Venous Stasis and Forearm Exercise During Venipuncture as Sources of Error in Plasma Electrolyte Determinations

A study was made of errors in plasma sodium, potassiu, chloride and calcium determinations caused by venous stasis and forearm exercise during venipuncture. Blood samples were taken from both arms of healthy young adults, one arm being used as a control. Analyses were performed in a routine hospital laboratory and the technicians were unaware of the identity of the samples. Laboratory precision was assessed at the same time.Venous stasis alone for two minutes caused no significant change, but the use of continuous slow forearm exercise for one minute caused mean elevations of 0.73 mEq./1. in potassium, and 0.4 mg. per 100 ml. in calcium, the maximum elevations being 1.1 mEq/1. and 1.3 mg. per 100 ml., respectively. A clinically unimportant but significant increase in sodium values of 1.40 mEq./1. was also observed. Chloride values were not affected. In addition there was a substantial error in calcium determinations in the laboratory, which emphasizes the need for repeated calcium determinations to avoid diagnostic error.The conclusion is reached that forearm exercise must be avoided during venipuncture.     

Venous plasma potassium is not associated with maintenance of the exercise pressor reflex in humans

Increases in the concentration of interstitial potassium concentration during exercise may play a role in the modulation of the cardiovascular response to exercise. However, it is not known if changes in potassium correlate with indexes of muscle reflex engagement. Eight healthy subjects performed dynamic [rhythmic handgrip (RHG)] and static handgrip (SHG) exercise at 40% of maximal voluntary contraction. Forearm circulatory arrest was performed to assess the metaboreceptor component of the exercise pressor reflex. Mean arterial pressure (MAP) and muscle sympathetic nerve activity (MSNA) were measured during each exercise paradigm. Venous plasma potassium concentrations ([K(+)](V)) were measured and used as a surrogate marker for interstitial potassium. [K(+)](V) were measured at baseline and at 1-min intervals during dynamic handgrip. During SHG, [K(+)](V) were measured at baseline, 30 and 90 s of exercise, and twice during forearm circulatory arrest. Mean [K(+)](V) was 3.6 mmol/l at rest before both paradigms. During RHG, [K(+)](V) rose by approximately 1.0 mmol/l by min 2 and remained constant throughout the rest of handgrip. During SHG, [K(+)](V) rose significantly at 30 s and rose an additional approximately 1.0 mmol/l by peak exercise. MAP and MSNA rose during both exercise paradigms. During posthandgrip circulatory arrest (PHG-CA), MSNA and blood pressure remained above baseline. [K(+)](V) and MSNA did not correlate during either exercise paradigm. Moreover, during PHG-CA, there was clear dissociation of MSNA from [K(+)](V). These data suggest that potassium does not play a direct role in the maintenance of the exercise pressor reflex.     

Effects of combined inhibition of ATP-sensitive potassium channels, nitric oxide, and prostaglandins on hyperemia during moderate exercise.

ATP-sensitive potassium (KATP) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that KATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the KATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 microg.dl(-1).min(-1)), followed by saline infusion during the final 10 min of exercise (n = 9). Exercise increased FBF from 71 +/- 11 to 239 +/- 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by approximately 50%, whereas blood glucose was unchanged (88 +/- 2 vs. 90 +/- 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of NG-nitro-L-arginine methyl ester (L-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L-NAME + ketorolac (i.e., triple blockade) reduced FBF by approximately 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of KATP channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and KATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals.     

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.     

Exercise hyperemia and vasoconstrictor responses in humans with cystic fibrosis.

