Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure

Jacobsen , T. N., Nielsen , H. V., Kassis , E. & Amtorp o S. 1992. Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure. Acta Physiol Scand 144 , 247–252. Received 8 March 1991, accepted 7 Novcmber 1991. ISSN 0001–6772. Department of Cardiology, Gentofte Hospital, University of Copenhagen, Denmark Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [¹³³Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at —10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 ± 2% (mean ± SEM) and in skeletal muscle by 16 ± l%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 ± 3% in subcutaneous tissue and of 30 ± 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.     

Circulatory and respiratory responses to lower body negative pressure in man

Circulatory and ventilatory responses to lower body negative pressure (LBNP) were simultaneously investigated in 8 healthy men before, during, and after the application of -20, -40, and -60 mmHg pressure. Minute ventilation (VE) decreased during LBNP due to a fall in respiratory frequency with sustained tidal volume. The cardiac output (Q) was reduced in proportion to the applied LBNP exposure, while VE decreased to almost the same level at all LBNP applications. In spite of decreased VE, end-tidal PO2 and PCO2 were increased and decreased, respectively, indicating a relative alveolar hyperventilation. The ventilation equivalent for O2 (VE/VO2) increased, while the cardiac output equivalent for O2 (Q/VO2) decreased. The relation between VE/VO2 and Q/VO2 showed a significant negative correlation (r = -0.93, p less than 0.01). The veno-arterial CO2 concentration difference (CvCO2--CaCO2) increased with LBNP, due to a fall in CaCO2 with constant CvCO2. The constant CvCO2 indicated a constant tissue acid-base balance. These observations suggest the existence of a ventilatory mechanism improving the efficiency of respiration in order to compensate for the sustained LBNP depression of Q at a given gas exchange.     

Skeletal muscle vascular responses in human limbs to isometric handgrip

Studies of whole limb blood flow have shown that static handgrip elicits a vasodilatation in the resting forearm and vasoconstriction in the resting leg. We asked if these responses occur in the skeletal muscle vascular bed, and if so, what is the relative contribution of local metabolic versus other mechanisms to these vascular responses. Blood flow recordings were made simultaneously in the skeletal muscle of the resting arm and leg using the Xenon-washout method in ten subjects during 3 min of isometric handgrip at 30% of maximal voluntary contraction. In the arm, skeletal muscle vascular resistance (SMVR) decreased transiently at the onset of exercise followed by a return to baseline levels at the end of exercise. In the leg SMVR remained unchanged during the 1st min of handgrip, but had increased to exceed baseline levels by the end of exercise. During exercise electromyography (EMG) recordings from nonexercising limbs demonstrated a progressive 20-fold increase in activity in the arm, but remained at baseline in the leg. During EMG-signal modelled exercise performed to mimic the inadvertent muscle activity, decreases in forearm SMVR amounted to 57% of the decrease seen with controlateral handgrip. The present study would seem to indicate that vascular tone in nonexercising skeletal muscle in the arm and leg are controlled differently during the early stages of static handgrip. Metabolic vasodilatation due to involuntary contraction could significantly modulate forearm skeletal muscle vascular responses, but other factors, most likely neural vasodilator mechanisms, must make major contributions. During the later stages of contralateral sustained handgrip, vascular adjustments in resting forearm skeletal muscle would seem to be the final result of reflex sympathetic vasoconstrictor drive, local metabolic vasodilator forces and possibly neurogenic vasodilator mechanisms.     

Pharmacological manipulation of cardiovascular responses to lower body negative pressure

