Restrictions in systemic and locomotor skeletal muscle perfusion, oxygen supply and VO2 during high-intensity whole-body exercise in humans

Perfusion to exercising skeletal muscle is regulated to match O(2) delivery to the O(2) demand, but this regulation might be compromised during or approaching maximal whole-body exercise as muscle blood flow for a given work rate is blunted. Whether muscle perfusion is restricted when there is an extreme metabolic stimulus to vasodilate during supramaximal exercise remains unknown. To examine the regulatory limits of systemic and muscle perfusion in exercising humans, we measured systemic and leg haemodynamics, O(2) transport, and , and estimated non-locomotor tissue perfusion during constant load supramaximal cycling (498 +/- 16 W; 110% of peak power; mean +/- S.E.M.) in addition to both incremental cycling and knee-extensor exercise to exhaustion in 13 trained males. During supramaximal cycling, cardiac output (Q), leg blood flow (LBF), and systemic and leg O(2) delivery and reached peak values after 60-90 s and thereafter levelled off at values similar to or approximately 6% (P < 0.05) below maximal cycling, while upper body blood flow remained unchanged (approximately 5.5 l min(-1)). In contrast, Q and LBF increased linearly until exhaustion during one-legged knee-extensor exercise accompanying increases in non-locomotor tissue blood flow to approximately 12 l min(-1). At exhaustion during cycling compared to knee-extensor exercise, Q, LBF, leg vascular conductance, leg O(2) delivery and leg for a given power were reduced by 32-47% (P < 0.05). In conclusion, locomotor skeletal muscle perfusion is restricted during maximal and supramaximal whole-body exercise in association with a plateau in Q and limb vascular conductance. These observations suggest that limits of cardiac function and muscle vasoconstriction underlie the inability of the circulatory system to meet the increasing metabolic demand of skeletal muscles and other tissues during whole-body exercise.     

Oxygen tension and content in the regulation of limb blood flow

During submaximal exercise, muscle blood flow increases when arterial oxygen content (CaO2) is reduced. The increase in blood flow is brought about by elevating cardiac output (CO) and enhancing leg vascular conductance. Conversely, increased CaO2 elicits lower limb blood flow (LBF) and CO. During maximal exercise, the influence of CaO2 on muscle blood flow is modulated depending on the amount of muscle mass recruited. When a small muscle mass is activated and the pumping capacity of the heart is not limited, changes in CaO2 barely influence the level of blood flow attained at peak exercise. However, when a large muscle mass is engaged in the exercise, as occurs for example during cycling and running, muscle blood flow is decreased if maximal CO is reduced, as happens during exercise in severe hypoxia. In contrast, maximal muscle blood flow and CO are maintained at peak exercise when CaO2 is increased. As such, exercise intensity, muscle mass and CaO2 appear to be the critical factors determining muscle blood flow during exercise.     

The effect of resistive breathing on leg muscle oxygenation using near-infrared spectroscopy during exercise in men

The effect of added respiratory work on leg muscle oxygenation during constant-load cycle ergometry was examined in six healthy adults. Exercise was initiated from a baseline of 20 W and increased to a power output corresponding to 90% of the estimated lactate threshold (moderate exercise) and to a power output yielding a tolerance limit of 11.8 min (+/- 1.4, S.D.) (heavy exercise). Ventilation and pulmonary gas exchange were measured breath-by-breath. Profiles of leg muscle oxygenation were determined throughout the protocol using near-infrared (NIR) spectroscopy (Hamamatsu NIRO 500) with optodes aligned midway along the vastus lateralis of the dominant leg. Four conditions were tested: (i) control (Con) where the subjects breathed spontaneously throughout, (ii) controlled breathing (Con Br) where breathing frequency and tidal volume were matched to the Con profile, (iii) increased work of breathing (Resist Br) in which a resistance of 7 cmH2O l(-1) s(-1) was inserted into the mouthpiece assembly, and (iv) partial leg blood flow occlusion (Leg Occl), where muscle perfusion was reduced by inflating a pressure cuff (approximately 90 mmHg) around the upper right thigh. During Resist Br and Leg Occl, subjects controlled their breathing pattern to reproduce the ventilatory profile of Con. An approximately 3 min period with respiratory resistance or pressure cuff was introduced approximately 4 min after exercise onset. NIR spectroscopy data for reduced haemoglobin-myoglobin (delta[Hb]) were extracted from the continuous display at specific times prior to, during and after removal of the resistance or pressure cuff. While the delta[Hb] increased during moderate- and heavy-intensity exercise, there was no additional increase in delta[Hb] with Resist Br. In contrast, delta[Hb] increased further with Leg Occl, reflecting increased muscle O2 extraction during the period of reduced muscle blood flow. In conclusion, increasing the work of breathing did not increase leg muscle deoxygenation during heavy exercise. Assuming that leg muscle O2 consumption did not decrease, this implies that leg blood flow was not reduced consequent to a redistribution of flow away from the working leg muscle.     

