Middle cerebral artery blood velocity and plasma catecholamines during exercise

During dynamic exercise, mean blood velocity (V_mean) in the middle cerebral artery (MCA) demonstrates a graded increase to work rate and reflects regional cerebral blood flow. At a high work rate, however, vasoactive levels of plasma catecholamines could mediate vasoconstriction of the MCA and thereby elevate V_mean at a given volume flow. To evaluate transcranial Doppler-determined V_mean at high plasma catecholamine levels, seven elite cyclists performed a maximal performance test on a bicycle ergometer. Results were compared with those elicited during five incremental exercise bouts and during rhythmic handgrip when plasma catecholamines are low. During rhythmic handgrip the V_mean was elevated by 21±3% (mean±SE), which was not statistically different from that established during moderate cycling. However, at the highest submaximal and maximal work intensities on the bicycle ergometer, V_mean increased by 31±3% and 48±4%, respectively, and this was significantly higher compared to handgrip (P<0.05). During maximal cycling, plasma adrenaline increased from 0.21±0.04 nmol L^-1 at rest to 4.18±1.46 nmol L^-1, and noradrenaline increased from 0.79±0.08 to 12.70±1.79 nmol L^-1. These levels were 12- to 16-fold higher than those during rhythmic handgrip (adrenaline: 0.34±0.03 nmol L^-1; noradrenaline: 0.78±0.05 nmol L^-1). The increase in V_mean during intense ergometer cycling conforms to some middle cerebral artery constriction elicited by plasma catecholamines. Such an influence is unlikely during rhythmic handgrip compared with low intensity cycling.     

Middle cerebral artery blood velocity during exercise with β‐1 adrenergic and unilateral stellate ganglion blockade in humans

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V_mean) is attenuated during cycling with β‐1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocain; 8 mL; n=8) affects the attenuated exercise – MCA V_mean following cardio‐selective β‐1 adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V_mean were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V_mean increased to the same extent (11.4 ± 1.9 vs. 11.1 ± 1.9 cm s^?1). With the pharmacological intervention the exercise CO (10 ± 1 vs. 12 ± 1 L min^?1; n=5), HR (115 ± 4 vs. 134 ± 4 beats min^?1) and ΔMCA V_mean (8.7 ± 2.2 vs. 11.4 ± 1.9 cm s^?1) were reduced, and MAP was increased (100 ± 5 vs. 86 ± 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the β‐1 blockade induced attenuation in ΔMCA V_mean (10.2 ± 2.5 cm s^?1). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.     

Enhanced cerebral CO2 reactivity during strenuous exercise in man

Light and moderate exercise elevates the regional cerebral blood flow by ~20% as determined by ultrasound Doppler sonography (middle cerebral artery mean flow velocity; MCA V _mean). However, strenuous exercise, especially in the heat, appears to reduce MCA V _mean more than can be accounted for by the reduction in the arterial CO₂ tension (P _aCO₂). This study evaluated whether the apparently large reduction in MCA V _mean at the end of exhaustive exercise relates to an enhanced cerebrovascular CO₂ reactivity. The CO₂ reactivity was evaluated in six young healthy male subjects by the administration of CO₂ as well as by voluntary hypo- and hyperventilation at rest and during exercise with and without hyperthermia. At rest, P _aCO₂ was 5.1±0.2 kPa (mean ± SEM) and MCA V _mean 50.7±3.8 cm s⁻¹ and the relationship between MCA V _mean and P _aCO₂ was linear (double-log slope 1.1±0.1). However, the relationship became curvilinear during exercise (slope 1.8±0.1; P<0.01 vs. rest) and during exercise with hyperthermia (slope 2.3±0.3; P<0.05 vs. control exercise). Accordingly, the cerebral CO₂ reactivity increased from 30.5±2.7% kPa⁻¹ at rest to 61.4±10.1% kPa⁻¹ during exercise with hyperthermia (P<0.05). At exhaustion P _aCO₂ decreased 1.1±0.2 kPa during exercise with hyperthermia, which, with the determined cerebral CO₂ reactivity, accounted for the 28±10% decrease in MCA V _mean. The results suggest that during exercise changes in cerebral blood flow are dominated by the arterial carbon dioxide tension.     

