Enhanced brain natriuretic peptide response to peak exercise in heart transplant recipients

We investigatedthe atrial (ANP) and brain natriuretic peptides (BNP), catecholamines,heart rate, and blood pressure responses to graded upright maximalcycling exercise of eight matched healthy subjects andcardiac-denervated heart transplant recipients (HTR). Baseline heart rate and diastolic blood pressure, together with ANP(15.2 ± 3.7 vs. 4.4 ± 0.8 pmol/l;P < 0.01) and BNP (14.3 ± 2.6 vs. 7.4 ± 0.6 pmol/l; P < 0.01), were elevated in HTR, but catecholamine levels were similarin both groups. Peak exercise O₂uptake and heart rate were lower in HTR. Exercise-inducedmaximal ANP increase was similar in both groups (167 ± 34 vs. 216 ± 47%). Enhanced BNP increase was significant only in HTR (37 ± 8 vs. 16 ± 8%; P < 0.05).Similar norepinephrine but lower peak epinephrine levels were observedin HTR. ANP and heart rate changes from rest to 75% peak exercise werenegatively correlated (r = 0.76, P < 0.05),and BNP increase was correlated with left ventricular mass index(r = 0.83, P < 0.01) after hearttransplantation. Although ANP increase was notexaggerated, these data support the idea that the chronotropiclimitation secondary to sinus node denervation might stimulate ANPrelease during early exercise in HTR. Furthermore, the BNPresponse to maximal exercise, which is related to the left ventricularmass index of HTR, is enhanced after heart transplantation.

     

Age and gender dependency of baroreflex sensitivity in healthy subjects

Laitinen, Tomi, Juha Hartikainen, Esko Vanninen, LeoNiskanen, Ghislaine Geelen, and Esko Länsimies. Age andgender dependency of baroreflex sensitivity in healthy subjects.J. Appl. Physiol. 84(2): 576-583, 1998.We evaluated the correlates of baroreflex sensitivity (BRS) inhealthy subjects. The study consisted of 117 healthy, normal-weight,nonsmoking male and female subjects aged 23-77 yr. Baroreflexcontrol of heart rate was measured by using the phenylephrinebolus-injection technique. Frequency- and time-domain analysis of heartrate variability and an exercise test were performed. Plasmanorepinephrine, epinephrine, insulin, and arginine vasopressinconcentrations and plasma renin activity were measured. In theunivariate analysis, BRS correlated with age(r = 0.65,P < 0.001), diastolic blood pressure(r = 0.47, P < 0.001), exercise capacity(r = 0.60, P < 0.001), and the high-frequency component of heart rate variability (r = 0.64, P < 0.001). There was also asignificant correlation between BRS and plasma norepinephrine concentration (r = 0.22,P < 0.05) and plasma renin activity (r = 0.32, P < 0.001). According to themultivariate analysis, age and gender were the most importantphysiological correlates of BRS. They accounted for 52% ofinterindividual BRS variation. In addition, diastolic blood pressureand high-frequency component of heart rate variability were significantindependent correlates of BRS. BRS was significantly higher in men thanin women (15.0 ± 1.2 vs. 10.2 ± 1.1 ms/mmHg, respectively;P < 0.01). Twenty-four percent ofwomen >40 yr old and 18% of men >60 yr old had markedly depressedBRS (<3 ms/mmHg). We conclude that physiological factors, particularly age and gender, have significant impact on BRS in healthysubjects. In addition, we demonstrate that BRS values that have beenproposed to be useful in identifying postinfarction patients at highrisk of sudden death are frequently found in healthy subjects.

