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PubMed2003

Pathophysiology of orthostatic hypotension after bed rest: paradoxical sympathetic withdrawal.

Although orthostatic hypotension is a common clinical syndrome after spaceflight and its ground-based simulation model, 6 degrees head-down bed rest (HDBR), the pathophysiology remains unclear. The authors' hypothesis that a decrease in sympathetic nerve activity is the major pathophysiology underlying orthostatic hypotension after HDBR was tested in a study involving 14-day HDBR in 22 healthy subjects who showed no orthostatic hypotension during 15-min 60 degrees head-up tilt test (HUT) at baseline. After HDBR, 10 of 22 subjects demonstrated orthostatic hypotension during 60 degrees HUT. In subjects with orthostatic hypotension, total activity of muscle sympathetic nerve activity (MSNA) increased less during the first minute of 60 degrees HUT after HDBR (314% of resting supine activity) than before HDBR (523% of resting supine activity, P < 0.05) despite HDBR-induced reduction in plasma volume (13% of plasma volume before HDBR). The postural increase in total MSNA continued during several more minutes of 60 degrees HUT while arterial pressure was maintained. Thereafter, however, total MSNA was paradoxically suppressed by 104% of the resting supine level at the last minute of HUT (P < 0.05 vs. earlier 60 degrees HUT periods). The suppression of total MSNA was accompanied by a 22 +/- 4-mmHg decrease in mean blood pressure (systolic blood pressure <80 mmHg). In contrast, orthostatic activation of total MSNA was preserved throughout 60 degrees HUT in subjects who did not develop orthostatic hypotension. These data support the hypothesis that a decrease in sympathetic nerve activity is the major pathophysiological factor underlying orthostatic hypotension after HDBR. It appears that the diminished sympathetic activity, in combination with other factors associated with HDBR (e.g., hypovolemia), may predispose some individuals to postural hypotension.

Adult↗

PubMed2006

Abdominal aortic hemodynamics in young healthy adults at rest and during lower limb exercise: quantification using image-based computer modeling.

Localization of atherosclerotic lesions in the abdominal aorta has been previously correlated to areas of adverse hemodynamic conditions, such as flow recirculation, low mean wall shear stress, and high temporal oscillations in shear. Along with its many systemic benefits, exercise is also proposed to have local benefits in the vasculature via the alteration of these regional flow patterns. In this work, subject-specific models of the human abdominal aorta were constructed from magnetic resonance angiograms of five young, healthy subjects, and computer simulations were performed under resting and exercise (50% increase in resting heart rate) pulsatile flow conditions. Velocity fields and spatial variations in mean wall shear stress (WSS) and oscillatory shear index (OSI) are presented. When averaged over all subjects, WSS increased from 4.8 +/- 0.6 to 31.6 +/- 5.7 dyn/cm2 and OSI decreased from 0.22 +/- 0.03 to 0.03 +/- 0.02 in the infrarenal aorta between rest and exercise. WSS significantly increased, whereas OSI decreased between rest and exercise at the supraceliac, infrarenal, and suprabifurcation levels, and significant differences in WSS were found between anterior and posterior sections. These results support the hypothesis that exercise provides localized benefits to the cardiovascular system through acute mechanical stimuli that trigger longer-term biological processes leading to protection against the development or progression of atherosclerosis.

Adult↗

PubMed1989

Training increases cardiac glucose uptake during rest and exercise in rats.

The effect of chronic exercise on the regional glucose uptake in the left ventricle of the heart was studied in resting and swimming rats using the 2-deoxyglucose method. The left ventricular glucose uptake of untrained resting controls averaged 1.7 +/- 0.1 mumol.min-1.g protein-1 and that of chronically trained resting rats 3.5 +/- 0.3 mumol.min-1.g protein-1 (P less than 0.001). During a 20-min swimming period the glucose uptake rate of untrained rats was 2.3 +/- 0.1 mumol.min-1.g protein-1 and that of trained rats 3.4 +/- 0.3 mumol.min-1.g protein-1 (P less than 0.01). The subendocardial glucose uptake was 25% higher than the subepicardial uptake in the resting control group, whereas no gradient was observed in the other groups. The product of heart rate and blood pressure during swimming increased by 60-70% in the untrained and trained groups. The increase in total left ventricular glucose uptake and its transmural distribution by training seemed to be independent of the actual oxygen consumption or supply of major alternative myocardial substrates.

