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Quantitating exercise ventilatory and gas exchange dynamics affords insights into physiological control processes and cardiopulmonary dysfunction. We designed a novel waveform, the chirp waveform, to efficiently extract moderate-intensity exercise response dynamics. In the chirp waveform, work rate fluctuates sinusoidally with constant amplitude as sinusoidal period decreases progressively from ∼8.5 to 1.4 min over 30 min of cycle ergometry. We hypothesized that response dynamics of pulmonary ventilation (V̇ e) and gas exchange [oxygen uptake (V̇ o 2) and carbon dioxide output (V̇ co 2)] extracted from chirp waveform are similar to those obtained from stepwise transitions. Thirty-one participants [14 young healthy, 7 older healthy, and 10 patients with chronic obstructive pulmonary disease (COPD)] exercised on three occasions. Participants first performed ramp-incremental exercise for gas exchange threshold (GET) determination. In randomized order, the next two visits involved either chirp or stepwise waveforms. Work rate amplitude (20 W to ∼95% GET work rate) and exercise duration (30 min) were the same for both waveforms. A first-order linear transfer function with a single system gain (G) and time constant (τ) characterized response dynamics. Agreement between model parameters extracted from chirp and stepwise waveforms was established using Bland–Altman analysis and Rothery's concordance coefficient (RCC). V̇ e , V̇ o 2, and V̇ co 2Gs showed no systematic bias (P > 0.178) and moderate-to-good agreement (RCC > 0.772, P < 0.01) between waveforms. Similarly, no systematic bias (P = 0.815) and good agreement (RCC = 0.837, P < 0.001) was found for τV̇ o 2. Despite moderate agreement for τV̇ co 2 (RCC = 0.794, P < 0.001) and τV̇ e (RCC = 0.722, P = 0.083), chirp τ was less [−6.9(11.7) s and −12.2(22.5) s, respectively]. We conclude that the chirp waveform is a promising method for measuring exercise response dynamics and investigating physiological control mechanisms. NEW & NOTEWORTHY: We investigated the ability of a novel waveform to extract exercise ventilatory and gas exchange dynamics. In the chirp waveform, work rate fluctuates sinusoidally with constant amplitude as sinusoidal period decreases progressively over 30 min of exercise. In a study of 31 healthy individuals and patients with COPD, comparison of exercise dynamics derived from chirp to those from stepwise waveforms suggests that the chirp waveform is a promising method for derivation of exercise response dynamics. [ABSTRACT FROM AUTHOR]

This study compared cardiovascular and metabolic responses during concentric and eccentric stepping. Eight participants (5 m, 3f; 22 ± 2 years) performed maximal concentric and eccentric ramp incremental tests on a modified stepping ergometer. Subsequently, three randomized 15‐min constant‐power tests were performed (1) concentric stepping at 90% of the concentric lactate threshold (LT), (2) eccentric stepping at the same power, and (3) eccentric stepping at the same oxygen uptake (V̇O2). At equivalent power (36 ± 6 W, p = 0.62), eccentric stepping resulted in 46 ± 8% lower V̇O2, 16 ± 6% lower heart rate (HR), and 11 ± 5% lower mean arterial blood pressure compared to concentric (p < 0.01). Matching V̇O2 required 65 ± 19% more power during eccentric stepping (p < 0.01). During this test, eccentric V̇O2 and HR continued to increase, resulting in a 22 ± 29% higher V̇O2 and 19 ± 16% higher HR in the final minute (p < 0.001). Reduced cardiorespiratory demand during eccentric stepping at the same power as concentric demonstrates a higher eccentric power is required to produce the same V̇O2. However, despite being below the concentric LT, eccentric V̇O2 and HR continued to increase past the predicted steady state, indicating a higher exercise intensity. [ABSTRACT FROM AUTHOR]

