Reduction in extracellular muscle volume increases heart rate and blood pressure response to isometric exercise

To investigate the effect of local dehydration on heart rate and blood pressure during static exercise, six healthy male subjects performed exercise of the calf muscles with different extracellular volumes of the working muscles. Exercise consisted of 5 min of static calf muscle contractions at about 10% of maximal voluntary contraction. The body position during exercise was identical in all tests, i.e. supine with the knee joint 90 degrees flexed. During a 25-min pre-exercise period three different protocols were employed to manipulate the calf volume. In test A the subjects rested in the exercise position; in test B the body position was the same as in A but calf volumes were increased by venous congestion [cuffs inflated to 10.67 kPa (80 mmHg)]; in test C the calf volumes were decreased by lifting the calves about 40 cm above heart level with the subjects supine. To clamp the changed calf volumes in tests B and C, cuffs were inflated to 300 mmHg 5 min before the onset of exercise. This occlusion was maintained for 1 min after the termination of exercise. Compared to tests A and B, the reduced volume of test C led to significant increases in heart rate and blood pressure during exercise. Oxygen uptake did not exceed resting levels in tests B and C until the cuffs were deflated, indicating that only calf muscles contributed to the neurogenic peripheral drive. It is concluded that extracellular muscle volume plays a significant role in adjusting heart rate and blood pressure during static exercise.     

Venous occlusion to the lower limb attenuates vasoconstriction in the nonexercised limb during posthandgrip muscle ischemia.

We investigated the effects of increases in calf volume on cardiovascular responses during handgrip (HG) exercise and post-HG exercise muscle ischemia (PEMI). Seven subjects completed two trials: one control (no occlusion) and one venous occlusion (VO) session. Both trials included a baseline measurement followed by 15 min of rest (REST), 2 min of HG, and 2 min of PEMI. VO was applied at 100 mmHg via cuffs placed around both distal thighs during REST, HG, and PEMI. Mean arterial pressure, heart rate, forearm blood flow (FBF) in the nonexercised arm, and forearm vascular resistance (FVR) in the nonexercised arm (FVR) were measured. During REST and HG, there were no significant differences between trials in all parameters. During PEMI in the control trial, mean arterial pressure and FVR were significantly greater and FBF was significantly lower than baseline values (P < 0.05 for each). In contrast, in the VO trial, FBF and FVR responses were different from control responses. In the VO trial, FBF was significantly greater than in the control trial (4.7 +/- 0.5 vs. 2.5 +/- 0.3 ml x 100 ml(-1) x min(-1), P < 0.05) and FVR was significantly lower (28.0 +/- 4.8 vs. 49.1 +/- 4.6 units, respectively, P < 0.05). These results indicate that increases in vascular resistance in the nonexercised limb induced by activation of the muscle chemoreflex can be attenuated by increases in calf volume.     

The influence of muscle interstitial volume on K+-induced heart rate drive in rats

During exercise heart rate is influenced by reflexogenic drives which are elicited by receptors situated in the interstitial space. Since the structure of interstitial tissue is complex (e.g. fixed negative charges of glycosaminoglycans), the situation in the immediate surrounding of the receptors might differ from the free fluid phases of blood or lymph in which the concentrations of stimulating substances are usually determined. Physiological variations of the interstitial structure may be due to changes in interstitial volume induced by exercise or the hydrostatic effects on body fluids. The objective of the present study was to investigate the effect of the interstitial volume on the relationship between heart rate and K+ stimuli applied through the muscle blood vessels. The calves of 12 male Wistar rats were artificially perfused and separated from the rest of the body with the sciatic nerve remaining intact. In these preparations the heart rate (HR) responses to low (4 mM) and high (8 mM) potassium concentrations were determined at different interstitial volumes. Expansion of the interstitial volume was obtained by reducing the colloid-osmotic pressure of the perfusate. The combination of intracellular oedema and mechanical limitation of total volume expansion (tapeing) was utilized to decrease the interstitial volume. When switching between the low and high potassium concentrations, significant heart rate responses could be observed only with reduced interstitial volume. It is suggested that the interstitial structure surrounding the muscular receptors modifies the relationship between heart rate response and the K+ stimuli determined in blood or lymph.     