Animals↗

PubMed1992

Age-related decline in left ventricular filling at rest and exercise.

To determine whether the age-associated decline in resting left ventricular diastolic filling persists during aerobic exercise, rest and bicycle exercise filling indexes were measured from gated radionuclide blood pool scans in 88 healthy men aged 22-82 yr. To evaluate the effect of physical conditioning status on these age-related changes, a subset of the subjects consisted of endurance-trained senior athletes with a maximal O2 consumption of 50.5 +/- 5 compared with 32.6 +/- 7 ml.kg-1 x min-1 in age-matched controls. The contribution of beta-adrenergic stimulation to exercise-induced changes in filling was also evaluated by the administration of intravenous propranolol to another subset before testing. Peak filling rate increased progressively at all ages with increasing exercise work loads. The peak filling rates at rest, 50% maximal exercise, and maximum exercise inversely correlated with age (r = -0.64, -0.53, -0.64, respectively). Rest and exercise filling indexes in senior athletes were similar to those of sedentary older subjects. Propranolol decreased exercise peak filling rates in young (37.2 +/- 7.5 yr) but not in older (62.1 +/- 6 yr) subjects. Therefore, filling rates increase with exercise in both young and older healthy men, but age differences persist at comparable relative work loads. This decline is not secondary to a decline in physical conditioning status but appears to be related to a decrease in beta-adrenergic responsiveness in older individuals.

Adrenergic beta-Antagonists↗

PubMed1994

Muscle metaboreflex triggers parallel sympathetic activation in exercising and resting human skeletal muscle.

Activation of a metabolically generated reflex in exercising skeletal muscle (muscle metaboreflex) in humans is known to trigger increases in sympathetic nerve activity (SNA) to resting skeletal muscles. In seven healthy human subjects, to determine whether this reflex mechanism also increases SNA to the exercising muscles, we recorded muscle SNA with microelectrodes in the right peroneal nerve and in fascicles of the left peroneal nerve selectively innervating the exercising muscles of the left foot. Subjects performed static toe extension at 20% maximal voluntary contraction alone or in combination with foot ischemia. Only static toe extension at 20% MVC during ischemia activated the muscle metaboreflex. This paradigm caused increases in SNA to exercising muscle that paralleled those to the resting muscles: during the first minute of exercise SNA was unchanged, but during the second minute SNA increased from 29 +/- 2 to 38 +/- 2 bursts/min (P < 0.05) to the exercising muscles and from 30 +/- 3 to 40 +/- 2 bursts/min (P < 0.05) to the resting muscles. These bilateral increases in SNA were maintained when metaboreflex activation was sustained by postexercise foot ischemia. In conclusion, these data provide neurophysiological evidence that the muscle metaboreflex evokes parallel sympathetic activation in exercising and resting human skeletal muscle.

Adult↗

PubMed1998

Continuous release of vasodilator prostanoids contributes to regulation of resting forearm blood flow in humans.

