Prostaglandin production contributes to exercise-induced vasodilation in heart failure

Lang, Chim C., Don B. Chomsky, Javed Butler, Shiv Kapoor,and John R. Wilson. Prostaglandin production contributes toexercise-induced vasodilation in heart failure. J. Appl. Physiol. 83(6): 1933-1940, 1997.Endothelial release of prostaglandins may contribute toexercise-induced skeletal muscle arteriolar vasodilation in patientswith heart failure. To test this hypothesis, we examined the effect ofindomethacin on leg circulation and metabolism in eight chronic heartfailure patients, aged 55 ± 4 yr. Central hemodynamics and legblood flow, determined by thermodilution, and leg metabolic parameterswere measured during maximum treadmill exercise before and 2 h afteroral administration of indomethacin (75 mg). Leg release of6-ketoprostaglandin F₁ was alsomeasured. During control exercise, leg blood flow increased from 0.34 ± 0.03 to 1.99 ± 0.19 l/min(P < 0.001), legO₂ consumption from 13.6 ± 1.8 to 164.5 ± 16.2 ml/min (P < 0.001), and leg prostanoid release from 54.1 ± 8.5 to267.4 ± 35.8 pg/min (P < 0.001).Indomethacin suppressed release of prostaglandinF₁(P < 0.001) throughout exercise anddecreased leg blood flow during exercise(P < 0.05). This was associated witha corresponding decrease in leg O₂ consumption (P < 0.05) and a higher level offemoral venous lactate at peak exercise(P < 0.01). These data suggest thatrelease of vasodilatory prostaglandins contributes to skeletal musclearteriolar vasodilation in patients with heart failure.

     

Interleukin-1 potentiates basal and AVP-stimulated ACTH secretion in vitro--the role of CRH pre-incubation.

The acute-phase cytokine interleukin-1 (IL-1) is known to activate the hypothalamic pituitary adrenal axis, primarily via corticotropin releasing hormone (CRH). The aim of this study was to determine whether IL-1beta could directly stimulate ACTH secretion from perifused equine anterior pituitary cells, and whether CRH pre-incubation affected corticotroph responsiveness. Isolated equine anterior pituitary cells were pre-incubated with media containing 10 nM CRH or vehicle for 20 hours before being loaded onto columns and perifused with 0.02 nM CRH and 100 nM cortisol. Columns were given a 5-minute pulse of arginine vasopressin (AVP, 10 nM), perifused for 4 hours with 0 (control) or 1 nM IL-1beta, then given a further 5-minute pulse of AVP (10nM). ACTH was measured in 5 minute fractions. In the setting of CRH pre-incubation, cells perifused with IL-1beta for 4 hours showed increased basal ACTH secretion compared to control (114 +/- 6 pM vs. 86 +/- 4 pM [means +/- S.E.M.], p < 0.001) and a significantly greater ACTH response to the final AVP pulse (240 +/- 32% vs. 96 +/- 30%, p = 0.009, expressed as % of ACTH response to the initial AVP pulse). The potentiation of AVP-stimulated ACTH release by IL-1 was not observed in cells pre-incubated with vehicle alone. In conclusion, IL-1 increases ACTH release in equine corticotroph cells pre-incubated with CRH and potentiates responsivity to AVP.     

Free mobilization and low- to high-intensity exercise in immobilization-induced muscle atrophy

