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.

Effects of malate, lactate, and pyruvate on myoglobin redox stability in homogenates of three bovine muscles.

We investigated the effects of glycolytic and tricarboxylic acid cycle metabolic intermediates on myoglobin redox forms and meat colour stability. Eighteen combinations of malate (M), lactate (L), and pyruvate (P) were added to beef Longissimus lumborum, Psoas major, and Semitendinosus muscle homogenates to study their effect on metmyoglobin formation during incubation at 25 degrees C. Changes in surface colour at 0, 2, 4, 8, and 12 h were evaluated by using reflecto-spectrophotometry [both L*, a*, and b* and wavelengths specific for metmyoglobin (MMb)]. Addition of M, L, and P alone or in combinations stabilized (P < 0.05) L*, a*, and b* values and myoglobin redox forms in muscle homogenates; however, there was a trend for P to be least effective. At the 2% concentrations for the individual metabolites, L was most effective at retarding MMb formation in the Semitendinosus (M was intermediate and P was least effective), and M was most effective in the Psoas major and L. lumborum muscles (L was intermediate and P was least effective). Metmyoglobin was reduced most effectively with a combination of metabolites (M + L > M + P > L + P). Enhancing meat with these metabolites can effectively extend colour life of post-rigor meat, apparently by providing more reducing conditions for myoglobin, thus increasing myoglobin redox form stability.

Effects of fibre orientation, myoglobin redox form, and postmortem storage on NIR tissue oximeter measurements of beef longissimus muscle.

To determine near-infrared tissue oximeter responses to muscle fibre orientation, display time, and surface colour differences of beef longissimus lumborum steaks, beef loins were cut into steaks either perpendicular or parallel to the muscle fibre orientation. Surface colour differences were created by packaging steaks in vacuum (VAC), 80% O(2) and 20% CO(2) modified atmosphere packaging (HiOx MAP), polyvinyl chloride film overwrap (PVC), and HiOx MAP converted to PVC (HiOx-PVC) after 2days. Changes in surface colour and subsurface pigments during display (0, 2, 4, 10, and 15days at 2 degrees C) were characterized by using a reflectance-spectrophotometer and a near-infrared tissue oximeter, respectively. Fibre orientation, storage, and packaging affected (P<0.05) colour, total pigment, deoxymyoglobin, and oxymyoglobin content. Tissue oximetry measurements appear to have potential for real-time monitoring of myoglobin redox forms and oxygen status of packaged meat, but fibre orientation needs to be controlled.

Oxygen uptake kinetics during supra VO2max treadmill running in humans.

Accurate classification of VO2 kinetics is essential to correctly interpret its control mechanisms. The purpose of this study was to examine VO2 kinetics in severe and supra-maximal intensity running exercise using two modelling techniques. Nine subjects (mean +/- S.D: age, 27 +/- 7 years; mass, 69.8 +/- 9.0 kg; VO2max, 59.1 +/- 1.8 mL x kg x min(-1)) performed a series of "square-wave" exercise transitions to exhaustion at running speeds equivalent to 80% of the difference between the VO2 at LT and VO2max (delta), and at 100%, 110% and 120% VO2max. The VO2 response was modelled with an exponential model and with a semi-logarithmic transformation, the latter assuming a certain steady state VO2. With the exponential model there was a significant reduction in the "gain" of the primary component in supra-maximal exercise (167 +/- 5 mL x kg(-1) x km(-1) at 80% delta to 142 +/- 5 mL x kg(-1) x km(-1) at 120% VO2max, p = 0.005). The time constant of the primary component also reduced significantly with increasing intensity (17.8 +/- 1.1 s at 80% delta to 12.5 +/- 1.2 s at 120% VO2max, p < 0.05). However, in contrast, using the semi-log model, the time constant significantly increased with intensity (30.9 +/- 13.5 s at 80% delta to 72.2 +/- 23.9 s at 120% VO2max, p < 0.05). Not withstanding the need for careful interpretation of mathematically modelled data, these results demonstrate that neither the gain nor the time constant of the VO2 primary component during treadmill running are invariant across the severe and supra-maximal exercise intensity domains when fit with an exponential model. This suggests the need for a reappraisal of the VO2/work rate relationship in running exercise.

