Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712-717, 1997.Ten patients with preserved inotropic function having adual-chamber (right atrium and right ventricle) pacemaker placed forcomplete heart block were studied. They performed static one-leggedknee extension at 20% of their maximal voluntary contraction for 5 minduring three conditions: 1)atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HRfixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and3) HR fixed at peak exercise rate(DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode),mean arterial pressure (MAP) increased by 25 mmHg with no change instroke volume (SV) or systemic vascular resistance. During DOO-Rest andDOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of aSV-dependent increase in cardiac output (+1.3 and +1.8 l/min,respectively). The increase in SV during DOO-Rest utilized acombination of increased contractility and the Frank-Starling mechanism(end-diastolic volume 118-136 ml). However, during DOO-Ex, agreater left ventricular contractility (end-systolic volume 55-38ml) mediated the increase in SV.

     

Decreased energy metabolism in brain stem during central respiratory depression in response to hypoxia

LaManna, J. C., M. A. Haxhiu, K. L. Kutina-Nelson, S. Pundik, B. Erokwu, E. R. Yeh, W. D. Lust, and N. S. Cherniack.Decreased energy metabolism in brain stem during centralrespiratory depression in response to hypoxia. J. Appl. Physiol. 81(4): 1772-1777, 1996.Metabolic changes in the brain stem were measured at the time when oxygen deprivation-induced respiratory depression occurred. Eucapnic ventilation with 8% oxygen in vagotomized urethan-anesthetized ratsresulted in cessation of respiratory drive, monitored by recordingdiaphragm electromyographic activity, on average within 11 min (range5-27 min), presumably via central depressant mechanisms. At thattime, the brain stems were frozen in situ for metabolic analyses. Byusing 20-µm lyophilized sections from frozen-fixed brainstem, microregional analyses of ATP, phosphocreatine, lactate, andintracellular pH were made from 1)the ventral portion of the nucleus gigantocellularis and theparapyramidal nucleus; 2) thecompact and ventral portions of the nucleus ambiguus;3) midline neurons;4) nucleus tractus solitarii; and5) the spinal trigeminal nucleus. Atthe time of respiratory depression, lactate was elevated threefold inall regions. Both ATP and phosphocreatine were decreased to 50 and 25%of control, respectively. Intracellular pH was more acidic by0.2-0.4 unit in these regions but was relatively preserved in thechemosensitive regions near the ventral and dorsal medullary surfaces.These results show that hypoxia-induced respiratory depression wasaccompanied by metabolic changes within brain stem regions involved inrespiratory and cardiovascular control. Thus it appears that there wassignificant energy deficiency in the brain stem after hypoxia-inducedrespiratory depression had occurred.

     

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.

     

Effect of resistance exercise training on cortical and cancellous bone in mature male rats

Westerlind, Kim C., James D. Fluckey, Scott E. Gordon,William J. Kraemer, Peter A. Farrell, and Russell T. Turner.Effect of resistance exercise training on cortical and cancellousbone in mature male rats. J. Appl.Physiol. 84(2): 459-464, 1998.The effect ofresistance training on tibial cancellous and cortical bone wasevaluated in rats by using static histomorphometry and Northernanalysis. Five-month-old male Sprague-Dawley rats were randomlyassigned to exercise (Ex; n = 8) orcontrol (Con; n = 4) groups. Animalswere operantly conditioned to press two levers, facilitating fullextension and flexion of the hindlimbs ("squats"), while wearingan unweighted vest. After an 8-wk familiarization period, Ex animalsperformed 3 sessions/wk for 17-19 sessions with progressivelyincreased amounts of weight applied to the vest. Con rats completed thesame exercise protocol without applied resistance. No difference incross-sectional, medullary, or cortical bone area was observed betweenEx and Con rats in the tibial diaphysis. In contrast, the cancellousbone area in the proximal tibial metaphysis was significantly larger intrained rats. Trabecular number, trabecular thickness, and thepercentage of cancellous bone covered by osteoid were significantlygreater in the Ex animals compared with Con animals. In addition,steady-state mRNA levels for osteocalcin for the Ex group were 456%those expressed in the Con group. The data demonstrate that resistancetraining increases cancellous bone area in sexually mature male ratsand suggest that it does so, in part, by stimulating bone formation.