After 3 wk of immobilization, the effects offree cage activity and low- and high-intensity treadmill running (8 wk)on the morphology and histochemistry of the soleus and gastrocnemius muscles in male Sprague-Dawley rats were investigated. In both muscles,immobilization produced a significant(P < 0.001) increase in the meanpercent area of intramuscular connective tissue (soleus: 18.9% inimmobilized left hindlimb vs. 3.6% in nonimmobilized right hindlimb)and in the relative number of muscle fibers with pathologicalalterations (soleus: 66% in immobilized hindlimb vs. 6% in control),with a simultaneous significant (P < 0.001) decrease in the intramuscular capillary density (soleus: mean capillary density in the immobilized hindlimb only 63% of that in thenonimmobilized hindlimb) and muscle fiber size (soleus type I fibers:mean fiber size in the immobilized hindlimb only 69% of that in thenonimmobilized hindlimb). Many of these changes could not be correctedby free remobilization, whereas low- and high-intensity treadmillrunning clearly restored the changes toward control levels, the effectbeing most complete in the high-intensity running group. Collectively,these findings indicate that immobilization-induced pathologicalstructural and histochemical alterations in rat calf muscles are, to agreat extent, reversible phenomena if remobilization is intensified byphysical training. In this respect, high-intensity exercise seems morebeneficial than low-intensity exercise.

     

Effects of four different single exercise sessions on lipids, lipoproteins, and lipoprotein lipase

The purpose ofthis study was to determine the threshold of exercise energyexpenditure necessary to change blood lipid and lipoproteinconcentrations and lipoprotein lipase activity (LPLA) in healthy,trained men. On different days, 11 men (age, 26.7 ± 6.1 yr; bodyfat, 11.0 ± 1.5%) completed four separate, randomly assigned,submaximal treadmill sessions at 70% maximalO₂ consumption. During eachsession 800, 1,100, 1,300, or 1,500 kcal were expended. Compared withimmediately before exercise, high-density lipoprotein cholesterol(HDL-C) concentration was significantly elevated 24 h after exercise(P < 0.05) in the 1,100-, 1,300-, and 1,500-kcal sessions. HDL-C concentration was also elevated(P < 0.05) immediately after and 48 h after exercise in the 1,500-kcal session. Compared with values 24 hbefore exercise, LPLA wassignificantly greater (P < 0.05) 24 h after exercise in the 1,100-, 1,300-, and 1,500-kcal sessions andremained elevated 48 h after exercise in the 1,500-kcal session. Thesedata indicate that, in healthy, trained men, 1,100 kcal of energyexpenditure are necessary to elicit increased HDL-C concentrations.These HDL-C changes coincided with increased LPLA.

     

Hormonal and metabolic responses to exercise across time of day and menstrual cycle phase

Galliven, E. A., A. Singh, D. Michelson, S. Bina, P. W. Gold, and P. A. Deuster. Hormonal and metabolic responses to exercise across time of day and menstrual cycle phase.J. Appl. Physiol. 83(6):1822-1831, 1997.Two studies, each utilizing short-term treadmillexercise of a different intensity, assessed the metabolic and hormonalresponses of women to exercise in the morning (AM) and late afternoon(PM). In study 1, plasmaconcentrations of growth hormone, arginine vasopressin, catecholamines,adrenocorticotropic hormone, cortisol, lactate, and glucose weremeasured before, during, and after high-intensity exercise (90%maximal O₂ uptake) in the AM andPM. In study 2, plasma concentrationsof adrenocorticotropic hormone, cortisol, lactate, andglucose were measured before, during, and aftermoderate-intensity exercise (70% maximalO₂ uptake) in the AM and PM in thefollicular (days 3-9), midcycle (days 10-16), and luteal(days 18-26) phases of themenstrual cycle. The results of studies1 and 2 revealed nosignificant diurnal differences in the magnitude of responses for anymeasured variable. In addition, study2 revealed a significant time-by-phase interaction forglucose (P = 0.014). However, netintegrated responses were similar across cycle phases. These datasuggest that metabolic and hormonal responses to short-term,high-intensity exercise can be assessed with equal reliability in theAM and PM and that there are subtle differences in blood glucoseresponses to moderate-intensity exercise across menstrual cycle phase.

     

Atrial natriuretic factor inhibits the CRH-stimulated secretion of ACTH and cortisol in man.