Interactions between β-adrenergic vasodilation and cervical sympathetic nerves are mediated by α<Subscript>2</Subscript>-adrenoceptors in the rat masseter muscle

Neural and humoral autonomic mechanisms may be important in the maintenance of blood flow in the masseter muscle (MBF). However, their interactions remain unclear. In this study, we examined interactions between neural and humoral regulation of MBF and investigated the mechanisms mediating these interactions in urethane-anesthetized rats. Stimulation of the adrenal nerve (AN) projecting to the adrenal medulla increased MBF, and this increase was mediated by β-adrenoceptors. Sectioning of the superior cervical sympathetic trunk (CST) significantly inhibited increases in MBF induced by AN stimulation during high activity in the CST, but not during low activity. AN stimulation with clonidine after CST sectioning induced a significant increased in MBF, however phenylephrine had no observable effect. Pretreatment with yohimbine or propranolol significantly inhibited the increase in the MBF. Our results suggest an interaction between β-adrenergic vasodilation evoked by circulating adrenaline and the cervical sympathetic nerves that is mediated by α₂-adrenoceptors in the masseter muscle.     

The influence of circulatory difference on muscle oxygenation and fatigue during intermittent static dorsiflexion

This study aimed to examine the influences of circulatory difference on the utilization of O₂ and the progression of fatigue in the tibialis anterior (TA) muscle during dorsiflexion exercise, with reference to different body postures. The subjects performed intermittent static dorsiflexion at 50% of maximal voluntary contraction (MVC) up to exhaustion with the right leg either up or down relative to the heart. These exercises were performed with and without occluding muscle blood flow. Simultaneously with the surface electromyogram (EMG) measurement, total hemoglobin volume change and tissue oxygenation (S _tO₂) of TA were measured using near-infrared spectroscopy (NIRS). When the subjects performed an exhaustive intermittent dorsiflexion exercise at 50% MVC, the endurance time decreased in the leg up position. Also, the progression of fatigue in TA detected using EMG signals (i.e. integrated EMG and mean power frequency of EMG) was faster with the leg elevated. The NIRS data indicated a lower blood volume and S _tO₂ with the leg up than with the leg down during the exercise, which suggests that the deficit in the O₂ supply to exercising muscles demand was more apparent in the leg up position. However, these differences in EMG and NIRS data disappeared when the blood flow was restricted in both positions. From these results it is concluded that the difference in exercising muscle oxygenation between two different body postures influenced the progression of muscle fatigue and caused the difference in endurance performance.     

Effects of propranolol and verapamil on plasma ionized calcium and parathyroid hormone in short-term intense isokinetic leg exercise

Physical exercise, beta-adrenergic stimulation and calcium channel blockade can affect calcium homeostasis. The present study investigated, in eight healthy males, the effects of orally administered propranolol or verapamil during a 2-min maximal, isokinetic, leg exercise. Immediately after exercise the plasma ionized calcium concentrations were increased, in control and drug tests, by 5-6%, and within 5 min of recovery they were almost returned to baseline. Serum parathyroid hormone (PTH) concentrations were unchanged at termination of exercise, but they increased during the first 5 min of recovery, coincident with the decline in calcium concentrations, which, however, were still elevated. Neither verapamil nor propranolol selectively changed basal or exercise plasma ionized calcium or serum PTH concentrations. Muscle strength, blood pH, lactate concentrations and plasma volume changes were not affected by any drug. Verapamil did not have any specific effect on the concentrations of plasma magnesium, phosphate, potassium or sodium while propranolol increased the concentrations of plasma potassium and decreased those of phosphate during exercise as well as recovery.     