ATP released from circulating erythrocytes is a potential signal regulating muscle blood flow during exercise (exercise hyperemia), and intravascular ATP appears to blunt sympathetic vasoconstriction during exercise. Erythrocytes from patients with cystic fibrosis (CF) do not release ATP. The goal of the present study was to determine whether increases in forearm blood flow during exercise are blunted in CF patients and whether CF patients exhibit greater vasoconstrictor responsiveness during exercise. Nine control subjects and 10 CF patients who were free of other disease complications (approximately 96% O2 saturation) performed incremental rhythmic forearm exercise at 5, 10, and 15% of maximum handgrip strength for 21 min (7 min at each workload). We used a cold pressor test to evoke sympathetic vasoconstriction under resting conditions and at each exercise workload. As a control, subjects performed a second exercise bout without the cold pressor test. Continuous brachial artery blood velocity was monitored beat-to-beat, and vessel diameter was assessed by Doppler ultrasound. Artery diameter, as well as blood pressure, heart rate, and O2 saturation, was measured at steady-state exercise and at 1 min into the cold pressor stimulus. Blood pressure and heart rate responses to the forearm exercise and each cold pressor test were similar in both groups (P > 0.05). Contrary to our hypothesis, forearm blood flow (P = 0.91) and forearm vascular conductance (P = 0.82) were similar at rest and at each level of exercise between CF patients and controls. Additionally, there was no difference in the degree of sympathetic vasoconstriction between groups at rest and at each level of exercise (P = 0.22). Our results suggest that ATP released from the deformation of erythrocytes is not an obligatory signal for exercise hyperemia in human skeletal muscle.     

Dependence on exercise intensity of changes in electrolyte secretion from the skin sampled by a simple method

Secreta from the palm and forearm was sampled for 1-min periods by a new technique, using a glass cylinder. Subjects exercised for 10-min periods at successive intensities of 40%, 50% and 65% VO2max with a leg ergometer operated in the supine position. Changes in the concentrations (values) of Na+, K+ and Cl- in their secreta during exercise were investigated. Significant positive correlations were found between the values of any two electrolytes in samples from the palm or the forearm, but the correlations between values for any one of the three electrolytes from the two sites were not significant. Values for concentrations of the electrolytes were significantly higher in samples from the palm than in those from the forearm at rest, 10 min after the beginning of exercise and at the end of exercise. No significant correlation was found between values for electrolytes in samples from the palm and the exercise intensity, but values for Na+ in samples from the forearm increased stepwise with increase in exercise intensity, and similar tendencies were observed for values of K+ and Cl-. The values for the three electrolytes in samples from the forearm, but not the palm, were significantly correlated with values for blood lactate, the percentage of VO2max and the heart rate. These results suggest that the present technique is suitable for successive samplings of secreta from the forearm, and that values for the electrolytes in samples are useful indices of exercise intensity.     

Physiological effects of micropauses in isometric handgrip exercise

The physiological response to continuous and intermittent handgrip exercise was evaluated. Three experiments were performed until exhaustion at 25% of maximal voluntary contraction (MVC): experiment 1, continuous handgrip (CH) (n = 8); experiment 2, intermittent handgrip with 10-s rest pause every 3 min (IH) (n = 8); and experiment 3, as IH but with electrical stimulation (ES) of the forearm extensors in the pauses (IHES) (n = 4). Before, during, and after exercise, recordings were made of heart rate (HR), arterial blood pressure (BP), exercising forearm blood flow, and concentrations of potassium [K+] and lactate [La-] in venous blood from both arms. The electromyogram (EMG) of the exercising forearm extensors and perceived exertion were monitored during exercise. Before and up to 24 h after exercise, observations were made of MVC, of force response to electrical stimulation and of the EMG response to a 10-s test contraction (handgrip) at 25% of the initial MVC. Maximal endurance time (tlim) was significantly longer in IH (23.1 min) than in CH (16.2 min). The ES had no significant effect on tlim. During exercise, no significant differences were seen between CH and IH in blood flow, venous [K+] and [La-], or EMG response. The HR and BP increased at the same rate in CH and IH but, because of the longer duration of IH, the levels at exhaustion were higher in this protocol. The subjects reported less subjective fatigue in IH. During recovery, return to normal MVC was slower after CH (24 h) than after IH (4 h).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral leucine uptake and protein synthesis in the near-term ovine fetus: relation to fetal behavioral state