Corticotrophic secretion of ACTH is stimulated by corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), and suppressed by glucocorticoids. In vitro and preclinical studies suggest that atrial natriuretic factor (ANF) may be a peptidergic inhibitor of pituitary-adrenocortical activity. The aim of this study was to elucidate a possible role of ANF as a modulator of ACTH release in humans. A bolus injection of 100 micrograms human CRH (hCRH) during a 30 min intravenous infusion of 5 micrograms/min human alpha atrial natriuretic factor (h alpha ANF) was administered at 19:00 to six healthy male volunteers. In comparison to saline, a blunted CRH-stimulated secretion of ACTH (mean maximum plasma level +/- SD 45 min after hCRH: saline 46.2 +/- 14.2 pg/ml, h alpha ANF 34.6 +/- 13.8 pg/ml, p-value = 0.007) and a delayed rise (10 min) in cortisol were detected. The maximum plasma cortisol levels remained nearly unchanged between saline and h alpha ANF administration (mean maximum plasma level +/- SD 60 min after hCRH: saline 182 +/- 26 ng/ml, h alpha ANF 166 +/- 54 ng/ml). No effects of h alpha ANF on basal cortisol levels were observed; in contrast, basal ACTH plasma levels were slightly reduced. Basal blood pressure and heart rate remained unaffected. In the control experiment, infusion of 3 IU AVP in the same experimental paradigm increased basal and stimulated ACTH and cortisol levels significantly in comparison to saline. These observations suggest that intravenously administered haANF inhibits the CRH-stimulated release of ACTH in man.     

Bed rest decreases mechanically induced myofiber wounding and consequent wound-mediated FGF release

Using a terrestrial model of spaceflight (i.e., bed rest), weinvestigated the amount of myofiber wounding and fibroblast growthfactor (FGF) release that occurs during unloading.Myofiber wounding was determined by serum levels of the creatine kinase MM (CKMM) isoform before and after bed rest. Serum levels of both acidic FGF (aFGF) and basic FGF were also determined. A second group ofsubjects was treated in an identical fashion except that they underwenta resistive exercise program during bed rest. Bed rest alone causedsignificant (P < 0.05;n = 7) reductions in post-bed-restserum levels of both CKMM and aFGF, which were paralleled by asignificant (P < 0.05;n = 7) decrease in myofiber size. Incontrast, bed rest plus resistive exercise resulted in significant (P < 0.05;n = 7) increases in post-bed-restserum levels of both CKMM and aFGF, which were paralleled by inhibitionof the atrophic response. These results suggest that mechanicallyinduced, myofiber wound-mediated FGF release may play an important rolein the etiology of unloading-induced skeletal muscle atrophy.

     

Pulmonary blood flow distribution during partial liquid ventilation

Regionalpulmonary blood flow was investigated with radiolabeled microspheres infour supine lambs during the transition from conventional mechanicalventilation (CMV) to partial liquid ventilation (PLV) and withincremental dosing of perfluorocarbon liquid to a cumulative dose of 30 ml/kg. Four lambs supported with CMV served as controls.Formalin-fixed, air-dried lungs were sectioned according to a grid;activity was quantitated with a multichannel scintillation counter,corrected for weight, and normalized to mean flow. During CMV, flow inapical and hilar regions favored dependent lung(P < 0.001), with no gradient acrosstransverse planes from apex to diaphragm. During PLV the gradientwithin transverse planes found during CMV reversed, most notably in thehilar region, favoring nondependent lung(P = 0.03). Also during PLV, flow wasprofoundly reduced near the diaphragm(P < 0.001), and across transverse planes from apex to diaphragm a dose-augmented flow gradient developed favoring apical lung (P < 0.01). Weconclude that regional flow patterns during PLV partially reverse thosenoted during CMV and vary dramatically within the lung from apex todiaphragm.