To evaluate influences on blood volume distribution, atrial natriuretic peptide concentrations (ANP) and thoracic and leg electrical impedance at 2.5 (TI_2.5 and LI_2.5, respectively) and 100 kHz (TI₁₀₀ and LI₁₀₀, respectively) were monitored during administration of ketanserin, noradrenaline and trimetaphan combined with lower body negative pressure (LBNP) in 12 subjects. Administration of clinically relevant doses of ketanserin alone did not induce changes in mean arterial pressure (MAP) or in the central blood volume, as electrical impedance and ANP concentrations did not change. During continued infusion of ketanserin an increase in MAP from a mean of 90 (range 83–108) to 113 (range 98–138) mmHg was induced by noradrenaline, but TI_2.5 [mean 45.6 (range 39.3–54.2)] and TI₁₀₀ [mean 33.8 (range 27.5–38.5) ] remainded stable until ganglionic blockade and LBNP were applied, when they increased by a mean of 3.1 (range 2.0–6.1) and 2.7 (range 1.1–4.2) , respectively (P < 0.05). Conversely, LI_2.5 [mean 79.6 (range 74.1–89.4)] and LI₁₀₀ [mean 56.7 (range 52.4–63.3) ] decreased by a mean of 3.2 (range 1.2–8.0) and 2.3 (range 0.9–3.9) ANP from a mean of 27.7 (range 10.2–62.7) to 12.7 (range 7.1–27.5) pmol· 1^–1 and MAP fell to a mean of 62 (range 42–70) mmHg (P < 0.05). The heart rate was a mean of 75 (range 69–77) beats -min-' and did not change until LBNP, when it increased to a mean of 102 (range 78–104) beats · min^–1, as presyncopal symptoms appeared. The data indicated that serotonergic blockade by ketanserin and -sympathetic stimulation by noradrenaline did not affect blood volume distribution in normal humans, but that ganglionic blockade combined with LBNP reduced the central blood volume as leg volume increased; during central hypovolaemia tachycardia induced by ganglionic blockade did not prevent the fall in MAP, and thereby the appearance of presyncopal symptoms.     

Cardiac responses to lower body negative pressure and dynamic leg exercise

Summary Cardiac responses to dynamic leg exercise at 0, 50, and 100 W in the supine position were investigated with and without the lower portion of the body exposed to a pressure of –6.6 kPa (Lower Body Negative Pressure, LBNP). Resting values for heart rate (HR) and stroke volume (SV) were considerably higher and lower, respectively, during LBNP than in the control condition. At the transition from rest to the mildest exercise during LBNP SV showed a prompt increase by about 40%, but no significant change in the control condition. HR, which increased by 17 beats · min^–1 in the control condition, showed during LBNP no change initially and subsequently a small but significant drop below its resting value. Steady-state values for HR at the various levels of exercise were not significantly affected by LBNP, whereas corresponding values for SV were considerably lowered, so that exercise values for cardiac output were about 3 l · min^–1 less during LBNP than in the control condition. The reductions in SV and cardiac output indicate residual pooling of blood in intra- and extramuscular capacitance vessels of the legs. With a change from rest to exercise at 100 W during LBNP mean systolic ejection rate (MSER) increased by 67%, the relations between SV and MSER suggesting that ventricular performance was maintained by a combination of the Frank-Starling mechanism and enhanced contractile strength.     

Vasoactive neuroendocrine responses associated with tolerance to lower body negative pressure in humans.

The purpose of this investigation was to test the hypothesis that peripheral vasoconstriction and orthostatic tolerance are associated with increased circulating plasma concentrations of noradrenaline, vasopressin and renin-angiotensin. Sixteen men were categorized as having high (HT, n=9) or low (LT, n=7) tolerance to lower body negative pressure (LBNP) based on whether the endpoint of their pre-syncopal-limited LBNP (peak LBNP) exposure exceeded -60 mmHg. The two groups were matched for age, height, weight, leg volume, blood volume and maximal oxygen uptake, as well as baseline blood volume and plasma concentrations of vasoactive hormones. Peak LBNP induced similar reductions in mean arterial pressure in both groups. The reduction in leg arterial pulse volume (measured by impedance rheography), an index of peripheral vascular constriction, from baseline to peak LBNP was greater (P<0.05) in the HT group (-0.041 +/- 0.005 ml 100 ml-1) compared to the reduction in the LT group (-0. 025 +/- 0.003 ml 100 ml-1). Greater peak LBNP in the HT group was associated with higher (P<0.05) average elevations in plasma concentrations of vasopressin (pVP, Delta=+7.2 +/- 2.0 pg ml-1) and plasma renin-angiotensin (PRA, Delta=+2.9 +/- 1.3 ng Ang II ml-1 h-1) compared to average elevations of pVP (+2.2 +/- 1.0 pg ml-1) and PRA (+0.1 +/- 0.1 ng Ang II ml-1 h-1) in the LT group. Plasma noradrenaline concentrations were increased (P<0.05) from baseline to peak LBNP in both HT and LT groups, with no statistically distinguishable difference between groups. These data suggest that the renin-angiotensin and vasopressin systems may contribute to sustaining arterial pressure and orthostatic tolerance by their vasoconstrictive actions.     