Dynamics of microvascular oxygen partial pressure in contracting skeletal muscle of rats with chronic heart failure.

OBJECTIVE: This investigation tested the hypothesis that the dynamics of muscle microvascular O(2) pressure (PO(2)m, which reflects the ratio of O(2) utilization [V*O(2)] to O(2) delivery [Q*O(2)]) following the onset of contractions would be altered in chronic heart failure (CHF). METHODS: Female Sprague-Dawley rats were subjected to a myocardial infarction (MI) or a sham operation (Sham). Six to 10 weeks post Sham (n=6) or MI (n=17), phosphorescence quenching techniques were utilized to determine PO(2)m dynamics at the onset of spinotrapezius muscle contractions (1 Hz). RESULTS: MI rats were separated into groups with Moderate (n=10) and Severe (n=7) CHF based upon the degree of left ventricular (LV) dysfunction as indicated by structural abnormalities (increased right ventricle weight and lung weight normalized to body weight). LV end-diastolic pressure was elevated significantly in both CHF groups compared with Sham (Sham, 3+/-1; Moderate CHF, 9+/-2; Severe CHF, 27+/-4 mmHg, P<0.05). The PO(2)m response was modeled using time delay and exponential components to fit the PO(2)m response to the steady-state. Compared with Shams, the time constant (tau) of the primary PO(2)m response was significantly speeded in Moderate CHF (tau, Sham, 19.0+/-1.5; Moderate CHF, 13.2+/-1.9 s, P<0.05) and slowed in Severe CHF (tau, 28.2+/-3.4 s, P<0.05). Within the Severe CHF group, tau increased linearly with the product of right ventricular and lung weight (r=0.83, P<0.05). CONCLUSIONS: These results suggest that CHF alters the dynamic matching of muscle V*O(2)-to-Q*O(2) across the transition from rest to contractions and that the nature of that perturbation is dependent upon the severity of cardiac dysfunction.

Effect of contraction frequency on leg blood flow during knee extension exercise in humans.

Previous studies in isolated muscle preparations have shown that muscle blood flow becomes compromised at higher contraction frequencies. The purpose of this study was to examine the effect of increases in contraction frequency and muscle tension on mean blood flow (MBF) during voluntary exercise in humans. Nine male subjects [23.6 +/- 3.7 (SD) yr] performed incremental knee extension exercise to exhaustion in the supine position at three contraction frequencies [40, 60, and 80 contractions/min (cpm)]. Mean blood velocity of the femoral artery was determined beat by beat using Doppler ultrasound. MBF was calculated by using the diameter of the femoral artery determined at rest using echo Doppler ultrasound. The work rate (WR) achieved at exhaustion was decreased (P < 0.05) as contraction frequency increased (40 cpm, 16.2 +/- 1.4 W; 60 cpm, 14.8 +/- 1.4 W; 80 cpm, 13.2 +/- 1.3 W). MBF was similar across the contraction frequencies at rest and during the first WR stage but was higher (P < 0.05) at 40 than 80 cpm at exercise intensities >5 W. MBF was similar among contraction frequencies at exhaustion. In humans performing knee extension exercise in the supine position, muscle contraction frequency and/or muscle tension development may appreciably affect both the MBF and the amplitude of the contraction-to-contraction oscillations in muscle blood flow.

Effect of muscle mass on V(O(2)) kinetics at the onset of work.