Objectives: Fatigue is a prominent feature of long COVID (LC) and may be related to several pathophysiologic mechanisms, including immune hyperstimulation. Aerobic endurance exercise training may be a useful therapy, with appropriate attention to preventing post-exertional malaise. Methods: Fourteen participants completed a pilot study of aerobic exercise training (twenty 1.5 h sessions of over 10 weeks). Cardiorespiratory fitness, 6 min walk distance, quality of life, symptoms, 7-day physical activity, immunophenotype, and inflammatory biomarkers were measured before and after exercise training. Results: The participant characteristics at baseline were as follows: 53.5 ± 11.6 yrs, 53% f, BMI 32.5 ± 8.4, 42% ex-smokers, 15.1 ± 8.8 months since initial COVID-19 infection, low normal pulmonary function testing, V. O2peak 19.3 ± 5.1 mL/kg/min, 87 ± 17% predicted. After exercise training, participants significantly increased their peak work rate (+16 ± 20 W, p = 0.010) and V. O2peak (+1.55 ± 2.4 mL/kg/min, p = 0.030). Patients reported improvements in fatigue severity (−11%), depression (−42%), anxiety (−29%), and dyspnea level (−46%). There were no changes in 6MW distance or physical activity. The circulating number of CD3+, CD4+, CD19+, CD14++CD16, and CD16++CD14+ monocytes and CD56+ cells (assessed with flow cytometry) increased with acute exercise (rest to peak) and was not diminished or augmented by exercise training. Plasma concentrations of TNF-α, IL-6, IL-8, IL-10, INF-γ, and INF-λ were normal at study entry and not affected by training. Conclusions: Aerobic endurance exercise training in individuals with LC delivered beneficial effects on cardiorespiratory fitness, quality of life, anxiety, depression, and fatigue without detrimental effects on immunologic function. [ABSTRACT FROM AUTHOR]

We investigated the effect of exercise intensity and tolerable duration on the development of exercise-induced diaphragm and expiratory muscle fatigue. Ten healthy adults (25 ± 5 yr; 2 females) cycled to intolerance on three separate occasions: 1) 5% below critical power (tw) and gastric (Pgatw) twitch pressures, respectively. Exercise time was 34.5 ± 6.2 min, 10.2 ± 2.6 min, and 4.9 ± 0.7 min for 2) at end-exercise was lower during 2peak) relative to Δ25 (97 ± 4% V̇ o 2peak) and Δ50 (99 ± 4% V̇ o 2peak) (P < 0.001). The pre- to postexercise decrease in Pditw was greater after Δ25 (−22 ± 12%) versus tw from pre- to postexercise was not different between trials ( 0.05). In conclusion, the magnitude of exercise-induced diaphragm fatigue was greater after longer-duration severe exercise than after shorter-duration severe and heavy exercise. By contrast, the magnitude of exercise-induced expiratory muscle fatigue was unaffected by exercise intensity and tolerable duration. NEW & NOTEWORTHY: Exercise-induced respiratory muscle fatigue contributes to limiting exercise tolerance. Accordingly, better understanding the exercise conditions under which respiratory muscle fatigue occurs is warranted. Although heavy-intensity as well as short- and long-duration severe-intensity exercise performed to intolerance elicit diaphragm and expiratory muscle fatigue, we find, for the first time, that the relationship between exercise intensity, exercise duration, and the magnitude of exercise-induced fatigue is different for the diaphragm compared with the expiratory muscles. [ABSTRACT FROM AUTHOR]

Identification of the breathing cycle forms the basis of any breath-by-breath gas exchange analysis. Classically, the breathing cycle is defined as the time interval between the beginning of two consecutive inspiration phases. Based on this definition, several research groups have developed algorithms designed to estimate the volume and rate of gas transferred across the alveolar membrane ("alveolar gas exchange"); however, most algorithms require measurement of lung volume at the beginning of the ith breath (VLi-1; i.e., the end-expiratory lung volume of the preceding i th breath). The main limitation of these algorithms is that direct measurement of VLi-1 is challenging and often unavailable. Two solutions avoid the requirement to measure VLi-1 by redefining the breathing cycle. One method defines the breathing cycle as the time between two equal fractional concentrations of lung expired oxygen (FO2) (or carbon dioxide; FCO2), typically in the alveolar phase, whereas the other uses the time between equal values of the FO2/FN2 (or FCO2/FN2) ratios [i.e., the ratio of fractional concentrations of lung expired O2 (or CO2) and nitrogen (N2)]. Thus, these methods identify the breathing cycle by analyzing the gas fraction traces rather than the gas flow signal. In this review, we define the traditional approach and two alternative definitions of the human breathing cycle and present the rationale for redefining this term. We also explore the strengths and limitations of the available approaches and provide implications for future studies. [ABSTRACT FROM AUTHOR]