Forearm vascular responses to combined muscle metaboreceptor activation in the upper and lower limbs in humans

Our previous studies showed that venous occlusion or passive stretch of the lower limb, assuming a mechanical stimulus, attenuates the vasoconstriction in the non-exercised forearm during postexercise muscle ischaemia (PEMI) of the upper limb. In this study, we investigated whether a metabolic stimulus to the lower limb induces a similar response. Eight subjects performed a 2 min static handgrip exercise at 30% maximal voluntary contraction (MVC) followed by 3 min PEMI of the upper limb, concomitant with or without 2 min static ankle dorsiflexion at 30% MVC followed by 2 min PEMI of the lower limb. During PEMI of the upper limb alone, forearm blood flow (FBF) and forearm vascular conductance (FVC) in the non-exercised arm decreased significantly, whereas during combined PEMI of the upper and lower limbs, the decreases in FBF and FVC produced by PEMI of the upper limb was attenuated. Forearm blood flow and FVC were significantly greater during combined PEMI of the upper and lower limbs than during PEMI of the upper limb alone. When PEMI of the lower limb was released after combined PEMI of the upper and lower limbs (only PEMI of the upper limb was maintained continuously), the attenuated decreases in FBF and FVC observed during combined PEMI of the upper and lower limbs was not observed. Thus, forearm vascular responses differ when muscle metaboreceptors are activated in the upper limb and when there is combined activation of muscle metaboreceptors in both the upper and lower limbs.     

Effects of resistance training on cardiovascular responses to lower body negative pressure in the elderly.

The purpose of the present study was to determine whether resistance training alters the cardiovascular responses to submaximal lower body negative pressure (LBNP) in the elderly. Twenty-one subjects were randomized into a control (C: n=10; 70 +/- 3 years, mean +/- SD) or a resistance training (TR: n=11; 67 +/- 7 years) group. Subjects in the TR underwent 12 weeks of training consisting of three sets of 8-12 contractions at approximately 60-80% of their initial maximal one repetition, three times per week, on 10 different machines. Before (Pre) and after (Post) training, all subjects underwent exposures of LBNP of -10, -20 and -40 Torr and muscle biopsy sampling at the vastus lateralis. TR increased (P< or =0.05) knee extension (Pre=379 +/- 140 N, Post=534 +/- 182 N) and chest press (Pre=349 +/- 137 N, Post=480 +/- 192 N) strength. Neither body weight nor percentage body fat were altered (P >0.05) by training. Resistance training increased (P< or =0.05) cross-sectional area in both Type I (4203 +/- 1196 to 5248 +/- 1728 microm2) and Type II (3375 +/- 1027 to 4286 +/- 1892 microm2) muscle fibres. Forearm blood flow, forearm vascular conductance, mean arterial pressure, and heart-rate responses to LBNP were not altered by the training. These data suggest that the cardiovascular responses of elderly to LBNP are unaffected by 12 weeks of whole-body resistance training despite increases in muscle strength and size.     

Reproducibility of the heart rate variability responses to graded lower body negative pressure

The reproducibility of heart rate variability (HRV) measures during graded lower body negative pressure (LBNP) have not been studied in sufficient detail. Active college age men (n=14) underwent an orientation exposure and two trials of graded LBNP to presyncope or –100 mmHg, separated by 1 week. Heart rate, stroke volume (impedance cardiography), blood pressure (Finapres), and forearm blood flow were assessed, as was HRV in both time and frequency domains. The trial-to-trial responses to LBNP common to all subjects (LBNP–60 mmHg and at test termination) showed parallel changes, suggesting similar responses between both trials. Good reproducibility estimates were found for the resting HRV data (lowest: R=0.62 for low frequency/high frequency ratio; highest: R=0.94 for standard deviation of normal R-R intervals). During LBNP, reproducibility estimates varied but were generally similar to that seen at rest. At test termination, they were unacceptably low (R<0.41) for the HRV data assessed in the frequency domain and expressed in absolute units. LBNP tolerance was lower in the first trial [LBNP tolerance index: 404 (21) versus 437 (15) mmHg min^–1; P<0.05] but the intraclass correlation coefficient was high (R=0.87). These data suggest that (1) HRV responses to submaximal LBNP up to –60 mmHg are consistent across trials, (2) the considerable variability seen in the HRV parameters at maximal LBNP can be reduced by expressing these data in either the time domain or using normalized units in the frequency domain, and (3) cardiovascular responses to sub- and maximal LBNP are reproducible. Data are presented as mean (SEM) unless otherwise stated.     