Influence of upper body position on middle cerebral artery blood velocity during continuous positive airway pressure breathing

Continuous positive airway pressure (CPAP) is a treatment modality for pulmonary oxygenation difficulties. CPAP impairs venous return to the heart and, in turn, affects cerebral blood flow (CBF) and augments cerebral blood volume (CBV). We considered that during CPAP, elevation of the upper body would prevent a rise in CBV, while orthostasis would challenge CBF. To determine the body position least affecting indices of CBF and CBV, the middle cerebral artery mean blood velocity (MCA V _mean) and the near-infrared spectroscopy determined frontal cerebral hemoglobin content (cHbT) were evaluated in 11 healthy subjects during CPAP at different body positions (15° head-down tilt, supine, 15°, 30° and 45° upper body elevation). In the supine position, 10 cmH₂O of CPAP reduced MCA V _mean by 9 ± 3% and increased cHbT by 4 ± 2 μmol/L (mean ± SEM); (P < 0.05). In the head-down position, CPAP increased cHbT to 13 ± 2 μmol/L but left MCA V _mean unchanged. Upper body elevation by 15° attenuated the CPAP associated reduction in MCA V _mean (−7 ± 2%), while cHbT returned to baseline (1 ± 2 μmol/L). With larger elevation of the upper body MCA V _mean decreased progressively to −17 ± 3%, while cHbT remained unchanged from baseline. These results suggest that upper body elevation by ∼15° during 10 cmH₂O CPAP prevents an increase in cerebral blood volume with minimal effect on cerebral blood flow.     

Contribution of pH,diprotonated phosphate and potassium for the reflex increase in blood pressure during handgrip

The relative importance of pH, diprotonated phosphate (H₂PO₄^?) and potassium (K⁺) for the reflex increase in mean arterial pressure (MAP) during exercise was evaluated in seven subjects during rhythmic handgrip at 15 and 30% maximal voluntary contraction (MVC), followed by post-exercise muscle ischaemia (PEMI). During 15% MVC, MAP rose from 92 ± 1 to 103 ± 2 mmHg, [K⁺] from 4.1 ± 0.1 to 5.1 ± 0.1 mmol L^?1, while the intracellular (7.00 ± 0.01 to 6.80 ± 0.06) and venous pH fell (7.39 ± 0.01 to 7.30 ± 0.01) (P < 0.05). The intracellular [H₂PO₄^?] increased 8.4 ± 2 mmol kg^?1 and the venous [H₂PO₄^?] from 0.14 ± 0.01 to 0.16 ± 0.01 mmol L^?1 (P < 0.05). During PEMI, MAP remained elevated along with the intracellular [H₂PO₄^?] as well as a low intracellular and venous pH. However, venous [K⁺] and [H₂PO₄^?] returned to the level at rest. During 30% MVC handgrip, MAP rose to 130 ± 3 mmHg, [K⁺] to 5.8 ± 0.2 mmol L^?1, the intracellular and extracellular [H₂PO₄^?] by 20 ± 5 mmol kg^?1 and to 0.20 ± 0.02 mmol L^?1, respectively, while the intracellular (6.33 ± 0.06) and venous pH fell (7.23 ± 0.02) (P < 0.05). During post-exercise muscle ischaemia all variables remained close to the exercise levels. Analysis of each variable as a predictor of blood pressure indicated that only the intracellular pH and diprotonated phosphate were linked to the reflex elevation of blood pressure during handgrip.     

Resistance exercise training enhances sympathetic nerve activity during fatigue-inducing isometric handgrip trials

Muscle sympathetic nerve activity (MSNA) was investigated 1 week before (pre-training), 1 week after, and 4–6 weeks after strength training using fatigue-inducing handgrip exercises and post-exercise forearm occlusion. Eighteen volunteers underwent forearm training, which consisted of 30 maximal effort, 10-s-duration static handgrips, 4 days per week for 4 weeks. A second group of 18 volunteers served as a control. MSNA was recorded from the tibial nerve by microneurography. Maximal handgrip force increased at 1 week post-training. The MSNA response during fatigued handgrip also increased at 1 week post-training, as compared to pre-training (52.6 ± 5.8 vs. 40.6 ± 4.4 bursts min⁻¹ (mean ± SEM), respectively). However, at 4 weeks post-training, MSNA activity returned to the pre-training level (44.0 ± 5.2 bursts min⁻¹; p < 0.0001 by ANOVA), while the control group showed no changes throughout this period. The MSNA response during post-exercise forearm occlusion was constant throughout the experiment in both groups. Our results indicate that an increased MSNA response after strength training is likely to be the result of central neural factors rather than the muscle metaboreflex.     