Thermal and circulatory responses during prolonged exercise at different levels of hydration

After a control experiment under initial normal hydration (N), five healthy unacclimated subjects were studied to investigate the effects of initial hypo- and hyperhydration on cardiovascular and thermo-regulatory responses to prolonged intermittent exercise in the heat (To = 36 degrees C; Tdp = 10 degrees C; Va = 0.6 m.s-1). Prior hydrohydration (O) was obtained by diuretics and prior hyperhydration (R) by ingestion of 0.5 L of isotonic (ISO) electrolyte sucrose solution 30 min before the experiments (4 h) started. Exercise (70 W) lasted 3 hours, and was periodically interrupted by resting periods (5-10 min). Three dehydration (D) runs were thus performed under the three initial hydration states (O,N,R) without fluid replacement during the exercise period. Four additional rehydration runs were carried out: 2 in each initial hydration level (O, R) included ingestion (at 36 degrees C) of water or ISO-solution during the first 3 hours. Physiological measurements were continuously recorded and hourly blood samples (15 ml) were obtained. Results showed that dehydration increased core temperature and heart rate and provoked blood hypovolemia and hyperosmolarity, the latter being somewhat prevented by prior ISO-ingestion. Dehydration reduced significantly the overall sweat rate only in hypohydrated subjects and the large hyperosmolarity seemed to be responsible for this. The significant Tcore rise during dehydration is unlikely to be the result of a decrease in evaporative heat transfer, which was found only in the case of initial hypohydration. Rehydration during exercise with water or ISO-solution induced different dynamic responses depending on the initial hydration level, but it never restored plasma volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fluid balance in exercise dehydration and rehydration with different glucose-electrolyte drinks

After exercise dehydration (3% of body weight) the restoration of water and electrolyte balance was followed in 6 male subjects. During a 2 h rest period after exercise, a drink of one of four solutions was given as 9 X 300 ml portions at 15 min intervals: control (C-drink), high potassium (K-drink), high sodium (Na-drink) or high sugar (S-drink). An exercise test (submaximal and supramaximal work) was performed before dehydration and after rehydration. Dehydration reduced plasma volume by 16%, a process reversed on resting even before fluid ingestion began, due to release of water accumulated in the muscles during exercise. After 2 h rehydration, plasma volume was above the initial resting value with all 4 drinks. The final plasma volumes after the Na-drink (+14%) and C-drink (+9%) were significantly higher than after the K- and S-drinks. The Na-drink favoured filling of the extracellular compartment, whereas the K- and S-drinks favoured intracellular rehydration. In spite of the higher than normal plasma volume after rehydration, mean heart rate during the submaximal test was 10 bpm higher after rest and rehydration than in the initial test, and was not different between the drinks. The amount of work which could be performed in the supramaximal test (105% VO2max) was 20% less after exercise dehydration and subsequent rest and rehydration than before. This reduction was similar for all drinks, and may be due to a decreased muscle glycogen content (70% of initial) at the time of the second test.     

Differential control of forearm and calf vascular resistance during one-leg exercise