Continuous release of nitric oxide contributes to the maintenance of resting tone in the human forearm and coronary circulations; however, evidence for a similar role of vasodilator prostanoids such as prostacyclin is lacking. We examined whether continuous release of prostacyclin contributes to basal forearm blood flow. Flow was measured using venous occlusion plethysmography in 38 healthy volunteers [mean age 21.3 +/- 2.5 yr (+/- SD); 13 female, 25 male] at rest, after administration of three incremental intra-arterial infusions of either the cyclooxygenase inhibitor aspirin or placebo, and before and after administration of the endothelium-dependent and -independent dilators acetylcholine (30 micrograms/min) and nitroprusside (1 microgram/min). To assess the effect of aspirin on the production of prostacyclin, plasma 6-keto prostaglandin F1 alpha (6-keto-PGF1 alpha; the stable metabolite of prostacyclin) was measured by simultaneous arterial and venous sampling. Aspirin produced a time- and dose-dependent reduction in forearm blood flow, resulting in a 32% decrease at the highest dose. The effect was maximal after 10 min. Flow at rest and after aspirin doses of 1, 3, and 10 mg/min was 2.6 +/- 0.2, 2.3 +/- 0.2, 2.1 +/- 0.2, and 1.8 +/- 0.2 ml.100 ml forearm tissue-1.min-1, respectively (means +/- SE, P < 0.001). Commensurate with these data, the net forearm production of 6-keto-PGF1 alpha was 52.9 +/- 16.4, 11.7 +/- 8.6, 18.7 +/- 8.5, and 12.0 +/- 12.5 pg.100 ml forearm tissue-1.min-1 for the respective doses (P = 0.04). No time-dependent reduction in flow was seen in subjects with vehicle infusion. Aspirin did not affect the responses to acetylcholine or nitroprusside. These data suggest that continuous release of prostacyclin plays a role in the maintenance of resting forearm blood flow. There appears to be a direct link between the reduction in flow with aspirin and inhibition of prostacyclin production.

6-Ketoprostaglandin F1 alpha↗

PubMed2001

eNOS 894T allele and coronary blood flow at rest and during adenosine-induced hyperemia.

The 894T allele of a G894T polymorphism in the endothelial nitric oxide synthase (eNOS) gene is associated with decreased eNOS activity, cleavage of the protein, and endothelial dysfunction. The present study evaluated the association with coronary blood flow (CBF) at rest and during adenosine (ADO)-induced hyperemia. CBF was determined by Doppler flow wire and angiography in 97 left anterior descending arteries of individuals without coronary artery disease. At rest, average peak velocity (APV) was lower and coronary vascular resistance (CVR) was higher in homozygous carriers of the 894T allele than in heterozygotes and individuals without the 894T allele. CBF tended to be lower in eNOS 894T allele carriers. During ADO-induced hyperemia (18 microg ic), APV, CVR, and CBF were not statistically different between the genotypes. The reduced APV at rest in conjunction with an increased CVR indicates a vasomotor dysfunction related to an increased microvascular resting tone in eNOS 894T allele carriers.

Adenosine↗

PubMed2004

The impact of aging and habitual physical activity on static respiratory work at rest and during exercise.

We investigated the effects of aging on the elastic properties of lung tissue and the chest wall, simultaneously quantifying the contribution of each component to static inspiratory muscle work in resting and exercising adults. We further evaluated the interaction of aging and habitual physical activity on respiratory mechanics. Static lung volumes and elastic properties of the lung and chest wall (pressure-volume relaxation maneuvers) in 29 chronically sedentary and 29 habitually active subjects, grouped by age, were investigated: young (Y, 20-30 years), middle-aged (M, 40-50 years), and older (O, >60 years). Using static pressure-volume data, we computed the elastic work of breathing (joules per liter, J.l(-1)), including inspiratory muscle work, over resting and exercising tidal volume excursions. Elastic work of the lung (Y = 0.79 +/- 0.05; M = 0.47 +/- 0.05; O = 0.43 +/- 0.05 J.l(-1)) and chest wall (Y = -0.49 +/- 0.06; M = -0.12 +/- 0.07; O = 0.04 +/- 0.05 J.l(-1) ) changed significantly with age (P < 0.05). With aging, a parallel displacement of the chest wall pressure-volume curve resulted in a shift from energy being stored primarily during expiration to energy storage during inspiration, and driving expiration, both at rest and during exercise. Although deviating significantly from young adults, this did not significantly elevate static inspiratory muscle work but resulted in a redistribution of the tissues on which this work was performed and the phase of the respiratory cycle in which it occurred. Nevertheless, static inspiratory muscle work remained similar across age groups, at rest and during exercise, and habitual physical activity failed to influence these changes.

