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.

     

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise

González-Alonso, José, RicardoMora-Rodríguez, Paul R. Below, and Edward F. Coyle.Dehydration markedly impairs cardiovascular function inhyperthermic endurance athletes during exercise. J. Appl. Physiol. 82(4): 1229-1236, 1997.Weidentified the cardiovascular stress encountered by superimposingdehydration on hyperthermia during exercise in the heat and themechanisms contributing to the dehydration-mediated stroke volume (SV)reduction. Fifteen endurance-trained cyclists [maximalO₂ consumption(O_{2 max}) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinkingfluids. Measurements were made after they continued exercise at 71%O_{2 max} for 30 minwhile 1) euhydrated with anesophageal temperature (T_es) of38.1-38.3°C (control); 2)euhydrated and hyperthermic (39.3°C);3) dehydrated and hyperthermic withskin temperature (T_sk) of34°C; 4) dehydrated withT_es of 38.1°C and T_sk of 21°C; and5) condition4 followed by restored blood volume. Compared withcontrol, hyperthermia (1°C T_esincrease) and dehydration (4% body weight loss) each separatelylowered SV 7-8% (11 ± 3 ml/beat;P < 0.05) and increased heart ratesufficiently to prevent significant declines in cardiac output.However, when dehydration was superimposed on hyperthermia, thereductions in SV were significantly (P < 0.05) greater (26 ± 3 ml/beat), and cardiac output declined 13% (2.8 ± 0.3 l/min). Furthermore, mean arterialpressure declined 5 ± 2%, and systemic vascular resistanceincreased 10 ± 3% (both P < 0.05). When hyperthermia wasprevented, all of the decline in SV with dehydration was due to reducedblood volume (~200 ml). These results demonstrate that thesuperimposition of dehydration on hyperthermia during exercise in theheat causes an inability to maintain cardiac output and blood pressurethat makes the dehydrated athlete less able to cope with hyperthermia.

     

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.

     

Hemodynamic and norepinephrine responses to pacing-induced heart failure in conscious sinoaortic-denervated dogs

Brändle, Marian, Kaushik P. Patel, Wei Wang, andIrving H. Zucker. Hemodynamic and norepinephrine responses topacing-induced heart failure in conscious sinoaortic-denervated dogs.J. Appl. Physiol. 81(4):1855-1862, 1996.The present study was undertaken to determinethe effects of chronic sinoaortic (baroreceptor) denervation (SAD) on the hemodynamic and sympathetic alterations thatoccur in the pacing-induced model of congestive heart failure. Twogroups of dogs were examined: intact(n = 9) and SAD(n = 9). Both groups of dogs werestudied in the control (prepace) state and each week after theinitiation of ventricular pacing at 250 beats/min. After the pacemakerwas turned off, hemodynamic and plasma norepinephrine levels returnedtoward control levels in the prepaced state and after 1 and 2 wk ofpacing. However, by 3 wk all hemodynamic and norepinephrine levelsremained relatively constant over the 10-min observation period withthe pacemaker off. With the pacemaker off, left ventricularend-diastolic pressure went from 2.7 ± 1.4 (SE) mmHg during theprepace state to 23.2 ± 2.9 mmHg in the heart failure state inintact dogs (P < 0.01). Leftventricular end-diastolic pressure increased to 27.1 ± 2.2 mmHgfrom a control level of 4.2 ± 1.9 mmHg in SAD dogs(P < 0.0003). Mean arterial pressuresignificantly decreased in intact and SAD dogs. Resting heart rate wassignificantly higher in SAD dogs and increased to 135.8 ± 8.9 beats/min in intact dogs and 136.1 ± 6.5 beats/min in SAD dogs.There were no significant differences in the hemodynamic parametersbetween intact and SAD dogs after pacing. Plasma norepinephrine wassignificantly lower in intact than in SAD dogs before pacing (197.7 ± 21.6 vs. 320.6 ± 26.6 pg/ml;P < 0.005). In the heart failurestate, plasma norepinephrine increased significantly in both intact(598.3 ± 44.2 pg/ml) and SAD (644.0 ± 64.6 pg/ml) groups. Therewere no differences in the severity or the magnitude of the developedheart failure state in SAD vs. intact dogs. We conclude from these datathat the arterial baroreflex is not the sole mechanism for the increasein sympathetic drive in heart failure.

     

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.

     

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.