Blood flow to exercising limbs varies with age, gender, and training status.

Understanding the effects of physiological aging on blood flow to active skeletal muscle and its regulation during exercise has important functional, hemodynamic, and metabolic implications for our rapidly expanding elderly population. During peak exercise involving a large muscle mass, blood flow to the legs is lower in healthy older compared to younger persons; this results from central (reduced cardiac output) and peripheral (reduced leg vascular conductance) limitations. There is considerable variability in the literature concerning age-related changes in leg blood flow during submaximal exercise, with reports of similar or reduced leg blood flow and vascular conductance in older vs. younger subjects depending on the exercise intensity and the gender and training status of the subjects. However, all the studies involving non-endurance-trained subjects are consistent in that older subjects achieve the requisite leg blood flow at higher arterial perfusion pressures than young subjects, suggesting altered local vasoregulatory mechanisms with aging. Although the nature of these age-related alterations is poorly understood, we have preliminary evidence for augmented sympathetic vasoconstrictor responsiveness in the legs of older men during exercise, and blunted leg vasodilator responsiveness in older women. Systematic research will be needed in order to define the central and local mechanisms underlying these age- and gender-specific differences in muscle vascular responsiveness. Such information will be important for designing future interventions aimed at improving muscle blood supply and functional capacity in older persons.     

The effects of beta-blockade on electrically stimulated contraction in fatigued human triceps surae muscle

The contractile characteristics of the triceps surae muscle group were examined before and after repeated isometric contractions in two groups of eight healthy young males. Single twitches and trains of stimuli at 10, 20, 50 and 100 Hz were delivered to the muscle using supramaximal voltages. Subjects were treated with beta-blockade (2 X 80 mg oral propranolol, beta-b) or matched placebo in a double-blind crossover design. Four different exercise conditions were studied: (I) maximal voluntary contraction (MVC); (II) MVC during circulatory occlusion; (III) electrical stimulation at 20 Hz using 50% of voltage required for maximal torque production; and (IV) electrical stimulation with occlusion. Each contraction was for 5 s with 5 s recovery. Total duration of exercise was 10 min for non-occluded contractions and to a 50% decline in torque output with occlusion. At rest prior to exercise, maximal voluntary contraction was significantly reduced (5.7%) by beta-b during 40 observations in 16 subjects. Following exercise without occlusion (I and III), the reduction in torque output of the muscle at 10 and 20 Hz stimulation was generally greater during beta-b than placebo. This low frequency fatigue was longer-lasting with beta-b. The shorter lasting reduction in torque at 50 and 100 Hz was generally not different between beta-b placebo. After exercise with occlusion (II and IV), the torque output at all stimulation frequencies was reduced to a similar extent in both placebo and beta-b at most comparison points. Twitch responses after exercise with occlusion showed decreases in peak tension and time to peak tension and a lengthening of one-half relaxation time in both placebo and beta-b. It was concluded that the greater reduction in torque output of the triceps surae muscle group at low frequencies during beta-b was probably a consequence of a reduction in blood flow relative to the placebo treatment. This relative low frequency fatigue could be responsible for the increased perception of effort in patients exercising during beta-blocker therapy.     

Haemodynamic and metabolic responses to prolonged exercise after chronic beta 1-adrenoceptor blockade in hypertensive man