Adult↗

PubMed2006

Disruption of adenosinergic modulation of ventilation at rest and during hypercapnia by neonatal caffeine in young rats: role of adenosine A(1) and A(2A) receptors.

Caffeine is commonly used to treat respiratory instabilities related to prematurity. However, the role of adenosinergic modulation and the potential long-term effects of neonatal caffeine treatment (NCT) on respiratory control are poorly understood. To address these shortcomings, we tested the following hypotheses: 1) adenosine A(1)- and A(2A)-receptor antagonists modulate respiratory activity at rest and during hypercapnia; 2) NCT has long-term consequences on adenosinergic modulation of respiratory control. Rat pups received by gavage either caffeine (15 mg/kg) or water (control) once a day from postnatal days 3 to 12. At day 20, rats received intraperitoneal injection with vehicle, DPCPX (A(1) antagonist, 4 mg/kg), or ZM-241385 (A(2A) antagonist, 1 mg/kg) before plethysmographic measurements of resting ventilation, hypercapnic ventilatory response (5% CO(2)), and occurrence of apneas in freely behaving rats. In controls, data show that A(2A), but not A(1), antagonist decreased resting ventilation by 31% (P = 0.003). A(1) antagonist increased the hypercapnic response by 60% (P < 0.001), whereas A(2A) antagonist increased the hypercapnic response by 42% (P = 0.033). In NCT rats, A(1) antagonist increased resting ventilation by 27% (P = 0.02), but the increase of the hypercapnic response was blunted compared with controls. A(1) antagonist enhanced the occurrence of spontaneous apneas in NCT rats only (P = 0.005). Finally, A(2A) antagonist injected in NCT rats had no effect on ventilation. These data show that hypercapnia activates adenosinergic pathways, which attenuate responsiveness (and/or sensitivity) to CO(2) via A(1) receptors. NCT elicits developmental plasticity of adenosinergic modulation, since neonatal caffeine persistently decreases ventilatory sensitivity to adenosine blockers.

Adenosine A1 Receptor Antagonists↗

PubMed1975

Assessment of the degradation of thyroid hormones in man during bed rest.

The effect of bed rest on the absolute turnover rates of thyroid hormones, thyroxine (T4) and triiodothyronine (T3), was evaluated in man. Bed rest resulted in physical deconditioning, measured by a decreased rate of maximal oxygen consumption; physical deconditioning was associated with no significant alterations in the metabolic clearance of T4 and T3. Plasma concentrations of these iodothyronines were not changed as a result of bed rest. Absolute hormone turnover rates were similar in control and bed-rest subjects. The data suggest that the degradation of thyroid hormones is not influenced by physical deconditioning or hypodynamia.

Adolescent↗

PubMed1980

Thermal effects of injecting norepinephrine into hypothalamus of the rat during rest and exercise.