Exercise training mode affects the hemodynamic responses to lower body negative pressure in women

To determine if different exercise modes used to improve cardiovascular fitness result in differing cardiovascular responses to lower body negative pressure (LBNP) in exercise-trained women, seven chronically exercising female runners (RUN) and 11 swimmers (SWIM) of similar fitness levels maximal oxygen uptake, [ , mean (SEM) = 50 (2) and 45 (2) ml·kg^–1·min^–1, respectively; P > 0.05] underwent serial exposures to LBNP at pressures of 0, –1.3, –2.7 and –5.3 kPa (referenced to ambient barometric pressure). Forearm vascular resistance (venous occlusion plethysmography) increased with LBNP but did not differ between groups at any level of LBNP. At 0 and –1.3 kPa, the total peripheral resistance index (TPRI; impedance cardiography) was significantly (P < 0.05) higher in RUN than SWIM [1.118 (0.028) vs 0.787 (0.040) at 0 kPa and 1.245 (0.100) vs 0.840 (0.040) kPa·1·min^–1 m^–2 at –1.3 kPa]. At an LBNP of –2.7 kPa, stroke index (SI) was significantly higher in SWIM than RUN [57.8 (4.6) vs 41.9 (4.0) ml·beat^–1 · m^–2] while TPRI remained greater in RUN than SWIM. At –5.3 kPa, SWIM exhibited a higher cardiac index [3.232 (0.209) vs 2.447 (0.189) 1·min^–1·m^–2] and SI [49.4 (4.4) vs 31.0 (4.5) ml·beat^–1·m^–2] but reduced heart rate [71 (3) vs 83 (5)beats·min^–1] and TPRI [0.968 (0.043) vs 1.655 (0.128) kPa·1·min^–1 · m^–2]. Mean arterial pressure declined significantly at an LBNP of –5.3 kPa in both groups; pulse pressure was lower (P < 0.05) in RUN than SWIM at LBNP values of –2.7 and –5.3 kPa. These data suggest that: (1) female runners experience a greater increase in systemic vasoconstriction even though female swimmers can better maintain their cardiac index at high levels of LBNP, and (2) training mode appears to affect the pulse pressure responses to LBNP in exercise-trained women.     

Noise-enhanced heart rate and sympathetic nerve responses to oscillatory lower body negative pressure in humans

By injecting noise into the carotid sinus baroreceptors, we previously showed that heart rate (HR) responses to weak oscillatory tilt were enhanced via a mechanism known as "stochastic resonance." It remains unclear, however, whether the same responses would be observed when using oscillatory lower body negative pressure (LBNP), which would unload the cardiopulmonary baroreceptors with physically negligible effects on the arterial system. Also, the vasomotor sympathetic activity directly controlling peripheral resistance against hypotensive stimuli was not observed. We therefore investigated the effects of weak (0 to approximately -10 mmHg) oscillatory (0.03 Hz) LBNP on HR and muscle sympathetic nerve activity (MSNA) while adding incremental noise to the carotid sinus baroreceptors via a pneumatic neck chamber. The signal-to-noise ratio of HR, cardiac interbeat interval, and total MSNA were all significantly improved by increasing noise intensity, while there was no significant change in the arterial blood pressure in synchronized with the oscillatory LBNP. We conclude that the stochastic resonance, affecting both HR and MSNA, results from the interaction of noise with the signal in the brain stem, where the neuronal inputs from the arterial and cardiopulmonary baroreceptors first come together in the nucleus tractus solitarius. Also, these results indicate that the noise could induce functional improvement in human blood pressure regulatory system in overcoming given hypotensive stimuli.     

Near-infrared spectroscopy provides an index of blood flow and vasoconstriction in calf skeletal muscle during lower body negative pressure