     

Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise

Saito, Mitsuru, Ryoko Sone, Masao Ikeda, and Tadaaki Mano.Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise. J. Appl.Physiol. 82(4): 1237 - 1243, 1997.Toinvestigate the effects of exercise duration on muscle sympatheticnerve activity (MSNA), heart rate, blood pressure (BP), tympanictemperature, blood lactate concentration, and thigh electromyogram weremeasured in eight volunteers during 30 min of cycling in the sittingposition at an intensity of 40% of maximal oxygen uptake. MSNA burstfrequency increased 18 min after exercise was begun (25 ± 4 bursts/min at baseline and 36 ± 5 bursts/min at 21 min ofexercise), reaching 41 ± 5 bursts/min at the end ofexercise. Heart rate and systolic BP increased during exercise. Twenty minutes after commencement of exercise, however, bothsystolic and diastolic BP values tended to drop compared with theinitial period of exercise. Tympanic temperature increased in atime-dependent manner, and the increment was significant 12 min afterexercise was begun. Blood lactate concentration and integratedelectromyogram showed no significant changes during exercise. Theincreased MSNA during prolonged light-intensity exercise may be asecondary effect of the drop in BP as a result of blood redistributioncaused by thermoregulation rather than by metaboreflex.

     

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

The cardiovascular adaptation at the onset of voluntary static exercise is controlled by the autonomic nervous system. Two neural mechanisms are responsible for the cardiovascular adaptation: one is central command descending from higher brain centers, and the other is a muscle mechanosensitive reflex from activation of mechanoreceptors in the contracting muscles. To examine which mechanism played a major role in producing the initial cardiovascular adaptation during static exercise, we studied the effect of intravenous administration of gadolinium (55 micromol/kg), a blocker of stretch-activated ion channels, on the increases in heart rate (HR) and mean arterial blood pressure (MAP) at the onset of voluntary static exercise (pressing a bar with a forelimb) in conscious cats. HR increased by 31 +/- 5 beats/min and MAP increased by 15 +/- 1 mmHg at the onset of voluntary static exercise. Gadolinium affected neither the baseline values nor the initial increases of HR and MAP at the onset of exercise, although the peak force applied to the bar tended to decrease to 65% of the control value before gadolinium. Furthermore, we examined the effect of gadolinium on the reflex responses in HR and MAP (18 +/- 7 beats/min and 30 +/- 6 mmHg, respectively) during passive mechanical stretch of a forelimb or hindlimb in anesthetized cats. Gadolinium significantly blunted the passive stretch-induced increases in HR and MAP, suggesting that gadolinium blocks the stretch-activated ion channels and thereby attenuates the reflex cardiovascular responses to passive mechanical stretch of a limb. We conclude that the initial cardiovascular adaptation at the onset of voluntary static exercise is predominantly induced by feedforward control of central command descending from higher brain centers but not by a muscle mechanoreflex.     

Growth hormone/IGF-I and/or resistive exercise maintains myonuclear number in hindlimb unweighted muscles