Norepinephrine (NE) was injected bilaterally through implanted guide cannulas into the anterior hypothalamus (AH) of conscious male Sprague-Dawley rats (300-360 g) at rest and just before treadmill exercise (21.5 m/min for 30 min). Colonic (Tc), tail-skin (Ts), and ambient (Ta) temperatures were monitored each minute by use of a telethermometer. At rest (Ta = 23 degrees C), intrahypothalamic injections of 0.5-40.0 micrograms of NE, in a total of 1.0 microliter delivered within 30 s, produced a dose-dependent hypothermia with a 3-5 degrees C rise in Ts. NE (10 micrograms) injected 2 min before exercise (Ta = 23 degrees C) caused an immediate rise in Ts and a mean decline in Tc of 0.9 +/- 0.1 degree C (SE) below resting levels during exercise. This decline in Tc was statistically the same as that observed after the injections of 10 micrograms of NE at rest. Under control exercise conditions, Tc rose approximately 1 degree C and was associated with an initial decline (0.5 degrees C) followed by a rise (4.0 degrees C) in Ts. When the alpha-adrenergic receptor blocker phentolamine was injected 5-15 min before exercise, it caused a significant (P < 0.01) elevation in Tc during the ensuing exercise compared with controls. These results indicate that 1) over a dose range 0.5-40.0 micrograms, NE microinjected into the AH of the rt produces only hypothermia; 2) alpha-adrenergic receptors in the AH participate in the mediation of heat dissipation when the thermoregulatory system is challenged by the endogenous heat stress of exercise; and 3) exercise per se provides a nonthermal input to the temperature regulatory system that enhances heat dissipation.

Animals↗

PubMed1982

Ventilatory responses at rest and during exercise in marathon runners.

Diminished ventilatory responsiveness to hypercapnia and hypoxia has been reported in athletes, but whether reduced chemosensitivity might lessen hyperpnea during exercise and facilitate performance is unknown. To evaluate ventilatory control and its possible role in athletic performance, we prospectively measured ventilatory responses to hypercapnia and hypoxia at rest and ventilatory equivalents for carbon dioxide (VE/VCO2) and oxygen (VE/VO2) during exercise in 20 accomplished marathon (42.2 km) runners (RUN) and 20 control subjects (CON). The athletes (mean age 27.8, range 18-41 yr) were all experienced runners with a mean best marathon time of 2 h, 36 min (range 2:14-2:55). There were no significant differences in the ventilatory responses at rest to hypercapnia (RUN, 2.23 +/- 0.73 vs. CON, 2.61 +/- 1.05 l X min-1 X Torr-1) and hypoxia (RUN, 0.57 +/- 0.40 vs. CON, 0.88 +/- 0.72 l X min-1 X 1% desat-1) (mean +/- SD). Similarly, there were no significant differences in VE/VCO2 and VE/VO2 between the two groups. Good correlation (r = 0.68; P less than 0.01) was observed between hypercapnic response at rest and exercise ventilation (VE/VCO2) in RUN. However, both hypercapnic and hypoxic ventilatory responses correlated poorly with marathon running time. These results demonstrate no differences in ventilatory responses at rest and during exercise between marathon runners and control subjects. The range of ventilatory responsiveness observed in this group of marathon runners indicates that a spectrum of ventilatory control is present in well-trained endurance athletes.

Adult↗

PubMed1984

VO2 kinetics of constant-load exercise following bed-rest-induced deconditioning.

The purpose of this study was to determine the effects of bed-rest-induced deconditioning on changes in O2 uptake (VO2) kinetics, O2 deficit, steady-state VO2, and recovery VO2 during the performance of constant-load exercise. Five male subjects (36-40 yr) underwent 7 days of continuous bed rest (BR) in the head-down (-6 degrees) position. Two days before (pre) and the day after (post) BR each subject performed one submaximal exercise test in the supine and one in the upright position consisting of 5 min of rest, 5 min of cycle ergometer exercise at 700 kg.m/min, and 10 min of recovery from exercise. VO2 was measured continuously in all tests from 2-liter aliquot gas samples collected every 30 s. Following BR steady-state VO2 was unchanged in supine and upright exercise. In the supine position BR did not change total exercise VO2, O2 deficit, or total recovery VO2. However, compared with pre-BR, total exercise VO2 decreased (P less than 0.05) from 7.41 +/- 0.11 to 7.23 +/- 0.17 liters, O2 deficit increased (P less than 0.05) from 1.15 +/- 0.05 to 1.41 +/- 0.07 liters, and total recovery VO2 increased (P less than 0.05) from 5.17 +/- 0.11 to 5.47 +/- 0.17 liters during the post-BR upright test. Despite the ability to attain similar steady-state VO2 within 5 min, bed-rest-induced deconditioning resulted in a reduction of total VO2 capacity and an increase in the O2 deficit during submaximal constant-load exercise. This change in VO2 kinetics is found only with exercise in the upright rather than supine position implicating orthostatic mechanisms in the delayed response to submaximal exercise.