The dependence of O(2) uptake (V(O(2))) kinetics on the muscle mass recruited under conditions when fiber and muscle recruitment patterns are similar following the onset of exercise has not been determined. We developed a motorized cycle ergometer that facilitated one-leg (1L) cycling in which the electromyographic (EMG) profile of the active muscles was not discernibly altered from that during two-leg (2L) cycling. Six subjects performed 1L and 2L exercise transitions from unloaded cycling to moderate [VT) exercise. The 1L condition yielded kinetics that was unchanged from the 2L condition [the phase 2 time constants (tau(1), in s) for 0.05; for >VT: 1L = 26.8 +/- 12.0; 2L = 27.8 +/- 16.1, P > 0.05]. The overall V(O(2)) kinetics (mean response time) was not significantly different for the two exercise conditions. However, the gain of the fast component (the amplitude/work rate) during the 1L exercise was significantly higher than that for the 2L exercise for both moderate and heavy work rates. The slow-component responses evident for heavy exercise were temporally and quantitatively unaffected by the 1L condition. These data demonstrate that, when leg muscle recruitment patterns are unchanged as assessed by EMG analysis, on-transient V(O(2)) kinetics for both moderate and heavy exercise are not dependent on the muscle mass recruited.

The slow component of O(2) uptake is not accompanied by changes in muscle EMG during repeated bouts of heavy exercise in humans.

1. We hypothesized that either the recruitment of additional muscle motor units and/or the progressive recruitment of less efficient fast-twitch muscle fibres was the predominant contributor to the additional oxygen uptake (VO2) observed during heavy exercise. Using surface electromyographic (EMG) techniques, we compared the VO2 response with the integrated EMG (iEMG) and mean power frequency (MPF) response of the vastus lateralis with the VO2 response during repeated bouts of moderate (below the lactate threshold, < LT) and heavy (above the lactate threshold, > LT) intensity cycle ergometer exercise. 2. Seven male subjects (age 29 +/- 7 years, mean +/- S.D.) performed three transitions to a work rate (WR) corresponding to 90 % LT and two transitions to a work rate that would elicit a VO2 corresponding to 50 % of the difference between peak VO2 and the LT (i.e. Delta50 %, > LT1 and > LT2). 3. The VO2 slow component was significantly reduced by prior heavy intensity exercise (> LT1, 410 +/- 196 ml min(-1); > LT2, 230 +/- 191 ml min-1). The time constant (tau), amplitude (A) and gain (DeltaVO2/DeltaWR) of the primary VO2 response (phase II) were not affected by prior heavy exercise when a three-component, exponential model was used to describe the V2 response. 4. Integrated EMG and MPF remained relatively constant and at the same level throughout both > LT1 and > LT2 exercise and therefore were not associated with the VO2 slow component. 5. These data are consistent with the view that the increased O2 cost (i.e. VO2 slow component) associated with performing heavy exercise is coupled with a progressive increase in ATP requirements of the already recruited motor units rather than to changes in the recruitment pattern of slow versus fast-twitch motor units. Further, the lack of speeding of the kinetics of the primary VO2 component with prior heavy exercise, thought to represent the initial muscle VO2 response, are inconsistent with O2 delivery being the limiting factor in V > O2 kinetics during heavy exercise.

Effect of endurance training on oxygen uptake kinetics during treadmill running.

The purpose of this study was to examine the effect of endurance training on oxygen uptake (VO(2)) kinetics during moderate [below the lactate threshold (LT)] and heavy (above LT) treadmill running. Twenty-three healthy physical education students undertook 6 wk of endurance training that involved continuous and interval running training 3-5 days per week for 20-30 min per session. Before and after the training program, the subjects performed an incremental treadmill test to exhaustion for determination of the LT and the VO(2 max) and a series of 6-min square-wave transitions from rest to running speeds calculated to require 80% of the LT and 50% of the difference between LT and maximal VO(2). The training program caused small (3-4%) but significant increases in LT and maximal VO(2) (P<0.05). The VO(2) kinetics for moderate exercise were not significantly affected by training. For heavy exercise, the time constant and amplitude of the fast component were not significantly affected by training, but the amplitude of the VO(2) slow component was significantly reduced from 321+/-32 to 217+/-23 ml/min (P<0.05). The reduction in the slow component was not significantly correlated to the reduction in blood lactate concentration (r = 0. 39). Although the reduction in the slow component was significantly related to the reduction in minute ventilation (r = 0.46; P<0.05), it was calculated that only 9-14% of the slow component could be attributed to the change in minute ventilation. We conclude that the VO(2) slow component during treadmill running can be attenuated with a short-term program of endurance running training.