max, LT or CR. Hence, no ergogenic effect was observed.

Physical and Physiological Determinants of Rock Climbing.

PURPOSE: Rock climbing performance relies on many characteristics. Herein, the authors identified the physical and physiological determinants of peak performance in rock climbing across the range from lower grade to elite. METHODS: Forty four male and 33 female climbers with onsight maximal climbing grades 5a-8a and 5a-7b+, respectively, were tested for physical, physiological, and psychological characteristics (independent variables) that were correlated and modeled by multiple regression and principal component analysis to identify the determinants of rock climbing ability. RESULTS: In males, 23 of 47 variables correlated with climbing ability (P < .05, Pearson correlation coefficients .773-.340), including shoulder endurance, hand and finger strength, shoulder power endurance, hip flexibility, lower-arm grip strength, shoulder power, upper-arm strength, core-body endurance, upper-body aerobic endurance, hamstrings and lower-back flexibility, aerobic endurance, and open-hand finger strength. In females, 10 of 47 variables correlated with climbing ability (P < .05, Pearson correlation coefficients .742-.482): shoulder endurance and power, lower-arm grip strength, balance, aerobic endurance, and arm span. Principal component analysis and univariate multiple regression identified the main explanatory variables. In both sexes, shoulder power and endurance measured as maximum pull-ups, average arm crank power, and bent-arm hang, emerged as the main determinants (P < .01; adjusted R2 = .77 in males and .62 in females). In males, finger pincer (P = .07) and grip strength also had trends (P = .09) toward significant effects. Finally, in test-of-principle training studies, they trained to increase main determinants 42% to 67%; this improved climbing ability 2 to 3 grades. CONCLUSIONS: Shoulder power and endurance majorly determines maximal climbing. Finger, hand, and arm strength, core-body endurance, aerobic endurance, flexibility, and balance are important secondary determinants.

Intensity-dependence of exercise and active recovery in high-intensity interval training.

BACKGROUND: High-intensity interval training (HIIT) with interspersing active recovery is an effective mode of exercise training in cohorts ranging from athletes to patients. Here, we assessed the intensity-dependence of the intervals and active recovery bouts for permitting a sustainable HIIT protocol. METHODS: Fourteen males completed 4x4-minute HIIT protocols where intensities of intervals ranged 80-100% of maximal oxygen uptake (VO2max) and active recovery ranged 60-100% of lactate (La-) threshold (LT). Blood La- measurements indicated fatigue, while tolerable duration of intervals indicated sustainability. RESULTS: HIIT at 100% of VO2max allowed 44±10% [30-70%] completion, i.e. fatigue occurred after 7minutes:6seconds of the intended 16 minutes of high intensity, whereas HIIT at 95-80% of VO2max was 100% sustainable (P<0.01). Measured intensity did not differ from intended intensity across the protocols (P>0.05). Blood La- concentration [La-] increased to 9.3±1.4mM during HIIT at 100% of VO2max, whereas at 80-95% of VO2max stabilized at 2-6mM in an intensity-dependent manner (P<0.01 vs. 100% of VO2max and P<0.05 vs. baseline). Active recovery at 60-70% of LT during HIIT associated with steady-state blood [La-] peaking at 6-7mM, whereas at 80-100% of LT, blood [La-] accumulated to 10-13mM (P<0.05). After HIIT, active recovery at 80-90% of LT cleared blood [La-] 90% faster than at 60-70% of LT (P<0.05). CONCLUSIONS: To permit highest exercise stress during 4x4-minute HIIT, exercise intensity should be set to 95% of VO2max, whereas active recovery should be set to 60-70% of LT during HIIT and 80-90% of LT after HIIT to most efficiently prevent excess La- and aid recovery.

Human cardiomyocyte calcium handling and transverse tubules in mid-stage of post-myocardial-infarction heart failure.

