Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip

Mostoufi-Moab, Sogol, Eric J. Widmaier, Jacob A. Cornett,Kristen Gray, and Lawrence I. Sinoway. Forearm training reduces the exercise pressor reflex during ischemic rhythmic handgrip. J. Appl. Physiol. 84(1): 277-283, 1998.We examined the effects of unilateral, nondominant forearmtraining (4 wk) on blood pressure and forearm metabolites duringischemic and nonischemic rhythmic handgrip (30 1-s contractions/min at25% maximal voluntary contraction). Contractions were performed by 10 subjects with the forearm enclosed in a pressurized Plexiglas tank toinduce ischemic conditions. Training increased the endurance time inthe nondominant arm by 102% (protocol1). In protocol 2,tank pressure was increased in increments of 10 mmHg/min to +50 mmHg.Training raised the positive-pressure threshold necessary to engage thepressor response. In protocol 3,handgrip was performed at +50 mmHg and venous blood samples wereanalyzed. Training attenuated mean arterial pressure (109 ± 5 and98 ± 4 mmHg pre- and posttraining, respectively, P < 0.01), venous lactate (2.9 ± 0.4 and 1.8 ± 0.3 mmol/l pre- and posttraining, respectively,P < 0.01), and the pH response (7.21 ± 0.02 and 7.25 ± 0.01, pre- and posttraining, respectively, P < 0.01). However, deep venousO₂ saturation was unchanged.Training increased the positive-pressure threshold for metaboreceptorengagement, reduced metabolite concentrations, and reduced meanarterial pressure during ischemic exercise.

     

Changes in leg vein filling and emptying characteristics and leg volumes during long-term head-down bed rest

Louisy, Francis, Philippe Schroiff, and Antonio Güell.Changes in leg vein filling and emptying characteristics and legvolumes during long-term head-down bed rest. J. Appl.Physiol. 82(6): 1726-1733, 1997.Leg venoushemodynamics [venous distensibility index (VDI), arterial flowindex (AFI), half-emptying time(T_1/2)], and leg volumes(LV) were assessed by mercury strain-gauge plethysmography with venousocclusion and volometry, respectively, in seven men before, during, andafter 42 days of 6° head-down bed rest. Results showed a highincrease in VDI up to day 26 of bedrest (+50% vs. control at day 26,P < 0.05), which tended to subsidethereafter (+20% increase vs. control value at day41, P < 0.05). VDIchanges were associated with parallel changes inT_1/2 (+54% vs. control atday 26 of bed rest,P < 0.05, and +25% vs.control at day 41, P < 0.05) and with a decrease in AFI(49% at day 41 vs. control, P < 0.05). LV continuously decreasedthroughout bed rest (13% vs. control at day41, P < 0.05) but was correlated with VDI only during the first month ofbed rest. These results show that during long-term 6° head-down bedrest alterations of leg venous compliance are associated withimpairment of venous emptying capacities and arterial flow. Changes inskeletal muscle mass and fluid shifts may account for venous changesduring the first month of bed rest but, subsequently, otherphysiological factors, to be determined, may also be involved in legvenous hemodynamic alterations.

     

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

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

     

Augmentation of exercise-induced muscle sympathetic nerve activity during muscle heating

