Bronchial vasodilator pathways in the vagus nerve of dogs

Bronchialvasodilation in dogs is mediated largely by vagal pathways. To examinethe relative contribution of cholinergic and noncholinergicparasympathetic pathways and of sensory axon reflexes to vagalbronchial vasodilation, we electrically stimulated the peripheral vagusnerve in 10 chloralose-anesthetized dogs and measured bronchial arteryflow. Moderate-intensity electrical stimulation (which did not activateC-fiber axons) caused a rapid voltage- and frequency-dependentvasodilation. After atropine, vasodilation was slower in onset andreduced at all voltages and frequencies: bronchial vascular conductanceincreased by 9.0 ± 1.5 (SE)ml · min¹ · 100 mmHg¹ during stimulationbefore atropine and 5.5 ± 1.4 ml · min¹ · 100 mmHg¹ after(P < 0.02). High-intensitystimulation (sufficient to recruit C fibers) was not studied beforeatropine because of the resulting cardiac arrest. After atropine,high-intensity stimulation increased conductance by 12.0 ± 2.5 ml · min¹ · 100 mmHg¹. Subsequent blockadeof ganglionic transmission, with arterial blood pressure maintained bya pressure reservoir, abolished the response to moderate-intensitystimulation and reduced the increase to high-intensity stimulation by82 ± 5% (P < 0.01). In 13 other dogs, we measured vasoactive intestinalpeptide-like immunoreactivity in venous blood draining from thebronchial veins. High-intensity vagal stimulationincreased vasoactive intestinal peptide concentration from 5.7 ± 1.8 to 18.4 ± 4.1 fmol/ml (P = 0.001). The results suggest that in dogs cholinergic and noncholinergicparasympathetic pathways play the major role in vagal bronchial vasodilation.

     

Increased GLUT-4 translocation mediates enhanced insulin sensitivity of muscle glucose transport after exercise

The purpose of this study was to determinewhether the increase in insulin sensitivity of skeletal muscle glucosetransport induced by a single bout of exercise is mediated by enhancedtranslocation of the GLUT-4 glucose transporter to the cell surface.The rate of3-O-[³H]methyl-D-glucosetransport stimulated by a submaximally effective concentration ofinsulin (30 µU/ml) was approximately twofold greater in the musclesstudied 3.5 h after exercise than in those of the sedentary controls(0.89 ± 0.10 vs. 0.43 ± 0.05 µmol · ml¹ · 10 min¹; means ± SE forn = 6/group). GLUT-4 translocation wasassessed by using theATB-[2-³H]BMPAexofacial photolabeling technique. Prior exercise resulted in greatercell surface GLUT-4 labeling in response to submaximal insulintreatment (5.36 ± 0.45 dpm × 10³/g in exercised vs. 3.00 ± 0.38 dpm × 10³/g insedentary group; n = 10/group) thatclosely mirrored the increase in glucose transport activity. The signalgenerated by the insulin receptor, as reflected in the extent ofinsulin receptor substrate-1 tyrosine phosphorylation, was unchangedafter the exercise. We conclude that the increase in muscle insulinsensitivity of glucose transport after exercise is due to translocationof more GLUT-4 to the cell surface and that this effect is not due topotentiation of insulin-stimulated tyrosine phosphorylation.

     

Changes in maximum oxygen uptake during prolonged training, overtraining, and detraining in horses

Tyler, Catherine M., Lorraine C. Golland, David L. Evans,David R. Hodgson, and Reuben J. Rose. Changes in maximum oxygenuptake during prolonged training, overtraining, and detraining inhorses. J. Appl. Physiol. 81(5):2244-2249, 1996.Thirteen standardbred horses were trained asfollows: phase 1 (endurance training, 7 wk),phase 2 (high-intensity training, 9 wk),phase 3 (overload training, 18 wk), andphase 4 (detraining, 12 wk). Inphase 3, the horses were divided intotwo groups: overload training (OLT) and control (C). The OLT groupexercised at greater intensities, frequencies, and durations than groupC. Overtraining occurred after 31 wk of training and was defined as asignificant decrease in treadmill run time in response to astandardized exercise test. In the OLT group, there was a significantdecrease in body weight (P < 0.05).From pretraining values of 117 ± 2 (SE)ml ^· kg^{1 ·} min¹,maximal O₂ uptake(O_{2 max}) increased by15% at the end of phase 1, and when signs of overtraining werefirst seen in the OLT group,O_{2 max} was 29%higher (151 ± 2 ml ^· kg^{1 ·} min¹in both C and OLT groups) than pretraining values. There was nosignificant reduction inO_{2 max} until after 6 wk detraining whenO_{2 max} was 137 ± 2 ml ^· kg^{1 ·} min¹.By 12 wk detraining, meanO_{2 max} was134 ± 2 ml ^· kg^{1 ·} min¹,still 15% above pretraining values. When overtraining developed, O_{2 max} was notdifferent between C and OLT groups, but maximal values forCO₂ production (147 vs. 159 ml ^· kg^{1 ·} min¹)and respiratory exchange ratio (1.04 vs. 1.11) were lower in the OLTgroup. Overtraining was not associated with a decrease inO_{2 max} and, afterprolonged training, decreases inO_{2 max} occurredslowly during detraining.