BACKGROUND: Supplemental oxygen is designed to raise alveolar PO2 to facilitate diffusion into arterial blood. Oxygen is generally delivered by nasal cannula either by continuous or pulsatile flow. Battery-powered portable oxygen concentrators (POCs) facilitate ambulation in patients experiencing exertional hypoxemia. In the United States, the Food and Drug Administration (FDA) clears these devices to be sold by physician prescription. Recently, however, lower-cost devices described as POCs have been advertised by online retailers. These devices lack FDA clearance and are obtained over the counter (OTC) without prescription. This study determined whether a selected group of OTC POCs have oxygen delivery characteristics suitable for use by hypoxemic patients. METHODS: A metabolic simulator, capable of simulating a range of metabolic rates and minute ventilations, determined effects of oxygen supplementation delivered by a variety of devices on alveolar PO2. Devices tested included 3 OTC POCs, an FDA-cleared POC, and continuous-flow oxygen from a compressed oxygen cylinder. End-tidal PETO2, a surrogate of alveolar PO2, was determined at each of each device's flow settings at 3 metabolic rates. RESULTS: Continuous-flow tank oxygen yielded a linear PETO2 increase as flow increased, with progressively lower slope of increase for higher metabolic rate. The prescription POC device yielded similar PETO2 elevations, though with somewhat smaller elevations in pulse-dose operation. One OTC POC was only technically portable (no on-board battery); it provided only modest PETO2 elevation that failed to increase as flow setting was incremented. A second OTC POC produced only minimal PETO2 elevation. A third OTC POC, a pulsed-dose device, produced meaningful PETO2 increases, though not as great as the prescription device. CONCLUSIONS: Only one of 3 OTC POCs tested was potentially of use by patients requiring ambulatory oxygen. Physicians and respiratory therapists should inform patients requiring portable oxygen that OTC devices may not meet their oxygenation requirements. [ABSTRACT FROM AUTHOR]

This document is a reply to a letter from Drs. Francescato and Cettolo regarding a recent review on cardiopulmonary exercise testing (CPET). The authors clarify that their review does not support relating volumes computed using one definition of the breathing cycle to gas tensions measured using a different definition, as this would lead to misinterpretation of key CPET variables. Instead, the review emphasizes the physiological implications of using different definitions of the breathing cycle and suggests investigating an approach to identify an equivalent value for pulmonary ventilation. The authors also highlight the broader implications of different definitions on respiratory measurements in various fields, such as ventilator management and the diagnosis and treatment of certain conditions. They acknowledge the need for further research to understand the impact of alternative definitions on CPET interpretation. The document concludes by stating that while alternative breathing cycle definitions may enrich the information provided by gas exchange measurement, their applications remain limited due to a lack of comprehensive data. The authors disclose their funding sources and potential conflicts of interest. [Extracted from the article]

Augmented breaths promote respiratory instability and have been implicated in triggering periods of sleep-disordered breathing. Since respiratory instability is well known to be exacerbated by hypocapnia, we asked whether one of the destabilizing effects of hypocapnia might be related to an increased prevalence of augmented breaths. With this question in mind, we first sought to determine whether hypoxiainduced augmented breaths are more prevalent when hypocapnia is also present. To do this, we studied the breath-by-breath ventilatory responses of a group of freely behaving adult rats in a variety of different respiratory background conditions. We found that the prevalence of augmented breaths was dramatically increased during hypocapnic-hypoxia compared with room air conditions. When hypocapnia was prevented during exposure to hypoxia by adding 5% C[O.sub.2] to the inspired air, the rate of occurrence of augmented breaths was no greater than that observed in room air. The addition of C[O.sub.2] alone to room air had no effect on the prevalence of augmented breaths. We conclude that in spontaneously breathing rats, hypoxia promotes the generation of augmented breaths, but only in poikilocapnic conditions, where hypocapnia develops. Our results, therefore, reveal a means by which C[O.sub.2] exerts a stabilizing influence on breathing, which may be of particular relevance during sleep in conditions commonly associated with respiratory instability. sighs; carbon dioxide; hypocapnia; respiratory instability