Allen, David L., Jon K. Linderman, Roland R. Roy, Richard E. Grindeland, Venkat Mukku, and V. Reggie Edgerton. Growth hormone/IGF-I and/or resistive exercise maintains myonuclearnumber in hindlimb unweighted muscles. J. Appl.Physiol. 83(5): 1857-1861, 1997.In the presentstudy of rats, we examined the role, during 2 wk ofhindlimb suspension, of growth hormone/insulin-like growth factor I(GH/IGF-I) administration and/or brief bouts of resistance exercise in ameliorating the loss of myonuclei in fibers of the soleusmuscle that express type I myosin heavy chain. Hindlimb suspensionresulted in a significant decrease in mean soleus wet weight that wasattenuated either by exercise alone or by exercise plus GH/IGF-Itreatment but was not attenuated by hormonal treatment alone. Both meanmyonuclear number and mean fiber cross-sectional area (CSA) of fibersexpressing type I myosin heavy chain decreased after 2 wk of suspensioncompared with control (134 vs. 162 myonuclei/mm and 917 vs. 2,076 µm², respectively). NeitherGH/IGF-I treatment nor exercise alone affected myonuclear number orfiber CSA, but the combination of exercise and growth-factor treatmentattenuated the decrease in both variables. A significant correlationwas found between mean myonuclear number and mean CSA across allgroups. Thus GH/IGF-I administration and brief bouts of muscle loadinghad an interactive effect in attenuating the loss of myonuclei inducedby chronic unloading.

     

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.

     

Failure of prostaglandins to modulate the time course of blood flow during dynamic forearm exercise in humans

Shoemaker, J. K., H. L. Naylor, Z. I. Pozeg, and R. L. Hughson. Failure of prostaglandins to modulate the time course ofblood flow during dynamic forearm exercise in humans.J. Appl. Physiol. 81(4):1516-1521, 1996.The time course and magnitude of increases inbrachial artery mean blood velocity (MBV; pulsed Doppler), diameter(D; echo Doppler), mean perfusionpressure (MPP; Finapres), shear rate ( = 8 ^· MBV/D), andforearm blood flow (FBF = MBV ^· r²)were assessed to investigate the effect that prostaglandins (PGs) haveon the hyperemic response on going from rest to rhythmic exercise inhumans. While supine, eight healthy men performed 5 min of dynamichandgrip exercise by alternately raising and lowering a 4.4-kg weight(~10% maximal voluntary contraction) with a work-to-rest cycle of1:1 (s/s). When the exercise was performed with the arm positionedbelow the heart, the rate of increase in MBV and wasfaster compared with the same exercise performed above the heart.Ibuprofen (Ibu; 1,200 mg/day, to reduce PG-induced vasodilation) andplacebo were administered orally for 2 days before two separate testingsessions in a double-blind manner. Resting heart rate was reduced inIbu (52 ± 3 beats/min) compared with placebo (57 ± 3 beats/min)(P < 0.05) without change to MPP.With placebo, D increased in both armpositions from ~4.3 mm at rest to ~4.5 mm at 5 min of exercise(P < 0.05). This response was notaltered with Ibu (P > 0.05). Ibudid not alter the time course of MBV or forearm blood flow(P > 0.05) in either arm position. The was significantly greater in Ibu vs. placebo at 30 and 40 s of above the heart exercise and for all time points after 25 sof below the heart exercise (P < 0.05). Because PG inhibition altered the time course of at the brachial artery, but not FBF, it was concludedthat PGs are not essential in regulating the blood flow responses todynamic exercise in humans.

     