Aim: Near‐infrared spectroscopy (NIRS) has been used previously for forearm blood flow estimation at rest and during exercise. In this study we applied NIRS to selectively monitor deep calf oxygenated haemoglobin (Hb) responses in order to estimate blood flow changes in the calf muscle during lower body negative pressure (LBNP). The purpose of this study was to test the hypothesis that changes in calf skeletal muscle oxygenated‐Hb, after the removal of superficial tissue responses, were related to blood flow changes during orthostatic stress, and to determine the efficacy of using NIRS measurements as an index of vasoconstriction. Methods: Twenty‐nine subjects participated in this study. All attempted a graded LBNP trial from baseline (0 mmHg) to ?60 mmHg LBNP in 10 mmHg steps at 5‐min intervals. Calf blood flow changes were estimated by oxygenated‐Hb responses in relation to changes in mercury strain gauge plethysmography and muscle sympathetic nerve activity (MSNA). Results: Calf selective deep oxygenated‐Hb decreased continuously from ?10 mmHg LBNP. Regression analysis showed that oxygenated‐Hb was significantly related to declines in plethysmography evaluations of blood flow [oxygenated‐Hb = (?1.57 ± 0.26) + (1.86 ± 0.49) plethysmography, r² = 0.87 ± 0.09]. Changes in MSNA (total activity) were also inversely related to oxygenated‐Hb (slope < 0, P = 0.037; r² = 0.52 ± 0.15). Conclusion: These results suggest that changes in selective deep calf oxygenated‐Hb can be utilized to estimate calf muscle blood flow changes that are most likely caused by vasoconstriction during graded LBNP.     

The effects of lower body negative pressure on baroreceptor responses in humans

In healthy human subjects the immediate responses of pulse interval and the steady-state responses of arterial blood pressure and cardiac output to changes in carotid sinus transmural pressure were determined before and during the application of a subatmospheric pressure to the lower part of the body. Increases in carotid sinus transmural pressure, effected by applications of subatmospheric pressure to the neck (neck suction) resulted in prolongation of pulse interval and decrease in blood pressure; opposite responses were obtained to application of a positive pressure (neck pressure). Application of lower body negative pressure resulted in a decrease in pulse interval (heart rate increase) but little change in blood pressure. During lower body negative pressure, the responses of pulse interval to neck pressure were reduced but those to neck suction were unaffected; the responses of blood pressure to neck suction were enhanced but those to neck pressure were unaffected. From experiments in which cardiac output was also determined, it was seen that lower body negative pressure reduced cardiac output, increased calculated total body vascular resistance and augmented the resistance response to neck suction although not to neck pressure. These results are compatible with the view that application of lower body negative pressure does not change the sensitivity of the baroreceptor reflex and that the changes in the responses are due to non-linearities of the stimulus-response curves.     

Haemodynamic responses to nonhypotensive central hypovolaemia induced by lower body negative pressure in men and women

Summary Haemodynamic responses to low levels of lower body negative pressure (LBNP) were investigated in two groups of healthy, normotensive volunteers (8 men and 8 women) during two repeated experimental runs on two occasions, the latter determined by the different phases of the menstrual cycle in the women. The data consisted of systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean blood pressure (MBP), pulse rate (f _c), forearm blood flow (FBF) and forearm vascular conductance (FC). The resting cardiovascular status was similar in men and women, except that women had a significantly higher f _c than men. LBNP (1.3, 2.7 and 4 kPa) had no significant effect on any BP variable or on f _c. However, FBF and FC were reduced at all levels of LBNP. Significant overshoots in FBF and FC were seen in all subjects following the release of LBNP of 2.7 and 4 kPa and, in most cases, after release of LBNP of 1.3 kPa. There were no significant gender differences in any of the responses to LBNP. Furthermore, none of the cardiovascular variables measured showed significant differences between the follicular and luteal phases of the menstrual cycle in women, either at rest or during exposure to LBNP, and the responses in the men on the two occasions were not different. These findings indicate that gender differences in responses to LBNP hypothesized previously are not apparent during and after exposure to low levels of LBNP.     

Regulation of arterial blood pressure in humans during isometric muscle contraction and lower body negative pressure

Previous studies have shown that the blood pressure response to isometric handgrip remains unchanged during reductions in preload induced by lower body negative pressure (LBNP). The purpose of the present study was to assess the beat-by-beat haemodynamic mechanisms allowing for precise control of mean arterial pressure (MAP). We have followed the cardiovascular variables involved in the regulation of MAP during isometric handgrip with and without additional application of LBNP during defined periods of the ongoing contraction. Sixteen subjects participated. Mean arterial blood pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO), blood flow velocity in the brachial artery, acral skin blood flow, as well as total (TPR) and local (LPR) peripheral resistance were continuously recorded/calculated before, during and after 2 min of handgrip both with and without concomitant LBNP. The main finding was that MAP increased at the same rate and to the same absolute level whether or not LBNP was applied. A uniform increase in MAP was observed even though the cardiovascular variables evolved differently in the periods with and without LBNP. At the onset of LBNP at –20 mmHg, there was a transient drop in MAP and a transient increase in HR, but within seconds, MAP was regulated back to the slope caused by the isometric handgrip proper. CO and SV, which were declining gradually, showed an additional marked but gradual reduction upon LBNP application. At the same time, both LPR and TPR increased markedly and continuously. In summary, the increase in MAP during isometric handgrip remained essentially unchanged by LBNP-induced alterations in preload. The increase in MAP was caused by a marked increase in peripheral resistance. This supports the concept of a central set point, continuously regulated upwards as long as the isometric handgrip persists. Furthermore, it reveals a considerable flexibility in the cardiovascular control mechanisms used to achieve the desired arterial pressure.     