The purpose of this study was to determine whether blood flow (BF) and vascular resistance (VR) are controlled differently in the nonactive arm and leg during submaximal rhythmic exercise. In eight healthy men we simultaneously measured BF to the forearm and calf (venous occlusion plethysmography) and arterial blood pressure (sphygmomanometry) and calculated whole limb VR before (control) and during 3 min of cycling with the contralateral leg at 38, 56, and 75% of peak one-leg O2 uptake (VO2). During the initial phase of exercise (0-1.5 min) at all work loads, BF increased and VR decreased in the forearm (P less than 0.05), whereas calf BF and VR remained at control levels. Thereafter, BF decreased and VR increased in parallel and progressive fashion in both limbs. At end exercise, forearm BF and VR were not different from control values (P greater than 0.05); however, in the calf, BF tended to be lower (P less than 0.05 at 75% peak VO2 only) and VR was higher (23 +/- 9, 44 +/- 14, and 88 +/- 23% above control at 38, 56, and 75% of peak VO2, respectively, all P less than 0.05). In a second series of studies, forearm and calf skin blood flow (laser-Doppler velocimetry) and arterial pressure were measured during the same levels of exercise in six of the subjects. Compared with control, skin BF was unchanged and VR was increased (P less than 0.05) in the forearm by end exercise at all work loads, whereas calf skin BF increased (P less than 0.05) and VR decreased (P less than 0.05). The present findings indicate that skeletal muscle and skin VR are controlled differently in the nonactive forearm and calf during the initial phase of rhythmic exercise with the contralateral leg. Skeletal muscle vasodilation occurs in the forearm but not in the calf; forearm skin vasoconstricts, whereas calf skin vasodilates. Finally, during exercise a time-dependent vasoconstriction occurs in the skeletal muscle of both limbs.     

On physiological edema in man's lower extremity

To examine whether the so-called musculovenous pump counteracts the development of interstitial edema in the lower extremities of man in the upright position, the volume changes in the calf which occurred during twenty minutes of rhythmic muscular exercise were measured in twenty-three subjects by impedance-plethysmography. The results were compared with the volume increase found during quiet relaxed standing for the same length of time. Contrary to the hypothesis, and edema-protective effect of the musculovenous pump could only be shown in about half the number of the subjects. In the others, muscular exercise led to increases in calf volume which were higher than those measured in the normal upright position. These results show that the calf muscle pump does not generally have a edema-protective effect but rather that muscle contractions also activate mechanisms which stimulate the extravasation of fluid. In a second test-series with twenty subjects, changes in calf volume were measured during the course of the day. In nearly all cases, the calf volume was greater in the evening than in the morning. It could be shown that the volume increases in the evening are caused by an increase in extravascular fluid. Compared to the increase in extravascular volume occurring during twenty minutes, in a normal upright position, the accumulation of extravascular fluid during the day is, however, remarkably low. Although it is still unknown how interstitial edema in man's lower extremities is prevented during the day, these findings lead to the hypothesis that the edema-preventing mechanisms, for instance the muscle-lymphpump, do not become maximally effective until a certain volume has accumulated in the interstitial space.     

On the edema-preventing effect of the calf muscle pump

During motionless standing an increased hydrostatic pressure leads to increased transcapillary fluid filtration into the interstitial space of the tissues of the lower extremities. The resulting changes in calf volume were measured using a mercury-in-silastic strain gauge. Following a change in body posture from lying to standing or sitting a two-stage change in calf volume was observed. A fast initial filling of the capacitance vessels was followed by a slow but continuous increase in calf volume during motionless standing and sitting with the legs dependent passively. The mean rates of this slow increase were about 0.17%.min-1 during standing and 0.12%.min-1 during sitting, respectively. During cycle ergometer exercise the plethysmographic recordings were highly influenced by movement artifacts. These artifacts, however, were removed from the recordings by low-pass filtering. As a result the slow volume changes, i.e. changes of the extravascular fluid were selected from the recorded signal. Contrary to the increases during standing and sitting the calf volumes of all 30 subjects decreased during cycle ergometer exercise. The mean decrease during 18 min of cycling (2-20 min) was -1.6% at 50 W work load and -1.9% at 100 W, respectively. This difference was statistically significant (p less than or equal to 0.01). The factors which may counteract the development of an interstitial edema, even during quiet standing and sitting, are discussed in detail. During cycling, however, three factors are most likely to contribute to the observed reduction in calf volume: (1) The decrease in venous pressure, which in turn reduces the effective filtration pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enhanced slow caudad fluid shifts in orthostatic intolerance after 24-h bed-rest