The influence of chronic beta 1-adrenoceptor blockade on haemodynamic and metabolic responses was examined in eight young hypertensive subjects during a 40 min submaximal bicycle test at 50% of maximal capacity. The patients were randomly allocated to one placebo and one treatment period of 6 weeks. During treatment atenolol (Tenormin, 100 mg) was given twice daily. Arterial pressure, cardiac output, leg blood flow, oxygen uptake and different metabolites in the blood were determined. The heart rate was reduced by beta 1-adrenoceptor blockade by 30% during exercise, and the decrease was related to plasma concentration of the drug. Cardiac output was decreased by approximately 10%, but the negative chronotropic effect was partly compensated for by a higher stroke volume. Blockade leg blood flow was reduced by 10%, but more oxygen was extracted, giving an unchanged oxygen uptake. Blood concentration and leg uptake of glucose were not influenced by the treatment, but plasma free fatty acids were reduced by 30-40%. Leg lactate release was decreased to half the value in the unblocked situation. Plasma renin activity did not increase at the beginning of exercise, but after 40 min an increase was seen, though only to half of the pretreatment value. It is concluded that beta 1-adrenoceptor blockade during submaximal exercise reduces blood flow to the working muscles and that this reduction is the result of a lower cardiac output. Aerobic metabolism is unchanged as a result of increased oxygen extraction, but less fat is used as lipolysis is inhibited. Glucose uptake by the working muscles is unchanged by beta 1-blockade, but there is evidence for an increased carbohydrate metabolism. As for non-selective blockade, atenolol decreases lactate release but this could be the result of non-specific action on the beta 1-receptor and/or increased carbohydrate oxidation. Furthermore, the beta 1-adrenoceptors seem to have a major influence on the renin release during exercise.     

A single bout of exercise is followed by a prolonged decrease in the interstitial glucose concentration in skeletal muscle

AIM: The present study was performed to test the hypothesis that the interstitial glucose concentration in human skeletal muscle is decreased for a prolonged period following a single bout of exercise, while blood flow has returned to resting levels. METHODS: Muscle interstitial concentrations of glucose, lactate, pyruvate and urea were monitored in six healthy individuals during 8 h following a 2-h one-leg exercise session by microdialysis at low perfusion flow rate. Simultaneously the blood flow was measured by the microdialysis ethanol technique. RESULTS: The blood glucose and the control leg interstitial glucose concentrations were stable during the experiment averaging 5.7 +/- 0.1 and 4.1 +/- 0.3 mm, respectively. In contrast, the interstitial glucose concentration in the exercise leg was markedly decreased, averaging 1.9 +/- 0.5 mm, during the first 5.5 h following exercise (P < 0.01), after which it returned towards normal values. Muscle blood flow at the site of the microdialysis catheter, measured as the ethanol outflow-to-inflow ratio, did not change significantly over time in the control or exercise leg and did not differ significantly between the two legs. Interstitial concentrations of lactate, pyruvate and urea were not significantly different between the control and exercise leg. CONCLUSION: The study shows that the interstitial glucose concentration in skeletal muscle is markedly decreased for several hours following a single exercise session. The decreased interstitial glucose concentration may serve to limit the rate of post-exercise muscle glucose uptake to a rate compatible with normal blood glucose levels and may also be speculated to have a positive long-term health implication by augmenting muscle insulin sensitivity.     

Importance of hemoglobin concentration to exercise: acute manipulations

An acute reduction of blood hemoglobin concentration ([Hb]), even when the circulating blood volume is maintained, results in lower (.)V(O(2)(max) and endurance performance, due to the reduction of the oxygen carrying capacity of blood. Conversely, an increase of [Hb] is associated with enhanced (.)V(O(2)(max) and endurance capacity, that is also proportional to the increase in the oxygen carrying capacity of blood. The effects on endurance capacity appear more pronounced and prolonged than on (.)V(O(2)(max). During submaximal exercise, there is a tight coupling between O(2) demand and O(2) delivery, such that if [Hb] is acutely decreased muscle blood flow is increased proportionally and vice versa. During maximal exercise with either a small or a large muscle mass, neither peak cardiac output nor peak leg blood flow are affected by reduced [Hb]. An acute increase of [Hb] has no effect on maximal exercise capacity or (.)V(O(2)(max) during exercise in acute hypoxia. Likewise, reducing [Hb] in altitude-acclimatized humans to pre-acclimatization values has no effect on (.)V(O(2)(max) during exercise in hypoxia.     