Background: Menopause represents a turning point where vascular damage begins to outweigh reparative processes, leading to increased cardiovascular disease (CVD) risk. Exercise training reduces CVD risk in postmenopausal females via improvements in traditional risk factors and direct changes to the vasculature. We assessed the effect of moderate (MODERATE‐IT) versus heavy (HEAVY‐IT) intensity interval exercise training upon markers of cardiovascular health and vascular repair in postmenopausal females. Methods: Twenty‐seven healthy postmenopausal females (56 ± 4 yr) were assigned to 12 weeks of either MODERATE‐IT or HEAVY‐IT, twice per week. MODERATE‐IT consisted of 10s work, and 10s active recovery repeated for 30 min. HEAVY‐IT comprised 30s work, and 30s active recovery repeated for 21 ± 2 min. Endothelial function (flow‐mediated dilation), arterial stiffness (pulse wave velocity), and V̇O2peak were assessed pre‐training and post‐training. Blood samples were obtained pre‐training and post‐training for enumeration of circulating angiogenic cells (CACs), culture of CACs, and lipoprotein profile. Results: V̇O2peak increased 2.4 ± 2.8 ml/kg/min following HEAVY‐IT only (p < 0.05). Brachial blood pressure and endothelial function were unchanged with exercise training (p > 0.05). Peripheral pulse wave velocity reduced 8% with exercise training, irrespective of intensity (p < 0.05). Exercise training had no effect on lipoprotein profile or endothelin‐1 (p > 0.05). CAC adhesion to vascular smooth muscle cells (VSMC) increased 30 min post plating following MODERATE‐IT only (p < 0.05). Conclusions: HEAVY‐IT was more effective at increasing V̇O2peak in postmenopausal females. The ability of CACs to adhere to VSMC improved following MODERATE‐IT but not HEAVY‐IT. Interval training had the same effect on endothelial function (no change) and arterial stiffness (reduced), regardless of exercise intensity. [ABSTRACT FROM AUTHOR]

We hypothesize that the V˙O2 time constant (τV˙O2) determines exercise tolerance by defining the power output associated with a "critical threshold" of intramuscular metabolite accumulation (e.g., inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V˙O2 "slow component" and its consequences (increased pulmonary, circulatory, and neuromuscular demands) determine performance limits. [ABSTRACT FROM AUTHOR]

Aims: Heart failure with reduced ejection fraction (HFrEF) induces skeletal muscle mitochondrial abnormalities that contribute to exercise limitation; however, specific mitochondrial therapeutic targets remain poorly established. This study quantified the relationship and contribution of distinct mitochondrial respiratory states to prognostic whole‐body measures of exercise limitation in HFrEF. Methods and results: Male patients with HFrEF (n = 22) were prospectively enrolled and underwent ramp‐incremental cycle ergometry cardiopulmonary exercise testing to determine exercise variables including peak pulmonary oxygen uptake (V̇O2peak), lactate threshold (V̇O2LT), the ventilatory equivalent for carbon dioxide (V̇E/V̇CO2LT), peak circulatory power (CircPpeak), and peak oxygen pulse. Pectoralis major was biopsied for assessment of in situ mitochondrial respiration. All mitochondrial states including complexes I, II, and IV and electron transport system (ETS) capacity correlated with V̇O2peak (r = 0.40–0.64; P < 0.05), V̇O2LT (r = 0.52–0.72; P < 0.05), and CircPpeak (r = 0.42–0.60; P < 0.05). Multiple regression analysis revealed that combining age, haemoglobin, and left ventricular ejection fraction with ETS capacity could explain 52% of the variability in V̇O2peak and 80% of the variability in V̇O2LT, respectively, with ETS capacity (P = 0.04) and complex I (P = 0.01) the only significant contributors in the model. Conclusions: Mitochondrial respiratory states from skeletal muscle biopsies of patients with HFrEF were independently correlated to established non‐invasive prognostic cycle ergometry cardiopulmonary exercise testing indices including V̇O2peak, V̇O2LT, and CircPpeak. When combined with baseline patient characteristics, over 50% of the variability in V̇O2peak could be explained by the mitochondrial ETS capacity. These data provide optimized mitochondrial targets that may attenuate exercise limitations in HFrEF. [ABSTRACT FROM AUTHOR]