Middle cerebral artery blood velocity depends on cardiac output during exercise with a large muscle mass

We tested the hypothesis that pharmacological reduction of the increase in cardiac output during dynamic exercise with a large muscle mass would influence the cerebral blood velocity/perfusion. We studied the relationship between changes in cerebral blood velocity (transcranial Doppler), rectus femoris blood oxygenation (near-infrared spectroscopy) and systemic blood flow (cardiac output from model flow analysis of the arterial pressure wave) as induced by dynamic exercise of large (cycling) vs. small muscle groups (rhythmic handgrip) before and after cardioselective β₁ adrenergic blockade (0.15 mg kg^?1 metoprolol i.v.). During rhythmic handgrip, the increments in systemic haemodynamic variables as in middle cerebral artery mean blood velocity were not influenced significantly by metoprolol. In contrast, during cycling (e.g. 113 W), metoprolol reduced the increase in cardiac output (222 ± 13 vs. 260 ± 16%), heart rate (114 ± 3 vs. 135 ± 7 beats min^?1) and mean arterial pressure (103 ± 3 vs.112 ± 4 mmHg), and the increase in cerebral artery mean blood velocity also became lower (from 59 ± 3 to 66 ± 3 vs. 60 ± 2 to 72 ± 3 cm s^?1; P < 0.05). Likewise, during cycling with metoprolol, oxyhaemoglobin in the rectus femoris muscle became reduced (compared to rest; ?4.8 ± 1.8 vs. 1.2 ± 1.7 μmol L^?1, P < 0.05). Neither during rhythmic handgrip nor during cycling was the arterial carbon dioxide tension affected significantly by metoprolol. The results suggest that as for the muscle blood flow, the cerebral circulation is also affected by a reduced cardiac output during exercise with a large muscle mass.     

The postural reduction in middle cerebral artery blood velocity is not explained by PaCO2

In the normocapnic range, middle cerebral artery mean velocity (MCA V _mean) changes ∼ 3.5% per mmHg carbon-dioxide tension in arterial blood (PaCO₂) and a decrease in PaCO₂ will reduce the cerebral blood flow by vasoconstriction (the CO₂ reactivity of the brain). When standing up MCA V _mean and the end-tidal carbon-dioxide tension (PETCO₂) decrease, suggesting that PaCO₂ contributes to the reduction in MCA V _mean. In a fixed body position, PETCO₂ tracks changes in the PaCO₂ but when assuming the upright position, cardiac output decreases and its distribution over the lung changes, while ventilation increases suggesting that PETCO₂ decreases more than PaCO₂. This study evaluated whether the postural reduction in PaCO₂ accounts for the postural decline in MCA V _mean. From the supine to the upright position, PETCO₂, PaCO₂, MCA V _mean, and the near-infrared spectrophotometry determined cerebral tissue oxygenation (CO₂Hb) were followed in seven subjects. When standing up, MCA V _mean (from 65.3±3.8 to 54.6±3.3 cm s⁻¹ ; mean ± SEM; P<0.05) and cO₂Hb (−7.2±2.2 μmol l⁻¹ ; P<0.05) decreased. At the same time, the ratio increased 49±14% (P<0.05) with the postural reduction in PETCO₂ overestimating the decline in PaCO₂ (−4.8±0.9 mmHg vs. −3.0±1.1 mmHg; P<0.05). When assuming the upright position, the postural decrease in MCA V _mean seems to be explained by the reduction in PETCO₂ but the small decrease in PaCO₂ makes it unlikely that the postural decrease in MCA V _mean can be accounted for by the cerebral CO₂ reactivity alone.     

Modulation of arterial baroreflex dynamic response during muscle metaboreflex activation in humans

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflexes (as reflected by alterations in the dynamic responses shown by muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) in humans. In nine healthy subjects (eight male, one female) who performed a sustained 1 min handgrip exercise at 50 % maximal voluntary contraction followed by forearm occlusion, a 5 s period of neck pressure (NP) (30 and 50 mmHg) or neck suction (NS)(-30 and -60 mmHg) was used to evaluate carotid baroreflex function at rest (CON) and during post-exercise muscle ischaemia (PEMI). In PEMI (as compared with CON): (a) the augmentations in MSNA and MAP elicited by 50 mmHg NP were both greater; (b) MSNA seemed to be suppressed by NS for a shorter period, (c) the decrease in MAP elicited by NS was smaller, and (d) MAP recovered to its initial level more quickly after NS. However, the HR responses to NS and NP were not different between PEMI and CON. These results suggest that during muscle metaboreflex activation, the dynamic arterial baroreflex response is modulated, as exemplified by the augmentation of the MSNA response to arterial baroreflex unloading (i.e. NP) and the reduction in the suppression of MSNA induced by baroreceptor stimulation (i.e. NS).     