     

Sympathetic drive to liver and nonhepatic splanchnic tissue during heavy exercise

Coker, Robert H., Mahesh G. Krishna, D. Brooks Lacy, Eric J. Allen, and David H. Wasserman. Sympathetic drive to liver andnonhepatic splanchnic tissue during heavy exercise. J. Appl. Physiol. 82(4): 1244-1249, 1997.Thecontribution of sympathetic drive and vascular catecholamine deliveryto the splanchnic bed during heavy exercise was studied in dogs thatunderwent a laparotomy during which flow probes were implanted onto theportal vein and hepatic artery and catheters were inserted into thecarotid artery, portal vein, and hepatic vein. At least 16 days aftersurgery, dogs completed a 20-min heavy exercise protocol (mean workrate of 5.7 ± 1 miles/h, 20 ± 2% grade). Arterial epinephrine(Epi) and norepinephrine (NE) increased by ~500 and ~900 pg/ml,respectively, after 20 min of heavy exercise. Because Epi is notreleased from the splanchnic bed and because Epi fractional extraction(FX) = NE FX, NE uptake by splanchnic tissue can be calculated despite simultaneous release of NE. Basal nonhepatic splanchnic (NHS) FXincreased from a basal rate of 0.52 ± 0.09 to a peak of 0.64 ± 0.05 at 10 min of exercise. Hepatic Epi FX increased froma basal rate of 0.68 ± 0.10 to 0.81 ± 0.09 at 20 min of exercise. Even though NHS extraction of Epi reduced portal veinEpi levels by ~60%, the release of NE from NHS tissue maintainedportal vein NE at levels similar to those in arterial blood. NHS NEspillover increased from a basal rate of 5.7 ± 1.4 to 11.7 ± 2.8 ng · kg¹ · min¹at 20 min of exercise. Hepatic NE spillover increased from a basal rateof 5.0 ± 1.2 ng · kg¹ · min¹to a peak of 14.2 ± 2.8 ng · kg¹ · min¹at 15 min of exercise. These results show that1) approximately two- and threefoldincreases in NHS and hepatic NE spillover occur during heavy exercise,demonstrating that sympathetic drive to these tissues contributes tothe increase in circulating NE; 2) the high catecholamine FX by the NHS tissues results in an Epi level atthe liver that is considerably lower than that in the arterial blood;and 3) circulating NE delivery tothe liver is sustained despite high catecholamine FX due tosimultaneous NHS NE release.

     

Effect of hypohydration on gastric emptying and intestinal absorption during exercise