     

Intravenous vs. oral rehydration: effects on subsequent exercise-heat stress

Castellani, John W., Carl M. Maresh, Lawrence E. Armstrong,Robert W. Kenefick, Deborah Riebe, Marcos Echegaray, Douglas Casa, andV. Daniel Castracane. Intravenous vs. oral rehydration: effects onsubsequent exercise-heat stress. J. Appl.Physiol. 82(3): 799-806, 1997.This studycompared the influence of intravenous vs. oral rehydration afterexercise-induced dehydration during a subsequent 90-min exercisebout. It was hypothesized that cardiovascular, thermoregulatory, and hormonal variables would be the same between intravenous and oral rehydration because of similar restoration ofplasma volume (PV) and osmolality (Osmo). Eight non-heat-acclimated menreceived three experimental treatments (counterbalanced design) immediately after exercise-induced dehydration (33°C) to 4%body weight loss. Treatments were intravenous 0.45% NaCl (iv; 25 ml/kg), no fluid (NF), and oral saline (Oral; 25 ml/kg).After rehydration and rest (2 h total), subjects walked at 50% maximalO₂ consumption for up to 90 min at36°C. The following observations were made: 1) heart rate was higher(P < 0.05) in Oral vs. ivat minutes 45, 60, and75 of exercise;2) rectal temperature, sweat rate, percent change in PV, and change in plasma Osmo were similar between ivand Oral; 3) change in plasmanorepinephrine decreased less (P < 0.05) in Oral compared with iv at minute45; 4) changes in plasma adrenocorticotropic hormone and cortisol were similar between ivand Oral after exercise was initiated; and5) exercise time was similar betweeniv (77.4 ± 5.4 min) and Oral (84.2 ± 2.3 min). These datasuggest that after exercise-induced dehydration, iv and Oral wereequally effective as rehydration treatments. Thermoregulation, changein adrenocorticotropic hormone, and change in cortisol were notdifferent between iv and Oral after exercise began; this is likely dueto similar percent change in PV and change in Osmo.

     

Exercise training reduces skeletal muscle membrane arachidonate in the obese (fa/fa) Zucker rat

Compared with the lean(Fa/) genotype, obese(fa/fa) Zucker rats have arelative deficiency of muscle phospholipid arachidonate, and skeletalmuscle arachidonate in humans is positively correlated with insulinsensitivity. To assess the hypothesis that the positive effects ofexercise training on insulin sensitivity are mediated by increasedmuscle arachidonate, we randomized 20 lean and 20 obese weanling maleZucker rats to sedentary or treadmill exercise groups. After 9 wk,fasting serum, three skeletal muscles (white gastrocnemius, soleus, andextensor digitorum longus), and heart were obtained. Fasting insulinwas halved by exercise training in the obese rat. In whitegastrocnemius and extensor digitorum longus (fast-twitch muscles), butnot in soleus (a slow-twitch muscle) or heart, phospholipidarachidonate was lower in obese than in lean rats(P < 0.001). In all muscles,exercise in the obese rats reduced arachidonate(P < 0.03, by ANOVA contrast). Weconclude that improved insulin sensitivity with exercise in the obesegenotype is not mediated by increased muscle arachidonate and thatreduced muscle arachidonate in obese Zucker rats is unique tofast-twitch muscles.

     

Neuromuscular fatigue after maximal stretch-shortening cycle exercise

Strojnik, V., and P. V. Komi. Neuromuscular fatigueafter maximal stretch-shortening cycle exercise. J. Appl. Physiol. 84(1): 344-350, 1998.To examinesome possible sites of fatigue during short-lasting maximally intensivestretch-shortening cycle exercise, drop jumps on an inclined sledgeapparatus were analyzed. Twelve healthy volunteers performed jumpsuntil they were unable to maintain jumping height >90% of theirmaximum. After the workout, the increases in the blood lactateconcentration and serum creatine kinase activation were statisticallysignificant (P < 0.001 and P < 0.05, respectively) but rathersmall in physiological terms. The major changes after the workout wereas follows: the single twitch was characterized by smaller peak torque(P < 0.05) and shorter time to peak(P < 0.05) and half-relaxation time(P < 0.01). The double-twitch torqueremained at the same level (P > 0.05), but with a steeper maximal slope of torque rise(P < 0.05); during 20- and 100-Hzstimulation the torque declined (both P < 0.01) and the maximal voluntarytorque changed nonsignificantly but with a smaller maximal slope oftorque rise (P < 0.01) and a higheractivation level (P < 0.05),accompanied by an increased electromyogram amplitude. These findingsindicate that the muscle response after the short-lasting consecutivemaximum jumps on the sledge apparatus may involve two distinctmechanisms acting in opposite directions:1) The contractile mechanism seemsto be potentiated through a shorterCa²⁺ transient and fastercross-bridge cycling, as implied by twitch changes.2) High-frequency action potentialpropagation shows an impairment, which is suggested as the possibledominant reason for fatigue in exercise of this type.