Ray, Chester A., and Kathryn H. Gracey. Augmentation ofexercise-induced muscle sympathetic nerve activity during muscle heating. J. Appl. Physiol. 82(6):1719-1725, 1997.The muscle metabo- and mechanoreflexes have beenshown to increase muscle sympathetic nerve activity (MSNA) duringexercise. Group III and IV muscle afferents, which are believed tomediate this response, have been shown to be thermosensitive inanimals. The purpose of the present study was to evaluate the effect ofmuscle temperature on MSNA responses during exercise. Eleven subjectsperformed ischemic isometric handgrip at 30% of maximal voluntarycontraction to fatigue, followed by 2 min of postexercise muscleischemia (PEMI), with and without local heating of the forearm. Localheating of the forearm increased forearm muscle temperature from 34.4 ± 0.2 to 38.9 ± 0.3°C(P = 0.001). Diastolic andmean arterial pressures were augmented during exercise in the heat.MSNA responses were greater during ischemic handgrip with local heatingcompared with control (no heating) after the first 30 s. MSNA responsesat fatigue were greater during local heating. MSNA increased by 16 ± 2 and 20 ± 2 bursts per 30 s for control and heating,respectively (P = 0.03). Whenexpressed as a percent change in total activity (total burstamplitude), MSNA increased 531 ± 159 and 941 ± 237% forcontrol and heating, respectively (P = 0.001). However, MSNA was not different during PEMI between trials.This finding suggests that the augmentation of MSNA during exercisewith heat was due to the stimulation of mechanically sensitive muscleafferents. These results suggest that heat sensitizes skeletal muscleafferents during muscle contraction in humans and may play a role inthe regulation of MSNA during exercise.

     

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.

     

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.

     

Comparison of leucine kinetics in endurance-trained and sedentary humans

Whole body leucine kinetics was compared inendurance-trained athletes and sedentary controls matched for age,gender, and body weight. Kinetic studies were performed during 3 h ofrest, 1 h of exercise (50% maximal oxygen consumption), and 2 h ofrecovery. When leucine kinetics were expressed both per unit of bodyweight and per unit of fat-free mass, both groups demonstrated anincrease in leucine oxidation during exercise(P < 0.01). Trained athletes had agreater leucine rate of appearance during exercise and recovery compared with their sedentary counterparts(P < 0.05) and an increased leucineoxidation at all times on the basis of body weight(P < 0.05). However, all of thesebetween-group differences were eliminated when leucine kinetics werecorrected for fat-free tissue mass. Therefore, correctionof leucine kinetics for fat-free mass may be important whencross-sectional investigations on humans are performed. Furthermore,leucine oxidation, when expressed relative to whole-body oxygenconsumption during exercise, was similar between groups. It isconcluded that there was no difference between endurance-trained andsedentary humans in whole body leucine kinetics during rest, exercise,or recovery when expressed per unit of fat-free tissue mass.

     

Effect of episodic eucapnic and hypocapnic hypoxia on systemic blood pressure in hypertension-prone rats

Fletcher, Eugene C., and Gang Bao. Effect of episodiceucapnic and hypocapnic hypoxia on systemic blood pressure in hypertension-prone rats. J. Appl. Physiol. 81(5):2088-2094, 1996.Repetitive episodic (18-24 s twice perminute) hypocapnic hypoxia (HH) administered chronically (7 h/day, 35 days) to Sprague-Dawley or Wistar-Kyoto rats results in a sustainedincrease in daytime blood pressure (BP). We examined acute and chronicBP response to episodic HH and eucapnic hypoxia (EH) in borderlinehypertensive rats [first generation (F1) cross between spontaneouslyhypertensive and Wistar-Kyoto rats]. We hypothesized that episodic HHand EH would create a greater increase in acute and chronic BP in thisbreed of rat than in previously studied strains. We also examinedneural mechanisms by which BP changes from hypoxia are induced. BP andheart rate were examined acutely in nine F1 rats during baseline, HH,EH, EH with prazosin, and EH with prazosin and atropine. Five groups ofmale F1 rats were studied after 35-day exposure to the following: Unhandled (n = 8): no treatment; Sham (n = 10):episodic compressed air; HH (n = 14): daily episodic hypoxia(2.7%); EH1 (n = 12): hypoxia 2.9%, CO₂ 8.4%;and EH2 (n = 11): hypoxia 2.8% and CO₂ 10.5%.Under acute conditions, HH caused a 34.2-mmHg and EH a 77.9-mmHgincrease in mean BP. Prazosin partially blocked the increase in BP.Under chronic conditions, HH caused a 10.3-mmHg increase in daytimemean BP, whereas EH caused a fall in mean BP of 16.6 and 9.3 mmHg inthe two separately studied groups. In the F1 rat, acute EH causes anelevation of BP but chronic EH causes a fall in BP. The acute responseto EH is not predictive of what occurs after chronic exposure in thehypertension-prone F-1 rat.