The effect of hypoxia on pulmonary O2 uptake, leg blood flow and muscle deoxygenation during single-leg knee-extension exercise

The effect of hypoxic breathing on pulmonary O(2) uptake (VO(2p)), leg blood flow (LBF) and O(2) delivery and deoxygenation of the vastus lateralis muscle was examined during constant-load single-leg knee-extension exercise. Seven subjects (24 +/- 4 years; mean +/-s.d.) performed two transitions from unloaded to moderate-intensity exercise (21 W) under normoxic and hypoxic (P(ET)O(2)= 60 mmHg) conditions. Breath-by-breath VO(2p) and beat-by-beat femoral artery mean blood velocity (MBV) were measured by mass spectrometer and volume turbine and Doppler ultrasound (VingMed, CFM 750), respectively. Deoxy-(HHb), oxy-, and total haemoglobin/myoglobin were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). VO(2p) data were filtered and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. MBV data were filtered and averaged to 2 s bins (1 contraction cycle). LBF was calculated for each contraction cycle and averaged to 5 s bins at 20, 40, 60, 120, 180 and 300 s. VO(2p) was significantly lower in hypoxia throughout the period of 20, 40, 60 and 120 s of the exercise on-transient. LBF (l min(-1)) was approximately 35% higher (P > 0.05) in hypoxia during the on-transient and steady-state of KE exercise, resulting in a similar leg O(2) delivery in hypoxia and normoxia. Local muscle deoxygenation (HHb) was similar in hypoxia and normoxia. These results suggest that factors other than O(2) delivery, possibly the diffusion of O(2,) were responsible for the lower O(2) uptake during the exercise on-transient in hypoxia.     

Effect of electrical stimulation of leg muscles on physiological responses during arm-cranking exercise in healthy men

The purpose of this study was to investigate the hypothesis that changes in physiological responses during arm-cranking exercise using electrical stimulation of the leg muscles (ACE-ES) compared to arm-cranking exercise alone (ACE) in able-bodied subjects (ABS) are based on an increase in active muscle mass rather than the enhancing effect of the leg muscle pump. In ABS the sympathetic nervous system induced vasoconstriction and activity of the leg muscle pump are intact, therefore, a normal redistribution of blood takes place during exercise. Consequently, ES should have no additional effect on the redistribution of blood in these ABS during exercise and, thus, changes in physiological responses will be based on an increase in active muscle mass. A group of 11 ABS performed three maximal arm-cranking tests. In the first test peak power output (PO _peak) was determined. The other tests were both submaximal and maximal ACE, once with ACE-ES and once with ACE. The PO _peak was not significantly different between ACE-ES and ACE. Oxygen uptake ( O₂) increased significantly during ACE-ES compared to ACE. Cardiac output ( ), stroke volume (SV), heart rate and ventilation were not significantly different during ACE-ES compared to ACE. Respiratory exchange ratios were significantly lower during ACE-ES compared to ACE at 60% PO _peak and at maximal exercise. In conclusion, ACE-ES caused significant increases in O₂ with a lack of elevation in and SV during submaximal and maximal exercise in ABS. The results of this study suggest that changes in physiological responses during ACE-ES are based on an increase in the active muscle mass rather than stimulation of the leg muscle pump.     

Comparison in eccentric exercise-induced muscle damage among four limb muscles

This study tested the hypothesis that changes in indirect markers of muscle damage following maximal eccentric exercise would be smaller for the knee extensors (KE) and flexors (KF) compared with the elbow flexors (EF) and extensors (EE). A total of 17 sedentary men performed five sets of six maximal isokinetic (90°?s^?1) eccentric contractions of EF (range of motion, ROM: 90°?C0°, 0?=?full extension), EE (55°?C145°), KF (90°?C0°), and KE (30°?C120°) using a different limb with a 4?C5-week interval in a counterbalanced order. Changes in maximal isometric and concentric isokinetic strength, optimum angle, limb circumference, ROM, plasma creatine kinase activity and myoglobin concentration, muscle soreness, and echo-intensity of B-mode ultrasound images before and for 5?days following exercise were compared amongst the four exercises using two-way repeated-measures ANOVA. All variables changed significantly following EF, EE, and KF exercises, but KE exercise did not change the optimum angle, limb circumference, and echo-intensity. Compared with KF and KE, EF and EE showed significantly greater changes in all variables, without significant differences between EF and EE. Changes in all variables were significantly greater for KF than KE. For the same subjects, the magnitude of change in the dependent variables following exercise varied among the exercises. These results suggest that the two arm muscles are equally more susceptible to muscle damage than leg muscles, but KF is more susceptible to muscle damage than KE. The difference in the susceptibility to muscle damage seems to be associated with the use of muscles in daily activities.     