To investigate quantitatively how sweating and cutaneous blood flow responses at the onset of dynamic exercise are affected by increasing exercise intensity in mildly heated humans, 18 healthy male subjects performed cycle exercise at 30, 50, and 70% of maximal O2 uptake (VO2 max) for 60 s in a warm environment. The study was conducted in a climatic chamber with a regulated ambient temperature of 35 degrees C and relative humidity of 50%. The subjects rested in the semisupine position in the chamber for 60 min, and then sweating rate (SR) and skin blood flow were measured during cycle exercise at three different intensities. Changes in the heart rate, rating of perceived exertion, and mean arterial blood pressure were proportional to increasing exercise intensity, whereas esophageal and mean skin temperatures were essentially constant throughout the experiment. The SR on the chest, forearm, and thigh, but not on the palm, increased significantly with increasing exercise intensity (P < 0.05). The mean SR of the chest, forearm, and thigh increased 0.05 mg.cm-2.min-1 with an increase in exercise intensity equivalent to 10% VO2 max. On the other hand, the cutaneous vascular conductance (CVC) on the chest, forearm, and palm decreased significantly with increasing exercise intensity (P < 0.05). The mean CVC of the chest and forearm decreased 5.5% and the CVC on the palm decreased 8.0% with an increase in exercise intensity equivalent to 10% VO2 max. In addition, the reduction in CVC was greater on the palm than on the chest and forearm at all exercise intensities (P < 0.01). We conclude that nonthermal sweating and cutaneous blood flow responses are exercise intensity dependent but directionally opposite at the onset of dynamic exercise in mildly heated humans. Furthermore, cutaneous blood flow responses to increased exercise intensity are greater in glabrous (palm) than in nonglabrous (chest and forearm) skin.     

Local bone mineral response to brief exercise that stresses the skeleton.

OBJECTIVE--To compare grip strength and bone mineral content in the forearm in women and to test the effects on bone mineral content of short periods of exercise that stresses the skeleton. DESIGN--Assessment of both wrists in 69 volunteers and of the non-fractured wrist in 30 patients followed by an exercise regimen entailing squeezing a tennis ball as hard as possible for 30 seconds each day for six weeks. SETTING--Old people''s homes and outpatient departments of Hammersmith and Northampton general hospitals. PATIENTS--99 Women, of whom 69 were volunteers and 30 had a fractured forearm. MAIN OUTCOME MEASURE--Grip strength and bone mineral content after six weeks and at six months after the exercises had stopped. RESULTS--The bone mineral content of the women''s forearms was measured with a densitometer and the grip strength with a semi-inflated bag connected to an anaeroid barometer. Measurements before exercise showed that the two variables correlated closely, irrespective of age, and that there were significant differences in both between the dominant and non-dominant arms of the volunteers. After six weeks of exercise there was a mean increase in grip strength of 14.5% (95% confidence interval 9.9 to 19.2%) and in bone mineral content of 3.4% (1.4 to 5.3%) in the stressed forearms of the 77 women who attended for examination. After six months without exercise the improvements in the 33 women who attended for follow up had reversed. Women who had had a fractured forearm (n = 13), however, had continued to gain grip strength and bone mineral content in the arm that had not been injured. CONCLUSIONS--Grip strength in the forearm is a good indicator of bone mineral content. Both variables may be increased by brief periods of stressful exercise. If this principle can be applied to the whole skeleton it may provide a means of reversing osteoporosis.     