     

Effects of hydration state on hormonal and renal responses during moderate exercise in the heat

The effects of hydromineral hormones and catecholamines on renal concentrating ability at different hydration states were examined in five male volunteers while they performed three trials. Each of these trials comprised a 60-min exercise bout on a treadmill (at 50% of maximal oxygen uptake) in a warm environment (dry bulb temperature, 35°C; relative humidity, 20–30%). In one session, subjects were euhydrated before exercise (C). In the two other sessions, after thermal dehydration (loss of 3% body mass) which markedly reduced plasma volume (PV) and increased plasma osmolality (osm_pl), the subjects exercised either not rehydrated (Dh) or rehydrated (Rh) by drinking 600 ml of mineral water before and 40 min after the onset of exercise. During exercise in the Dh compared to C state, plasma renin, aldosterone, arginine vasopressin (AVP), noradrenaline and adrenaline concentrations were increased (P < 0.05). A reduction in creatinine clearance and urine flow was also observed (P < 0.05) together with a decrease in urine osmolality, osmolar clearance and sodium excretion, while free water clearance increased (P < 0.05). However, compared to Dh, Rh partially restored PV and osm_pl and induced a marked reduction in the time courses of both the plasma AVP and catecholamine responses (P < 0.05). Values for renal water and electrolyte excretion were intermediate between those of Dh and C. Plasma atrial natriuretic peptide presented similar changes whatever the hydration state. These results demonstrate that during moderate exercise in the heat, renal concentrating ability is paradoxically reduced by prior dehydration in spite of high plasma AVP levels, and might be the result of marked activation of the sympatho-adrenal system. Rehydration, by reducing this activation, could partially restore the renal concentrating ability despite the lowered plasma AVP. Accepted: 23 April 1997     

Effects of N2O narcosis on breathing and effort sensations during exercise and inspiratory resistive loading

Fothergill, D. M., and N. A. Carlson. Effects ofN₂O narcosis on breathing andeffort sensations during exercise and inspiratory resistive loading.J. Appl. Physiol. 81(4):1562-1571, 1996.The influence of nitrous oxide(N₂O) narcosis on the responses toexercise and inspiratory resistive loading was studied in thirteen maleUS Navy divers. Each diver performed an incremental bicycle exercisetest at 1 ATA to volitional exhaustion while breathing a 23%N₂O gas mixture and a nonnarcoticgas of the same PO₂, density, andviscosity. The same gas mixtures were used during four subsequent30-min steady-state submaximal exercise trials in which the subjectsbreathed the mixtures both with and without an inspiratory resistance(5.5 vs. 1.1 cmH₂O ^· s ^· l¹at 1 l/s). Throughout each test, subjective ratings of respiratory effort (RE), leg exertion, and narcosis were obtained with acategory-ratio scale. The level of narcosis was rated between slightand moderate for the N₂O mixturebut showed great individual variation. Perceived leg exertion and thetime to exhaustion were not significantly different with the twobreathing mixtures. Heart rate was unaffected by the gas mixture andinspiratory resistance at rest and during steady-state exercise but wassignificantly lower with the N₂O mixture during incremental exercise (P < 0.05). Despite significant increases in inspiratory occlusionpressure (13%; P < 0.05),esophageal pressure (12%; P < 0.001), expired minute ventilation (4%;P < 0.01), and the work rate ofbreathing (15%; P < 0.001) when the subjects breathed the N₂O mixture,RE during both steady-state and incremental exercise was 25% lowerwith the narcotic gas than with the nonnarcotic mixture(P < 0.05). We conclude that the narcotic-mediated changes in ventilation, heart rate, and RE induced by23% N₂O are not of sufficientmagnitude to influence exercise tolerance at surface pressure.Furthermore, the load-compensating respiratory reflexes responsible formaintaining ventilation during resistive breathing are not depressed byN₂O narcosis.