Near-infrared spectrophotometry determined brain oxygenation during fainting

During orthostatic hypotension we evaluated whether presyncopal symptoms relate to a reduced brain oxygenation. Nine subjects performed 50° head-up tilt for 1 h and eight subjects were followed during 2 h of supine rest and during 1 h of 10° head-down tilt. Cerebral perfusion was assessed by transcranial Doppler determined middle cerebral artery blood velocity (MCA v_mean), while brain blood oxygenation was assessed by near-infrared spectrophotometry determined concentration changes for oxygenated (ΔHbO₂) and deoxygenated haemoglobin and brain cell oxygenation by the oxidized cytochrome c concentration (ΔCytO₂). During head-up tilt, six volunteers developed presyncopal symptoms and mean arterial pressure (88 (78–103) to 68 (57–79) mmHg; median and range), heart rate (96 (72–111) to 65 (50–107) beats min^?1), MCA v_mean (59 (51–82) to 41 (29–56) cm s^?1), ΔHbO₂ (by ?5.3 (?3.0 to ?14.8) μmol l^?1) and ΔCytO₂ were reduced (by ?0.2 (?0.1 to ?0.4) μmol l^?1; P < 0.05). During tilt down the cardiovascular variables recovered immediately and ΔHbO₂ increased to 2.2 (?0.9–12.0) mmol L^?1 above the resting value and also ΔCytO₂ recovered. In the nonsyncopal head-up tilted subjects as in the controls, blood pressure, heart rate, MCA v_mean and brain oxygenation indices remained stable. The results suggest that during orthostasis, presyncopal symptoms relate not only to cerebral hypoperfusion but also to reduced brain oxygenation.     

Effects of digoxin on muscle reflexes in normal humans

Blockade of the skeletal muscle Na⁺–K⁺-ATPase pump by digoxin could result in a more marked hyperkaliema during a forearm exercise, which in turn could stimulate the mechano- and metaboreceptors. In a randomized, double-blinded, placebo-controlled, and cross-over-design study, we measured mean blood pressure (MBP), heart rate (HR), ventilation (V _E), oxygen saturation (SpO₂), muscle sympathetic nerve activity (MSNA), venous plasma potassium and lactic acid during dynamic handgrip exercises, and local circulatory arrest in 11 healthy subjects. Digoxin enhanced MBP during exercise but not during the post-handgrip ischemia and had no effect on HR, V _E, SpO₂, and MSNA. Venous plasma potassium and lactic acid were also not affected by digoxin-induced skeletal muscle Na⁺–K⁺-ATPase blockade. We conclude that digoxin increased MBP during dynamic exercise in healthy humans, independently of changes in potassium and lactic acid. A modest direct sensitization of the muscle mechanoreceptors is unlikely and other mechanisms, independent of muscle reflexes and related to the inotropic effects of digoxin, might be implicated.     

Central modulation of exercise-induced muscle pain in humans

The purpose of the current study was to determine if exercise-induced muscle pain is modulated by central neural mechanisms (i.e. higher brain systems). Ratings of muscle pain perception (MPP) and perceived exertion (RPE), muscle sympathetic nerve activity (MSNA), arterial pressure, and heart rate were measured during fatiguing isometric handgrip (IHG) at 30% maximum voluntary contraction and postexercise muscle ischaemia (PEMI). The exercise trial was performed twice, before and after administration of naloxone (16 mg intravenous; n = 9) and codeine (60 mg oral; n = 7). All measured variables increased with exercise duration. During the control trial in all subjects ( n = 16), MPP significantly increased during PEMI above ratings reported during IHG (6.6 ± 0.8 to 9.5 ± 1.0; P < 0.01). However, MSNA did not significantly change compared with IHG (7 ± 1 to 7 ± 1 bursts (15 s)⁻¹), whereas mean arterial blood pressure was slightly reduced (104 ± 4 to 100 ± 3 mmHg; P < 0.05) and heart rate returned to baseline values during PEMI (83 ± 3 to 67 ± 2 beats min⁻¹; P < 0.01). These responses were not significantly altered by the administration of naloxone or codeine. There was no significant relation between arterial blood pressure and MSNA with MPP during either IHG or PEMI. A second study ( n = 8) compared MPP during ischaemic IHG to MPP during PEMI. MPP was greater during PEMI as compared with ischaemic IHG. These findings suggest that central command modulates the perception of muscle pain during exercise. Furthermore, endogenous opioids, arterial blood pressure and MSNA do not appear to modulate acute exercise-induced muscle pain.     