AIMS: Cellular processes in the heart rely mainly on studies from experimental animal models or explanted hearts from patients with terminal end-stage heart failure (HF). To address this limitation, we provide data on excitation contraction coupling, cardiomyocyte contraction and relaxation, and Ca2+ handling in post-myocardial-infarction (MI) patients at mid-stage of HF. METHODS AND RESULTS: Nine MI patients and eight control patients without MI (non-MI) were included. Biopsies were taken from the left ventricular myocardium and processed for further measurements with epifluorescence and confocal microscopy. Cardiomyocyte function was progressively impaired in MI cardiomyocytes compared with non-MI cardiomyocytes when increasing electrical stimulation towards frequencies that simulate heart rates during physical activity (2 Hz); at 3 Hz, we observed almost total breakdown of function in MI. Concurrently, we observed impaired Ca2+ handling with more spontaneous Ca2+ release events, increased diastolic Ca2+ , lower Ca2+ amplitude, and prolonged time to diastolic Ca2+ removal in MI (P < 0.01). Significantly reduced transverse-tubule density (-35%, P < 0.01) and sarcoplasmic reticulum Ca2+ adenosine triphosphatase 2a (SERCA2a) function (-26%, P < 0.01) in MI cardiomyocytes may explain the findings. Reduced protein phosphorylation of phospholamban (PLB) serine-16 and threonine-17 in MI provides further mechanisms to the reduced function. CONCLUSIONS: Depressed cardiomyocyte contraction and relaxation were associated with impaired intracellular Ca2+ handling due to impaired SERCA2a activity caused by a combination of alteration in the PLB/SERCA2a ratio and chronic dephosphorylation of PLB as well as loss of transverse tubules, which disrupts normal intracellular Ca2+ homeostasis and handling. This is the first study that presents these mechanisms from viable and intact cardiomyocytes isolated from the left ventricle of human hearts at mid-stage of post-MI HF.

Exercise training reverses myocardial dysfunction induced by CaMKIIδC overexpression by restoring Ca2+ homeostasis.

Several conditions of heart disease, including heart failure and diabetic cardiomyopathy, are associated with upregulation of cytosolic Ca(2+)/calmodulin-dependent protein kinase II (CaMKIIδC) activity. In the heart, CaMKIIδC isoform targets several proteins involved in intracellular Ca(2+) homeostasis. We hypothesized that high-intensity endurance training activates mechanisms that enable a rescue of dysfunctional cardiomyocyte Ca(2+) handling and thereby ameliorate cardiac dysfunction despite continuous and chronic elevated levels of CaMKIIδC CaMKIIδC transgenic (TG) and wild-type (WT) mice performed aerobic interval exercise training over 6 wk. Cardiac function was measured by echocardiography in vivo, and cardiomyocyte shortening and intracellular Ca(2+) handling were measured in vitro. TG mice had reduced global cardiac function, cardiomyocyte shortening (47% reduced compared with WT, P < 0.01), and impaired Ca(2+) homeostasis. Despite no change in the chronic elevated levels of CaMKIIδC, exercise improved global cardiac function, restored cardiomyocyte shortening, and reestablished Ca(2+) homeostasis to values not different from WT. The key features to explain restored Ca(2+) homeostasis after exercise training were increased L-type Ca(2+) current density and flux by 79 and 85%, respectively (P < 0.01), increased sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA2a) function by 50% (P < 0.01), and reduced diastolic SR Ca(2+) leak by 73% (P < 0.01), compared with sedentary TG mice. In conclusion, exercise training improves global cardiac function as well as cardiomyocyte function in the presence of a maintained high CaMKII activity. The main mechanisms of exercise-induced improvements in TG CaMKIIδC mice are mediated via increased L-type Ca(2+) channel currents and improved SR Ca(2+) handling by restoration of SERCA2a function in addition to reduced diastolic SR Ca(2+) leak.

Application of the speed-duration relationship to normalize the intensity of high-intensity interval training.