     

Effects of emphysema on diaphragm blood flow during exercise

Chronichyperinflation of the lung in emphysema displaces the diaphragmcaudally, thereby placing it in a mechanically disadvantageous positionand contributing to the increased work of breathing. We tested thehypothesis that total and regional diaphragm blood flows are increasedin emphysema, presumably reflecting an increased diaphragm energeticdemand. Male Syrian Golden hamsters were randomly divided intoemphysema (E; intratracheal elastase 25 units/100 g body wt) andcontrol (C; saline) groups, and experiments were performed 16-20wk later. The regional distribution of blood flow withinthe diaphragm was determined by using radiolabeled microspheres inhamsters at rest and during treadmill exercise (walking at 20 feet/min,20% grade). Consistent with pronounced emphysema, lung volume per unitbody weight was greater in E hamsters (C, 59.3 ± 1.8; E, 84.5 ± 5.0 ml/kg; P < 0.001) and arterialPO₂ was lower both at rest (C, 74 ± 3; E, 59 ± 2 Torr; P < 0.001) and during exercise (C, 93 ± 3; E, 69 ± 4 Torr; P < 0.001). At rest, total diaphragm blood flow was not different between C and Ehamsters (C, 47 ± 4; E, 38 ± 4 ml · min¹ · 100 g¹;P = 0.18). In both C and E hamsters,blood flow at rest was lower in the ventral costal region of thediaphragm than in the dorsal and medial costal regions and the cruraldiaphragm. During exercise in both C and E hamsters, blood flowsincreased more in the dorsal and medial costal regions and in thecrural diaphragm than in the ventral costal region. Total diaphragmblood flow was greater in E hamsters during exercise (C, 58 ± 7; E,90 ± 14 ml · min¹ · 100 g¹;P = 0.03), as a consequence ofsignificantly higher blood flows in the medial and ventral costalregions and crural diaphragm. In addition, exercise-induced increasesin intercostal (P < 0.005) andabdominal (P < 0.05) muscle bloodflows were greater in E hamsters. The finding that diaphragm blood flowwas greater in E hamsters during exercise supports the contention thatemphysema increases the energetic requirements of the diaphragm.

     

Metabolic effects of low cortisol during exercise in humans

This studyexamined the physiological effect of reduced plasma cortisol (C) duringprolonged exercise in humans. The effects of normal C (NC) werecompared with metyrapone-induced low C (LC) on plasma substrateavailability and the respiratory exchange ratio during 2 h of exerciseat ~60% peak O₂ consumption innine subjects. The C responses were compared with preexercise (Pre) levels and with a rest day (Con). At rest, C was attenuated by ~70%for LC compared with NC. At rest, plasma glucose, lactate, glycerol,-hydroxybutyrate, alanine, branched-chain amino acids, insulin,glucagon, growth hormone, epinephrine, and norepinephrine were similarunder LC and NC (P > 0.05). Duringexercise under NC, plasma C increased compared with Pre, whereas itremained unchanged during LC. During NC, plasma C was elevated at 90 min (compared with Con) and at 120 min (compared with Con and Pre). During exercise, plasma glucose decreased to the same extent and lactate was similar under both conditions, whereas plasma glycerol, -hydroxybutyrate, alanine, and branched-chain amino acids were higher (P < 0.01) under NC. Plasmainsulin declined (P = 0.01) to agreater extent under LC, whereas growth hormone, epinephrine, andnorepinephrine tended to be higher (0.05  P  0.10). Plasma glucagon increasedunder both conditions (P < 0.01).The respiratory exchange ratio did not differ between conditions. Weconclude that, during exercise, 1) Caccelerates lipolysis, ketogenesis, and proteolysis;2) under LC, glucoregulatory hormoneadjustments maintain glucose homeostasis; and3) LC does not alter whole body substrate utilization or the ability to complete 2 h of moderate exercise.