To evaluate mechanisms of late orthostatic intolerance, slow fluid shifts along the body axis were studied during deconditioning by 24-h bed-rest and during 13-min upright tilts before and after this manoeuvre. In 11 healthy male subjects the fluid volumes of a thorax and a calf segment (impedance plethysmography) as well as tissue thickness at the forehead and the tibia (miniature ultrasonic plethysmograph) were recorded. Cardiovascular performance was monitored by recording heart rate (electrocardiogram), brachial and finger arterial pressure (by the Riva Rocci method and by the Finapres technique) as well as stroke volume (by impedance cardiography). Bed-rest led to a cephalad fluid shift with a mean interstitial leg dehydration of 2.2 ml·-100 ml^–1 with no changes in body mass and plasma volume. No syncope during the tilt occurred before bed-rest, while after bed-rest 8 subjects fainted between min 2.1 and 9.0 of the tilt. Bed-rest resulted in an augmented initial heart rate response to tilting which was similar in all subjects. In later orthostasis, bed-rest caused two- to threefold faster caudad fluid shifts with higher calf filtration rates in fainters (prior to hypotension) than in nonfainters. Through bed-rest the estimated extravasation within 10 min into general lower body tissue spaces increased by 192 ml in (late) fainters as opposed to only 23 ml in nonfainters. It was concluded that contributing factors to orthostatic intolerance may be slow transcapillary fluid shifts which are easily underestimated and whose quantity and time course call for further investigation after various deconditioning manoeuvres. In particular, the postflight fluid shifts in astronauts who will have markedly dehydrated legs, may impose a circulatory stress which needs to be evaluated. In general, the filtration rate in relevant areas appears to be an integrative and easily determined parameter, reflecting hormonal and neurogenic vascular as well as local interstitial control of the Starling forces.     

Fluid replacement and glucose infusion during exercise prevent cardiovascular drift.

This study examined the influence of both hydration and blood glucose concentration on cardiovascular drift during exercise. We first determined if the prevention of dehydration during exercise by full fluid replacement prevents the decline in stroke volume (SV) and cardiac output (CO) during prolonged exercise. On two occasions, 10 endurance-trained subjects cycled an ergometer in a 22 degrees C room for 2 h, beginning at 70 +/- 1% maximal O2 uptake (VO2max) and in a euhydrated state. During one trial, no fluid (NF) replacement was provided and the subject's body weight declined 2.09 +/- 0.19 kg or 2.9%. During the fluid replacement trial (FR), water was ingested at a rate that prevented body weight from declining after 2 h of exercise (i.e., 2.34 +/- 0.17 1/2 h). SV declined 15% and CO declined 7% during the 20- to 120-min period of the NF trial while heart rate (HR) increased 10% and O2 uptake (VO2) increased 6% (all P less than 0.05). In contrast, SV was maintained during the 20- to 120-min period of FR while HR increased 5% and thus CO actually increased 7% (all P less than 0.05). Rectal temperature, SV, and HR were similar during the 1st h of exercise during NF and FR. However, after 2 h of exercise, rectal temperature was 0.6 degree C higher (P less than 0.05) and SV and CO were 11-16% lower (P less than 0.05) during NF compared with FR.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular responses to military antishock trouser inflation during standing arm exercise

Military antishock trousers (MAST) inflated to 50 mmHg were used with 12 healthy males (mean age 28 +/- 1 yr) to determine the effects of lower-body positive pressure on cardiac output (Q), stroke volume (SV), heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MABP), total peripheral resistance (TPR), and O2 uptake (VO2) during graded arm-cranking exercise. Subjects were studied while standing at rest and at 25, 50, and 75% of maximal arm-cranking VO2. At each level, rest or work was continued for 6 min with MAST inflated and for 6 min with MAST deflated. Order of inflation and deflation was alternated at each experimental rest or exercise level. Measurements were obtained during the last 2 min at each level. Repeated-measures analysis of variance revealed significant increases (P less than 0.001) in Q, SV, and MABP and a consistent decrease in HR with MAST inflation. There was no apparent change in Q/VO2 between inflated and control conditions. There was no effect of MAST inflation on VO2 or TPR. MAST inflation counteracts the gravitational effect of venous return in upright exercise, restoring central blood volume and thereby increasing Q and MABP from control. HR is decreased consequent to increased MABP through arterial baroreflexes. The associated decrease in TPR is not observed, being offset by the mechanical compression of leg vasculature with MAST inflation.     