In 11 healthy adults (25 ± 4 yr; 2 female, 9 male subjects), we investigated the effect of expiratory resistive loaded breathing [65% maximal expiratory mouth pressure (MEP), 15 breaths·min−1, duty cycle 0.5; ERLPm] on mean arterial pressure (MAP), leg vascular resistance (LVR), and leg blood flow (Q̇L). On a separate day, a subset of five male subjects performed ERL targeting 65% of maximal expiratory gastric pressure (ERLPga). ERL-induced expiratory muscle fatigue was confirmed by a 17 ± 5% reduction in MEP (P < 0.05) and a 16 ± 12% reduction in the gastric twitch pressure response to magnetic nerve stimulation (P = 0.09) from before to after ERLPm and ERLPga, respectively. From rest to task failure in ERLPm and ERLPga, MAP increased (ERLPm = 31 ± 10 mmHg, ERLPga = 18 ± 9 mmHg, both P < 0.05), but group mean LVR and Q̇L were unchanged (ERLPm: LVR = 0.78 ± 0.21 vs. 0.97 ± 0.36 mmHg·mL−1·min, Q̇L = 133 ± 34 vs. 152 ± 74 mL·min−1; ERLPga: LVR = 0.70 ± 0.21 vs. 0.84 ± 0.33 mmHg·mL−1·min, Q̇L = 160 ± 48 vs. 179 ± 110 mL·min−1) (all P ≥ 0.05). Interestingly, Q̇L during ERLPga oscillated within each breath, increasing (∼66%) and decreasing (∼50%) relative to resting values during resisted expirations and unresisted inspirations, respectively. In conclusion, fatiguing expiratory muscle work did not affect group mean LVR or Q̇L in otherwise resting humans. We speculate that any sympathetically mediated peripheral vasoconstriction was counteracted by transient mechanical effects of high intra-abdominal pressures during ERL. NEW & NOTEWORTHY Fatiguing expiratory muscle work in otherwise resting humans elicits an increase in sympathetic motor outflow; whether limb blood flow (Q̇L) and leg vascular resistance (LVR) are affected remains unknown. We found that fatiguing expiratory resistive loaded breathing (ERL) did not affect group mean Q̇L or LVR. However, within-breath oscillations in Q̇L may reflect a sympathetically mediated vasoconstriction that was counteracted by transient increases in Q̇L due to the mechanical effects of high intra-abdominal pressure during ERL. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The asymptote of the hyperbolic power-duration relationship, critical power (CP), demarcates sustainable from non-sustainable exercise. CP is a salient parameter within the theoretical framework determining exercise tolerance. However, measuring CP is time consuming – typically 4 constant-power exercise tests to intolerance, or a 3-min all-out sprint is required. To determine whether 30 s of maximal isokinetic cycling, immediately following the limit of tolerance, approximates CP. Fifteen participants (7 women, 8 men, 23±5 yr, 71±12 kg, V̇O2peak 4.39±1.04 L·min−1 ; 61±9 mL·kg·min−1) completed 4 constant supra-CP exercise tests to intolerance. Each test was followed immediately by a 30 s maximal isokinetic effort at 80 rpm. Mean isokinetic power was compared to the known CP. Mean±SD CP was 159±47 W (CI95 133, 185 W). Maximal isokinetic power immediately following intolerance was greater (p< 0.05) than CP in all but one comparison (181±51 vs. 159±47 W; p> 0.07). However, this closest estimation, following the longest duration constant-power test, resulted in 21 W of mean bias and wide limits of agreement (±84 W). Isokinetic power measured immediately following intolerance consistently overestimated critical power. Thus, an adjunct of 30 s maximal isokinetic cycling immediately following the limit of tolerance does not approximate critical power. [ABSTRACT FROM AUTHOR]

The article discusses a study on patients with chronic obstructive pulmonary disease (COPD) and the differentiation between critical power (CP) and the respiratory compensation point (RCP) during exercise tests, emphasizing that despite some physiological similarities.

Phase 2 pulmonary oxygen uptake kinetics (ϕ2 τV̇o2P) reflect muscle oxygen consumption dynamics and are sensitive to changes in state of training or health. This study identified an unbiased method for data collection, handling, and fitting to optimize V̇o2P kinetics estimation. A validated computational model of V̇o2P kinetics and a Monte Carlo approach simulated 2 × 105 moderate-intensity transitions using a distribution of metabolic and circulatory parameters spanning normal health. Effects of averaging (interpolation, binning, stacking, or separate fitting of up to 10 transitions) and fitting procedures (biexponential fitting, or ϕ2 isolation by time removal, statistical, or derivative methods followed by monoexponential fitting) on accuracy and precision of V̇o2P kinetics estimation were assessed. The optimal strategy to maximize accuracy and precision of τV̇o2P estimation was 1-s interpolation of 4 bouts, ensemble averaged, with the first 20 s of exercise data removed. Contradictory to previous advice, we found optimal fitting procedures removed no more than 20 s of ϕ1 data. Averaging method was less critical: interpolation, binning, and stacking gave similar results, each with greater accuracy compared with analyzing repeated bouts separately. The optimal procedure resulted in ϕ2 τV̇o2P estimates for transitions from an unloaded or loaded baseline that averaged 1.97 ± 2.08 and 1.04 ± 2.30 s from true, but were within 2 s of true in only 47–62% of simulations. Optimized 95% confidence intervals for τV̇o2P ranged from 4.08 to 4.51 s, suggesting a minimally important difference of ~5 s to determine significant changes in τV̇o2P during interventional and comparative studies. NEW & NOTEWORTHY We identified an unbiased method to maximize accuracy and precision of oxygen uptake kinetics (τV̇o2P) estimation. The optimum number of bouts to average was four; interpolation, bin, and stacking averaging methods gave similar results. Contradictory to previous advice, we found that optimal fitting procedures removed no more than 20 s of phase 1 data. Our data suggest a minimally important difference of ~5 s to determine significant changes in τV̇o2P during interventional and comparative studies. [ABSTRACT FROM AUTHOR]