Transient increase in femoral arterial blood flow to the contralateral non-exercising limb during one-legged exercise

We studied the effect of exercise intensity and duration on blood flow to the non-exercising leg during one-legged dynamic knee extension. Femoral arterial blood flow (FBF) to the non-exercising leg, blood pressure (BP), and heart rate (HR) were monitored during one-legged dynamic knee extension exercise at 15, 30, and 45% maximal voluntary contraction (MVC) in seven healthy females. There was an interaction between exercise intensity and duration for FBF and FVC (P < 0.01). During the initial phase of contralateral leg exercise at all intensities, FBF and femoral vascular conductance (FVC) of non-exercising leg increased, and the increase was larger at higher intensities (P < 0.01). After initial vasodilatation, FBF and FVC decreased to baseline, which suggests the vasoconstriction. However, FBF and FVC gradually increased during exercise at 15% MVC. We conclude that transient vasodilatation at the onset of exercise is followed by gradual change to vasoconstriction in non-exercising limb during dynamic one-legged exercise and these changes are exercise intensity- and duration-dependent.     

Ischemic preconditioning improves maximal performance in humans

Repeated episodes of ischemia followed by reperfusion, commonly referred to as ischemic preconditioning (IPC), represent an endogenous protective mechanism that delays cell injury. IPC also increases blood flow and improves endothelial function. We hypothesize that IPC will improve physical exercise performance and maximal oxygen consumption. The purpose of the study was to examine the effect of ischemic preconditioning in leg skeletal muscles on cycling exercise performance in healthy individuals. Fifteen healthy, well-trained subjects performed two incremental maximal exercise tests on a bicycle ergometer. Power output, oxygen consumption, ventilation, respiratory quotient, and heart rate were measured continuously. Blood pressure and blood lactate were measured before and after the test. One exercise test was performed after the application of ischemic preconditioning, using a protocol of three series of 5-min ischemia at both legs with resting periods of 5 min in between. The other maximal cycling test served as a control. Tests were conducted in counterbalanced order, at least 1 week apart, at the same time of the day. The repeated ischemic periods significantly increased maximal oxygen consumption from 56.8 to 58.4 ml/min per kg (P = 0.003). Maximal power output increased significantly from 366 to 372 W (P = 0.05). Ischemic preconditioning had no effect on ventilation, respiratory quotient, maximal heart rate, blood pressure or on blood lactate. Repeated short-term leg ischemia prior to an incremental bicycle exercise test improves maximal oxygen consumption by 3% and power output by 1.6%. This protocol, which is suggested to mimic the effects of ischemic preconditioning, may have important implications for exercise performance.     

The effect of beta-adrenergic blockade on leg blood flow with repeated maximal contractions of the triceps surae muscle group in man

Summary The effect of -adrenergic blockade on torque output and leg blood flow was examined in seven healthy young men during repeated maximal isometric voluntary contractions of the triceps surae muscle group. Exercise was performed in either a bent- or straight-leg position during each of four drug treatments: placebo, propranolol, metoprolol, oxprenolol. Contractions were sustained for 5 s with 5 s relaxation for a total of 10 min followed by a 10-min recovery. Leg blood flow was measured during the 5 s relaxation separating contractions using strain gauge plethysmography. Torque output decreased during the 10-min contractions with no differences between the four drug treatments. Leg blood flow was lower with -blockade during the initial stages of exercise and recovery in the bent-leg position but no differences were observed after 3 min exercise or recovery. Leg blood flow in the straight-leg position was not different between any of the four drug treatments, but it was significantly less than in bent-leg exercise. The lower blood flows during the initial stages of exercise in the -blocked conditions probably reflect a slowing of the central cardiovascular response because of ₁-receptor blockade of the heart rather than on the ₂-receptors effects on peripheral vacular resistance. It is concluded that local vasodilator substances released from the working muscle may play a more important role than ₂-receptor stimulation of smooth muscle in skeletal muscle resistance vessels in regulating local muscle blood flow during maximal exercise of the triceps surae muscle group.     

