Heart failure with preserved ejection fraction diminishes peripheral hemodynamics and accelerates exercise-induced neuromuscular fatigue.

This study investigated the impact of HFpEF on neuromuscular fatigue and peripheral hemodynamics during small muscle mass exercise not limited by cardiac output. Eight HFpEF patients (NYHA II-III, ejection-fraction: 61 ± 2%) and eight healthy controls performed dynamic knee extension exercise (80% peak workload) to task failure and maximal intermittent quadriceps contractions (8 × 15 s). Controls repeated knee extension at the same absolute intensity as HFpEF. Leg blood flow (QL) was quantified using Doppler ultrasound. Pre/postexercise changes in quadriceps twitch torque (ΔQtw; peripheral fatigue), voluntary activation (ΔVA; central fatigue), and corticospinal excitability were quantified. At the same relative intensity, HFpEF (24 ± 5 W) and controls (42 ± 6 W) had a similar time-to-task failure (∼10 min), ΔQtw (∼50%), and ΔVA (∼6%). This resulted in a greater exercise-induced change in neuromuscular function per unit work in HFpEF, which was significantly correlated with a slower QL response time. Knee extension exercise at the same absolute intensity resulted in an ∼40% lower QL and greater ΔQtw and ΔVA in HFpEF than in controls. Corticospinal excitability remained unaltered during exercise in both groups. Finally, despite a similar ΔVA, ΔQtw was larger in HFpEF versus controls during isometric exercise. In conclusion, HFpEF patients are characterized by a similar development of central and peripheral fatigue as healthy controls when tested at the same relative intensity during exercise not limited by cardiac output. However, HFpEF patients have a greater susceptibility to neuromuscular fatigue during exercise at a given absolute intensity, and this impairs functional capacity. The patients' compromised QL response to exercise likely accounts, at least partly, for the patients' attenuated fatigue resistance.NEW & NOTEWORTHY The susceptibility to neuromuscular fatigue during exercise is substantially exaggerated in individuals with heart failure with a preserved ejection fraction. The faster rate of fatigue development is associated with the compromised peripheral hemodynamic response characterizing these patients during exercise. Given the role of neuromuscular fatigue as a factor limiting exercise, this impairment likely accounts for a significant portion of the exercise intolerance typical for this population.

Decreases in maximal oxygen uptake following long-duration spaceflight: Role of convective and diffusive O2 transport mechanisms.

We have previously predicted that the decrease in maximal oxygen uptake (V̇o2max) that accompanies time in microgravity reflects decrements in both convective and diffusive O2 transport to the mitochondria of the contracting myocytes. The aim of this investigation was therefore to quantify the relative changes in convective O2 transport (Q̇o2) and O2 diffusing capacity (Do2) following long-duration spaceflight. In nine astronauts, resting hemoglobin concentration ([Hb]), V̇o2max, maximal cardiac output (Q̇Tmax), and differences in arterial and venous O2 contents ([Formula: see text]-[Formula: see text]) were obtained retrospectively for International Space Station Increments 19-33 (April 2009-November 2012). Q̇o2 and Do2 were calculated from these variables via integration of Fick's Principle of Mass Conservation and Fick's Law of Diffusion. V̇o2max significantly decreased from pre- to postflight (-53.9 ± 45.5%, P = 0.008). The significant decrease in Q̇Tmax (-7.8 ± 9.1%, P = 0.05), despite an unchanged [Hb], resulted in a significantly decreased Q̇o2 (-11.4 ± 10.5%, P = 0.02). Do2 significantly decreased from pre- to postflight by -27.5 ± 24.5% (P = 0.04), as did the peak [Formula: see text]-[Formula: see text] (-9.2 ± 7.5%, P = 0.007). With the use of linear regression analysis, changes in V̇o2max were significantly correlated with changes in Do2 (R2 = 0.47; P = 0.04). These data suggest that spaceflight decreases both convective and diffusive O2 transport. These results have practical implications for future long-duration space missions and highlight the need to resolve the specific mechanisms underlying these spaceflight-induced changes along the O2 transport pathway.NEW & NOTEWORTHY Long-duration spaceflight elicited a significant decrease in maximal oxygen uptake. Given the adverse physiological adaptations to microgravity along the O2 transport pathway that have been reported, an integrative approach to the determinants of postflight maximal oxygen uptake is needed. We demonstrate that both convective and diffusive oxygen transport are decreased following ~6 mo International Space Station missions.