Effects of aging on the cerebrovascular orthostatic response

When healthy subjects stand up, it is associated with a reduction in cerebral blood velocity and oxygenation although cerebral autoregulation would be considered to prevent a decrease in cerebral perfusion. Aging is associated with a higher incidence of falls, and in the elderly falls may occur particularly during the adaptation to postural change. This study evaluated the cerebrovascular adaptation to postural change in 15 healthy younger (YNG) vs. 15 older (OLD) subjects by recordings of the near-infrared spectroscopy-determined cerebral oxygenation (cO₂Hb) and the transcranial Doppler-determined mean middle cerebral artery blood velocity (MCA V_mean). In OLD (59 (52-65) years) vs. YNG (29 (27-33) years), the initial postural decline in mean arterial pressure (−52 ± 3% vs. −67 ± 3%), cO₂Hb (−3.4 ± 2.5 μmol l⁻¹ vs. −5.3 ± 1.7 μmol l⁻¹) and MCA V_mean (−16 ± 4% vs. −29 ± 3%) was smaller. The decline in MCA V_mean was related to the reduction in MAP. During prolonged orthostatic stress, the decline in MCA V_meanand cO₂Hb in OLD remained smaller. We conclude that with healthy aging the postural reduction in cerebral perfusion becomes less prominent.     

Reduced arterial diameter during static exercise in humans

In eight subjects luminal diameter of the resting limb radial and dorsalis pedis arteries was determined by high-resolution ultrasound (20 MHz). This measurement was followed during rest and during 2 min of static handgrip or of one-leg knee extension at 30% of maximal voluntary contraction of another limb. Static exercise increased heart rate and mean arterial pressure, which were largest during one-leg knee extension. After exercise heart rate and mean arterial pressure returned to the resting level. No changes were recorded in arterial carbon dioxide tension, and the rate of perceived exertion was ? 15 units after both types of exercise. The dorsalis pedis arterial diameter was 1.50±0.20 mm (mean and SE) and the radial AD 2.45±0.12 mm. During both types of contractions the luminal diameters decreased ? 3.5% within the first 30 s (P< 0.05), and during one-leg knee extension they continued to decrease to a final exercise value 7.6±1.1% lower than at rest (P < 0.05). Thus, they became smaller than during the handgrip. After exercise resting values were reestablished. When the arterial diameter was expressed in relation to mean arterial pressure for the radial and dorsalis pedis artery was 22±3 and 28±3% lower during handgrip than the relation during rest, respectively. After one-leg knee extension both arteries reached 30±4% lower values. This study demonstrated arterial constriction in the resting limbs within the first 30 s of static exercise, and continued constriction during one-leg knee extension. These results support to the hypothesis that central command and/or muscle mechano- receptors influence arterial tone, and that the exercise pressor reflex becomes important with the involvement of a large muscle mass.     

Rate of oxidative phosphorylation in isolated mitochondria from human skeletal muscle: effect of training status