Plasma volume changes during and after acute variations of body hydration level in humans

This study examined plasma volume changes (deltaPV) in humans during periods with or without changes in body hydration: exercise-induced dehydration, heat-induced dehydration and glycerol hyperhydration. Repeated measurements of plasma volume were made after two injections of Evans blue. Results were compared to deltaPV calculated from haematocrit (Hct) and blood haemoglobin concentration ([Hb]). Eight well-trained men completed four trials in randomized order: euhydration (control test C), 2.8% dehydration of body mass by passive controlled hyperthermia (D) and by treadmill exercise (60% of their maximal oxygen uptake, VO2max) (E), and hyperhydration (H) by glycerol ingestion. The Hct, [Hb], plasma protein concentrations and plasma osmolality were measured before, during and after the changes in body hydration. Different Hct and [Hb] reference values were obtained to allow for posture-induced variations between and during trials. The deltaPV values calculated after two Evans blue injections were in good agreement with deltaPV calculated from Hct and [Hb]. Compared to the control test, mean plasma volume declined markedly during heat-induced dehydration [-11.4 (SEM 1.7)%] and slightly during exercise-induced dehydration [-4.2 (SEM 0.9)%] (P < 0.001 compared to D), although hyperosmolality was similar in these two trials. Conversely, glycerol hyperhydration induced an increase in plasma volume [+7.5 (SEM 1.0)%]. These results would indicate that, for a given level of dehydration, plasma volume is dramatically decreased during and after heat exposure, while it is better maintained during and after exercise.     

Muscle chemoreflex elevates muscle blood flow and O2 uptake at exercise onset in nonischemic human forearm.

We tested the hypothesis that increases in forearm blood flow (FBF) during the adaptive phase at the onset of moderate exercise would allow a more rapid increase in muscle O2 uptake (VO2 mus). Fifteen subjects completed forearm exercise in control (Con) and leg occlusion (Occ) conditions. In Occ, exercise of ischemic calf muscles was performed before the onset of forearm exercise to activate the muscle chemoreflex evoking a 25-mmHg increase in mean arterial pressure that was sustained during forearm exercise. Eight subjects who increased FBF during Occ compared with Con in the adaptation phase by >30 ml/min were considered "responders." For the responders, a higher VO2 mus accompanied the higher FBF only during the adaptive phase of the Occ tests, whereas there was no difference in the baseline or steady-state FBF or VO2 mus between Occ and Con. Supplying more blood flow at the onset of exercise allowed a more rapid increase in VO2 mus supporting our hypothesis that, at least for this type of exercise, O2 supply might be limiting.     

Hypohydration affects forearm vascular conductance independent of heart rate during exercise.

Elevated body core temperature stimulates cutaneous vasodilation, which can be modified by nonthermal factors. To test whether hypohydration affects forearm vascular conductance discretely from relative alterations in heart rate (HR), eight trained cyclists exercised progressively for 20 min each at 60, 120, and 180 W [approximately 22, 37, and 55% of maximal cycling O2 consumption (VO2peak), respectively] in a warm humid environment (dry bulb temperature 30 degrees C; wet bulb temperature 24 degrees C). Esophageal temperature and forearm blood flow were measured every 30 s, and mean arterial pressure and HR were measured at rest and during each exercise intensity (minutes 15, 35, and 55). In the hypovolemic (HP) compared with the euvolemic (EU) state, blood volume was contracted by 24-h fluid restriction an average of 510 ml, and this difference was sustained throughout exercise. The esophageal temperature and HR responses were similar between EU and HP states at 60 and 120 W but were significantly (P < 0.05) higher in HP by the end of 180 W. In contrast, the forearm blood flow response was significantly (P < 0.05) depressed during exercise at 120 and 180 W in HP, whereas mean arterial pressure remained similar between conditions. When body core temperature is elevated in a hypohydrated state, forearm vascular conductance is reduced at exercise intensities of approximately 37% VO2peak, which is independent of relative changes in HR. These findings are consistent with the notion that during exercise an attenuated cutaneous vasodilation is elicited by alterations in regionalized sympathetic outflow, which is unaccompanied by activation of cardiac pacemaker cells.     