Use of electromyography to detect muscle exhaustion in finishing barrows fed ractopamine HCl.

The objectives of this study were to determine the effects of dietary ractopamine HCl (RAC) on muscle fiber characteristics and electromyography (EMG) measures of finishing barrow exhaustion when barrows were subjected to increased levels of activity. Barrows ( = 34; 92 ± 2 kg initial BW) were assigned to 1 of 2 treatments: a conventional swine finishing diet containing 0 mg/kg ractopamine HCl (CON) or a diet formulated to meet the requirements of finishing barrows fed 10 mg/kg RAC (RAC+). After 32 d on feed, barrows were individually moved around a track at 0.79 m/s until subjectively exhausted. Wireless EMG sensors were affixed to the deltoideus (DT), triceps brachii lateral head (TLH), tensor fasciae latae (TFL), and semitendinosus (ST) muscles to measure median power frequency (MdPF) and root mean square (RMS) as indicators of action potential conduction velocity and muscle fiber recruitment, respectively. After harvest, samples of each muscle were collected for fiber type, succinate dehydrogenase (SDH), and capillary density analysis. Speed was not different ( = 0.82) between treatments, but RAC+ barrows reached subjective exhaustion earlier and covered less distance than CON barrows ( < 0.01). There were no treatment × muscle interactions or treatment effects for end-point MdPF values ( > 0.29). There was a treatment × muscle interaction ( = 0.04) for end-point RMS values. The RAC diet did not change end-point RMS values in the DT or TLH ( > 0.37); however, the diet tended to decrease and increase end-point RMS in the ST and TFL, respectively ( < 0.07). There were no treatment × muscle interactions for fiber type, SDH, or capillary density measures ( > 0.10). Muscles of RAC+ barrows tended to have less type I fibers and more capillaries per fiber ( < 0.07). Type I and IIA fibers of RAC+ barrows were larger ( < 0.07). Compared with all other muscles, the ST had more ( < 0.01) type IIB fibers and larger type I, IIA, and IIX fibers ( < 0.01). Type I, IIA, and IIX fibers of the ST also contained less SDH compared with the other muscles ( < 0.01). Barrows fed a RAC diet had increased time to subjective exhaustion due to loss of active muscle fibers in the ST, possibly due to fibers being larger and less oxidative in metabolism. Size increases in type I and IIA fibers with no change in oxidative capacity could also contribute to early exhaustion of RAC+ barrows. Overall, EMG technology can measure real-time muscle fiber loss to help explain subjective exhaustion in barrows.

Discrepancy between femoral and capillary blood flow kinetics during knee extension exercise.

Capillary blood flow (QCAP) kinetics have previously been shown to be significantly slower than femoral artery (QFA) kinetics following the onset of dynamic knee extension exercise. If the increase in QCAP does not follow a similar time course to QFA, then a substantial proportion of the available blood flow is not distributed to the working muscle. One possible explanation for this discrepancy is that blood flow also increases to the nonworking lower leg muscles. Therefore, the present study aimed to determine if a reduction in lower limb blood flow, via arterial occlusion below the knee, alters the kinetics of QFA and QCAP during knee extension exercise, and thus provide insight into the potential mechanisms controlling the rapid increase in QFA. Subjects performed a ramp max test to determine the work rate at which gas exchange threshold (GET) occurred. At least four constant work rate trials with and without below-knee occlusion were conducted at work rates eliciting ∼ 80% GET. Pulmonary gas exchange, near-infrared spectroscopy and QFA measurements were taken continuously during each exercise bout. Muscle oxygen uptake (VO2m) and deoxy[hemoglobin+myoglobin] were used to estimate QCAP. There was no significant difference between the uncuffed and cuffed conditions in any response (P>0.05). The mean response times (MRT) of QFA were 18.7 ± 14.2s (uncuffed) and 24.6 ± 14.9s (cuffed). QCAP MRTs were 51.8 ± 23.4s (uncuffed) and 56.7 ± 23.2s (cuffed), which were not significantly different from the time constants (τ) of VO2m (39.7 ± 23.2s (uncuffed) and 46.3 ± 24.1s (cuffed). However, the MRT of QFA was significantly faster (P<0.05) than the MRT of QCAP and τVO2m. τVO2m and MRT QCAP were significantly correlated and estimated QCAP kinetics tracked VO2m following exercise onset. Cuffing below the knee did not significantly change the kinetics of QFA, QCAP or VO2m, although an effect size of 1.02 suggested that a significant effect on QFA may have been hidden by small subject number.