     

Both physical fitness and acute exercise regulate nitric oxide formation in healthy humans

Jungersten, Lennart, Anneli Ambring, Björn Wall, andÅke Wennmalm. Both physical fitness and acute exerciseregulate nitric oxide formation in healthy humans. J. Appl. Physiol. 82(3): 760-764, 1997.We analyzednitrate, a major stable end product of nitric oxide (NO) metabolism invivo in plasma and urine from groups of healthy subjects with differentworking capacities. Resting plasma nitrate was higher in athleticsubjects than in nonathletic controls [45 ± 2 vs. 34 ± 2 (SE) µM; P < 0.01]. In other subjects, both the resting plasma nitrate level(r = 0.53; P < 0.01) and the urinary excretionof nitrate at rest (r = 0.46; P < 0.01) correlated to thesubjects' peak work rates, as determined by bicycle ergometry. Twohours of physical exercise elevated plasma nitrate by 18 ± 4 (P < 0.01) and 16 ± 6%(P < 0.01), respectively, in athletes and nonathletes, compared with resting nitrate before exercise. We conclude that physical fitness and formation of NO at restare positively linked to each other. Furthermore, a single session ofexercise elicits an acute elevation of NO formation. The observedpositive relation between physical exercise and NO formation may helpto explain the beneficial effects of physical exercise oncardiovascular health.

     

Fuel metabolism in men and women during and after long-duration exercise

This study aimed to determine gender-baseddifferences in fuel metabolism in response to long-duration exercise.Fuel oxidation and the metabolic response to exercise were compared inmen (n = 14) and women(n = 13) during 2 h (40% of maximalO₂ uptake) of cycling and 2 h ofpostexercise recovery. In addition, subjects completed a separatecontrol day on which no exercise was performed. Fuel oxidation wasmeasured using indirect calorimetry, and blood samples were drawn forthe determination of circulating substrate and hormone levels. Duringexercise, women derived proportionally more of the total energyexpended from fat oxidation (50.9 ± 1.8 and 43.7 ± 2.1% forwomen and men, respectively, P < 0.02), whereas men derived proportionally more energy from carbohydrateoxidation (53.1 ± 2.1 and 45.7 ± 1.8% for men and women,respectively, P < 0.01). Thesegender-based differences were not observed before exercise, afterexercise, or on the control day. Epinephrine(P < 0.007) and norepinephrine(P < 0.0009) levels weresignificantly greater during exercise in men than in women (peakepinephrine concentrations: 208 ± 36 and 121 ± 15 pg/ml in menand women, respectively; peak norepinephrine concentrations: 924 ± 125 and 659 ± 68 pg/ml in men and women, respectively). Ascirculating glycerol levels were not different between the two groups,this suggests that women may be more sensitive to the lipolytic action of the catecholamines. In conclusion, these data support the view thatdifferent priorities are placed on lipid and carbohydrate oxidationduring exercise in men and women and that these gender-based differences extend to the catecholamine response to exercise.

     

Metabolic effects of low cortisol during exercise in humans

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

     

Physical exercise and normobaric hypoxia: independent modulators of peripheral cholecystokinin metabolism in man

The purpose ofthe present investigation was to determine the independent effects ofhypoxia and physical exercise on peripheral cholecystokinin (CCK)metabolism in humans. Thirty-two physically active men wererandomly assigned in a double-blind manner to either a normoxic (N;n = 14) or hypoxic (H; n = 18) group.During the acute study, subjects in the H group only participated in two tests, separated by 48 h, which involved a cycling test to exhaustion in normobaric normoxia and normobaric hypoxia (inspired O₂ fraction = 0.21 and 0.16, respectively). In theintermittent study, N and H groups cycle-trained for 4 wk at the samerelative exercise intensity in both normoxia and hypoxia. Acutenormoxic exercise consistently raised plasma CCK during both studies by 290-723%, which correlated with increases in the plasma ratio offree tryptophan to branched chain amino acids (r = 0.58-0.71, P < 0.05). In contrast, acute hypoxicexercise decreased CCK by 7.0 ± 5.5 pmol/l, which correlated withthe decrease in arterial oxygen saturation (r = 0.56, P < 0.05). In the intermittent study, plasma CCKresponse at rest and after normoxic exercise was not altered afterphysical training, despite a slight decrease in adiposity. We concludethat peripheral CCK metabolism 1) is more sensitive to acutechanges than chronic changes in energy expenditure and 2) ispotentially associated with acute changes in tissue PO₂ and metabolic precursors of cerebralserotoninergic activity.