Background--Cardiac remodeling occurs in response to regular athletic training, and the degree of remodeling is associated with fitness. Understanding the myocardial structural changes in athlete's heart is important to develop tools that differentiate athletic from cardiomyopathic change. We hypothesized that athletic left ventricular hypertrophy is a consequence of increased myocardial cellular rather than extracellular mass as measured by cardiovascular magnetic resonance. Methods and Results--Forty-five males (30 athletes and 15 sedentary age-matched healthy controls) underwent comprehensive cardiovascular magnetic resonance studies, including native and postcontrast T1 mapping for extracellular volume calculation. In addition, the 30 athletes performed a maximal exercise test to assess aerobic capacity and anaerobic threshold. Participants were grouped by athleticism: untrained, low performance, and high performance (VO2max <60 or>60 mL/kg per min, respectively). In athletes, indexed cellular mass was greater in high- than low-performance athletes 60.7±7.5 versus 48.6±6.3 g/m²; P<0.001), whereas extracellular mass was constant (16.3±2.2 versus 15.3±2.2 g/m²; P=0.20). Indexed left ventricular end-diastolic volume and mass correlated with VO2max (r=0.45, P=0.01; r=0.55, P=0.002) and differed significantly by group (P=0.01; P<0.001, respectively). Extracellular volume had an inverse correlation with VO2max (r=-0.53, P=0.003 and left ventricular mass index (r=-0.44, P=0.02). Conclusions--Increasing left ventricular mass in athlete's heart occurs because of an expansion of the cellular compartment while the extracellular volume becomes relatively smaller: a difference which becomes more marked as left ventricular mass increases. Athletic remodeling, both on a macroscopic and cellular level, is associated with the degree of an individual's fitness. Cardiovascular magnetic resonance ECV quantification may have a future role in differentiating athlete's heart from change secondary to cardiomyopathy. [ABSTRACT FROM AUTHOR]

During whole body exercise in health, maximal oxygen uptake (VO2max) is typically attained at or immediately before the limit of tolerance (LoT). At the VO2max and LoT of incremental exercise, a fundamental, but unresolved, question is whether maximal evocable power can be increased above the task requirement, i.e., whether there is a "power reserve" at the LoT. Using an instantaneous switch from cadence-independent (hyperbolic) to isokinetic cycle ergometry, we determined maximal evocable power at the limit of ramp-incremental exercise. We hypothesized that in endurance-trained men at LoT, maximal (4 s) isokinetic power would not differ from the power required by the task. Baseline isokinetic power at 80 rpm (Piso; measured at the pedals) and summed integrated EMG from five leg muscles (ΣEMG) were measured in 12 endurance-trained men (VO2max = 4.2 ± 1.0 l/min). Participants then completed a ramp incremental exercise test (20-25 W/min), with instantaneous measurement of Piso and ΣiEMG at the LoT. Piso decreased from 788 ± 103 W at baseline to 391 ± 72 W at LoT, which was not different from the required ramp-incremental flywheel power (352 ± 58 W; P > 0.05). At LoT, the relative reduction in Piso was greater than the relative reduction in the isokinetic ΣiEMG (50 ± 9 vs. 63 ± 10% of baseline; P < 0.05). During maximal ramp incremental exercise in endurance-trained men, maximum voluntary power is not different from the power required by the task and is consequent to both central and peripheral limitations in evocable power. The absence of a power reserve suggests both the perceptual and physiological limits of maximum voluntary power production are not widely dissociated at LoT in this population. [ABSTRACT FROM AUTHOR]