Adaptive responses of human skeletal muscle to vibration exposure.

The aim of this study was to investigate the effects of whole-body vibrations (WBV) on the mechanical behaviour of human skeletal muscle. For this purpose, six female volleyball players at national level were recruited voluntarily. They were tested with maximal dynamic leg press exercise on a slide machine with extra loads of 70, 90, 110 and 130 kg. After the testing, one leg was randomly assigned to the control treatment (C) and the other to the experimental treatment (E) consisting of vibrations. The subjects were then retested at the end of the treatment using the leg press. Results showed remarkable and statistically significant enhancement of the experimental treatment in average velocity (AV), average force (AF) and average power (AP) (P < 0.05-0.005). Consequently, the velocity-force and power-force relationship shifted to the right after the treatment. In conclusion, it was affirmed that the enhancement could be caused by neural factors, as athletes were well accustomed to the leg press exercise and the learning effect was minimized.     

Hemodynamic and hormonal responses to lower body negative pressure in men with varying profiles of strength and aerobic power

Hemodynamic, cardiac, and hormonal responses to lower-body negative pressure (LBNP) were examined in 24 healthy men to test the hypothesis that responsiveness of reflex control of blood pressure during orthostatic challenge is associated with interactions between strength and aerobic power. Subjects underwent treadmill tests to determine peak oxygen uptake ( O_2max) and isokinetic dynamometer tests to determine knee extensor strength. Based on predetermined criteria, subjects were classified into one of four fitness profiles of six subjects each, matched for age, height, and body mass: (a) low strength/average aerobic fitness, (b) low strength/high aerobic fitness, (c) high strength/average aerobic fitness, and (d) high strength/high aerobic fitness. Following 90 min of 0.11 rad (6°) head-down tilt (HDT), each subject underwent graded LBNP to –6.7 kPa or presyncope, with maximal duration 15 min, while hemodynamic, cardiac, and hormonal responses were measured. All groups exhibited typical hemodynamic, hormonal, and fluid shift responses during LBNP, with no intergroup differences between high and low strength characteristics. Subjects with high aerobic power exhibited greater (P < 0.05) stroke volume and lower (P < 0.05) heart rate, vascular peripheral resistance, and mean arterial pressure during rest, HDT, and LBNP. Seven subjects, distributed among the four fitness profiles, became presyncopal. These subjects showed greatest reduction in mean arterial pressure during LBNP, had greater elevations in vasopressin, and lesser increases in heart rate and peripheral resistance. Neither O_2max nor leg strength were associated with fall in arterial pressure or with syncopal episodes. We conclude that interactions between aerobic and strength fitness characteristics do not influence responses to LBNP challenge.     

Synaptic connections from large muscle afferents to motoneurones in human lower limbs

OBJECTIVES: Our study was undertaken to investigate reciprocal inhibition in humans both from ankle flexors to extensors and from ankle extensors to flexors. METHODES: Changes in the firing probability of single motor units in response to electrical stimulation of muscle nerves (the peristimulus time histogram technique) were used to derive the reciprocal projections of muscle spindle Ia afferents to the motoneurones of ankle muscles. Discharges of units in ankle flexors (the tibialis anterior muscle [TA]) and extensors (soleus [SOL] and medial gastrocnemius [MG] muscles) were investigated respectively after stimulation of the posterior tibial (PTN) and common peroneal (CPN) nerves (predominantly on the deep branch). In eight normal subjects aged 24 to 40 years, one motor unit per each muscle was studied. RESULTS: CPN stimulation produced reciprocal Ia inhibition in the SOL of 5 of 7 of them and in the MG of 3 of 5, whereas PTN stimulation produced reciprocal Ia inhibition in the TA of only 2 of 6 subjects. CONCLUSIONS: These findings suggest that at low level contraction reciprocal Ia inhibition from ankle flexors to extensors may be stronger than that from ankle extensors to flexors.