Effect of heat stress on glucose kinetics during exercise

Hargreaves, Mark, Damien Angus, Kirsten Howlett, Nelly MarmyConus, and Mark Febbraio. Effect of heat stress on glucose kinetics during exercise. J. Appl.Physiol. 81(4): 1594-1597, 1996.To identify themechanism underlying the exaggerated hyperglycemia during exercise inthe heat, six trained men were studied during 40 min of cyclingexercise at a workload requiring 65% peak pulmonary oxygen uptake(O_{2 peak}) on twooccasions at least 1 wk apart. On one occasion, the ambient temperaturewas 20°C [control (Con)], whereas on the other, it was40°C [high temperature (HT)]. Rates ofglucose appearance and disappearance were measured by using a primedcontinuous infusion of[6,6-²H]glucose. Nodifferences in oxygen uptake during exercise were observed betweentrials. After 40 min of exercise, heart rate, rectal temperature,respiratory exchange ratio, and plasma lactate were all higher in HTcompared with Con (P < 0.05). Plasmaglucose levels were similar at rest (Con, 4.54 ± 0.19 mmol/l; HT,4.81 ± 0.19 mmol/l) but increased to a greater extent duringexercise in HT (6.96 ± 0.16) compared with Con (5.45 ± 0.18;P < 0.05). This was the result of ahigher glucose rate of appearance in HT during the last 30 min ofexercise. In contrast, the glucose rate of disappearance and metabolicclearance rate were not different at any time point during exercise.Plasma catecholamines were higher after 10 and 40 min of exercise in HTcompared with Con (P < 0.05),whereas plasma glucagon, cortisol, and growth hormone were higher in HTafter 40 min. These results indicate that the hyperglycemia observedduring exercise in the heat is caused by an increase in liver glucoseoutput without any change in whole body glucoseutilization.

     

Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea

Zinkovska, Sophia, and Debra A. Kirby.Intracerebroventricular propranolol prevented vascular resistanceincreases on arousal from sleep apnea. J. Appl.Physiol. 82(5): 1637-1643, 1997.Despite theincreased risk of sudden cardiac death associated with sleep apnea,little is known about mechanisms controlling cardiovascular responsesto sleep apnea and arousal. Chronically instrumented pigs were used toinvestigate the effects of airway obstruction (AO) duringrapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on meanarterial pressure (MAP), heart rate (HR), cardiac output (CO), andtotal peripheral resistance (TPR). A stainless steelcannula was implanted in the lateral cerebral ventricle. During REMsleep, HR was 133 ± 10 beats/min, MAP was 65 ± 3 mmHg, CO was1,435 ± 69 ml/min, and TPR was 0.046 ± 0.004 mmHg · ml¹ · min.During AO, CO decreased by 90 ± 17 ml/min(P < 0.05). On arousal from AO, MAPincreased by 15 ± 3 mmHg, HR increased by 10 ± 3 beats/min, andTPR increased by 0.008 ± 0.001 mmHg · ml¹ · min(all P < 0.05). Changes during NREMwere similar but were more modest during AO. After theintracerebroventricular administration of propranolol (50 µg/kg; a-adrenoreceptor blocking agent), decreases in CO during AO andincreases in HR during arousal were intact, but increases in MAP andTPR were no longer significant. These data suggest thatvascular responses to AO during sleep may be regulated in part by-adrenergic receptors in the central nervous system.

     

Effects of chronic exercise and deconditioning on platelet function in women

Wang, Jong-Shyan, Chauying J. Jen, and Hsiun-Ing Chen.Effects of chronic exercise and deconditioning on plateletfunction in women. J. Appl. Physiol.83(6): 2080-2085, 1997.To investigate the effects of chronicexercise and deconditioning on platelet function in women, 16 healthysedentary women were divided into control and exercise groups. Theexercise group cycled on an ergometer at 50% maximal oxygenconsumption for 30 min/day, 5 days/wk, for two consecutive menstrualcycles and then were deconditioned for three menstrual cycles. Duringthis period, platelet adhesiveness on a fibrinogen-coated surface,ADP-induced platelet aggregation and intracellular calciumconcentration elevation, guanosine 3,5-cyclic monophosphate (cGMP) content in platelets, and plasma nitric oxide metabolite levels were measured before and immediately after a progressive exercise test in the midfollicular phase. Ourresults indicated that, after exercise training,1) resting heart rates and bloodpressures were reduced, and exercise performance was improved;2) resting platelet function wasdecreased, whereas plasma nitrite and nitrate levels and platelet cGMPcontents were enhanced; and 3) thepotentiation of platelet function by acute strenuous exercise wasdecreased, whereas the increases in plasma nitrite and nitrate levelsand platelet cGMP contents were enhanced by acuteexercise. Furthermore, deconditioning reversed these training effects. This implies that training-induced platelet functional changes in women in the midfollicular phase may be mediatedby nitric oxide.