Dehydration and hyperthermia may impair gastricemptying (GE) during exercise; the effect of these alterations onintestinal water flux (WF) is unknown. Thus the purpose of this studywas to determine the effect of hypohydration (~2.7% body weight) on GE and WF of a water placebo (WP) during cycling exercise (85 min, 65%maximal oxygen uptake) in a cool environment (22°C) and to alsocompare GE and WF of three carbohydrate-electrolyte solutions (CES)while the subjects were hypohydrated. GE and WF were determined simultaneously by a nasogastric tube placed in the gastric antrum andvia a multilumen tube that spanned the duodenum and the first 25 cm ofjejunum. Hypohydration was attained 12-16 h before experiments bylow-intensity exercise in a hot (45°C), humid (relative humidity 50%) environment. Seven healthy subjects (age 26.7 ± 1.7 yr,maximal oxygen uptake 55.9 ± 8.2 ml · kg¹ · min¹)ingested either WP or a 6% (330 mosmol), 8% (400 mosmol), or a 9%(590 mosmol) CES the morning following hypohydration. For comparison,subjects ingested WP after a euhydration protocol. Solutions (~2.0liters total) were ingested as a large bolus (4.6 ml/kg body wt) 5 minbefore exercise and as small serial feedings (2.3 ml/kg body wt) every10 min of exercise. Average GE rates were not different amongconditions (P > 0.05). Mean(±SE) values for WF were also similar(P > 0.05) for the euhydration (15.3 ± 1.7 ml · cm¹ · h¹)and hypohydration (18.3 ± 2.6 ml · cm¹ · h¹)experiments. During exercise after hypohydration, waterabsorption was greater (P < 0.05)with ingestion of WP (18.3 ± 2.6) and the 6% CES (16.5 ± 3.7),compared with the 8% CES (6.9 ± 1.5) and the 9% CES (1.8 ± 1.7). Mean values for final core temperature (38.6 ± 0.1°C),heart rate (152 ± 1 beats/min), and change in plasma volume(5.7 ± 0.7%) were similar among experimental trials. Weconclude that 1) hypohydration to~3% body weight does not impair GE or fluid absorption duringmoderate exercise when ingesting WP, and2) hyperosmolality (>400 mosmol)reduced WF in the proximal intestine.

     

Importance of the lactate anion in control of breathing

Hardarson, Thorir, Jon O. Skarphedinsson, and TorarinnSveinsson. Importance of the lactate anion in control ofbreathing. J. Appl. Physiol. 84(2):411-416, 1998.The purpose of this study was to examine theeffects of raising the arterialLa andK⁺ levels on minute ventilation(E) in rats. EitherLa or KCl solutions wereinfused in anesthetized spontaneously breathing Wistar rats to raisethe respective ion arterial concentration ([La] and[K⁺]) gradually tolevels similar to those observed during strenuous exercise.E, blood pressure, and heart rate wererecorded continuously, and arterial[La],[K⁺], pH, and bloodgases were repeatedly measured from blood samples. To prevent changesin pH during the Lainfusions, a solution of sodium lactate and lactic acid was used. Raising [La] to13.2 ± 0.6 (SE) mM induced a 47.0 ± 4.0% increase inE without any concomitant changes ineither pH or PCO₂. Raising[K⁺] to 7.8 ± 0.11 mM resulted in a 20.3 ± 5.28% increase inE without changes in pH. Thus ourresults show that Laitself, apart from lactic acidosis, may be important in increasing E during strenuous exercise, and weconfirm earlier results regarding the role of arterial[K⁺] in the control ofE during exercise.

     

Ocular and regional cerebral blood flow in aging Fischer-344 rats

Vascularremodeling and changes in vascular responsiveness occur in the ratcerebrum with old age. This includes reductions in cerebral arteriolarnumerical density, cross-sectional area, distensibility, the relativeproportion of distensible elements in the cerebral arteriolar wall, andreduced endothelium-dependent relaxation. The purpose of this study wasto test the hypothesis that old age results in an increase in vascularresistance and, correspondingly, a decrease in blood flow to ocular,regional cerebral, and spinal tissue in the rat. Blood flow wasmeasured in the eye, olfactory bulb, left and right cerebrum, pituitary gland, midbrain, pons, cerebellum, medulla, and spinal cord of juvenile(2-mo-old, n = 6), adult (6-mo-old,n = 7), and aged (24-mo-old,n = 7) male Fischer-344 rats. Arterialpressure and blood flow were used to calculate vascular resistance.Vascular resistance in the eye of aged rats (6.03 ± 1.08 mmHg · ml¹ · min · 100 g) was higher than that in juvenile (3.83 ± 0.38 mmHg · ml¹ · min · 100 g) and adult rats (3.12 ± 0.24 mmHg · ml¹ · min · 100 g). Similarly, resistance in the pons of older rats (2.24 ± 0.55 mmHg · ml¹ · min · 100 g) was greater than in juvenile (0.66 ± 0.06 mmHg ·ml¹ · min · 100 g) and adult rats (0.80 ± 0.11 mmHg · ml¹ · min · 100 g). In contrast, vascular resistance in the pituitary gland was lowerin the aged rats (juvenile, 3.09 ± 0.22; adult, 2.79 ± 0.42;aged, 1.73 ± 0.32 mmHg · ml¹ · min · 100 g, respectively). Vascular resistance was not different in othercerebral tissues or in the spinal cord in the aged rats. These datasuggest that regional cerebral and spinal blood flow and vascularresistance remain largely unchanged in conscious aged rats at rest butthat elevations in ocular vascular resistance and, correspondingly,decreases in ocular perfusion with advanced age could have seriousadverse effects on visual function.