Influence of blood flow occlusion on the development of peripheral and central fatigue during small muscle mass handgrip exercise.

Critical power represents an important threshold for neuromuscular fatigue development and may, therefore, dictate intensities for which exercise tolerance is determined by the magnitude of fatigue accrued. Peripheral fatigue appears to be constant across O2 delivery conditions for large muscle mass exercise, but this consistency is equivocal for smaller muscle mass exercise. We sought to determine the influence of blood flow occlusion during handgrip exercise on neuromuscular fatigue development and to examine the relationship between neuromuscular fatigue development and W '. Blood flow occlusion influenced the development of both peripheral and central fatigue, thus providing further evidence that the magnitude of peripheral fatigue is not constant across O2 delivery conditions for small muscle mass exercise. W ' appears to be related to the magnitude of fatigue accrued during exercise, which may explain the reported consistency of intramuscular metabolic perturbations and work performed for severe-intensity exercise. The influence of the muscle metabolic milieu on peripheral and central fatigue is currently unclear. Moreover, the relationships between peripheral and central fatigue and the curvature constant (W ') have not been investigated. Six men (age: 25 ± 4 years, body mass: 82 ± 10 kg, height: 179 ± 4 cm) completed four constant power handgrip tests to exhaustion under conditions of control exercise (Con), blood flow occlusion exercise (Occ), Con with 5 min post-exercise blood flow occlusion (Con + Occ), and Occ with 5 min post-exercise blood flow occlusion (Occ + Occ). Neuromuscular fatigue measurements and W ' were obtained for each subject. Each trial resulted in significant peripheral and central fatigue. Significantly greater peripheral (79.7 ± 5.1% vs. 22.7 ± 6.0%) and central (42.6 ± 3.9% vs. 4.9 ± 2.0%) fatigue occurred for Occ than for Con. In addition, significantly greater peripheral (83.0 ± 4.2% vs. 69.0 ± 6.2%) and central (65.5 ± 14.6% vs. 18.6 ± 4.1%) fatigue occurred for Occ + Occ than for Con + Occ. W ' was significantly related to the magnitude of global (r = 0.91) and peripheral (r = 0.83) fatigue. The current findings demonstrate that blood flow occlusion exacerbated the development of both peripheral and central fatigue and that post-exercise blood flow occlusion prevented the recovery of both peripheral and central fatigue. Moreover, the current findings suggest that W ' may be determined by the magnitude of fatigue accrued during exercise.

Influence of blood flow occlusion on muscle oxygenation characteristics and the parameters of the power-duration relationship.

It was previously (Monod H, Scherrer J. Ergonomics 8: 329-338, 1965) postulated that blood flow occlusion during exercise would reduce critical power (CP) to 0 Watts (W), while not altering the curvature constant (W'). We empirically assessed the influence of blood flow occlusion on CP, W', and muscle oxygenation characteristics. Ten healthy men (age: 24.8 ± 2.6 yr; height: 180 ± 5 cm; weight: 84.6 ± 10.1 kg) completed four constant-power handgrip exercise tests during both control blood flow (control) and blood flow occlusion (occlusion) for the determination of the power-duration relationship. Occlusion CP (-0.7 ± 0.4 W) was significantly (P < 0.001) lower than control CP (4.1 ± 0.7 W) and significantly (P < 0.001) lower than 0 W. Occlusion W' (808 ± 155 J) was significantly (P < 0.001) different from control W' (558 ± 129 J), and all 10 subjects demonstrated an increased occlusion W' with a mean increase of ∼49%. The present findings support the aerobic nature of CP. The findings also demonstrate that the amount of work that can be performed above CP is constant for a given condition, but can vary across conditions. Moreover, this amount of work that can be performed above CP does not appear to be the determinant of W', but rather a consequence of the depletion of intramuscular energy stores and/or the accumulation of fatigue-inducing metabolites, which limit exercise tolerance and determine W'.

The relationship between critical speed and the respiratory compensation point: Coincidence or equivalence.