     

Cardiovascular adaptations to 10days of cycle exercise

Mier, Constance M., Michael J. Turner, Ali A. Ehsani, andRobert J. Spina. Cardiovascular adaptations to 10 days of cycleexercise. J. Appl. Physiol. 83(6):1900-1906, 1997.We hypothesized that 10 days of training wouldenhance cardiac output (CO) and stroke volume (SV) during peak exerciseand increase the inotropic response to -adrenergic stimulation. Tensubjects [age 26 ± 2 (SE) yr] trained on a cycleergometer for 10 days. At peak exercise, training increasedO₂ uptake, CO, and SV(P < 0.001). Left ventricular (LV)size and function at rest were assessed with two-dimensional echocardiography before (baseline) and after atropine injection (1.0 mg) and during four graded doses of dobutamine. LV end-diastolic diameter increased with training (P < 0.02), whereas LV wall thickness was unchanged. LV contractileperformance was assessed by relating fractional shortening (FS) to theestimated end-systolic wall stress(_ES). Training increased theslope of the FS-_ES relationship (P < 0.05), indicating enhancedsystolic function. The increase in slope correlated with increases inCO (r = 0.71,P < 0.05) and SV(r = 0.70,P < 0.05). The increase in bloodvolume also correlated with increases in CO(r = 0.80, P < 0.01) and SV (r = 0.85, P < 0.004). These datashow that 10 days of training enhance the inotropic response to-adrenergic stimulation, associated with increases in CO and SVduring peak exercise.

     

Improving energy expenditure estimation by using a triaxial accelerometer

Chen, Kong Y., and Ming Sun. Improving energyexpenditure estimation by using a triaxial accelerometer.J. Appl. Physiol. 83(6):2112-2122, 1997.In our study of 125 subjects (53 men and 72 women) for two 24-h periods, we validated energy expenditure (EE),estimated by a triaxial accelerometer (Tritrac-R3D), by using awhole-room indirect calorimeter under close-to-normal livingconditions. The estimated EE was correlated with the measured total EEfor the 2 days (r = 0.925 andr = 0.855;P < 0.001) and in minute-by-minuteEE (P < 0.01). Resting EE formulatedby the Tritrac was found to be similar to the measured values[standard errors of estimation (SEE) = 0.112 W/kg;P = 0.822]. The Tritrac significantly underestimated total EE, EE for physical activities, EEof sedentary and light-intensity activities, and EE for exercise suchas stepping (all P < 0.001). Wedeveloped a linear and a nonlinear model to predict EE by using theacceleration components from the Tritrac. Predicted EE wassignificantly improved with both models in estimating total EE, totalEE for physical activities, EE in low-intensity activities,minute-by-minute averaged relative difference, and minute-by-minute SEE(all P < 0.05). Furthermore, withour generalized models and by using subjects' physical characteristics and body acceleration, EE can be estimated with higher accuracy (averaged SEE = 0.418 W/kg) than with the Tritrac model.

     

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

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

     

More tetanic contractions are required for activating glucose transport maximally in trained muscle