     

Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy

Colin, Patrice, Michel Slama, Alec Vahanian, YvesLecarpentier, Gilbert Motté, and Denis Chemla. Hemodynamiccorrelates of effective arterial elastance in mitral stenosis beforeand after balloon valvotomy. J. Appl.Physiol. 83(4): 1083-1089, 1997.This study hadthe purpose of documenting the hemodynamic correlates of effectivearterial elastance (Ea; i.e., an accurate estimate of hydraulic load)in mitral stenosis (MS) patients. The main hypothesis tested was thatEa relates to the total vascular resistance (R)-to-pulse intervalduration (T) ratio(R/T) in MS patients both before andafter successful balloon mitral valvotomy (BMV). High-fidelity aorticpressure recordings were obtained in 10 patients (40 ± 12 yr)before and 15 min after BMV. Ea value was calculated as the ratio ofthe steady-state end-systolic aortic pressure (ESAP) to stroke volume(thermodilution). Ea increased after BMV (from 1.55 ± 0.63 to 1.83 ± 0.71 mmHg/ml; P < 0.05). Throughout the procedure, there was a strong linearrelationship between Ea and R/T: Ea = 1.09R/T  0.01 mmHg/ml,r = 0.99, P = 0.0001. This ultimately dependedon the powerful link between ESAP and mean aortic pressure [MAP;r = 0.99, 95% confidence interval for the difference (MAP  ESAP) from 18.5 to +4.5 mmHg].Ea was also related to total arterial compliance (area method) and towave reflections (augmentation index), although to a lesser extent. After BMV, enhanced and anticipated wave reflections were observed, andthis was likely to be explained by decreased arterial compliance. Thepresent study indicated that Ea depended mainly on the steady componentof hydraulic load (i.e., R) and on heart period (i.e., T) in MS patients.

     

Muscle metaboreflex control of coronary blood flow

We investigated the effect of muscle metaboreflex activation on left circumflex coronary blood flow (CBF) and vascular conductance (CVC) in conscious, chronically instrumented dogs during treadmill exercise ranging from mild to severe workloads. Metaboreflex responses were also observed during mild exercise with constant heart rate (HR) of 225 beats/min and beta(1)-adrenergic receptor blockade to attenuate the substantial reflex increases in cardiac work. The muscle metaboreflex was activated via graded partial occlusion of hindlimb blood flow. During mild exercise, with muscle metaboreflex activation, hindlimb ischemia elicited significant reflex increases in mean arterial pressure (MAP), HR, and cardiac output (CO) (+39.0 +/- 5.2 mmHg, +29.9 +/- 7.7 beats/min, and +2.0 +/- 0.4 l/min, respectively; all changes, P < 0.05). CBF increased from 51.9 +/- 4.3 to 88.5 +/- 6.6 ml/min, (P < 0.05), whereas no significant change in CVC occurred (0.56 +/- 0.06 vs. 0.59 +/- 0.05 ml. min(-1). mmHg(-1); P > 0.05). Similar responses were observed during moderate exercise. In contrast, with metaboreflex activation during severe exercise, no further increases in CO or HR occurred, the increases in MAP and CBF were attenuated, and a significant reduction in CVC was observed (1.00 +/- 0.12 vs. 0.90 +/- 0.13 ml. min(-1). mmHg(-1); P < 0.05). Similarly, when the metaboreflex was activated during mild exercise with the rise in cardiac work lessened (via constant HR and beta(1)-blockade), no increase in CO occurred, the MAP and CBF responses were attenuated (+15.6 +/- 4.5 mmHg, +8.3 +/- 2 ml/min), and CVC significantly decreased from 0.63 +/- 0.11 to 0.53 +/- 0.10 ml. min(-1). mmHg(-1). We conclude that the muscle metaboreflex induced increases in sympathetic nerve activity to the heart functionally vasoconstricts the coronary vasculature.     

Effects of renal denervation on cardiovascular and renal responses to ACE inhibition in conscious lambs