     

Albumin synthesis after intense intermittent exercise in human subjects

Yang, Roger C., Gary W. Mack, Robert R. Wolfe, and Ethan R. Nadel. Albumin synthesis after intense intermittent exercise inhuman subjects. J. Appl. Physiol.84(2): 584-592, 1998.We measured hepatic albumin synthesis infive volunteers (4 men and 1 woman) at 3 and 6 h after recovery fromintense exercise. A primed-constant infusion of a stable isotopictracer of phenylalanine was used to determine hepatic fractionalsynthetic rate (FSR) and absolute synthetic rate (ASR) of albumin fromthe enrichment of phenylalanine in albumin. The infusion of the stableisotope tracer began 2 h after upright exercise or upright rest.Albumin FSR and ASR were 6.39 ± 0.48%/day and 120 ± 9 mg · kg bodywt¹ · day¹,respectively, 3-6 h after recovery from exercise; the FSR and ASRon the time control study day were 5.94 ± 0.47%/day and 104 ± 9 mg · kg bodywt¹ · day¹,respectively. The 6 and 16% increases(P < 0.05) in FSR and ASR afterexercise were associated with an elevated plasma albumin content at 5 and 6 h of recovery (P < 0.05), anincreased total protein content throughout recovery(P < 0.05), and a negative freewater clearance (P < 0.05) at 2, 3, and 6.5 h of recovery compared with baseline values; these variableswere unchanged from their baselines on the time control study day.Increased albumin content and reduced free water clearance contributeto a retention of fluid within the circulation after intense exercise. The measured increase in albumin synthesis could not account for theentire increase in albumin content at 6 h of recovery from exercise.However, we estimate that if the increased activity was maintained forthe next 18 h, it could account for the expected increase in albumincontent at 24 h of recovery.

     

Muscle protein metabolism in female swimmers after a combination of resistance and endurance exercise

Tipton, Kevin D., Arny A. Ferrando, Bradley D. Williams, andRobert R. Wolfe. Muscle protein metabolism in female swimmers after a combination of resistance and endurance exercise.J. Appl. Physiol. 81(5):2034-2038, 1996.There is little known about the responses ofmuscle protein metabolism in women to exercise. Furthermore, the effectof adding resistance training to an endurance training regimen on netprotein anabolism has not been established in either men or women. Thepurpose of this study was to quantify the acute effects of combinedswimming and resistance training on protein metabolism in femaleswimmers by the direct measurement of muscle protein synthesis andwhole body protein degradation. Seven collegiate female swimmers wereeach studied on four separate occasions with a primed constant infusionofring-[¹³C₆]phenylalanine(Phe) to measure the fractional synthetic rate (FSR) of the posteriordeltoid and whole body protein breakdown. Measurements were made over a5-h period at rest and after each of three randomly ordered workouts:1) 4,600 m of intense interval swimming (SW); 2) a whole bodyresistance-training workout with no swimming on that day (RW); and3) swimming and resistance training combined (SR). Whole body protein breakdown was similar for all treatments (0.75 ± 0.04, 0.69 ± 0.03, 0.69 ± 0.02, and 0.71 ± 0.04 µmol ^· min^{1 ·} kg¹for rest, RW, SW, and SR, respectively). The FSR of the posterior deltoid was significantly greater (P < 0.05) after SR (0.082 ± 0.015%/h) than at rest (0.045 ± 0.006%/h). There was no significant difference in the FSR after RW(0.048 ± 0.004%/h) or SW (0.064 ± 0.008%/h) from rest or fromSR. These data indicate that the combination of swimming and resistanceexercise stimulates net muscle protein synthesis above resting levelsin female swimmers.