The tolerable duration of continuous high-intensity exercise is determined by the hyperbolic Speed-tolerable duration (S-tLIM) relationship. However, application of the S-tLIM relationship to normalize the intensity of High-Intensity Interval Training (HIIT) has yet to be considered, with this the aim of present study. Subjects completed a ramp-incremental test, and series of 4 constant-speed tests to determine the S-tLIM relationship. A sub-group of subjects (n = 8) then repeated 4 min bouts of exercise at the speeds predicted to induce intolerance at 4 min (WR4), 6 min (WR6) and 8 min (WR8), interspersed with bouts of 4 min recovery, to the point of exercise intolerance (fixed WR HIIT) on different days, with the aim of establishing the work rate that could be sustained for 960 s (i.e. 4×4 min). A sub-group of subjects (n = 6) also completed 4 bouts of exercise interspersed with 4 min recovery, with each bout continued to the point of exercise intolerance (maximal HIIT) to determine the appropriate protocol for maximizing the amount of high-intensity work that can be completed during 4×4 min HIIT. For fixed WR HIIT tLIM of HIIT sessions was 399±81 s for WR4, 892±181 s for WR6 and 1517±346 s for WR8, with total exercise durations all significantly different from each other (P<0.050). For maximal HIIT, there was no difference in tLIM of each of the 4 bouts (Bout 1: 229±27 s; Bout 2: 262±37 s; Bout 3: 235±49 s; Bout 4: 235±53 s; P>0.050). However, there was significantly less high-intensity work completed during bouts 2 (153.5±40. 9 m), 3 (136.9±38.9 m), and 4 (136.7±39.3 m), compared with bout 1 (264.9±58.7 m; P>0.050). These data establish that WR6 provides the appropriate work rate to normalize the intensity of HIIT between subjects. Maximal HIIT provides a protocol which allows the relative contribution of the work rate profile to physiological adaptations to be considered during alternative intensity-matched HIIT protocols.

Subepicardial action potential characteristics are a function of depth and activation sequence in isolated rabbit hearts.

BACKGROUND: Electric excitability in the ventricular wall is influenced by cellular electrophysiology and passive electric properties of the myocardium. Action potential (AP) rise time, an indicator of myocardial excitability, is influenced by conduction pattern and distance from the epicardial surface. This study examined AP rise times and conduction velocity as the depolarizing wavefront approaches the epicardial surface. METHODS AND RESULTS: Two-photon excitation of di-4-aminonaphthenyl-pyridinum-propylsulfonate was used to measure electric activity at discrete epicardial layers of isolated Langendorff-perfused rabbit hearts to a depth of 500 µm. Endo-to-epicardial wavefronts were studied during right atrial or ventricular endocardial pacing. Similar measurements were made with epi-to-endocardial, transverse, and longitudinal pacing protocols. Results were compared with data from a bidomain model of 3-dimensional (3D) electric propagation within ventricular myocardium. During right atrial and endocardial pacing, AP rise time (10%-90% of upstroke) decreased by ≈50% between 500 and 50 µm from the epicardial surface, whereas conduction velocity increased and AP duration was only slightly shorter (≈4%). These differences were not observed with other conduction patterns. The depth-dependent changes in rise time were larger at higher pacing rates. Modeling data qualitatively reproduced the behavior seen experimentally and demonstrated a parallel reduction in peak I(Na) and electrotonic load as the wavefront approaches the epicardial surface. CONCLUSIONS: Decreased electrotonic load at the epicardial surface results in more rapid AP upstrokes and higher conduction velocities compared with the bulk myocardium. Combined effects of tissue depth and pacing rate on AP rise time reduce conduction safety and myocardial excitability within the ventricular wall.

Chronic CaMKII inhibition blunts the cardiac contractile response to exercise training.

Activation of the multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) plays a critical role modulating cardiac function in both health and disease. Here, we determined the effect of chronic CaMKII inhibition during an exercise training program in healthy mice. CaMKII was inhibited by KN-93 injections. Mice were randomized to the following groups: sham sedentary, sham exercise, KN-93 sedentary, and KN-93 exercise. Cardiorespiratory function was evaluated by ergospirometry during treadmill running, echocardiography, and cardiomyocyte fractional shortening and calcium handling. The results revealed that KN-93 alone had no effect on exercise capacity or fractional shortening. In sham animals, exercise training increased maximal oxygen uptake by 8% (p < 0.05) compared to a 22% (p < 0.05) increase after exercise in KN-93 treated mice (group difference p < 0.01). In contrast, in vivo fractional shortening evaluated by echocardiography improved after exercise in sham animals only: from 25 to 32% (p < 0.02). In inactive mice, KN-93 reduced rates of diastolic cardiomyocyte re-lengthening (by 25%, p < 0.05) as well as Ca(2+) transient decay (by 16%, p < 0.05), whereas no such effect was observed after exercise training. KN-93 blunted exercise training response on cardiomyocyte fractional shortening (63% sham vs. 18% KN-93; p < 0.01 and p < 0.05, respectively). These effects could not be solely explained by the Ca(2+) transient amplitude, as KN-93 reduced it by 20% (p < 0.05) and response to exercise training was equal (64% sham and 47% KN-93; both p < 0.01). We concluded that chronic CaMKII inhibition increased time to 50% re-lengthening which were recovered by exercise training, but paradoxically led to a greater increase in maximal oxygen uptake compared to sham mice. Thus, the effect of chronic CaMKII inhibition is multifaceted and of a complex nature.