Prolonged decrease in cardiac volumes after maximal upright bicycle exercise

Sequential exercise-gated cardiac blood pool scintigrams provide a noninvasive technique for evaluating the effect of therapeutic interventions on cardiac volumes and function only if both exercise periods are equivalent in the absence of an intervention. To assess whether they are indeed equivalent, 14 healthy subjects underwent gated blood pool scintigraphy during two maximal upright exercise periods separated by 60 min without changing position. Although resting cardiac output and blood pressure returned to base-line values 60 min after the first exercise period, mean resting heart rate was markedly higher (89.4 +/- 2.7 vs. 66.5 +/- 2.5 beats/min, P less than 0.001) and upright cardiac volumes lower [39.1 +/- 4.9 vs. 56.3 +/- 6.0 ml, P less than 0.001, for end-systolic volume (ESV) and 112.6 +/- 8.0 vs. 144.9 +/- 9.0 ml, P less than 0.001, for end-diastolic volume (EDV)] than before the first exercise period. These differences persisted during low levels of the subsequent exercise but not at high and maximum work loads. Cardiac volumes and heart rate 60 min after an identical exercise protocol in a second group of 22 subjects who received propranolol, 0.15 mg/kg iv, after their initial exercise, however, were the same as those preexercise. Thus higher sympathetic tone may be responsible for the persistently higher heart rate and decreased cardiac volumes after exercise, and the assumption that cardiac volumes and function are similar during two closely spaced sequential exercise studies is not always valid.     

Ventilatory control studied with circulatory occlusion during exercise recovery

Mechanisms involved in the control of pulmonary ventilation were studied in seven male subjects following 6 min of exercise on a cycle ergometer at 98w. Circulation to the legs was occluded by thigh cuffs (27 kPa) during the last 15 s of exercise and the subsequent 4 min of recovery. Respiratory gas exchange and the tidal partial pressures of O2 and CO2 were measured breath-by-breath. The results were compared to control studies without occlusion. There was a significant increase in both systolic and diastolic blood pressures during occluded recovery. Following occlusion systolic pressure remained elevated while diastolic pressure returned to control values. Occlusion during recovery caused hyperventilation during the first 1.5 min after exercise as evidenced by significantly higher VE/VCO2, VE/VO2, PETO2, and lower PETCO2. Following the release of the cuffs PETCO2, VE, VCO2, VO2, and heart rate all increased significantly above control values, while PETO2 decreased. PETCO2 rose abruptly 14.5 +/- 0.9 s after the release of the cuffs. Marked increases in VE and heart rate were seen, and occurred 30.8 +/- 1.5 s and 12.8 +/- 1.3 s, respectively, after cuff release. The 16.3 +/- 1.4 s lag between the increase in PETCO2 and VE after occlusion suggests that the ventilatory response to a sudden load of hypercapnic blood is not mediated by a pulmonary chemoreceptor. Other receptors, probably the peripheral chemoreceptors, appear to be responsible for hypercapnic hyperventilation.     

Effect of graded erythrocythemia on cardiovascular and metabolic responses to exercise

The effects of graded induced erythrocythemia on cardiovascular and metabolic responses to intense treadmill running were studied in four highly trained endurance runners. Three autologous infusions of 1 unit (U) whole blood (450 ml/U) were administered sequentially 2-7 days apart. Maximal O2 consumption (VO2max) increased from 5.04 l/min at control (C) to 5.24 l/min after 2 U (R2) and 5.38 l/min after 3 U (R3). Cardiac output during treadmill running at 91% control VO2max was 28.2 l/min at C, 29.8 l/min at R2, and 33.1 l/min at R3. Corresponding heart rates were unchanged, and stroke volume was increased at R3. Peak lactate concentration was reduced, and arterial acid-base status improved at R2 and R3 after standardized bouts of intense exercise. Arterial blood pressures and electrocardiograms during exercise were not affected by erythrocythemia. We conclude that the reinfusion of up to 3 U of autologous blood into highly trained endurance runners who have normal hematology does not adversely affect their cardiovascular response to maximal exercise. In addition, the increases in VO2max following reinfusion of 2 U, and again after 3 U, suggest that the aerobic power of the working muscles was not surpassed at these levels of erythrocythemia.     