Smith, Francine G., Suzanne Chan, and Saskia N. De Wildt.Effects of renal denervation on cardiovascular and renal responsesto ACE inhibition in conscious lambs. J. Appl.Physiol. 83(2): 414-419, 1997.Cardiovascular andrenal effects of either the angiotensin-converting enzyme inhibitorcaptopril or vehicle were measured in chronically instrumented lambs inthe presence (intact; n = 6) andabsence of renal sympathetic nerves (denervated; n = 5) to determine whether there wasan interaction between the renin-angiotensin system and renalsympathetic nerves early in life. Captopril caused a similar decreasein mean arterial pressure (P < 0.001) in intact and denervated lambs, predominantly through a decreasein diastolic pressure. Heart rate was increased from 177 ± 34 to213 ± 22 (SD) beats/min during captopril compared with vehicleinfusion in intact lambs. In denervated lambs, basal heart rates wereelevated to 218 ± 33 beats/min; there was no further increase inheart rate during captopril compared with vehicle infusion. Captoprilinfusion caused a decrease in renal vascular resistance but only in theabsence of renal nerves. These findings provide evidence to suggestthat early in life there is an interaction between renal sympatheticnerves and the renin-angiotensin system in regulating renalhemodynamics and the baroreflex control of the heart.

     

Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise

Sinoway, Lawrence, Jeffrey Shenberger, Gretchen Leaman,Robert Zelis, Kristen Gray, Robert Baily, and Urs Leuenberger. Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise. J. Appl.Physiol. 81(4): 1778-1784, 1996.We previouslydemonstrated that nonfatiguing rhythmic forearm exercise at 25%maximal voluntary contraction (12 2-s contractions/min) evokessympathoexcitation without significant engagement ofmetabolite-sensitive muscle afferents (B. A. Batman, J. C. Hardy, U. A. Leuenberger, M. B. Smith, Q. X. Yang, and L. I. Sinoway.J. Appl. Physiol. 76: 1077-1081,1994). This is in contrast to the sympathetic nervous system responsesobserved during fatiguing static forearm exercise wheremetabolite-sensitive afferents are the key determinants of sympatheticactivation. In this report we examined whether forearm exercisetraining would attenuate sympathetic nervous system responses torhythmic forearm exercise. We measured heart rate, mean arterial bloodpressure (MAP), muscle sympathetic nerve activity (microneurography),plasma norepinephrine (NE), and NE spillover and clearance (tritiatedNE kinetics) during nonfatiguing rhythmic forearm exercise before andafter a 4-wk unilateral forearm training paradigm. Training had noeffect on forearm mass, maximal voluntary contraction, or heart ratebut did attenuate the increase in MAP (increase in MAP: from 15.2 ± 1.8 before training to 11.4 ± 1.4 mmHg after training;P < 0.017), muscle sympathetic nerve activity (increase in bursts: from 10.8 ± 1.4 before training to6.2 ± 1.1 bursts/min after training;P < 0.030), and the NE spillover(increase in arterial spillover: from 1.3 ± 0.2 before training to0.6 ± 0.2 nmol ^· min^{1 ·} m²after training, P < 0.014; increasein venous spillover: from 2.0 ± 0.6 beforetraining to 1.0 ± 0.5 nmol ^· min^{1 ·} m²after training, P < 0.037) seen inresponse to exercise performed by the trained forearm. Thus forearmtraining reduces sympathetic responses during a nonfatiguing rhythmichandgrip paradigm that does not engage muscle metaboreceptors. Wespeculate that this effect is due to a conditioning-inducedreduction in mechanically sensitive muscle afferentdischarge.

     

Sympathetic discharge and vascular resistance after bed rest

Shoemaker, J. Kevin, Cynthia S. Hogeman, Urs A. Leuenberger,Michael D. Herr, Kristen Gray, David H. Silber, and Lawrence I. Sinoway. Sympathetic discharge and vascular resistance after bedrest. J. Appl. Physiol. 84(2):612-617, 1998.The effect of 6° head-down-tilt bedrest (HDBR) for 14 days on supine sympathetic discharge andcardiovascular hemodynamics at rest was assessed. Mean arterialpressure, heart rate (n = 25), musclesympathetic nerve activity (MSNA; n = 16) burst frequency, and forearm blood flow(n = 14) were measured, and forearmvascular resistance (FVR) was calculated. Stroke distance,our index of stroke volume, was derived from measurements of aorticmean blood velocity (Doppler) and R-R interval(n = 7). With these data, an index oftotal peripheral resistance was determined. Heart rate at rest wasgreater in the post (71 ± 2 beats/min)- compared with the pre-HDBRtest (66 ± 2 beats/min; P < 0.003), but mean arterial pressure was unchanged. Aortic strokedistance during post-HDBR (15.5 ± 1.1 cm/beat) was reduced frompre-HDBR levels (20.0 ± 1.5 cm/beat)(P < 0.03). Also, MSNA burstfrequency was reduced in the post (16.7 ± 2.8 beats/min)- comparedwith the pre (25.2 ± 2.6 beats/min)-HDBR condition(P < 0.01). Bed rest did not alterforearm blood flow, FVR, or total peripheral resistance. Thusreductions in MSNA with HDBR were not associated with a decrease inFVR.