Exercise training corrects control of spontaneous calcium waves in hearts from myocardial infarction heart failure rats.

Impaired cardiac control of intracellular diastolic Ca(2+) gives rise to arrhythmias. Whereas exercise training corrects abnormal cyclic Ca(2+) handling in heart failure, the effect on diastolic Ca(2+) remains unstudied. Here, we studied the effect of exercise training on the generation and propagation of spontaneous diastolic Ca(2+) waves in failing cardiomyocytes. Post-myocardial infarction heart failure was induced in Sprague-Dawley rats by coronary artery ligation. Echocardiography confirmed left ventricular infarctions of 40 ± 5%, whereas heart failure was indicated by increased left ventricular end-diastolic pressures, decreased contraction-relaxation rates, and pathological hypertrophy. Spontaneous Ca(2+) waves were imaged by laser linescanning confocal microscopy (488 nm excitation/505-530 nm emission) in 2 µM Fluo-3-loaded cardiomyocytes at 37°C and extracellular Ca(2+) of 1.2 and 5.0 mM. These studies showed that spontaneous Ca(2+) wave frequency was higher at 5.0 mM than 1.2 mM extracellular Ca(2+) in all rats, but failing cardiomyocytes generated 50% (P < 0.01) more waves compared to sham-operated controls at Ca(2+) 1.2 and 5.0 mM. Exercise training reduced the frequency of spontaneous waves at both 1.2 and 5.0 mM Ca(2+) (P < 0.05), although complete normalization was not achieved. Exercise training also increased the aborted/completed ratio of waves at 1.2 mM Ca(2+) (P < 0.01), but not 5.0 mM. Finally, we repeated these studies after inhibiting the nitric oxide synthase with L-NAME. No differential effects were found; thus, mediation did not involve the nitric oxide synthase. In conclusion, exercise training improved the cardiomyocyte control of diastolic Ca(2+) by reducing the Ca(2+) wave frequency and by improving the ability to abort spontaneous Ca(2+) waves after their generation, but before cell-wide propagation.

Intrinsic aerobic capacity sets a divide for aging and longevity.

RATIONALE: Low aerobic exercise capacity is a powerful predictor of premature morbidity and mortality for healthy adults as well as those with cardiovascular disease. For aged populations, poor performance on treadmill or extended walking tests indicates closer proximity to future health declines. Together, these findings suggest a fundamental connection between aerobic capacity and longevity. OBJECTIVES: Through artificial selective breeding, we developed an animal model system to prospectively test the association between aerobic exercise capacity and survivability (aerobic hypothesis). METHODS AND RESULTS: Laboratory rats of widely diverse genetic backgrounds (N:NIH stock) were selectively bred for low or high intrinsic (inborn) treadmill running capacity. Cohorts of male and female rats from generations 14, 15, and 17 of selection were followed for survivability and assessed for age-related declines in cardiovascular fitness including maximal oxygen uptake (VO(2max)), myocardial function, endurance performance, and change in body mass. Median lifespan for low exercise capacity rats was 28% to 45% shorter than high capacity rats (hazard ratio, 0.06; P<0.001). VO(2max), measured across adulthood was a reliable predictor of lifespan (P<0.001). During progression from adult to old age, left ventricular myocardial and cardiomyocyte morphology, contractility, and intracellular Ca(2+) handling in both systole and diastole, as well as mean blood pressure, were more compromised in rats bred for low aerobic capacity. Physical activity levels, energy expenditure (Vo(2)), and lean body mass were all better sustained with age in rats bred for high aerobic capacity. CONCLUSIONS: These data obtained from a contrasting heterogeneous model system provide strong evidence that genetic segregation for aerobic exercise capacity can be linked with longevity and are useful for deeper mechanistic exploration of aging.

The effect of exercise training on transverse tubules in normal, remodeled, and reverse remodeled hearts.