     

Arginine-induced pancreatic hormone secretion during exercise in rats

Trabelsi, Fethi, and Jean-Marc Lavoie. Arginine-inducedpancreatic hormone secretion during exercise in rats.J. Appl. Physiol. 81(6):2528-2533, 1996.The aim of the present investigation was to1) determine whetherarginine-induced pancreatic hormone secretion can be modified during anexercise bout, and 2) verify whetherthe sectioning of the hepatic branch of the vagus nerve can alter thearginine-induced insulin and glucagon secretion during exercise inrats. To this end, we studied the effects of an intraperitonealinjection of arginine (1 g/kg body mass) during an exercise bout (30 min, 26 m/min, 0% grade) on the pancreatic hormone responses. Theseeffects were determined in one group of sham-operated exercising ratsand compared with three control groups: one group of resting rats, onegroup of saline-injected exercising rats, and one group ofhepatic-vagotomized exercising rats. Five minutes after the injectionof arginine, significant (P < 0.05)increases in insulin, glucagon, and C-peptide concentrations wereobserved in exercising as well as in resting rats. These responses werenot, however, altered by the hepatic vagotomy and/or by theexercise bout. It is concluded that arginine is a potent stimulus ofpancreatic hormone secretion during exercise, even though thesympathoadrenal system is activated. These results also indicate that ahepatic vagotomy does not seem to influence arginine-inducedhormonal pancreatic responses and question the role of the putativehepatic arginoreceptors in the control of the pancreatic hormonesecretion during exercise.

     

Influence of voluntary exercise on hypothalamic norepinephrine

We combined hypothalamic tissue and plasma determinations ofnorepinephrine, dihydroxyphenylalanine, and dihydroxyphenylglycol withmeasurements of abdominal fat in voluntary running rats to examine therelationship among exercise training, hypothalamic and sympatheticnervous function, and body fat stores. The hypothalamic concentrationsof norepinephrine, dihydroxyphenylalanine, and dihydroxyphenylglycolwere reduced after exercise training(P < 0.01), with the amount ofnorepinephrine being strongly associated with the plasma norepinephrine(r = 0.58, P < 0.05) and dihydroxyphenylglycol (r = 0.65, P = 0.01) concentrations. Exercisetraining resulted in a diminution in abdominal fat mass(P < 0.01). A strongrelationship existed between fat mass and hypothalamic norepinephrinecontent (r = 0.83, P < 0.001). The presence of apositive relationship between the arterial and hypothalamicnorepinephrine levels provides presumptive evidence of an associationbetween noradrenergic neuronal activity of the hypothalamus andsympathetic nervous function. The observation that abdominal fat massis linked with norepinephrine in the hypothalamus raises thepossibility that alterations in body fat stores provide an afferentsignal linking hypothalamic function and the activity of thesympathetic nervous system.

     

Altered mechanisms of sympathetic activation during rhythmic forearm exercise in heart failure

In congestive heart failure (CHF), themechanisms of exercise-induced sympathoexcitation are poorly defined.We compared the responses of sympathetic nerve activity directed tomuscle (MSNA) and to skin (SSNA, peroneal microneurography) duringrhythmic handgrip (RHG) at 25% of maximal voluntary contraction andduring posthandgrip circulatory arrest (PHG-CA) in CHF patients with those of an age-matched control group. During RHG, the CHF patients fatigued prematurely. At end exercise, the increase in MSNA was similarin both groups (CHF patients, n = 12;controls, n = 10). However, duringPHG-CA, in the controls MSNA returned to baseline, whereas it remainedelevated in CHF patients (P < 0.05).Similarly, at end exercise, the increase in SSNA was comparable in bothgroups (CHF patients, n = 11;controls, n = 12), whereas SSNAremained elevated during PHG-CA in CHF patients but not in the controls (P < 0.05). In a separate controlgroup (n = 6), even high-intensity static handgrip was not accompanied by sustained elevation of SSNAduring PHG-CA. ³¹P-nuclear magneticresonance spectroscopy during RHG demonstrated significant muscleacidosis and accumulation of inorganic phosphate in CHF patients(n = 7) but not in controls(n = 9). We conclude that in CHFpatients rhythmic forearm exercise leads to premature fatigue andaccumulation of muscle metabolites. The prominent PHG-CA response ofMSNA and SSNA in CHF patients suggests activation of the musclemetaboreflex. Because, in contrast to controls, in CHF patients bothMSNA and SSNA appear to be under muscle metaboreflex control, themechanisms and distribution of sympathetic outflow during exerciseappear to be different from normal.