     

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.

     

Cardiovascular responses during spontaneous overground locomotion in freely moving decerebrate cats

Sadamoto, Tomoko, and Kanji Matsukawa. Cardiovascularresponses during spontaneous overground locomotion in freely movingdecerebrate cats. J. Appl. Physiol.83(5): 1454-1460, 1997.To examine whether the cerebrum isessential for producing the rapid cardiovascular adjustment at thebeginning of overground locomotion, we examined heart rate (HR), meanarterial blood pressure (MAP), and integrated electromyogram (iEMG) ofthe forelimb triceps brachialis muscle in freely moving decerebratecats during locomotion. Two to four days after decerebration surgeryperformed at the level of the precollicular-premammillary body, theanimals spontaneously produced coordinated overground locomotion,supporting body weight. HR began to increase immediately before theonset of iEMG, and MAP began to rise almost simultaneously with theiEMG onset. Their increases in HR and MAP (24 ± 3 beats/min and 22 ± 4 mmHg) were sustained during locomotion. Sinoaortic denervation(SAD) did not affect the abrupt changes in HR and MAP at the beginningof locomotion (0-4 s from the onset of iEMG), whereas SAD had acontrasting effect during the subsequent period, a decrease in the HRresponse (9 ± 1 beats/min) and an increase in the MAP response (30 ± 3 mmHg). These results suggest that the cerebrum and the rostral part of the diencephalon are not essential for producing the rapid cardiovascular adjustment at the beginning of spontaneous overground locomotion. The arterial baroreflex does not contribute to this rapidadjustment but plays an important role in regulating the cardiovascularresponses during the later period of spontaneous locomotion.

     

Effect of endurance exercise training on muscle glycogen supercompensation in rats

Nakatani, Akira, Dong-Ho Han, Polly A. Hansen, Lorraine A. Nolte, Helen H. Host, Robert C. Hickner, and John O. Holloszy. Effect of endurance exercise training on muscle glycogensupercompensation in rats. J. Appl.Physiol. 82(2): 711-715, 1997.The purpose of this study was to test the hypothesis that the rate and extent ofglycogen supercompensation in skeletal muscle are increased byendurance exercise training. Rats were trained by using a 5-wk-long swimming program in which the duration of swimming was gradually increased to 6 h/day over 3 wk and then maintained at 6 h/day for anadditional 2 wk. Glycogen repletion was measured in trained anduntrained rats after a glycogen-depleting bout of exercise. The ratswere given a rodent chow diet plus 5% sucrose in their drinking waterad libitum during the recovery period. There were remarkabledifferences in both the rates of glycogen accumulation and the glycogenconcentrations attained in the two groups. The concentration ofglycogen in epitrochlearis muscle averaged 13.1 ± 0.9 mg/g wet wtin the untrained group and 31.7 ± 2.7 mg/g in the trained group(P < 0.001) 24 h after the exercise.This difference could not be explained by a training effect on glycogensynthase. The training induced ~50% increases in muscle GLUT-4glucose transporter protein and in hexokinase activity inepitrochlearis muscles. We conclude that endurance exercise trainingresults in increases in both the rate and magnitude of muscle glycogensupercompensation in rats.