Muscle oxidative function has been investigated in subjects with various training status (VO _{2 max}, 41–72 mL O₂ kg^?1 body wt min^?1, n=10). Mitochondria were isolated from biopsies taken from m. vastus lateralis. Maximal mitochondrial oxygen consumption (QO ₂) and ATP production (MAPR) were measured with polarographic and bioluminometric techniques, respectively. The yield of mitochondria, calculated from the fractional activity of citrate synthase (CS), averaged 26%. With pyruvate + malate, the respiratory control ratio was 5.7 ± 0.4 (X ± SE) and the P/O ratio was 2.83 ± 0.02, which demonstrates that the isolated mitochondria were functionally intact. QO ₂ was significantly correlated to aerobic training status expressed as muscle CS activity (r=0.86), VO _{2 max} (r=0.84) and lactate threshold (r=0.83) but not to the fibre type composition. A highly significant correlation (r=0.93) was observed between ATP production calculated from QO ₂ and MAPR, but ATP production derived from QO ₂ was higher than MAPR both for pyruvate + malate (255%) and for α-ketoglutarate (23%). QO ₂ extrapolated to a temperature of 38 °C averaged 68 mL O₂ min^?1 kg^?1 wet wt, which is similar to previous findings in vitro and in vivo during the post-exercise period. However, calculated muscle O₂ utilization during exercise was three- to fivefold higher than QO ₂ measured on isolated mitochondria. It is suggested that additional factors exist for activation of mitochondrial respiration during exercise. It is concluded that muscle oxidative function can be quantitatively assessed from the respiration of mitochondria isolated from needle biopsy specimens and that QO ₂ is closely correlated to whole-body VO _{2 max}.     

Skin blood flow influences cerebral oxygenation measured by near-infrared spectroscopy during dynamic exercise

Purpose

Near-infrared spectroscopy (NIRS) is widely used to investigate cerebral oxygenation and/or neural activation during physiological conditions such as exercise. However, NIRS-determined cerebral oxygenated hemoglobin (O₂Hb) may not necessarily correspond to intracranial blood flow during dynamic exercise. To determine the selectivity of NIRS to assess cerebral oxygenation and neural activation during exercise, we examined the influence of changes in forehead skin blood flow (SkBF_head) on NIRS signals during dynamic exercise.

Methods

In ten healthy men (age: 20 ± 1 years), middle cerebral artery blood flow velocity (MCA V _mean, via transcranial Doppler ultrasonography), SkBF_head (via laser Doppler flowmetry), and cerebral O₂Hb (via NIRS) were continuously measured. Each subject performed 60 % maximum heart rate moderate-intensity steady-state cycling exercise. To manipulate SkBF_head, facial cooling using a mist of cold water (~4 °C) was applied for 3 min during steady-state cycling.

Results

MCA V _mean significantly increased during exercise and remained unchanged with facial cooling. O₂Hb and SkBF_head were also significantly increased during exercise; however, both of these signals were lowered with facial cooling and returned to pre-cooling values with the removal of facial cooling. The changes in O₂Hb correlated significantly with the relative percent changes in SkBF_head in each individual (r = 0.71–0.99).

Conclusions

These findings suggest that during dynamic exercise NIRS-derived O₂Hb signal can be influenced by thermoregulatory changes in SkBF_head and therefore, may not be completely reflective of cerebral oxygenation or neural activation.     

Skeletal muscle blood flow in humans and its regulation during exercise

Regional limb blood flow has been measured with dilution techniques (cardio-green or thermodilution) and ultrasound Doppler. When applied to the femoral artery and vein at rest and during dynamical exercise these methods give similar reproducible results. The blood flow in the femoral artery is ～0.3 L min^?1 at rest and increases linearly with dynamical knee-extensor exercise as a function of the power output to 6–10 L min^?1 (Q = 1.94 + 0.07 load). Considering the size of the knee-extensor muscles, perfusion during peak effort may amount to 2–3 L kg^?1 min^?1, i.e. ～100-fold elevation from rest. The onset of hyperaemia is very fast at the start of exercise with T_½ of 2–10 s related to the power output with the muscle pump bringing about the very first increase in blood flow. A steady level is reached within ～10–150 s of exercise. At all exercise intensities the blood flow fluctuates primarily due to the variation in intramuscular pressure, resulting in a phase shift with the pulse pressure as a superimposed minor influence. Among the many vasoactive compounds likely to contribute to the vasodilation after the first contraction adenosine is a primary candidate as it can be demonstrated to (1) cause a change in limb blood flow when infused i.a., that is similar in time and magnitude as observed in exercise, and (2) become elevated in the interstitial space (microdialysis technique) during exercise to levels inducing vasodilation. NO appears less likely since NOS blockade with L -NMMA causing a reduced blood flow at rest and during recovery, it has no effect during exercise. Muscle contraction causes with some delay (60 s) an elevation in muscle sympathetic nerve activity (MSNA), related to the exercise intensity. The compounds produced in the contracting muscle activating the group III–IV sensory nerves (the muscle reflex) are unknown. In small muscle group exercise an elevation in MSNA may not cause vasoconstriction (functional sympatholysis). The mechanism for functional sympatholysis is still unknown. However, when engaging a large fraction of the muscle mass more intensely during exercise, the MSNA has an important functional role in maintaining blood pressure by limiting blood flow also to exercising muscles.     