Kawanaka, Kentaro, Izumi Tabata, and MitsuruHiguchi. More tetanic contractions are requiredfor activating glucose transport maximally in trained muscle.J. Appl. Physiol. 83(2): 429-433, 1997.Exercise training increases contraction-stimulated maximalglucose transport and muscle glycogen level in skeletal muscle.However, there is a possibility that more muscle contractions arerequired to maximally activate glucose transport in trained than inuntrained muscle, because increased glycogen level after training mayinhibit glucose transport. Therefore, the purpose of this study was toinvestigate the relationship between the increase in glucose transportand the number of tetanic contractions in trained and untrained muscle.Male rats swam 2 h/day for 15 days. In untrained epitrochlearis muscle,resting glycogen was 26.6 µmol glucose/g muscle. Ten, 10-s-longtetani at a rate of 1 contraction/min decreased glycogen level to 15.4 µmol glucose/g muscle and maximally increased2-deoxy-D-glucose(2-DG) transport. Training increasedcontraction-stimulated maximal 2-DG transport (+71%;P < 0.01), GLUT-4 protein content(+78%; P < 0.01), and restingglycogen level (to 39.3 µmol glucose/g muscle;P < 0.01) on the next day after thetraining ended, although this training effect might be due, at least inpart, to last bout of exercise. In trained muscle, 20 tetani werenecessary to maximally activate glucose transport. Twenty tetanidecreased muscle glycogen to a lower level than 10 tetani (18.9 vs.24.0 µmol glucose/g muscle; P < 0.01). Contraction-stimulated 2-DG transport was negatively correlatedwith postcontraction muscle glycogen level in trained (r = 0.60;P < 0.01) and untrained muscle(r = 0.57;P < 0.01).

     

Myosin molecular motor dysfunction in dystrophic mouse diaphragm

Cross-bridge properties and myosin heavy chain (MHC) compositionwere investigated in isolated diaphragm from 6-mo-old control (n = 12) andmdx(n = 12) mice. Compared with control,peak tetanic tension fell by 50% inmdx mice(P < 0.001). The total number ofcross bridges per square millimeter(×10⁹), the elementaryforce per cross bridge, and the peak mechanical efficiency were lowerin mdx than in control mice (eachP < 0.001). The duration of thecycle and the rate constant for cross-bridge detachment weresignificantly lower in mdx than incontrol mice. In the overall population, there was a linearrelationship between peak tetanic tension and either total number ofcross bridges per square millimeter or elementary force per crossbridge (r = 0.996 andr = 0.667, respectively, eachP < 0.001). Themdx mice presented a higher proportionof type IIA MHC (P < 0.001) thancontrol mice and a reduction in type IIX MHC(P < 0.001) and slowmyosin isoforms (P < 0.01) comparedwith control mice. We concluded that, inmdx mice, impaired diaphragm strengthwas associated with qualitative and quantitative changes in myosin molecular motors. It is proposed that reduced force generated per crossbridge contributed to diaphragm weakness inmdx mice.

     

Influence of diet and exercise on skeletal muscle and visceral adipose tissue in men

Ross, Robert, John Rissanen, Heather Pedwell, JenniferClifford, and Peter Shragge. Influence of diet and exercise onskeletal muscle and visceral adipose tissue in men. J. Appl. Physiol. 81(6): 2445-2455, 1996.Theeffects of diet only (DO) and diet combined with either aerobic (DA) orresistance (DR) exercise on subcutaneous adipose tissue (SAT), visceraladipose tissue (VAT), lean tissue (LT), and skeletal muscle (SM) tissue were evaluated in 33 obese men (DO, n = 11; DA, n = 11; DR,n = 11). All tissues were measured byusing a whole body multislice magnetic resonance imaging (MRI) model.Within each group, significant reductions were observed for bodyweight, SAT, and VAT (P < 0.05). Thereductions in body weight (~10%) and SAT (~25%) and VAT volume (~35%) were not different between groups(P > 0.05). For alltreatments, the relative reduction in VAT was greater than in SAT(P < 0.05). For the DA and DR groupsonly, the reduction in abdominal SAT (~27%) was greater(P < 0.05) than thatobserved for the gluteal-femoral region (~20%). Conversely, thereduction in VAT was uniform throughout the abdomen regardless oftreatment (P > 0.05). MRI-LT andMRI-SM decreased both in the upper and lower body regions for the DO group alone (P < 0.05). PeakO₂ uptake (liters) wassignificantly improved (~14%) in the DA group as was muscularstrength (~20%) in the DR group (P < 0.01). These findings indicate that DA and DR result in a greaterpreservation of MRI-SM, mobilization of SAT from the abdominal region,by comparison with the gluteal-femoral region, and improved functionalcapacity when compared with DO in obese men.