Adult↗

PubMed1986

Ventilatory responses to partial cardiopulmonary bypass at rest and exercise in dogs.

We determined the role of blood flow-induced changes in CO2 load to the lungs on ventilatory control, at rest and in the steady-state of electrically induced exercise, in the anesthetized dog. A portion of the vena caval blood was diverted to the descending aorta following "arterialization" through an extracorporeal gas exchanger. Ventilation typically decreased, both at rest and during exercise (i.e., at 2 different levels of mixed venous CO2), in proportion to the CO2 loss; arterial PCO2 was consequently regulated. There were concomitant increases of the pulmonary and peripheral vascular resistance. Bilateral cervical vagosympathectomy markedly attenuated the ventilatory response at rest, thus disrupting arterial PCO2 homeostasis, but not so during exercise. The results therefore provide evidence for and support the suggestion of CO2 flow-related hyperpnea both at rest and during muscular exercise.

Animals↗

PubMed1987

Effect of resting smooth muscle length on contractile response in resistance airways.

We studied the effect of resting smooth muscle length on the contractile response of the major resistance airways (generations 0-5) in 18 mongrel dogs in vivo using tantalum bronchography. Dose-response curves to 10(-10) to 10(-7) mol/kg methacholine (MCh) were generated [at functional residual capacity (FRC)] by repeated intravenous bolus administration using tantalum bronchography after each dose. Airway constriction varied substantially with dose-equivalent stimulation and varied sequentially from trachea (8.8 +/- 2.2% change in airway diam) to fifth-generation bronchus (49.8 +/- 3.0%; P less than 0.001). Length-tension curves were generated for each airway to determine the airway diameter (i.e., resting in situ smooth muscle length) at which maximal constriction was elicited using bolus intravenous injection of 10(-8) mol/kg MCh. A Frank-Starling relationship was obtained for each airway; the transpulmonary pressure at which maximal constriction was elicited increased progressively from 2.50 +/- 1.12 cmH2O for trachea (approximately FRC) to 18.3 +/- 1.05 cmH2O for fifth-generation airways (approximately 50% TLC) (P less than 0.001). A similar relationship was obtained when change in airway diameter was plotted as a function of airway radius. We demonstrate substantial heterogeneity in the lung volumes at which maximal constriction is elicited and in distribution of parasympathomimetic constriction within the first few generations of resistance bronchi. Our data also suggest that lung hyperinflation may lead to augmented airway contractile responses by shifting resting smooth muscle length toward optimum resting smooth muscle length.

Airway Resistance↗

PubMed1988

Breathing strategy of the adult horse (Equus caballus) at rest.

To investigate the mechanism underlying the polyphasic airflow pattern of the equine species, we recorded airflow, tidal volum, rib cage and abdominal motion, and the sequence of activation of the diaphragm, intercostal, and abdominal muscles during quiet breathing in nine adult horses standing at rest. In addition, esophageal, abdominal, and transdiaphragmatic pressures were simultaneously recorded using balloon-tipped catheters. Analysis of tidal flow-volume loops showed that, unlike humans, the horse at rest breathes around, rather than from, the relaxed volume of the respiratory system (Vrx). Analysis of the pattern of electromyographic activities and changes in generated pressures during the breathing cycle indicate that the first part of expiration is passive, as in humans, with deflation toward Vrx, but subsequent abdominal activity is responsible for a second phase of expiration: active deflation to below Vrx. From this end-expiratory volume, passive inflation occurs toward Vrx, followed by a second phase of inspiration: active inflation to above Vrx, brought about by inspiratory muscle contraction. Under these conditions the abdominal muscles appear to share the principal pumping duties with the diaphragm. Adoption of this breathing strategy by the horse may relate to its peculiar thoracoabdominal anatomic arrangement and to its very low passive chest wall compliance. We conclude that there is a passive and active phase to both inspiration and expiration due to the coordinated action of the respiratory pump muscles responsible for the resting adult horse's biphasic inspiratory and expiratory airflow pattern. This unique breathing pattern perhaps represents a strategy of minimizing the high elastic work of breathing in this species, at least at resting breathing frequencies.