     

Training intensity-dependent and tissue-specific increases in lactate uptake and MCT-1 in heart and muscle

We investigatedthe effects of 3 wk of moderate- (21 m/min, 8% grade) andhighintensity treadmill training (31 m/min, 15% grade) on1) monocarboxylate transporter 1 (MCT-1) content in rat hindlimb muscles and the heart and2) lactate uptake in isolated soleus(Sol) muscles and perfused hearts. In the moderately trained groupMCT-1 was not increased in any of the muscles [Sol, extensor digitorum longus (EDL), and red (RG) and white gastrocnemius(WG)] (P > 0.05). Similarly,lactate uptake in Sol strips was also not increased(P > 0.05). In contrast, in theheart, MCT-1 (+36%, P < 0.05) andlactate uptake (+72%, P < 0.05)were increased with moderate training. In the highly trained group,MCT-1 (+70%, P < 0.05) and lactateuptake (+79%, P < 0.05) wereincreased in Sol. MCT-1 was also increased in RG (+94%,P < 0.05) but not in WG and EDL(P > 0.05). In the highly trainedgroup, heart MCT-1 (+44%, P < 0.05)and lactate uptake (+173%, P < 0.05) were increased. In conclusion, it has been shown that1) in both heart and skeletal musclelactate uptake is increased only when MCT-1 is increased; 2) training-induced increases inMCT-1 occurred at a lower training intensity in the heart than inskeletal muscle; 3) in the heart, lactate uptake was increased much more after high-intensity training than after moderate-intensity training, despite similar increases inheart MCT-1 with these two training intensities; and4) the increases in MCT-1 occurredindependently of any changes in the heart's oxidative capacity (asmeasured by citrate synthase activity).

     

A 33-yr follow-up of peak oxygen uptake and related variables of former physical education students

Åstrand, Per-Olof, Ulf Bergh, and ÅsaKilbom. A 33-yr follow-up of peak oxygen uptake and relatedvariables of former physical education students. J. Appl. Physiol. 82(6): 1844-1852, 1997.In 1949, 27 female and 26 male physical education students were studied at amean age of 22 and 25 yr, respectively. They were restudied in 1970 and1982. Measurements included oxygen uptake, heart rate, and pulmonaryventilation during submaximal and maximal exercise on a cycle ergometerand treadmill. After 21 yr, peak aerobic power was significantlyreduced, from 2.90 to 2.18 l/min and from 4.09 to 3.28 l/min for womenand men, respectively. After another 12 yr, the 1970 maxima were notreduced further. From 1949 to 1982 there was a decrease in peak heartrate from 196 to 177 beats/min in women and from 190 to 175 beats/minin men (P < 0.05). Highest pulmonaryventilation did not change significantly. At an oxygen uptake of 1.5 l/min, the heart rate was the same in 1949 as in 1982. In conclusion,the physical fitness level of the subjects was well above average forthese ages. From 1970 to 1982 there was no decline in the average peakaerobic power, a finding possibly related to increased habitualphysical activity.

     

Beat-to-beat modulation of heart rate is coupled to coronary perfusion pressure in the isolated heart

A goal ofclinicians caring for heart transplant recipients has been to use heartrate variability as a noninvasive means of diagnosing graftrejection. The determinants of beat-to-beat variability inthe surgically denervated heart have yet to be elucidated. We used anisolated, blood buffer-perfused porcine heart preparation toquantitatively assess the relationship between coronary perfusion andsinus node automaticity. Hearts(n = 9) were suspended in aLangendorff preparation, and heart rate (HR) fluctuations werequantified while perfusion pressure was modulated between 70/50, 80/60,90/70, and 100/80 mmHg at 0.067 Hz. In 32 of 32 recordings, the crossspectrum of perfusion pressure vs. HR showed the largest peak centeredat 0.067 Hz. In eight of nine experiments during nonpulsatileperfusion, HR accelerated as perfusion pressure was increased from 40 to 110 mmHg (mean increase 24.2 ± 3.0 beats/min). HR increased 0.34 beats/min per mmHg increase in perfusion pressure (least squares linearregression y = 25.8 mmHg + 0.34x;r = 0.88, P < 0.0001). Administration of low-and high-dose nitroglycerin (Ntg) resulted in a modest increase in flowbut produced a significant decrease in HR and blunted the response ofHR to changes in perfusion pressure (HR increase 0.26 beats · min¹ · mmHg¹,r = 0.87, P < 0.0001 after low-dose Ntg; 0.25 beats · min¹ · mmHg¹,r = 0.78, P < 0.0001 after high-dose Ntg).These experiments suggest that sinus node discharge in the isolatedperfused heart is mechanically coupled to perfusion pressure on abeat-to-beat basis.     

Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure

Delp, Michael D., Changping Duan, John P. Mattson, andTimothy I. Musch. Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure.J. Appl. Physiol. 83(4):1291-1299, 1997.One of the primary consequences of leftventricular dysfunction (LVD) after myocardial infarction is adecrement in exercise capacity. Several factors have been hypothesizedto account for this decrement, including alterations in skeletal musclemetabolism and aerobic capacity. The purpose of this study was todetermine whether LVD-induced alterations in skeletal muscle enzymeactivities, fiber composition, and fiber size are1) generalized in muscles orspecific to muscles composed primarily of a given fiber type and2) related to the severity of theLVD. Female Wistar rats were divided into three groups: sham-operatedcontrols (n = 13) and rats withmoderate (n = 10) and severe(n = 7) LVD. LVD was surgicallyinduced by ligating the left main coronary artery and resulted inelevations (P < 0.05) in leftventricular end-diastolic pressure (sham, 5 ± 1 mmHg; moderate LVD,11 ± 1 mmHg; severe LVD, 25 ± 1 mmHg). Moderate LVDdecreased the activities of phosphofructokinase (PFK) and citratesynthase in one muscle composed of type IIB fibers but did not modifyfiber composition or size of any muscle studied. However, severe LVDdiminished the activity of enzymes involved in terminal and-oxidation in muscles composed primarily of type I fibers, type IIAfibers, and type IIB fibers. In addition, severe LVD induced areduction in the activity of PFK in type IIB muscle, a 10% reductionin the percentage of type IID/X fibers, and a corresponding increase inthe portion of type IIB fibers. Atrophy of type I fibers, type IIAfibers, and/or type IIB fibers occurred in soleus and plantarismuscles of rats with severe LVD. These data indicate that rats withsevere LVD after myocardial infarction exhibit1) decrements in mitochondrialenzyme activities independent of muscle fiber composition,2) a reduction in PFK activity in type IIB muscle, 3) transformationof type IID/X to type IIB fibers, and4) atrophy of type I, IIA, and IIBfibers.

     

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.

     

Restoration of fluid balance after exercise-induced dehydration: effects of alcohol consumption

Shirreffs, Susan M., and Ronald J Maughan. Restorationof fluid balance after exercise-induced dehydration: effects of alcoholconsumption. J. Appl. Physiol. 83(4):1152-1158, 1997.The effect of alcohol consumption on therestoration of fluid and electrolyte balance after exercise-induceddehydration [2.01 ± 0.10% (SD) of body mass] wasinvestigated. Drinks containing 0, 1, 2, and 4% alcohol were consumedover 60 min beginning 30 min after the end of exercise; a differentbeverage was consumed in each of four trials. The volume consumed(2,212 ± 153 ml) was equivalent to 150% of body mass loss. Peakurine flow rate occurred later (P = 0.024) with the 4% beverage. The total volume of urine produced overthe 6 h after rehydration, although not different between trials(P = 0.307), tended to increase as thequantity of alcohol ingested increased. The increase in blood(P = 0.013) and plasma(P = 0.050) volume with rehydrationwas slower when the 4% beverage was consumed and did not increase tovalues significantly greater than the dehydrated level(P = 0.013 andP = 0.050 for blood volume and plasmavolume, respectively); generally, the increase was an inverse functionof the quantity of alcohol consumed. These results suggest that alcoholhas a negligible diuretic effect when consumed in dilute solution aftera moderate level of hypohydration induced by exercise in the heat.There appears to be no difference in recovery from dehydration whetherthe rehydration beverage is alcohol free or contains up to 2% alcohol,but drinks containing 4% alcohol tend to delay the recovery process.