     

Isolated mouse pancreatic beta-cells show cell-specific temporal response pattern

The length of the silent lag time beforeelevation of the cytosolic free Ca²⁺ concentration([Ca²⁺]_i) differs between individualpancreatic -cells. One important question is whether thesedifferences reflect a random phenomenon or whether the length of lagtime is inherent in the individual -cell. We compared the lag times,initial dips, and initial peak heights for[Ca²⁺]_i from two consecutive glucosestimulations (with either 10 or 20 mM glucose) in individualob/ob mouse -cells with the fura 2 technique in amicrofluorimetric system. There was a strong correlation between thelengths of the lag times in each -cell (10 mM glucose:r = 0.94, P < 0.001; 20 mM glucose:r = 0.96, P < 0.001) as well as between theinitial dips in [Ca²⁺]_i (10 mM glucose:r = 0.93, P < 0.001; 20 mM glucose:r = 0.79, P < 0.001) and between theinitial peak heights (10 mM glucose: r = 0.51, P < 0.01; 20 mM glucose: r = 0.77, P < 0.001). These data provide evidence that theresponse pattern, including both the length of the lag time and thedynamics of the subsequent [Ca²⁺]_i, isspecific for the individual -cell.

     

Effect of exercise timing on postprandial lipemia and HDL cholesterol subfractions

The purpose ofthe study was to examine the effect of exercise timing on postprandiallipemia responses. Subjects were 21 recreationally trained men (ages 27 ± 1.7 yr). Each subject performed four trials:1) Control (fat meal only),2) Post (exercise 1 h after a fat meal), 3) 1 h-Pre(exercise 1 h before a fat meal), and4) 12 h-Pre (exercise 12 h before afat meal). In each trial, subjects had a standard fat meal to inducepostprandial hypertriglyceridemia. Blood samples were taken at 0 h(immediately before the fat meal) and at 2, 4, 6, 8, and 24 h after themeal. In the exercise trials, each subject exercised at 60% of maximalO₂ consumption for 1 h. Theresults indicated that triglyceride area under the curve scores inpremeal-exercise trials were lower (P < 0.05) than those in Post and Control. At 24 h, total high-densitylipoprotein (HDL)-cholesterol in the premeal-exercise trials was higher(P < 0.05) than that at 0 h, whereastotal HDL-cholesterol was not changed in Control and Post. At 24 h, HDLsubtype 2-cholesterol was higher (P < 0.05) in the premeal-exercise trials than in Control, which did not differ from Post. These results suggest that exercising before a fatmeal may have a beneficial effect on the triglyceride response and HDLmetabolism, which may blunt atherosclerotic process induced by the fatmeal.

     

Aerobic exercise maintains regional bone mineral density during weight loss in postmenopausal women

This studyexamines the effects of weight loss by caloric restriction (WL) andaerobic exercise plus weight loss (AEx+WL) on total and regional bonemineral density (BMD) in older women. Healthy,postmenopausal women [age 63 ± 1 (SE) yr] not onhormone-replacement therapy underwent 6 mo of WL(n = 15) consisting of dietarycounseling one time per week with a caloric deficit (250-350kcal/day) or AEx+WL (n = 15)consisting of treadmill exercise three times per week in addition tothe weight loss. Maximal aerobic capacity increased only in the AEx+WLgroup (P < 0.001). Body weight,percent fat, and fat mass decreased similarly in both groups(P < 0.005), with no changesin fat-free mass. Total body BMD (by dual-energy X-rayabsorptiometry) decreased in both groups(P < 0.05). Femoral neck, Ward'striangle, and greater trochanter BMD decreased in the WL group(P  0.05) but were not significantlydifferent after AEx+WL.L₂-L₄BMD did not significantly change in either group. Thus WL andAEx+WL both result in losses of totalbody BMD; however, AEx+WL appears to prevent the loss in regional BMDseen with WL alone in healthy, older women. This suggests that theaddition of exercise to weight-loss programs may reduce the risk forbone loss.