     

Learned control of heart rate during dynamic exercise in nonhuman primates

The purpose of this study was to describe an animal model to test the relationships among the cardiovascular, pulmonary, and somatomotor command systems during exercise. Using operant conditioning, three chronically chaired monkeys (Macaca mulatta) were trained to exercise (to lift weights repeatedly), to attenuate their heart rate responses, and finally, both conditions were combined so that the animals were required to exercise and attenuate their heart rates. Heart rate, systolic and diastolic blood pressure, rate-pressure product, O2 and CO2 concentration in expired air, and number of weight lifts were recorded and compared between the two conditions, i.e., exercise only and combined exercise and heart rate slowing. In all animals heart rate increases in response to exercise were significantly less (P less than 0.05) during combined conditions than during exercise only: the mean heart rate increase was 41 beats/min less during combined sessions than during exercise only sessions for monkey 1, 13.5 beats/min less for monkey 2, and 9 beats/min less for monkey 3. Rate-pressure product showed a consistent difference across animals paralleling the heart rate differences. This acquired response did not involve other cardiovascular and pulmonary parameters, which did not change systematically across animals. However, the pattern of cardiovascular reactivity in relation to O2 consumption (linear regression of heart rate and systolic or diastolic blood pressure on change in O2 consumption over many experiments) was attenuated during combined sessions relative to exercise only experiments. The relative attenuation of heart rate during combined sessions also remained significant when both experimental conditions were equated on the basis of work done. Therefore, this animal model shows a dissociation of cardiovascular, somatomotor, and pulmonary effects of central command.     

Oral glucose ingestion increases endurance capacity in normal and diabetic (type I) humans

Ramires, P. R., C. L. M. Forjaz, C. M. C. Strunz, M. E. R. Silva, J. Diament, W. Nicolau, B. Liberman, and C. E. Negrão. Oral glucose ingestion increases endurance capacity in normal anddiabetic (type I) humans. J. Appl.Physiol. 83(2): 608-614, 1997.The effects of anoral glucose administration (1 g/kg) 30 min before exercise onendurance capacity and metabolic responses were studied in 21 type Idiabetic patients [insulin-dependent diabetes mellitus(IDDM)] and 23 normal controls (Con). Cycle ergometer exercise (55-60% of maximalO₂ uptake) was performed untilexhaustion. Glucose administration significantly increased endurancecapacity in Con (112 ± 7 vs. 125 ± 6 min,P < 0.05) but only in IDDM patientswhose blood glucose decreased during exercise (70.8 ± 8.2 vs. 82.8 ± 9.4 min, P < 0.05).Hyperglycemia was normalized at 15 min of exercise in Con (7.4 ± 0.2 vs. 4.8 ± 0.2 mM) but not in IDDM patients (12.4 ± 0.7 vs.15.6 ± 0.9 mM). In Con, insulin and C-peptide levels werenormalized during exercise. Glucose administration decreased growthhormone levels in both groups. In conclusion, oral glucose ingestion 30 min before exercise increases endurance capacity in Con and in someIDDM patients. In IDDM patients, in contrast with Con, exercise to exhaustion attenuates hyperglycemia but does not bring blood glucose levels to preglucose levels.

     

Gut and liver fat metabolism in depancreatized dogs: effects of exercise and acute insulin infusion

Namdaran, Kiarash, Deanna P. Bracy, D. Brooks Lacy, JaniceL. Johnson, Jennifer L. Bupp, and David H. Wasserman. Gut andliver fat metabolism in depancreatized dogs: effects of exercise andacute insulin infusion. J. Appl.Physiol. 83(4): 1339-1347, 1997.Excessivecirculating fat levels are a defining feature of poor metabolic controlin diabetes. Splanchnic adipose tissue is a source of free fatty acids(FFA), and the liver is a key site of FFA utilization and the solesource of ketones. Despite the role of splanchnic tissues in fatmetabolism, little is known about how these tissues respond to diabetesunder divergent metabolic conditions. Therefore, splanchnic fatmetabolism was studied in poorly controlled diabetes under twoconditions. First, it was studied during exercise, a stimulus thatenhances FFA flux. Second, it was studied while insulin was beingacutely infused to achieve levels normally present during exercise, atreatment that may be expected to inhibit lipolysis. For this purpose,liver and gut arteriovenous differences were used during rest and 2.5 h of treadmill exercise in insulin-deficient(n = 6) and acutely insulin-infused(n = 4) depancreatized (PX) dogs. Thedata show that 1) exercise, ininsulin-deficient PX dogs, leads to an increase in net FFA release frommesenteric fat that is equal in magnitude to the response innondiabetic dogs; 2) net hepaticfractional FFA extraction is increased twofold during exercise in bothinsulin-deficient PX dogs and nondiabetic control dogs;3) during exercise, ~40 and 75%of the FFA consumed by the liver is effectively transferred from fatstores mobilized from splanchnic adipose tissue in insulin-deficient PXand nondiabetic dogs, respectively;4) hepatic ketogenic efficiency iselevated during rest three- to fourfold in insulin-deficient PX dogscompared with nondiabetic control dogs and remains elevated duringexercise; and 5) surprisingly, acuteinsulin replacement is ineffective in normalizing net gut, hepatic, orsplanchnic FFA or ketone body balances in PX dogs.