Measurement of forearm blood flow by venous occlusion plethysmography: influence of hand blood flow during sustained and intermittent isometric exercise

The requirement for using an arterial occlusion cuff at the wrist when measuring forearm blood flows by plethysmography was tested on a total of 8 subjects at rest and during and after sustained and intermittent isometric exercise. The contribution of the venous effluent from the hand to the forearm flow during exercise was challenged by immersing the arm in water at 20, 34, and 40 degrees C. Occlusion of the circulation to the hand reduced the blood flow through the resting forearm at all water temperatures. There was an inverse relationship between the temperature of the water and the proportion in the reduction of forearm blood flow upon inflation of the wrist-cuff, ranging from 45 to 19% at 20 degrees to 40 degrees C, respectively. However, during sustained isometric exercise at 10% of the subjects maximum voluntary contraction (MVC) there was no reduction in the measured forearm flow when an arterial occlusion cuff was inflated aroung the wrist. Similarly, there was no alteration in the blood flow measured 2 s after each of a series of intermittent isometric contractions exerted at 20% or 60% MVC for 2 s whether or not circulation to the hand was occluded nor of the post-exercise hyperemia following 1 min of sustained contraction at 40% MVC. These results indicate that a wrist-cuff is not required for accurate measurement of forearm blood flows during or after isometric exercise.     

Blood flow and muscle oxygen uptake at the onset and end of moderate and heavy dynamic forearm exercise

We hypothesized that forearm blood flow (FBF) during moderate intensity dynamic exercise would meet the demands of the exercise and that postexercise FBF would quickly recover. In contrast, during heavy exercise, FBF would be inadequate causing a marked postexercise hyperemia and sustained increase in muscle oxygen uptake (VO(2musc)). Six subjects did forearm exercise (1-s contraction/relaxation, 1-s pause) for 5 min at 25 and 75% of peak workload. FBF was determined by Doppler ultrasound, and O(2) extraction was estimated from venous blood samples. In moderate exercise, FBF and VO(2musc) increased within 2 min to steady state. Rapid recovery to baseline suggested adequate O(2) supply during moderate exercise. In contrast, FBF was not adequate during heavy dynamic exercise. Immediately postexercise, there was an approximately 50% increase in FBF. Furthermore, we observed for the first time in the recovery period an increase in VO(2musc) above end-exercise values. During moderate exercise, O(2) supply met requirements, but with heavy forearm exercise, inadequate O(2) supply during exercise caused accumulation of a large O(2) deficit that was repaid during recovery.     

Localized β-adrenergic receptor blockade does not affect sweating during exercise

The purpose of the current study was to determine the effect of a locally administered nonselective β-adrenergic antagonist on sweat gland function during exercise. Systemically administered propranolol has been reported to increase, decrease, or not alter sweat production during exercise. To eliminate the confounding systemic effects associated with orally administered propranolol, we used iontophoresis to deliver it to the eccrine sweat glands within a localized area on one forearm prior to exercise. This allowed for determination of the direct effect of β-adrenergic receptor blockade on sweating during exercise. Subjects (n = 14) reported to the laboratory (23 ± 1°C, 35 ± 3% relative humidity) after having refrained from exercise for ≥12 h. Propranolol (1% solution) was administered to a 5-cm(2) area of the flexor surface of one forearm via iontophoresis (1.5 mA) for 5 min. A saline solution was administered to the opposing arm via iontophoresis. Each subject then exercised on a motor-driven treadmill at 75% of their age-predicted maximal heart rate for 20 min, while sweat rate was measured simultaneously in both forearms. Immediately after cessation of exercise, the number of active sweat glands was measured by application of iodine-impregnated paper to each forearm. The sweat rate for the control and propranolol-treated forearm was 0.62 ± 41 and 0.60 ± 0.44 (SD) mg·cm(-2)·min(-1), respectively (P = 0.86). The density of active sweat glands for the control and propranolol-treated forearm was 130 ± 6 and 134 ± 5 (SD) glands/cm(2), respectively, (P = 0.33). End-exercise skin temperature was 32.9 ± 0.2 and 33.1 ± 0.3°C for the control and propranolol-treated forearm, respectively (P = 0.51). Results of the current study show that when propranolol is administered locally, thus eliminating the potential confounding systemic effects of the drug, it does not directly affect sweating during the initial stages of high-intensity exercise in young, healthy subjects.     