     

Ultrasound Doppler estimates of femoral artery blood flow during dynamic knee extensor exercise in humans

Rådegran, G. Ultrasound Dopplerestimates of femoral artery blood flow during dynamic knee extensorexercise in humans. J. Appl. Physiol.83(4): 1383-1388, 1997.Ultrasound Doppler has been used tomeasure arterial inflow to a human limb during intermittent staticcontractions. The technique, however, has neither been thoroughlyvalidated nor used during dynamic exercise. In this study, the inherentproblems of the technique have been addressed, and the accuracy wasimproved by storing the velocity tracings continuously and calculatingthe flow in relation to the muscle contraction-relaxation phases. Thefemoral arterial diameter measurements were reproducible with a meancoefficient of variation within the subjects of 1.2 ± 0.2%. Thediameter was the same whether the probe was fixed or repositioned atrest (10.8 ± 0.2 mm) or measured during dynamic exercise. The bloodvelocity was sampled over the width of the diameter and the parabolicvelocity profile, since sampling in the center resulted in anoverestimation by 22.6 ± 9.1% (P < 0.02). The femoral arterial Doppler blood flow increased linearly(r = 0.997, P < 0.001) with increasing load [Doppler blood flow = 0.080 · load (W) + 1.446 l/min] and was correlated positively with simultaneousthermodilution venous outflow measurements(r = 0.996, P < 0.001). The two techniques werelinearly related (Doppler = thermodilution · 0.985 + 0.071 l/min; r = 0.996, P < 0.001), with a coefficient ofvariation of ~6% for both methods.

     

Fluid and electrolyte hormonal responses to exercise and acute plasma volume expansion

Grant, S. M., H. J. Green, S. M. Phillips, D. L. Enns, andJ. R. Sutton. Fluid and electrolyte hormonal responses to exerciseand acute plasma volume expansion. J. Appl.Physiol. 81(6): 2386-2392, 1996.To investigatethe effect of acute graded increases in plasma volume (PV) on fluid andregulatory hormone levels, eight untrained men (peak aerobic power 45.2 ± 2.2 ml ^· kg^{1 ·} min¹)performed prolonged cycle exercise (46 ± 4% maximal aerobic poweron three occasions, namely, with no PV expansion (Con) and after 14%(Low) and 21% (High) expansions, respectively. The exercise plasmalevels of aldosterone (Aldo), arginine vasopressin (AVP), and atrialnatriuretic peptide (ANP) were all altered by acute PV increases. Apronounced blunting (P < 0.05) ofthe Aldo response during exercise was observed, the magnitude of whichwas directly related to the amount of hypervolemia (Con < Low < High). At 120 min of exercise, Aldo concentrations were 660 ± 71, 490 ± 85, and 365 ± 78 pg/ml for Con, Low, and High conditions,respectively. In contrast, the lower AVP and the higher ANP observedduring exercise appeared to be due to the effect of PV expansion onresting concentrations. Because osmolality did not vary amongconditions, the results indicate that PV represents an importantprimary stimulus in the response of Aldo to exercise. The lowerexercise blood concentrations of both epinephrine and norepinephrineobserved with PV expansion would suggest that a lower sympathetic drive may be implicated at least in the lower Aldo responses.