     

Smaller lungs in women affect exercise hyperpnea

We subjected 29 healthy young women (age: 27 ± 1 yr) with a wide range of fitness levels [maximal oxygenuptake (O_{2 max}): 57 ± 6 ml · kg¹ · min¹;35-70ml · kg¹ · min¹]to a progressive treadmill running test. Our subjects had significantly smaller lung volumes and lower maximal expiratory flow rates, irrespective of fitness level, compared with predicted values for age-and height-matched men. The higher maximal workload in highly fit(O_{2 max} > 57 ml · kg¹ · min¹,n = 14) vs. less-fit(O_{2 max} < 56 ml · kg¹ · min¹,n = 15) women caused a higher maximalventilation (E) with increased tidal volume (VT)and breathing frequency (f_b) atcomparable maximal VT/vitalcapacity (VC). More expiratory flow limitation (EFL; 22 ± 4% ofVT) was also observed duringheavy exercise in highly fit vs. less-fit women, causing higherend-expiratory and end-inspiratory lung volumes and greater usage oftheir maximum available ventilatory reserves.HeO₂ (79% He-21%O₂) vs. room air exercise trialswere compared (with screens added to equalize external apparatusresistance). HeO₂ increasedmaximal expiratory flow rates (20-38%) throughout the range ofVC, which significantly reduced EFL during heavy exercise. When EFL wasreduced with HeO₂, VT,f_b, andE (+16 ± 2 l/min) weresignificantly increased during maximal exercise. However, in theabsence of EFL (during room air exercise),HeO₂ had no effect onE. We conclude that smaller lungvolumes and maximal flow rates for women in general, and especiallyhighly fit women, caused increased prevalence of EFL during heavyexercise, a relative hyperinflation, an increased reliance onf_b, and a greater encroachment onthe ventilatory "reserve." Consequently,VT andE are mechanically constrained duringmaximal exercise in many fit women because the demand for highexpiratory flow rates encroaches on the airways' maximum flow-volumeenvelope.

     

Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare theO₂ uptake(O₂) kinetics at the onsetof heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cyclingtask to determine peak O₂(O_{2 peak}).On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice bycycling at 50%O_{2 peak} for 3.5 min,once by cycling at 100%O_{2 peak} for 2 min,and once by cycling at 130%O_{2 peak} for 75 s.O₂ deficit was not significantlydifferent between boys and men (respectively, 50%O_{2 peak} task: 6.6 ± 11.1 vs. 5.5 ± 7.3 ml · min¹ · kg¹;100% O_{2 peak} task:28.5 ± 8.1 vs. 31.8 ± 6.3 ml · min¹ · kg¹;and 130%O_{2 peak}task: 30.1 ± 5.7 vs. 35.8 ± 5.3 ml · min¹ · kg¹).To assess the kinetics, phase I was excluded from analysis. Phase IIO₂ kinetics could bedescribed in all cases by a monoexponential function. ANOVA revealed nodifferences in time constants between boys and men (respectively, 50%O_{2 peak}task: 22.8 ± 5.1 vs. 26.4 ± 4.1 s; 100%O_{2 peak} task: 28.0 ± 6.0 vs. 28.1 ± 4.4 s; and 130%O_{2 peak} task: 19.8 ± 4.1 vs. 20.7 ± 5.7 s). In conclusion, O₂ deficit and fast-componentO₂ on-transientsare similar in boys and men, even at high exercise intensities, whichis in contrast to the findings of other studies employing simplermethods of analysis. The previous interpretation that children relyless on nonoxidative energy pathways at the onset of heavy exercise isnot supported by our findings.

     

Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume

Mann, Stephanie E., Mark J. M. Nijland, and Michael G. Ross.Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume. J. Appl.Physiol. 81(6): 2588-2594, 1996.Adequateamniotic fluid (AF) volume is maintained by a balance of fetal fluidproduction (lung liquid and urine) and resorption (swallowing andintramembranous flow). Because fetal urine is the principle source ofAF, alterations in urine flow and composition directly impact AFdynamics. Intra-amniotic 1-desamino-8-D-argininevasopressin (DDAVP) is rapidly absorbed into fetal plasma and induces amarked fetal urinary antidiuresis. To examine the effect ofintra-amniotic- DDAVP-induced fetal urinary responses on AF volume andcomposition, six chronically prepared ewes with singleton fetuses(gestation 128 ± 2 days) were studied for 72 h after a singleintra-amniotic DDAVP (50-µg) injection. After DDAVP, fetal urineosmolality significantly increased at 2 h (157 ± 13 to 253 ± 21 mosmol/kg) and remained elevated at 72 h (400 ± 13 mosmol/kg). Urinary sodium (33.0 ± 4.5 to 117.2 ± 9.7 meq/l)and chloride (26.0 ± 2.8 to 92.4 ± 8.1 meq/l) concentrations similarly increased. AF osmolality increased (285 ± 3 to 299 ± 4 mosmol/kgH₂O), although there was no change in fetalplasma osmolality (294 ± 2 mosmol/kg). Despite a 50% reductionin fetal urine flow (0.12 ± 0.03 to 0.05 ± 0.02 ml ^· kg^{1 ·} min¹at 2 h and 0.06 ± 0.01 ml ^· kg^{1 ·} min¹after 72 h), AF volume did not change (693 ± 226 to 679 ± 214 ml). There were no changes in fetal arterial blood pressures, pH,PCO₂, orPO₂ after DDAVP. We conclude the following. 1)Intra-amniotic DDAVP injection induces a prolonged decrease in fetalurine flow and increases in urine and AF osmolalities. 2) Despite decreased urine flow, AFvolume does not change. We speculate that, in response to DDAVP-inducedfetal oliguria, reversed intramembranous flow (from isotonic fetalplasma to hypertonic AF) preserves AF volume.