Kinetics of oxygen uptake during supine and upright heavy exercise.

It is presently unclear how the fast and slow components of pulmonary oxygen uptake (VO(2)) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (VO(2) equal to 50% of the difference between LT and peak VO(2)) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in VO(2) was similar in the two positions, but VO(2) kinetics were slower in the supine position. During heavy exercise, the rate of adjustment of VO(2) to the 6-min value was also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component of VO(2), without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exercise VO(2) was the same in the two positions. The changes in VO(2) kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component for VO(2) but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position.     

Lowering of interstitial fluid pressure in rat submandibular gland: a novel mechanism in saliva secretion

The submandibular gland transports fluid at a high rate through the interstitial space during salivation, but the exact level of all forces governing transcapillary fluid transport has not been established. In this study, our aim was to measure the relation between interstitial fluid volume (V(i)) and interstitial fluid pressure (P(if)) in salivary glands during active secretion and after systemically induced passive changes in gland hydration. We tested whether interstitial fluid could be isolated by tissue centrifugation to enable measurement of interstitial fluid colloid osmotic pressure. During control conditions, V(i) averaged 0.23 ml/g wet wt (SD 0.014), with a corresponding mean P(if) measured with micropipettes of 3.0 mmHg (SD 1.3). After induction of secretion by pilocarpine, P(if) dropped by 3.8 mmHg (SD 1.5) whereas V(i) was unchanged. During dehydration and overhydration of up to 20% increase of V(i) above control, a linear relation was found between volume and pressure, resulting in a compliance (DeltaV(i)/DeltaP(if)) of 0.012 ml.g wet wt(-1).mmHg(-1). Interstitial fluid was isolated, and interstitial fluid colloid osmotic pressure averaged 10.4 mmHg (SD 1.2), which is 64% of the corresponding level in plasma. We conclude that P(if) drops during secretion and, thereby, increases the net transcapillary pressure gradient, a condition that favors fluid filtration and increases the amount of fluid available for secretion. The reduction in P(if) is most likely induced by contraction of myoepithelial cells and suggests an active and new role for these cells in salivary secretion. The relatively low interstitial compliance of the organ will enhance the effect of the myoepithelial cells on P(if) during reduced V(i).     

Effect of fluid intake on renal function during exercise in the cold

The effect of an imposed drinking discipline versus ad libitum drinking was studied on 21 healthy, well-trained volunteers, during a continuous 4.5-h march at an altitude of 1,700 m and an ambient temperature of 0 degree C, SD 1. Group I (n = 13) was instructed to drink 250 ml of warmed, artificially sweetened fluid every 30 min, whereas group II (n = 8) drank plain water ad libitum. The median fluid intake in group I was significantly higher than in group II (P less than 0.0002). Serum urea and osmolality decreased during the march in group I (P less than 0.05; P less than 0.002, respectively) with no significant change in group II. In both groups, a similar increase in haemoglobin concentration concomitant with a reduction in calculated blood and plasma volume was observed after exercise and did not correlate with the state of hydration. Total urine volume, creatinine clearance, urea clearance and potassium excretion were significantly higher and urinary osmolality was lower in group I than in group II (P less than 0.05). These results reflect a state of extreme "voluntary dehydration" in the control group when no fluid intake was obligatory. Thus, during exercise in the cold, under conditions similar to those in this study, a fluid intake of 150 ml.h-1 should be maintained in order to keep a urinary flow of about 1 ml.kg-1.h-1 and to achieve a good state of hydration.