     

Hydration effects on physiological strain of horses during exercise-heat stress

This study examined the effects ofhyperhydration, exercise-induced dehydration, and oral fluidreplacement on physiological strain of horses during exercise-heatstress. On three occasions, six horses completed a 90-min exerciseprotocol (50% maximal O₂ uptake,34.5°C, 48% relative humidity) divided into two 45-min periods(exercise I andexercise II) with a 15-min recoverybetween exercise bouts. In random order, horses receivedno fluid (NF), 10 liters of water (W), or a carbohydrate-electrolytesolution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (), stroke volume (SV), corebody temperature, sweating rate (SR), or sweating sensitivity duringexercise I. In contrast, afterexercise II, exercise-induceddehydration in NF (decrease in body mass: NF, 5.6 ± 0.8%; W, 1.1 ± 0.4%; CE, 1.0 ± 0.2%) resulted in greater heat storage,with core body temperature ~1.0°C higher compared with W and CE.In exercise II, the greater thermalstrain in NF was associated with significant(P < 0.05) decreases in (10 ± 2%), SV (9 ± 3%), SR, and sweatingsensitivity. We concluded that 1)preexercise hyperhydration provided no thermoregulatory advantage;2) maintenance of euhydration byoral fluid replacement (~85% of sweat fluid loss) during exercise inthe heat was reflected in higher , SV, and SR withdecreased heat storage; and 3) W oran isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.

     

Reflex responses to regional venous pooling during lower body negative pressure in humans

Halliwill, John R., Lori A. Lawler, Tamara J. Eickhoff,Michael J. Joyner, and Sharon L. Mulvagh. Reflex responses toregional venous pooling during lower body negative pressure in humans.J. Appl. Physiol. 84(2): 454-458, 1998.Lower body negative pressure is frequently used to simulateorthostasis. Prior data suggest that venous pooling in abdominal orpelvic regions may have major hemodynamic consequences. Therefore, we developed a simple paradigm for assessing regional contributions tovenous pooling during lower body negative pressure. Sixteen healthy menand women underwent graded lower body negative pressure protocols to 60 mmHg while wearing medical antishock trousers to prevent venous poolingunder three randomized conditions:1) no trouser inflation (control),2) only the trouser legs inflated, and 3) the trouser legs andabdominopelvic region inflated. Without trouser inflation, heart rateincreased 28 ± 4 beats/min, mean arterial pressure fell 3 ± 2 mmHg, and forearm vascular resistance increased 51 ± 9 units at 60 mmHg lower body negative pressure. With inflation of eitherthe trouser legs or the trouser legs and abdominopelvic region, heartrate and mean arterial pressure did not change during lower bodynegative pressure. By contrast, although the forearm vasoconstrictorresponse to lower body negative pressure was attenuated by inflation ofthe trouser legs (forearm vascular resistance 33 ± 10 units,P < 0.05 vs. control), attenuation was greater with the inflation of the trouser legs and abdominopelvic region (forearm vascular resistance 16 ± 5 units,P < 0.05 vs. control and trouserlegs-only inflation). Thus the hemodynamic consequences of pooling inthe abdominal and pelvic regions during lower body negative pressureappear to be less than in the legs in healthy individuals.

     

Impaired muscle metaboreflex-induced increases in ventricular function in heart failure

We investigated to what extent heart failure alters the ability of the muscle metaboreflex to improve ventricular function. Dogs were chronically instrumented to monitor mean arterial pressure (MAP), cardiac output (CO), heart rate (HR), stroke volume (SV), and central venous pressure (CVP) at rest and during mild treadmill exercise (3.2 km/h) before and during reductions in hindlimb blood flow imposed to activate the muscle metaboreflex. These control experiments were repeated at constant heart rate (ventricular pacing 225 beats/min) and at constant heart rate coupled with a beta-adrenergic blockade (atenolol, 2 mg/kg iv) in normal animals and in the same animals after the induction of heart failure (HF, induced via rapid ventricular pacing). In control experiments in normal animals, metaboreflex activation caused tachycardia with no change in SV, resulting in large increases in CO and MAP. At constant HR, large increases in CO still occurred via significant increases in SV. Inasmuch as CVP did not change in this setting and that beta-adrenergic blockade abolished the reflex increase in SV at constant HR, this increase in SV likely reflects increased ventricular contractility. In contrast, after the induction of HF, much smaller increases in CO occurred with metaboreflex activation because, although increases in HR still occurred, SV decreased thereby limiting any increase in CO. At constant HR, no increase in CO occurred with metaboreflex activation even though CVP increased significantly. After beta-adrenergic blockade, CO and SV decreased with metaboreflex activation. We conclude that in HF, the ability of the muscle metaboreflex to increase ventricular function via both increases in contractility as well as increases in filling pressure are markedly impaired.