In situ demonstration of angiotensin-dependent and independent pathways for hyperaldosteronism during chronic extracellular fluid volume depletion.

In wild-type mice, 2-wk administration of losartan, an angiotensin (Ang) II type 1 (AT1) receptor antagonist, along with dietary sodium restriction, resulted in an elevation of plasma aldosterone greater than that seen with sodium restriction alone (2.75 +/- 0.35 vs. 1.38 +/- 0.16 ng/ml, P < 0.01). Plasma potassium increased in sodium-restricted, losartan-treated mice (6.0 +/- 0.2 mEq/liter), while potassium remained unchanged in mice with sodium restriction alone. To study the effect of Ang II on glomerulosa cells that may operate independently of plasma potassium in situ, we used chimeric mice made of cells with or without the intact AT1A gene (Agtr1a). When animals were fed a normal diet or chronically infused with Ang II, the aldosterone synthase mRNA was detectable only in Agtr1a+/+ but not Agtr1a-/- zona glomerulosa cells. After 2 wk of sodium restriction, plasma aldosterone increased (1.51 +/- 0.27 ng/ml) and potassium remained on average at 4.5 +/- 0.2 mEq/liter, with aldosterone synthase mRNA expressed intensively in Agtr1a+/+, but not detectable in Agtr1a-/- cells. Simultaneous sodium restriction and losartan treatment caused increases in plasma potassium (5.5 +/- 0.1 mEq/liter) and aldosterone (1.84 +/- 0.38 ng/ml), with both Agtr1a-/- and Agtr1a+/+ cells intensively expressing aldosterone synthase mRNA. Thus, aldosterone production is regulated by Ang II in the adrenal gland during chronic alterations in extracellular fluid volume when plasma potassium is maintained within the normal range. In the light of a previous observation that dietary potassium restriction superimposed on sodium restriction abolished secondary hyperaldosteronism in angiotensinogen null-mutant mice, the present findings demonstrate that when the renin-Ang system is compromised, plasma potassium acts as an effective alternative mechanism for the volume homeostasis through its capacity to induce hyperaldosteronism.     

Rectal temperature, distal sweat rate, and forearm blood flow following mild exercise at two phases of the circadian cycle

Changes in rectal temperature during mild exercise in the middle of the rising (11:00 h) and falling (23:00 h) phases of the circadian rhythm of resting core temperature have been compared. Seven healthy males were studied at rest, while exercising on a cycle ergometer (60 min at 80 W), and during the first 30 min of recovery. Rectal temperature, forearm blood flow, and forearm sweat rate were measured at 1 min intervals throughout. During exercise, there were significant time-of-day differences in the profiles of all three variables, and in the thresholds for increases in forearm blood flow and sweating. Forearm blood flow and sweat rate were recruited more rapidly and to a greater extent with evening exercise, and rectal temperature rose less. Analysis of covariance, with rectal temperature as the covariate, indicated the associations between it and forearm blood flow or sweating were significantly different (p<0.05) between the two times of day. There were also significant (p<0.05) time-of-day effects for forearm blood flow and sweating that were independent of rectal temperature. During recovery, rectal temperature fell more quickly in the late evening than late morning. Forearm blood flow and sweating also showed time-of-day differences, but these did not co-vary with rectal temperature. Control of rectal temperature during exercise and recovery appears to be more effective in the late evening than late morning, and differences in forearm blood flow and sweating, as well as factors independent of these two variables, contribute to this difference. The results support our "heat-gain/heat-loss modes" hypothesis.     

