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Introduction: Despite knowledge of cardiorespiratory fitness (CRF) training responders and nonresponders, it is not well understood how the exercise intensity prescription affects the incidence of response. The purpose of this study was to determine CRF training responsiveness based on cohort-specific technical error after 12 wk of standardized or individually prescribed exercise and the use of a verification protocol to confirm maximal oxygen uptake (V˙O2max)., Methods: Sedentary adult participants (9 men, 30 women; 48.2 ± 12.2 yr) completed exercise training on 3 d·wk for 12 wk, with exercise intensity prescribed based on standardized methods using heart rate reserve or an individualized approach using ventilatory thresholds. A verification protocol was used at baseline and 12 wk to confirm the identification of a true V˙O2max and subsequent relative percent changes to quantify CRF training responsiveness. A cohort-specific technical error (4.7%) was used as a threshold to identify incidence of response., Results: Relative V˙O2max significantly increased (P < 0.05) from 24.3 ± 4.6 to 26.0 ± 4.2 and 29.2 ± 7.5 to 32.8 ± 8.6 mL·kg·min for the standardized and individualized groups, respectively. Absolute V˙O2max significantly increased (P < 0.05) from 2.0 ± 0.6 to 2.2 ± 0.6 and 2.4 ± 0.8 to 2.6 ± 0.9 L·min for the standardized and individualized groups, respectively. A significant difference in responsiveness was found between the individualized and standardized groups with 100% and 60% of participants categorized as responders, respectively., Conclusions: A threshold model for exercise intensity prescription had a greater effect on the incidence of CRF training response compared with a standardized approach using heart rate reserve. The use of thresholds for intensity markers accounts for individual metabolic characteristics and should be considered as a viable and practical method to prescribe exercise intensity.

Purpose: The purpose of this study was to investigate the role of the group III/IV muscle afferents in the bioenergetics of exercising skeletal muscle beyond constraining the magnitude of metabolic perturbation., Methods: Eight healthy men performed intermittent isometric knee-extensor exercise to task failure at ~58% maximal voluntary contraction under control conditions (CTRL) and with lumbar intrathecal fentanyl to attenuate group III/IV leg muscle afferents (FENT). Intramuscular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), diprotonated phosphate (H2PO4), adenosine triphosphate (ATP), and pH were determined using phosphorous magnetic resonance spectroscopy (P-MRS)., Results: The magnitude of metabolic perturbation was significantly greater in FENT compared with CTRL for [Pi] (37.8 ± 16.8 vs 28.6 ± 8.6 mM), [H2PO4] (24.3 ± 12.2 vs 17.9 ± 7.1 mM), and [ATP] (75.8% ± 17.5% vs 81.9% ± 15.8% of baseline), whereas there was no significant difference in [PCr] (4.5 ± 2.4 vs 4.4 ± 2.3 mM) or pH (6.51 ± 0.10 vs 6.54 ± 0.14). The rate of perturbation in [PCr], [Pi], [H2PO4], and pH was significantly faster in FENT compared with CTRL. Oxidative ATP synthesis was not significantly different between conditions. However, anaerobic ATP synthesis, through augmented creatine kinase and glycolysis reactions, was significantly greater in FENT than in CTRL, resulting in a significantly greater ATP cost of contraction (0.049 ± 0.016 vs 0.038 ± 0.010 mM·min·N)., Conclusion: Group III/IV muscle afferents not only constrain the magnitude of perturbation in intramuscular Pi, H2PO4, and ATP during small muscle mass exercise but also seem to play a role in maintaining efficient skeletal muscle contractile function in men.

Background: In patients with left ventricular systolic dysfunction (LVSD), the rate at which oxygen uptake (VO2) increases on initiation of exercise is inadequate to match metabolic demands. To gain mechanistic insights into delayed VO2 kinetics in LVSD, we simultaneously assessed hemodynamic measurements, ventilatory parameters, and peripheral oxygen usage during exercise., Methods and Results: Forty-two patients with symptomatic LVSD (age, 59±2 years [mean±SEM]; LV ejection fraction, 30±1%) and 17 controls (LV ejection fraction, 68±1%) underwent maximum upright cycle ergometry cardiopulmonary exercise testing. Hemodynamic monitoring and first-pass radionuclide ventriculography were performed at rest and during exercise. VO2 kinetics were quantified by mean response time (MRT), which was significantly longer in patients with LVSD compared with controls (64±3 versus 45±5 s; P=0.004). In LVSD patients, MRT was associated with higher biventricular filling pressures and reduced cardiac output during early exercise. LVSD patients with MRT ≥60 s, compared with LVSD subjects with MRT <60 s, demonstrated greater impairment in right ventricular-pulmonary vascular function during exercise as evidenced by lower right ventricular ejection fraction (35±2 versus 45±2%; P=0.03), steeper increment in transpulmonary gradient relative to cardiac output (3.7 versus 2.2 mm Hg/L; P<0.001), and increased ventilatory dead-space fraction (17±1 versus 12±2%; P=0.03). In contrast, MRT was not associated with LV ejection fraction (rest, exercise), PaO2, hemoglobin, or resting pulmonary function test results., Conclusions: Delayed oxygen uptake on initiation of exercise (ie, MRT ≥60 s) in LVSD is closely related to impaired right ventricular-pulmonary vascular function and may represent an important surrogate for inability to augment RV performance during physical activity in patients with heart failure.