The response of transverse (T)-tubules to exercise training in health and disease remains unclear. Therefore, we studied the effect of exercise training on the density and spacing of left ventricle cardiomyocyte T-tubules in normal and remodeled hearts that associate with detubulation, by confocal laser scanning microscopy. First, exercise training in normal rats increased cardiomyocyte volume by 16% (P < 0.01), with preserved T-tubule density. Thus, the T-tubules adapted to the physiologic hypertrophy. Next, we studied T-tubules in a rat model of metabolic syndrome with pressure overload-induced concentric left ventricle hypertrophy, evidenced by 15% (P < 0.01) increased cardiomyocyte size. These rats had only 85% (P < 0.01) of the T-tubule density of control rats. Exercise training further increased cardiomyocyte volume by 8% (P < 0.01); half to that in control rats, but the T-tubule density remained unchanged. Finally, post-myocardial infarction heart failure induced severe cardiac pathology, with a 70% (P < 0.01) increased cardiomyocyte volume that included both eccentric and concentric hypertrophy and 55% (P < 0.01) reduced T-tubule density. Exercise training reversed 50% (P < 0.01) of the pathologic hypertrophy, whereas the T-tubule density increased by 40% (P < 0.05) compared to sedentary heart failure, but remained at 60% of normal hearts (P < 0.01). Physiologic hypertrophy associated with conserved T-tubule spacing (~1.8-1.9 µm), whereas in pathologic hypertrophy, T-tubules appeared disorganized without regular spacing. In conclusion, cardiomyocytes maintain the relative T-tubule density during physiologic hypertrophy and after mild concentric pathologic hypertrophy, whereas after severe pathologic remodeling with a substantial loss of T-tubules; exercise training reverses the remodeling and partly corrects the T-tubule density.

One-arm maximal strength training improves work economy and endurance capacity but not skeletal muscle blood flow.

Maximal strength training with a focus on maximal mobilization of force in the concentric phase improves endurance performance that employs a large muscle mass. However, this has not been studied during work with a small muscle mass, which does not challenge convective oxygen supply. We therefore randomized 23 adult females with no arm-training history to either one-arm maximal strength training or a control group. The training group performed five sets of five repetitions of dynamic arm curls against a near-maximal load, 3 days a week for 8 weeks. This training increased maximal strength by 75% and improved rate of force development during both strength and endurance exercise, suggesting that each arm curl became more efficient. This coincided with a 17-18% reduction in oxygen cost at standardized submaximal workloads (work economy), and a 21% higher peak oxygen uptake and 30% higher peak load during maximal arm endurance exercise. Blood flow assessed by Doppler ultrasound in the axillary artery supplying the working biceps brachii and brachialis muscles could not explain the training-induced adaptations. These data suggest that maximal strength training improved work economy and endurance performance in the skeletal muscle, and that these effects are independent of convective oxygen supply.

Blood lactate clearance during active recovery after an intense running bout depends on the intensity of the active recovery.

High-intensity exercise training contributes to the production and accumulation of blood lactate, which is cleared by active recovery. However, there is no commonly agreed intensity or mode for clearing accumulated blood lactate. We studied clearance of accumulated blood lactate during recovery at various exercise intensities at or below the lactate threshold after high-intensity interval runs that prompted lactate accumulation. Ten males repeated 5-min running bouts at 90% of maximal oxygen uptake (VO(2max)), which increased blood lactate concentration from 1.0 +/- 0.1 to 3.9 +/- 0.3 mmol l(-1). This was followed by recovery exercises ranging from 0 to 100% of lactate threshold. Repeated blood lactate measurements showed faster clearance of lactate during active versus passive recovery, and that the decrease in lactate was more rapid during higher (60-100% of lactate threshold) than lower (0-40% of lactate threshold) (P < 0.05) intensities. The more detailed curve and rate analyses showed that active recovery at 80-100% of lactate threshold had shorter time constants for 67% lactate clearance and higher peak clearance rates than 40% of lactate threshold or passive recovery (P < 0.05). Finally, examination of self-regulated intensities showed enhanced lactate clearance during higher versus lower intensities, further validating the intensity dependence of clearance of accumulated blood lactate. Therefore, active recovery after strenuous exercise clears accumulated blood lactate faster than passive recovery in an intensity-dependent manner. Maximum clearance occurred at active recovery close to the lactate threshold.

High-intensity interval training to maximize cardiac benefits of exercise training?

We hypothesized that high-intensity aerobic interval training results in a greater beneficial adaptation of the heart compared with that observed after low-to-moderate exercise intensity. This is supported by recent epidemiological, experimental, and clinical studies. Cellular and molecular mechanisms of myocardial adaptation to exercise training are discussed in this review.