     

Effect of sprint cycle training on activities of antioxidant enzymes in human skeletal muscle

Hellsten, Ylva, Fred S. Apple, and Bertil Sjödin.Effect of sprint cycle training on activities of antioxidantenzymes in human skeletal muscle. J. Appl.Physiol. 81(4): 1484-1487, 1996.The effect ofintermittent sprint cycle training on the level of muscle antioxidantenzyme protection was investigated. Resting muscle biopsies, obtainedbefore and after 6 wk of training and 3, 24, and 72 h after the finalsession of an additional 1 wk of more frequent training, were analyzedfor activities of the antioxidant enzymes glutathione peroxidase (GPX),glutathione reductase (GR), and superoxide dismutase (SOD). Activitiesof several muscle metabolic enzymes were determined to assess the effectiveness of the training. After the first 6-wk training period, nochange in GPX, GR, or SOD was observed, but after the 7th week oftraining there was an increase in GPX from 120 ± 12 (SE) to 164 ± 24 µmol ^· min^{1 ·} gdry wt¹(P < 0.05) and in GR from 10.8 ± 0.8 to 16.8 ± 2.4 µmol ^· min^{1 ·} gdry wt¹(P < 0.05). There was no significantchange in SOD. Sprint cycle training induced a significant(P < 0.05) elevation in the activity of phosphofructokinase and creatine kinase, implying an enhanced anaerobic capacity in the trained muscle. The present studydemonstrates that intermittent sprint cycle training that induces anenhanced capacity for anaerobic energy generation also improves thelevel of antioxidant protection in the muscle.

     

Rat hindlimb muscle blood flow during level and downhill locomotion

Duringeccentrically biased exercise (e.g., downhill locomotion), whole bodyoxygen consumption and blood lactate concentrations are lower thanduring level locomotion. These general systemic measurements indicatethat muscle metabolism is lower during downhill exercise. This studywas designed to test the hypothesis that hindlimb muscle blood flow iscorrespondingly lower during downhill vs. level exercise. Muscle bloodflow (determined by using radioactive microspheres) was measured inrats after 15 min of treadmill exercise at 15 m/min on the level (L,0°) or downhill (D, 17°). Blood flow to ankle extensormuscles was either lower (e.g., white gastrocnemius muscle: D, 9 ± 2; L, 15 ± 1 ml · min¹ · 100 g¹) or not different(e.g., soleus muscle: D, 250 ± 35; L, 230 ± 21 ml · min¹ · 100 g¹) in downhill vs. levelexercise. In contrast, blood flow to ankle flexor muscles was higher(e.g., extensor digitorum longus muscle: D, 53 ± 5; L, 31 ± 6 ml · min¹ · 100 g¹) during downhill vs.level exercise. When individual extensor and flexor muscle flows weresummed, total flow to the leg was lower during downhill exercise (D,3.24 ± 0.08; L, 3.47 ± 0.05 ml/min). These data indicate thatmuscle blood flow and metabolism are lower during eccentrically biasedexercise but are not uniformly reduced in all active muscles; i.e.,flows are equivalent in several ankle extensor muscles and higher inankle flexor muscles.     