     

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

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

     

Arginine-induced pancreatic hormone secretion during exercise in rats

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

     

Effects of training and a single session of exercise on lipids and apolipoproteins in hypercholesterolemic men

Crouse, Stephen F., Barbara C. O'Brien, Peter W. Grandjean,Robert C. Lowe, J. James Rohack, and John S. Green. Effects oftraining and a single session of exercise on lipids and apolipoproteins in hypercholesterolemic men. J. Appl.Physiol. 83(6): 2019-2028, 1997.To differentiatebetween transient (acute) and training (chronic) effects of exercise attwo different intensities on blood lipids and apolipoproteins (apo), 26 hypercholesterolemic men (cholesterol = 258 mg/dl, age = 47 yr, weight = 81.9 kg) trained three times per week for 24 wk, 350 kcal/session athigh (80% maximal O₂ uptake,n = 12) or moderate (50% maximalO₂ uptake, n = 14) intensity. Serum lipid andapolipoprotein (apo) concentrations (plasma volume adjusted) weremeasured before and immediately, 24, and 48 h after exercise on fourdifferent occasions corresponding to 0, 8, 16, and 24 wk of training.Data were analyzed using three-way repeated-measures multivariateanalysis of variance followed by analysis of variance and Duncan'sprocedures ( = 0.05). A transient 6% rise inlow-density-lipoprotein cholesterol measured before training at the24-h time point was no longer evident after training. Triglyceridesfell and total cholesterol, high-density-lipoprotein cholesterol(HDL-C), HDL₃-C, apo A-I, and apoB rose 24-48 h after exercise regardless of training or intensity.Total cholesterol, HDL₃-C, apoA-I, and apo B were lower andHDL₂-C was higher after trainingthan before training. Thus exercise training and a single session ofexercise exert distinct and interactive effects on lipids andapolipoproteins. These results support the practice of training atleast every other day to obtain optimal exercise benefits.

     

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.

     

Augmented sympathetic tone alters muscle metabolism with exercise: lack of evidence for functional sympatholysis

Shoemaker, J. Kevin, Prasant Pandey, Michael D. Herr, DavidH. Silber, Qing X. Yang, Michael B. Smith, Kristen Gray, and LawrenceI. Sinoway. Augmented sympathetic tone alters muscle metabolismwith exercise: lack of evidence for functional sympatholysis. J. Appl. Physiol. 82(6):1932-1938, 1997.It is unclear whether sympathetic tone opposesdilator influences in exercising skeletal muscle. We examined highlevels of sympathetic tone, evoked by lower body negative pressure(LBNP, 60 mmHg) on intramuscular pH and phosphocreatine (PCr)levels (³¹P-nuclear magnetic resonance spectroscopy) duringgraded rhythmic handgrip (30 contractions/min; ~17, 34, 52 and 69%maximal voluntary contraction). Exercise was performedwith LBNP and without LBNP (Control). At the end of exercise, LBNPcaused lower levels of muscle pH (6.59 ± 0.09) comparedwith Control (6.78 ± 0.05; P < 0.05). PCr recovery, an index of mitochondrial respiration, was lessduring the recovery phase of the LBNP trial. Exercise mean arterialpressure was not altered by LBNP. The protocols were repeated withmeasurements of forearm blood flow velocity and deep venous samples(active forearm) of hemoglobin (Hb) saturation, pH, and lactate. WithLBNP, mean blood velocity was reduced at rest, during exercise, andduring recovery compared with Control (P < 0.05). Also, venous Hbsaturation and pH levels during exercise and recovery were lower withLBNP and lactate was higher compared with Control(P < 0.05). We concludethat LBNP enhanced sympathetic tone and reduced oxygen transport. Athigh workloads, there was a greater reliance on nonoxidativemetabolism. In other words, sympatholysis did not occur.