     

Prolonged exercise increases peripheral plasma ACTH, CRH, and AVP in male athletes

We wished to determine whether the increased ACTH duringprolonged exercise was associated with changes in peripheralcorticotropin-releasing hormone (CRH) and/or argininevasopressin (AVP). Six male triathletes were studied during exercise: 1 h at 70% maximal oxygen consumption, followed by progressivelyincreasing work rates until exhaustion. Data obtained during theexercise session were compared with a nonexercise control session.Venous blood was sampled over a 2-h period for cortisol, ACTH, CRH,AVP, renin, glucose, and plasma osmolality. There were significantincreases by ANOVA on log-transformed data in plasma cortisol(P = 0.002), ACTH(P < 0.001), CRH(P < 0.001), and AVP(P < 0.03) during exercise comparedwith the control day. A variable increase in AVP was observed after the period of high-intensity exercise. Plasma osmolality rose with exercise(P < 0.001) and was related toplasma AVP during submaximal exercise(P < 0.03) but not with theinclusion of data that followed the high-intensity exercise. Thisindicated an additional stimulus to the secretion of AVP. The mechanismby which ACTH secretion occurs during exercise involves both CRH andAVP. We hypothesize that high-intensity exercise favors AVP release andthat prolonged duration favors CRH release.

     

Enhanced muscle glucose uptake facilitates nitrogen efflux from exercised muscle

The hypothesis that glucose ingestion inthe postexercise state enhances the synthesis of glutamine and alaninein the skeletal muscle was tested. Glucose was infused intraduodenallyfor 150 min (44.5 µmol · kg¹ · min¹)beginning 30 min after a 150-min period of exercise(n = 7) or an equivalent durationsedentary period (n = 10) in18-h-fasted dogs. Prior exercise caused a twofold greater increase inlimb glucose uptake during the intraduodenal glucose infusion compared with uptake in sedentary dogs. Arterial glutamine levels fell graduallywith the glucose load in both groups. Net hindlimb glutamine effluxincreased in response to intraduodenal glucose in exercised but notsedentary dogs (P < 0.05-0.01).Arterial alanine levels, depleted by 50% with exercise, rose withintraduodenal glucose in exercised but not sedentary dogs(P < 0.05-0.01). Net hindlimb alanine efflux also rose in exercised dogs in response to intraduodenal glucose (P < 0.05-0.01),whereas it was not different from baseline in sedentary controls forthe first 90 min of glucose infusion. Beyond this point,it, too, rose significantly. We conclude that oral glucosemay facilitate recovery of muscle from prolonged exercise by enhancingthe removal of nitrogen in the form of glutamine andalanine.

     

Expanded blood volumes contribute to the increased cardiovascular performance of endurance-trained older men