A comparison of blood gases and acid-base measurements in arterial,arterialized venous,and venous blood during short-term maximal exercise

Summary The purpose of this study was to determine the relationship between blood gases and acid-base measurements in arterial, arterialized venous, and venous blood measured simultaneously during short-term maximal exercise. Ten well-trained male cyclists performed a graded maximal exercise test on a cycle ergometer to determine the power output corresponding to their peak oxygen consumption (test I), and a short-term maximal test on a cycle ergometer at peak power output (test 11). During test 11 arterial, arterialized venous and venous blood were sampled simultaneously for determination of partial pressures of oxygen and carbon dioxide, pH, bicarbonate (HCO₃ ^–), base excess (BE), and lactate (La). Samples were taken at rest, the end of 1 min of exercise (1 ME), at the end of exercise (EE), and at 2 min of recovery (REC). During test II, subjects maintained a peak power output of 370.6 (62.1) W [mean (SD)] for 4.5, SD 1.6 min. Except at rest venous and arterialized venous measurements tended to be the same at all sampling intervals, but differed significantly from measurements in arterial blood (P<0.05). BE was the only variable that rendered consistently significant correlations between arterial and arterialized venous blood at each sampling interval. The pooled correlation coefficient between arterial and arterialized venous BE was r=0.83 [regression equation: BE_a=(0.84 BE_av)–0.51]. Arterial La was significantly higher than venous La at 1 ME (2.8, 0.7 vs 0.8, 0.3mmol · 1^–1) and higher than both venous and arterialized venous La at EE. At EE La concentration was 9.2, SD 2.0, 4.6, SD 0.4, and 5.1, SD 0.1 mmol · 1^–1 in arterial, venous, and arterialized venous blood respectively. It is concluded that except for base excess, blood gases and acid base measurements in venous and arterialized venous blood do not accurately reflect values found in arterial blood during short-term maximal exercise. We suggest that these differences may be due in part to clearance by inactive muscle near the sampling site or vasoconstriction at the inactive sampling site.     

Tissue oxygenation by near-infrared spectroscopy and muscle blood flow during isometric contractions of the forearm.

The relationship between tissue oxygenation measured by near-infrared spectroscopy (NIRS) and forearm muscle blood flow (FBF) measured by Doppler ultrasound was tested during isometric contractions at 10 and 30% maximal voluntary contraction (MVC) under conditions of normoxia and hypoxia (14% inspired O2). Six subjects maintained contractions at 10% MVC for 5 min and 30% for 2 min in both gas conditions. FBF was elevated during exercise at 10% MVC in hypoxia compared to normoxia, but there was no further increase in flow at 30% MVC. Median power frequency calculations from electromyographic recordings suggested progressive development of fatigue throughout both 10 and 30% MVC contractions. NIRS indicated no change in muscle oxygenation at 10% MVC, but deep venous blood O2 saturation was reduced in normoxia and more so in hypoxia. At 30% MVC, both NIRS and venous O2 saturation were reduced, with no effect of hypoxia on the NIRS signal. While NIRS might provide an indication of muscle oxygenation during isometric exercise, the conflicting findings for NIRS and direct venous blood sampling at 10 vs 30% MVC suggest caution in the application of this noninvasive technique.     

Intramuscular pressure and muscle blood flow in supraspinatus

Summary Intramuscular pressure and muscle blood flow was measured in the supraspinatus muscle in 6 healthy subjects. The recordings were performed at rest, during isometric exercise, during an isometric muscle contraction of 5.6 kPa (42 mm Hg) and 10.4 kPa (78 mm Hg), and at rest after the contraction. Intramuscular pressure was measured by the microcapillary infusion technique, and muscle blood flow by the Xenon-133 washout technique. Intramuscular pressure was 38.2 kPa (SD 12.0) (287 mm Hg) during maximal voluntary contraction. A muscle contraction pressure of 5.6 kPa (42 mm Hg), which is 16% of maximal voluntary contraction, reduces local muscle blood flow significantly. It is concluded that the high intramuscular pressures found in supraspinatus during work with the arms elevated impedes local muscle blood flow.