Effects of NaHCO3 loading on acid-base balance, lactate concentration, and performance in racing greyhounds

This investigation examined the effects ofNaHCO₃ loading on lactateconcentration ([La]), acid-base balance, and performance for a 603.5-m sprint task. Ten greyhounds completed aNaHCO₃ (300 mg/kg body weight) andcontrol trial in a crossover design. Results are expressed as means ± SE. Presprint differences (P < 0.05) were found for NaHCO₃ vs.control, respectively, for blood pH (7.47 ± 0.01 vs. 7.42 ± 0.01), HCO₃ (28.4 ± 0.4 vs. 23.5 ± 0.3 meq/l), and base excess (5.0 ± 0.3 vs. 0.2 ± 0.3 meq/l). Peak blood [La] increased(P < 0.05) inNaHCO₃ vs. control (20.4 ± 1.6 vs. 16.9 ± 1.3 mM, respectively). Relative to control,NaHCO₃ produced a greater(P < 0.05) reduction in blood baseexcess (18.5 ± 1.4 vs. 14.1 ± 0.8 meq/l) andHCO₃ (17.4 ± 1.2 vs.12.8 ± 0.7 meq/l) from presprint to postexercise. Postexercise peak muscle H⁺concentration ([H⁺])was higher (P < 0.05) inNaHCO₃ vs. control (158.8 ± 8.8 vs. 137.0 ± 5.3 nM, respectively). Muscle[H⁺] recoveryhalf-time (7.2 ± 1.6 vs. 11.3 ± 1.6 min) and time to predosevalues (22.2 ± 2.4 vs. 32.9 ± 4.0 min) were reduced(P < 0.05) inNaHCO₃ vs. control, respectively.No differences were found in blood[H⁺] or blood[La] recovery curves or performance times.NaHCO₃ increased postexerciseblood [La] but did not reduce the muscle or blood acid-basedisturbance associated with a 603.5-m sprint or significantly affectperformance.

     

Transcapillary escape rate of albumin in humans during exercise-induced hypervolemia

Haskell, Andrew, Ethan R. Nadel, Nina S. Stachenfeld, KeiNagashima, and Gary W. Mack. Transcapillary escape rate of albuminin humans during exercise-induced hypervolemia. J. Appl. Physiol. 83(2): 407-413, 1997.To test thehypotheses that plasma volume (PV) expansion 24 h after intenseexercise is associated with reduced transcapillary escape rate ofalbumin (TER_alb) and that localchanges in transcapillary forces in the previously active tissues favorretention of protein in the vascular space, we measured PV,TER_alb, plasma colloid osmoticpressure (COP_p), interstitialfluid hydrostatic pressure (Pi), and colloid osmotic pressure in legmuscle and skin and capillary filtration coefficient (CFC) in the armand leg in seven men and women before and 24 h after intense uprightcycle ergometer exercise. Exercise expanded PV by 6.4% at 24 h (43.9 ± 0.8 to 46.8 ± 1.2 ml/kg, P < 0.05) and decreased total protein concentration (6.5 ± 0.1 to6.3 ± 0.1 g/dl, P < 0.05) andCOP_p (26.1 ± 0.8 to 24.3 ± 0.9 mmHg, P < 0.05), although plasmaalbumin concentration was unchanged. TER_alb tended to decline (8.4 ± 0.5 to 6.5 ± 0.7%/h, P = 0.11) and was correlated with the increase in PV(r = 0.69,P < 0.05). CFC increased in the leg(3.2 ± 0.2 to 4.3 ± 0.5 µl · 100 g¹ · min¹ · mmHg¹,P < 0.05), and Pi showed a trend toincrease in the leg muscle (2.8 ± 0.7 to 3.8 ± 0.3 mmHg, P = 0.08). These datademonstrate that TER_alb isassociated with PV regulation and that local transcapillary forcesin the leg muscle may favor retention of albumin in the vascular spaceafter exercise.

     

High-energy phosphates and tension production in rabbit tibialis anterior/extensor digitorum longus muscles

Ryschon, T. W., J. C. Jarvis, S. Salmons, and R. S. Balaban.High-energy phosphates and tension production in rabbit tibialisanterior/extensor digitorum longus muscles. J. Appl. Physiol. 82(3): 1024-1029, 1997.The effects ofrepetitive muscle contraction on energy state and tension productionwere studied in rabbit tibialis anterior/extensor digitorum longusmuscles that had been subjected to 90 days of continuous indirectelectrical stimulation at 10 Hz. Anesthetized chronically stimulatedand control rabbits were challenged with 15 min of stimulation at 4 and15 tetani/min.P_i-to-phosphocreatine (PCr) ratio(P_i/PCr) was measured in vivo before, during, andafter acute stimulation by³¹P-magnetic resonancespectroscopy, and tension was recorded at the same time. AlthoughP_i/PCr was low at rest, it wassignificantly higher in chronically stimulated muscle than in controlmuscle (0.20 ± 0.02 vs. 0.05 ± 0.01, P < 0.05). Stimulation of control muscle for 15 min at both 4 and 15 tetani/min induced a significant rise in P_i/PCr, whereas the sameconditions in chronically stimulated muscle did not produce anysignificant departure from initial levels. The tension produced bycontrol muscle fell to 93 ± 3% of its initial value duringstimulation at 4 tetani/min and to 61 ± 7% at 15 tetani/min,respectively. In chronically stimulated muscle, on the other hand,tension was potentiated above its initial level at both stimulationrates (135 ± 15 and 138 ± 11%, respectively) and remainedsignificantly elevated throughout each trial. The ability ofchronically stimulated muscle to sustain high levels of activity withminimal perturbations in P_i/PCr ordecrement in tension is attributable to cellular adaptations thatinclude a well-documented increase in oxidative capacity.