     

Cerebral areas associated with motor control of speech in humans

Murphy, K., D. R. Corfield, A. Guz, G. R. Fink, R. J. S. Wise, J. Harrison, and L. Adams. Cerebral areas associated withmotor control of speech in humans. J. Appl.Physiol. 83(5): 1438-1447, 1997.We have definedareas in the brain activated during speaking, utilizing positronemission tomography. Six normal subjects continuously repeated thephrase "Buy Bobby a poppy" (requiring minimal languageprocessing) in four ways: A) spoken aloud, B) mouthed silently,C) without articulation, andD) thought silently. Statisticalcomparison of images from conditions Awith C andB withD highlighted areas associated witharticulation alone, because control of breathing for speech wascontrolled for; we found bilateral activations in sensorimotor cortexand cerebellum with right-sided activation in the thalamus/caudate nucleus. Contrasting images from conditionsA with B andC with D highlighted areas associated withthe control of breathing for speech, vocalization, and hearing, becausearticulation was controlled for; we found bilateral activations insensorimotor and motor cortex, close to but distinct from theactivations in the preceding contrast, together with activations inthalamus, cerebellum, and supplementary motor area. In neithersubtraction was there activation in Broca's area. These resultsemphasize the bilaterality of the cerebral control of "speaking"without language processing.

     

Exercise training increases sarcolemmal GLUT-4 protein and mRNA content in diabetic heart

Osborn, Brett A., June T. Daar, Richard A. Laddaga, Fred D. Romano, and Dennis J. Paulson. Exercise training increases sarcolemmal GLUT-4 protein and mRNA content in diabetic heart. J. Appl. Physiol. 82(3): 828-834, 1997.This study determined whether dynamic exercise training ofdiabetic rats would increase the expression of the GLUT-4 glucosetransport protein in prepared cardiac sarcolemmal membranes. Fourgroups were compared: sedentary control, sedentary diabetic, trainedcontrol, and trained diabetic. Diabetes was induced by intravenousstreptozotocin (60 mg/kg). Trained control and diabetic rats were runon a treadmill for 60 min, 27 m/min, 10% grade, 6 days/wk for 10 wk.Sarcolemmal membranes were isolated by using differentialcentrifugation, and the activity of sarcolemmalK⁺-p-nitrophenylphosphatase( pNPPase; an indicator ofNa⁺-K⁺-adenosinetriphosphataseactivity) was quantified. Hearts from the sedentary diabetic groupexhibited a significant depression of sarcolemmal pNPPaseactivity. Exercise training did not significantly alterpNPPase activity. Sedentary diabetic rats exhibited an 84 and 58% decrease in GLUT-4 protein and mRNA, respectively, relative tocontrol rats. In the trained diabetic animals, sarcolemmal GLUT-4protein levels were only reduced by 50% relative to control values,whereas GLUT-4 mRNA were returned to control levels. The increase inmyocardial sarcolemmal GLUT-4 may be beneficial to the diabetic heartby enhancing myocardial glucose oxidation and cardiac performance