It has previously been suggested that the respiratory compensation point (RCP) and critical speed (CS) parameters are equivalent and, therefore, like CS, RCP demarcates the boundary between the heavy- and severe-intensity domains. However, these findings are equivocal and therefore must be interpreted cautiously. Thus, we examined the relationship between CS and RCP across a wide range of subject fitness levels, in an attempt to determine if CS and RCP are equivalent. Forty men and 30 women (age: 23.2 ± 2.5 year, height: 174 ± 10 cm, body mass: 74.1 ± 15.7 kg) completed an incremental and four constant-speed protocols on a treadmill. RCP was determined as the point at which the minute ventilation increased disproportionately to CO2 production and the end-tidal CO2 partial pressure began to decrease. CS was determined from the constant-speed protocols using the linearized 1·time(-1) model. CS and RCP, expressed as speed or metabolic rate, were not significantly different (11.7 ± 2.3 km·h(-1) vs. 11.5 ± 2.3 km·h(-1), p = 0.208; 2.88 ± 0.80 l·min(-1) vs. 2.83 ± 0.72 l·min(-1), p = 0.293) and were significantly correlated (r(2) = 0.52, p < 0.0001; r(2) = 0.74, p < 0.0001, respectively). However, there was a high degree of variability between the parameters. The findings of the current study indicate that, while on average CS and RCP were not different, the high degree of variability between these parameters does not permit accurate estimation of one from the other variable and suggests that these parameters may not be physiologically equivalent.

Influence of pedal cadence on the respiratory compensation point and its relation to critical power.

It is not known if the respiratory compensation point (RCP) is a distinct work rate (Watts (W)) or metabolic rate V̇(O2) and if the RCP is mechanistically related to critical power (CP). To examine these relationships, 10 collegiate men athletes performed cycling incremental and constant-power tests at 60 and 100 rpm to determine RCP and CP. RCP work rate was significantly (p≤0.05) lower for 100 than 60 rpm (197±24 W vs. 222±24 W), while RCP V̇(O2) was not significantly different (3.00±0.33 l min(-1) vs. 3.12±0.41 l min(-1)). CP at 60 rpm (214±51 W; V̇(O2): 3.01±0.69 l min(-1)) and 100 rpm (196±46 W; V̇(O2): 2.95±0.54 l min(-1)) were not significantly different from RCP. However, RCP and CP were not significantly correlated. These findings demonstrate that RCP represents a distinct metabolic rate, which can be achieved at different power outputs, but that RCP and CP are not equivalent parameters and should not, therefore, be used synonymously.

Relationship between simulated extravehicular activity tasks and measurements of physical performance.

The purpose was to evaluate the relationships between tests of fitness and two activities that simulate components of Lunar- and Martian-based extravehicular activities (EVA). Seventy-one subjects completed two field tests: a physical abilities test and a 10km Walkback test. The relationships between test times and the following parameters were determined: running V˙O2max, gas exchange threshold (GET), speed at V˙O2max (s-V˙O2max), highest sustainable rate of aerobic metabolism [critical speed (CS)], and the finite distance that could be covered above CS (D'): arm cranking V˙O2peak, GET, critical power (CP), and the finite work that can be performed above CP (W'). CS, running V˙O2max, s-V˙O2max, and arm cranking V˙O2peak had the highest correlations with the physical abilities field test (r=0.66-0.82, P<0.001). For the 10km Walkback, CS, s-V˙O2max, and running V˙O2max were significant predictors (r=0.64-0.85, P<0.001). CS and to a lesser extent V˙O2max are most strongly associated with tasks that simulate aspects of EVA performance, highlighting CS as a method for evaluating astronaut physical capacity.

Influence of duty cycle on the power-duration relationship: observations and potential mechanisms.

The highest sustainable rate of aerobic metabolism [critical power (CP)] and the finite amount of work that can be performed above CP (W' [curvature constant]) were determined under two muscle contraction duty cycles. Eight men completed at least three constant-power handgrip tests to exhaustion to determine CP and W' for 50% and 20% duty cycles, while brachial artery blood flow (Q̇BA) and deoxygenated-[hemoglobin + myoglobin] (deoxy-[Hb+Mb]) were measured. CP was lower for the 50% duty cycle (3.9 ± 0.9 W) than the 20% duty cycle (5.1 ± 0.8 W; p < 0.001), while W' was not significantly different (50% duty cycle: 452 ± 141 J vs. 20% duty cycle: 432 ± 130 J; p > 0.05). At the same power output, Q̇BA and deoxy-[Hb + Mb] achieved higher end-exercise values for the 20% duty cycle (9.87 ± 1.73 ml·s(-1); 51.7 ± 4.7 µM) than the 50% duty cycle (7.37 ± 1.76 ml·s(-1), p < 0.001; 44.3 ± 2.4 µM, p < 0.03). These findings indicate that blood flow influences CP, but not W'.