The sympathetic and pressor responses to exercise are exaggerated in hypertension. Evidence suggests that an overactive exercise pressor reflex (EPR) contributes to this abnormal responsiveness. The mechanisms underlying this EPR overactivity are poorly understood. An increasing body of evidence suggests that aldosterone and excessive salt intake play a role in regulating resting sympathetic activity and blood pressure in hypertension. Therefore, each is a good candidate for the generation of EPR dysfunction in this disease. The purpose of this study was to examine whether excessive salt intake and chronic administration of aldosterone potentiate EPR function. Changes in mean arterial pressure and renal sympathetic nerve activity induced by EPR stimulation were examined in vehicle and aldosteronetreated (4 weeks via osmotic mini-pump) Sprague-Dawley rats given either water or saline (elevated salt load) to drink. When compared with vehicle/water-treated rats, stimulation of the EPR by muscle contraction evoked significantly greater increases in mean arterial pressure in vehicle/saline, aldosterone/water, and aldosterone/saline-treated animals (14±3, 29±3, 37±6, and 44±7 mm Hg/kg, respectively; P<0.01). A similar renal sympathetic nerve activity response profile was likewise produced (39±11%, 87±15%, 110±20%, and 151±25%/kg, respectively; P<0.01). The pressor and sympathetic responses to the individual activation of the mechanically and chemically sensitive components of the EPR were also augmented by both saline and aldosterone. These data provide the first direct evidence that both aldosterone and high salt intake elicit EPR overactivity. As such, each represents a potential mechanism by which sympathetic activity and blood pressure are augmented during exercise in hypertension. [ABSTRACT FROM AUTHOR]

Exposure to a microgravity environment decreases the maximal rate of O2 uptake (...O2max) in healthy individuals returning to a gravitational environment. The magnitude of this decrease in ...O2max is, in part, dependent on the duration of microgravity exposure, such that long exposure may result in up to a 38% decrease in ...O2max. This review identifies the components within the O2 transport pathway that determine the decrease in postmicrogravity ...O2max and highlights the potential contributing physiological mechanisms. A retrospective analysis revealed that the decline in ...O2max is initially mediated by a decrease in convective and diffusive O2 transport that occurs as the duration of microgravity exposure is extended. Mechanistically, the attenuation of O2 transport is the combined result of a deconditioning across multiple organ systems including decreases in total blood volume, red blood cell mass, cardiac function and mass, vascular function, skeletal muscle mass, and, potentially, capillary hemodynamics, which become evident during exercise upon re-exposure to the head-to-foot gravitational forces of upright posture on Earth. In summary, ...O2max is determined by the integration of central and peripheral O2 transport mechanisms, which, if not maintained during microgravity, will have a substantial long-term detrimental impact on space mission performance and astronaut health. [ABSTRACT FROM AUTHOR]

Background—Exercise oscillatory ventilation (EOV) is a noninvasive parameter that potently predicts outcomes in systolic heart failure (HF). However, mechanistic insights into EOV have been limited by the absence of studies relating EOV to invasive hemodynamic measurements and blood gases performed during exercise. Methods and Results—Fifty-six patients with systolic HF (mean±SEM age, 59±2 years; left ventricular ejection fraction, 30±1%) and 19 age-matched control subjects were studied with incremental cardiopulmonary exercise testing. Fick cardiac outputs, filling pressures, and arterial blood gases were measured at 1-minute intervals during exercise. We detected EOV in 45% of HF (HF+EOV) patients and in none of the control subjects. The HF+EOV group did not differ from the HF patients without EOV (HF-EOV) in age, sex, body mass index, left ventricular ejection fraction, or origin of HF. Univariate predictors of the presence of EOV in HF, among measurements performed during exercise, included higher right atrial pressure and pulmonary capillary wedge pressure and lower cardiac index (CI) but not Paco2 or Pao2. Multivariate logistic regression identified that low exercise CI is the strongest predictor of EOV (odds ratio, 1.39 for each 1.0-L · min-1 · m-2 decrement in CI; 95% confidence interval, 1.14-1.70; P=0.001). Among HF patients with EOV, exercise CI was inversely related to EOV cycle length (R=-0.71) and amplitude (R=-0.60; both P<0.001). In 11 HF+EOV subjects treated with 12 weeks of sildenafil, EOV cycle length and amplitude decreased proportionately to increases in CI. Conclusion—Exercise oscillatory ventilation is closely related to reduced CI and elevated filling pressures during exercise and may be an important surrogate for exercise-induced hemodynamic impairment in HF patients. [ABSTRACT FROM AUTHOR]

The article presents a study which characterized pulmonary arterial pressure (PAP) response patterns to exercise in left ventricular systolic dysfunction (LVSD). The study involved 19 controls and 60 LVSD patients who underwent maximum incremental cardiopulmonary exercise testing with simultaneous hemodynamic monitoring. Results revealed that related to decreased exercise capacity and survival in patients with LVSD was the discovery of a steep increment in PAP during exercise and the failure to augment PAP throughout the exercise.