Animals↗

PubMed1988

Regional heat flows of resting and exercising men immersed in cool water.

Trunk (HT), limb (HL), and whole-body (HDIR = HT + HL + Hforehead) skin-to-water heat flows were measured by heat flow transducers on nine men immersed head out in water at critical temperature (TCW = 30 +/- 2 degrees C) and below [overall water temperature (TW) range = 22-32 degrees C] after up to 3 h at rest and exercise. Body heat flow was also determined indirectly (HM) from metabolic rate corrected for changes in heat stores. At rest at TCW [O2 uptake (VO2) = 0.33 +/- 0.07 l/min, n = 7], HT = 52.3 +/- 14.2 (SD) W, HL = 56.4 +/- 14.6 W, HDIR = 120 +/- 27 W, and HM = 111 +/- 29 W (significantly different from HDIR). TW markedly affected HDIR but only slightly affected HM (n = 22 experiments at TW different from TCW plus 7 experiments at TCW). During light exercise (3 MET) at TCW (VO2 = 1.06 +/- 0.26 l/min, n = 9), HT = 122 +/- 43 W, HL = 130 +/- 27 W, HDIR = 285 +/- 69 W, and HM = 260 +/- 60 W. During severe exercise (7 MET) at TCW (VO2 = 2.27 +/- 0.50 l/min, n = 4), HT = 226 +/- 100 W, HL = 262 +/- 61 W, HDIR = 517 +/- 148 W, and HM = 496 +/- 98 W. Lowering TW at 7-MET exercise (n = 9, plus 4 at TCW) had no effect on HDIR and HM. In conclusion, resting HL and HT are equal. At TW less than TCW at rest, HDIR greater than HM, showing that unexpectedly the shell was still cooling. During exercise, HL increases more than HT but less than expected from the heat production of the working limbs. Therefore some heat produced by the limbs is probably transported by blood to the trunk. During heavy exercise, HDIR is constant at all considered TW; apparently it is regulated by some thermally dependent mechanism, such as a progressive cutaneous vasodilation occurring as TW increases.

Body Temperature Regulation↗

PubMed1988

Increased resting energy expenditure in cystic fibrosis.

To explore the hypothesis that there is an increased metabolic rate in cystic fibrosis, resting energy expenditure was measured by indirect calorimetry in 23 subjects with cystic fibrosis in a stable clinical state and in 42 normal control subjects. Resting energy expenditure was found to be elevated by an average of 0.45 MJ/24 h [95% confidence interval (CI) = 0.26-0.64, t = 4.91, P less than 0.001] (108 kcal/24 h), or 9.2% above expected values derived from the regression relating resting energy expenditure to whole body weight and sex in control subjects. When related to lean body mass, values were still elevated by 0.36 MJ/24 h (95% CI = 0.18-0.53, t = 4.15, P less than 0.001) (86 kcal/24 h), or 7.2%. The increased values were found to be independent of age, sex, or body size. There were significant correlations between increased values and poor pulmonary function as measured by the ratio of the forced expiratory volume in 1 s to forced vital capacity (r = -0.44, P less than 0.05) and subclinical infection as indicated by the blood leukocyte count (r = 0.40, P less than 0.05). However, the correlations were low, suggesting that other factors may contribute to the increased resting energy expenditure, possibly including the putative metabolic defect in cystic fibrosis.

Adolescent↗