     

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.

     

Skeletal muscle mass and the reduction of VO2 max in trained older subjects

Proctor, David N., and Michael J. Joyner. Skeletalmuscle mass and the reduction ofO_{2 max} in trainedolder subjects. J. Appl. Physiol.82(5): 1411-1415, 1997.The role of skeletal muscle mass in theage-associated decline in maximalO₂ uptake (O_{2 max}) is poorlydefined because of confounding changes in muscle oxidative capacity andin body fat and the difficulty of quantifying active muscle mass duringexercise. We attempted to clarify these issues byexamining the relationship between several indexes of muscle mass, asestimated by using dual-energy X-ray absorptiometry and treadmillO_{2 max} in 32 chronically endurance-trained subjects from four groups(n = 8/group): young men(20-30 yr), older men (56-72 yr), young women(19-31 yr), and older women (51-72 yr).O_{2 max} per kilogrambody mass was 26 and 22% lower in the older men (45.9 vs. 62.0 ml · kg¹ · min¹)and older women (40.0 vs. 51.5 ml · kg¹ · min¹).These age differences were reduced to 14 and 13%, respectively, whenO_{2 max} was expressedper kilogram of appendicular muscle. When appropriately adjusted forage and gender differences in appendicular muscle mass by analysis ofcovariance, whole body O_{2 max} was 0.50 ± 0.09 l/min less (P < 0.001) in theolder subjects. This effect was similar in both genders.These findings suggest that the reducedO_{2 max} seen in highlytrained older men and women relative to their younger counterparts isdue, in part, to a reduced aerobic capacity per kilogram of activemuscle independent of age-associated changes in body composition, i.e.,replacement of muscle tissue by fat. Because skeletal muscleadaptations to endurance training can be well maintained in oldersubjects, the reduced aerobic capacity per kilogram of muscle likelyresults from age-associated reductions in maximalO₂ delivery (cardiac outputand/or muscle blood flow).

     

Optical measurement of isolated canine lung filtration coefficients after alloxan infusion

In this study, lung filtration coefficient(K_fc) wasmeasured in eight isolated canine lung preparations by using threemethods: standard gravimetric (Std), blood-corrected gravimetric (BC), and optical. The lungs were held in zone III conditions and were subjected to an average venous pressure increase of 8.79 ± 0.93 (mean ± SD) cmH₂O. Thepermeability of the lungs was increased with an infusion of alloxan (75 mg/kg). The resultingK_fc values (inmilliliters · min¹ · cmH₂O¹ · 100 g dry lung weight¹)measured by using Std and BC gravimetric techniques before vs. afteralloxan infusion were statistically different: Std, 0.527 ± 0.290 vs. 1.966 ± 0.283; BC, 0.313 ± 0.290 vs. 1.384 ± 0.290. However, the optical technique did not show any statisticaldifference between pre- and postinjury with alloxan, 0.280 ± 0.305 vs. 0.483 ± 0.297, respectively. The alloxan injury, quantified byusing multiple-indicator techniques, showed an increase in permeability and a corresponding decrease in reflection coefficient for albumin (_f). Because the opticalmethod measures the product ofK_fc and _f, this study shows thatalbumin should not be used as an intravascular optical filtrationmarker when permeability is elevated. However, the optical technique,along with another means of measuringK_fc (such as BC),can be used to calculate the _fof a tracer (in this study, _fof 0.894 at baseline and 0.348 after injury). Another important findingof this study was that the ratio of baseline-to-injury K_fc values wasnot statistically different for Std and BC techniques, indicating thatthe percent contribution of slow blood-volume increases does not changebecause of injury.