Effects of body posture and exercise training on cardiorespiratory responses to exercise.

The primary aims of the present study were to evaluate cardiorespiratory responses to incremental head down tilt exercise and to determine if the cardiorespiratory adaptations obtained from endurance training in the head down tilt posture transfer to the upright posture. 22 men (25±3 years) performed V˙O2peak cycle exercise tests in the upright and head down tilt postures. Of these, 11 men were endurance trained on a cycle ergometer in the upright posture for 8 weeks (upright training group; UTG) or in the upright posture for 4 weeks followed by 4 weeks in the head down tilt posture (head down training group; HTG). During acute exercise, V˙O2peak was decreased in the head down tilt posture compared to upright (2.01±0.51 vs. 2.32±0.61l/min respectively, P<0.05). Stroke volume (SV) at 100 W was greater during head down tilt cycling compared to the upright (77±5 vs. 71±4 ml/beat, P<0.05). Following training V˙O2peak increased in both groups during upright exercise. However, V˙O2peak during head down tilt cycling was only increased in the HTG. Sub-maximal and peak SV in the HTG increased in both upright and head down tilt postures. SV in the UTG increased only in the upright posture and was unchanged during head down tilt cycling. In conclusion, acute head down tilt exercise increases sub-maximal SV compared to upright exercise. Furthermore, training in the head down tilt posture induces cardiorespiratory adaptations in both upright and head down tilt postures, while the adaptations to upright exercise training are primarily observed when upright exercise was performed.

A single test for the determination of parameters of the speed-time relationship for running.

A validated expeditious method is needed to determine critical speed (CS) and the finite distance that can be covered above CS (D'). We tested the hypothesis that a single all-out 3-min running test would accurately determine CS and D'. Seven healthy subjects completed three constant-speed runs on a treadmill for the determination of CS and D', as well as an all-out 3-min test on a track for the determination of end-test speed (ES) and the distance above end-test speed (DES). ES (13.4 ± 2.8 km h(-1)) was not significantly different from the speed-1/time model CS (13.3 ± 2.8 km h(-1)). While DES (141 ± 34 m) was not significantly different from D' (204 ± 103 m), it underestimated D' in 5 of 7 subjects. Thus, the speed-1/time model CS can be accurately determined using a single 3-min test, while caution should be used in relating DES to D'.

Anterograde and retrograde blood velocity profiles in the intact human cardiovascular system.

Current assessments of the effects of shear patterns on vascular function assume that a parabolic velocity profile is always present. Any substantial deviation in the profile away from this may result in misinterpretation of the importance that shear patterns have on vascular function. The present investigation tested the hypothesis that anterograde and retrograde blood flow would have a parabolic velocity profile at rest, during cold pressor test and exercise. Eight healthy subjects completed a cold pressor test and a graded knee-extension exercise test. Doppler ultrasound was used to determine time-averaged mean velocity (V(mean)) and time-averaged peak velocity (V(peak)) for both anterograde and retrograde flow in the femoral artery (FA) and brachial artery (BA). The V(mean)/V(peak) ratio was used to interpret the shape of the blood velocity profile (parabolic, V(mean)/V(peak) = 0.5; plug-like, V(mean)/V(peak) = 1.0). At rest, BA and FA V(mean)/V(peak) ratios of anterograde and retrograde flow were not significantly different from 0.5. During cold pressor test, anterograde V(mean)/V(peak) in the BA (0.56 ± 0.02) and FA (0.58 ± 0.03) were significantly greater than 0.5. During peak exercise, the V(mean)/V(peak) ratio of anterograde flow in the FA (0.53 ± 0.04) was not significantly different from 0.5. In all conditions, the retrograde V(mean)/V(peak) ratio was lower than anterograde. These data demonstrate that blood flow through two different conduit arteries during two different physiological stressors maintains a velocity profile that resembles a slightly blunted parabolic velocity profile.