To determine whether expanded intravascular volumes contributeto the older athlete's higher exercise stroke volume and maximal oxygen consumption(O_{2 max}),we measured peak upright cycle ergometry cardiac volumes(^99mTc ventriculography) andplasma (¹²⁵I-labeled albumin) andred cell (NaCr⁵¹) volumes in 7 endurance-trained and 12 age-matched lean sedentary men. The athleteshad ~40% higherO_{2 max} values thandid the sedentary men and larger relative plasma (46 vs. 38 ml/kg), red cell (30 vs. 26 ml/kg), and total blood volumes (76 vs. 64 ml/kg) (allP < 0.05). Athletes hadlarger peak cycle ergometer exercise stroke volume indexes (75 vs. 57 ml/m²,P < 0.05) and 17% largerend-diastolic volume indexes. In the total group,O_{2 max}correlated with plasma, red cell, and total blood volumes(r = 0.61-0.70,P < 0.01). Peakexercise stroke volume was correlated directly with the blood volumevariables (r = 0.59-0.67,P < 0.01). Multiple regressionanalyses showed that fat-free mass and plasma or total blood volume,but not red cell volume, were independent determinants ofO_{2 max} andpeak exercise stroke volume. Plasma and total blood volumes correlated with the stroke volume and end-diastolic volume changes from rest topeak exercise. This suggests that expanded intravascular volumes, particularly plasma and total blood volumes, contribute to the higherpeak exercise left ventricular end-diastolic volume, stroke volume, andcardiac output and hence the higherO_{2 max} in master athletes by eliciting both chronic volume overload and increased utilization of the Frank-Starling effect during exercise.

     

Plasma Catechols in Familial Dysautonomia: A Long-term Follow-up Study

This study tested whether familial dysautonomia (FD) involves progressive loss of noradrenergic nerves. Plasma levels of catechols, including dihydroxyphenylglycol (DHPG), norepinephrine (NE), dopamine (DA), and DOPA, were measured in 7 adult patients with FD and 50 healthy control subjects. FD patients were re-tested after a mean follow-up period of 13 years. Compared to controls, FD patients had low plasma levels of DHPG (P < 0.001), high DOPA and DA levels (P = 0.01, P = 0.0002), and high NE:DHPG (P < 0.0001), DA:NE (P = 0.0003), and DOPA:DHPG (P < 0.0001) ratios. At follow-up there were no changes in plasma levels of individual catechols; however, there were further increases in DOPA:DHPG ratios (mean 24 ± 7%, P = 0.01). In FD, plasma catechol profiles are sufficiently stable, at least over a decade, to be used as a biomarker of disease involvement. An increasing DOPA:DHPG ratio suggests slight but consistent, progressive loss of noradrenergic neurons.     

Plasma levels of trace elements and exercise induced stress hormones in well-trained athletes

This study analyzed the variation and relationship of several trace elements, metabolic substrates and stress hormones activated by exercise during incremental exercise. Seventeen well-trained endurance athletes performed a cycle ergometer test: after a warm-up of 10 min at 2.0 W kg⁻¹, the workload was increased by 0.5 W kg⁻¹ every 10 min until exhaustion. Prior diet, activity patterns, and levels of exercise training were controlled, and tests timed to minimize variations due to the circadian rhythm. Oxygen uptake, blood lactate concentration, plasma ions (Zn, Se, Mn and Co), serum glucose, non-esterified fatty acids (NEFAs) and several hormones were measured at rest, at the end of each stage and 3, 5 and 7 min post-exercise. Urine specific gravity was measured before and after the test, and participants drank water ad libitum.Significant differences were found in plasma Zn and Se levels as a function of exercise intensity. Zn was significantly correlated with epinephrine, norepinephrine and cortisol (r = 0.884, P < 0.01; r = 0.871, P < 0.01; and r = 0.808, P = 0.05); and Se showed significant positive correlations whit epinephrine and cortisol (r = 0.743, P < 0.05; and r = 0.776, P < 0.05). Neither Zn nor Se levels were associated with insulin or glucagon, and neither Mn nor Co levels were associated with any of the hormones or substrate metabolites studied. Further, while Zn levels were found to be associated only with lactate, plasma Se was significantly correlated with lactate and glucose (respectively for Zn: r = 0.891, P < 0.01; and for Se: r = 0.743, P < 0.05; r = 0.831, P < 0.05).In conclusion, our data suggest that there is a positive correlation between the increases in plasma Zn or Se and stress hormones variations induced by exercise along different submaximal intensities in well-hydrated well-trained endurance athletes.