Hypokalemia and alkalosis in adipsic hypernatremia are not associated with hyperaldosteronism

Idiopathic adipsic hypernatremia (AH) is a rare disorder associated with hypokalemia and alkalosis. Hypokalemic alkalosis has been presumed to be secondary to hyperaldosteronism. We evaluated plasma renin activity, serum aldosterone, serum and urine electrolytes in a 17-year-old patient with AH on several occasions. Despite evidence of mild dehydration, serum Na >160 and K <3.2, aldosterone levels were suppressed and plasma renin activity was not elevated. Urine Na and K were not conserved. We also examined electrolyte and hormone levels in previously reported cases of AH. Aldosterone levels were not increased in any of the cases when measured. Renin secretion was increased in 2 patients. Among the compiled cases serum K was inversely correlated with serum Na (r = -0.73, p < 0.002, n = 15). Hypokalemia and alkalosis occurring in AH are not associated with secondary hyperaldosteronism. Patients with AH may have chronic renal losses of potassium leading to hypokalemia and alkalosis.     

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.     

Vascular responses in forearm and calf to contralateral static exercises

Ten normal subjects performed a 90-s isometric exercise [20, 30, and 40% of maximal voluntary contraction (MVC) of the flexor muscle of the right index finger or quadriceps muscle of the right leg. Contralateral forearm and calf blood flows (strain gauge plethysmography) and arterial blood pressure (auscultation) were measured simultaneously. Each exercise caused a decrease in forearm vascular resistance and a progressive increase in calf resistance. These changes were greatest with the 40% MVC. With finger exercise at 20 and 40% MVC, the percentage decreases in forearm vascular resistance from control were 12.3 and 22.7%, respectively (P less than 0.01). Similar decreases (9.5 and 24.9%, respectively; P less than 0.01) were noted with exercise of the quadriceps muscle. By contrast, the corresponding increases in calf vascular resistance were greater (P less than 0.01) with quadriceps exercise (13.3 and 55.4%, respectively) than with finger exercise (6.0 and 36.0%). Arrest of the circulation to the exercising muscles just before the exercise ended caused an abrupt increase in forearm vascular resistance and a decrease in calf resistance. These studies provide further evidence of the heterogeneity of responses of forearm and calf resistance vessels to certain cardiovascular stimuli.     

The State of the Regional Blood Flow in the Upper Extremity after Dosed Physical Exercise

The effect of local isometric exercise on hand and forearm blood flow was studied. With maximum muscular exercise performed by both males and females, a decrease in hand and forearm blood flow was due to vasoconstriction caused by the mechanical pressure of working muscles. With 75 and 50% loads, marked hyperemia was observed in the main and microcirculatory vessels in the hand and forearm, which was rather long-lasting in the hand because of the difficulty of the forearm venous outflow. The minimum loads affected mainly the microcirculation, and no significant hemodynamic changes in main vessels were observed. The exercise performed at 50% of maximum muscular force was taken as an optimum load in kinesotherapeutic programs.     

Forearm metabolic asymmetry detected by 31P-NMR during submaximal exercise

This study evaluated the relationship of skeletal muscle energy metabolism to forearm blood flow and muscle mass in the dominant (D) and nondominant (ND) forearms of normal subjects. 31P-Magnetic resonance spectroscopy was used to determine intracellular pH and the ratio of inorganic phosphate to phosphocreatine (Pi/PCr), an index of energy metabolism. Forearm blood flow and muscle mass were measured by venous occlusion plethysmography and magnetic resonance imaging, respectively. Metabolic measurements and flow were determined at rest and during submaximal exercise in both forearms. After a warm-up period, six normal right-handed male subjects performed 7.5 min of wrist flexion exercise in the magnet (1 contraction every 5 s), first with the ND forearm and then with the D forearm, at 23, 46, and 69 J/min. At rest, there were no differences between forearms in Pi/PCr or pH. However, at each work load the D forearm demonstrated significantly lower Pi/PCr and higher pH than the ND forearm. Blood flow was not significantly different between the forearms at rest or during exercise. Because these subjects were not engaged in unilateral arm training, we conclude that 1) Pi/PCr is lower and pH is higher in the D compared with the ND forearm in normal subjects during submaximal exercise, 2) these differences are independent of muscle mass and blood flow, and 3) the cumulative effect of long-term, low-level daily activity provides an adequate training stimulus for muscular metabolic adaptations.     

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.