Differences in muscle sympathetic nerve response to isometric exercise in different muscle groups

The aim of this study was to examine the effects of muscle fibre composition on muscle sympathetic nerve activity (MSNA) in response to isometric exercise. The MSNA, recorded from the tibial nerve by a microneurographic technique during contraction and following arterial occlusion, was compared in three different muscle groups: the forearm (handgrip), anterior tibialis (foot dorsal contraction), and soleus muscles (foot plantar contraction) contracted separately at intensities of 20%, 33% and 50% of the maximal voluntary force. The increases in MSNA relative to control levels during contraction and occlusion were significant at all contracting forces for handgrip and at 33% and 50% of maximal for dorsal contraction, but there were no significant changes, except during exercise at 50%, for plantar contraction. The size of the MSNA response correlated with the contraction force in all muscle groups. Pooling data for all contraction forces, there were different MSNA responses among muscle groups in contraction forces (P = 0.0001, two-way analysis of variance), and occlusion periods (P = 0.0001). The MSNA increases were in the following order of magnitude: handgrip, dorsal, and plantar contractions. The order of the fibre type composition in these three muscles is from equal numbers of types I and II fibres in the forearm to increasing number of type I fibres in the leg muscles. The different MSNA responses to the contraction of different muscle groups observed may have been due in part to muscle metaboreflex intensity influenced by their metabolic capacity which is related to by their metabolic capacity which is related to the fibre type.     

Changes in muscle sympathetic nerve activity and calf blood flow during combined leg and forearm exercise

In order to examine efferent sympathetic nerve control of the peripheral circulation during exercise, muscle sympathetic nerve activity (MSNA), calf blood flow (CBF), heart rate (HR), blood pressure (BP) and oxygen uptake were measured during combined foot and forearm exercise. An initial period of rhythmic foot exercise (RFE) (60 min^-1 at 10% of maximal voluntary contraction (MVC) was followed by the addition of rhythmic handgrip exercise (RFE+OCCL) (60 min at 30% of MVC) and by forearm ischaemia after handgrip exercise while continuing RFE (RFE + OCCL). During RFE, CBF in the working leg, HR and oxygen increased respectively by 560%, 121% and 144% when compared with the control rest period, but MSNA (burst rate) was reduced by 13% (P > 0.05) and BP was unchanged. During RFE+RHG, HR, BP and oxygen uptake were greater than during RFE alone. There was no change in CBF, but a significant increase occurred in calf vascular resistance (CVR) and MSNA increased to 121% of the control level. During RFE + OCCL, MSNA, CVR and BP were all higher than during RFE alone, whereas HR and oxygen uptake decreased slightly, although they remained higher than the control values. The increase in CVR in the working leg and the rise in BP during RFE+RHG or RFE+OCCL might be linked to enhancement of MSNA, which may have been reflexly evoked by input from muscle metabolic receptors in the working forearm.     

Muscle sympathetic nerve activity at rest compared to exercise tolerance

Cardiovascular autonomic function is associated with physical performance and exercise training adaptation. The association between physical performance and sympathetic regulation is not well known. We hypothesized that sympathetic nervous system activity is associated with physical performance among male runners. The study population included 26 healthy male club runners [age 33 ± 5 years, body mass index (BMI) 24 ± 1 kg/m², VO_2max 58 ± 5 ml kg⁻¹ min⁻¹; mean ± SD]. Muscle sympathetic nerve activity (MSNA) was assessed from the peroneal nerve by the microneurography technique during 5 min of supine rest. Physical performance was assessed by time to exhaustion during treadmill running. The mean resting MSNA was 20 ± 6 bursts min⁻¹ (range 6–34). The mean time to exhaustion was 1,005 ± 136 s (range 720–1260). When the study group was divided into tertiles according to their running performance (866 ± 69, 994 ± 30 and 1154 ± 71 s in time to exhaustion, P < 0.0001 between the groups), MSNA was lower (P = 0.032) in the group with the best running performance (16 ± 5 bursts min⁻¹) compared to those with the worst running performance (23 ± 7 bursts min⁻¹). In conclusion, baseline sympathetic activity, measured by a microneurography at rest, may be associated with the maximal running performance of healthy subjects.