     

Long-term creatine intake is beneficial to muscle performance during resistance training

Vandenberghe, K., M. Goris, P. Van Hecke, M. Van Leemputte,L. Vangerven, and P. Hespel. Long-term creatine intake isbeneficial to muscle performance during resistance training. J. Appl. Physiol. 83(6):2055-2063, 1997.The effects of oral creatine supplementation onmuscle phosphocreatine (PCr) concentration, muscle strength, and bodycomposition were investigated in young female volunteers(n = 19) during 10 wk ofresistance training (3 h/wk). Compared with placebo, 4 days ofhigh-dose creatine intake (20 g/day) increased(P < 0.05) muscle PCr concentration by 6%. Thereafter, this increase was maintained during 10 wk of training associated with low-dose creatine intake (5 g/day).Compared with placebo, maximal strength of the muscle groups trained,maximal intermittent exercise capacity of the arm flexors, and fat-free mass were increased 20-25, 10-25, and 60% more(P < 0.05), respectively, duringcreatine supplementation. Muscle PCr and strength, intermittent exercise capacity, and fat-free mass subsequently remained at a higherlevel in the creatine group than in the placebo group during 10 wk ofdetraining while low-dose creatine was continued. Finally, on cessationof creatine intake, muscle PCr in the creatine group returned to normalwithin 4 wk. It is concluded that long-term creatine supplementationenhances the progress of muscle strength during resistance training insedentary females.

     

Exercise performance, red blood cell deformability, and lipid peroxidation: effects of fish oil and vitamin E

Oostenbrug, G. S., R. P. Mensink, M. R. Hardeman, T. DeVries, F. Brouns, and G. Hornstra. Exercise performance, red bloodcell deformability, and lipid peroxidation: effects of fish oil andvitamin E. J. Appl. Physiol. 83(3):746-752, 1997.Previous studies have indicated that fish oilsupplementation increases red blood cell (RBC) deformability, which mayimprove exercise performance. Exercise alone, or in combination with anincrease in fatty acid unsaturation, however, may enhance lipidperoxidation. Effects of a bicycle time trial of ~1 h on RBCcharacteristics and lipid peroxidation were, therefore, studied in 24 trained cyclists. After 3 wk of fish oil supplementation (6 g/day),without or with vitamin E (300 IU/day), trial performance,RBC characteristics, and lipid peroxidation were measuredagain. RBC deformability appeared to decrease duringendurance exercise. After correction for hemoconcentration, plasmatotal tocopherol concentrations decreased by 0.77 µmol/l(P = 0.012) or 2.9% and carotenoidconcentrations by 0.08 µmol/l (P = 0.0008) or 4.5%. Endurance exercise did not affect the lag time andrate of in vitro oxidation of low-density lipoproteins (LDLs), but themaximum amount of conjugated dienes formed decreased by 2.1 ± 1.0 µmol/mmol LDL cholesterol (P = 0.042) or 1.2%. Fish oil supplementation with andwithout vitamin E did not affect RBC characteristics or exerciseperformance. Both supplements decreased the rate of LDL oxidation, andfish oil supplementation with vitamin E delayed oxidation. The amountof dienes, however, was not affected. The supplements also did notchange effects of exercise. We conclude that the changes observedduring endurance exercise may indicate increased oxidative stress, butfurther research is necessary to confirm this. Fish oil supplementation does not improve endurance performance, but it also does not cause oraugment changes in antioxidant levels or LDL oxidation during exercise.

     

Physiological adaptations to a weight-loss dietary regimen and exercise programs in women

Kraemer, William J., Jeff S. Volek, Kristine L. Clark, ScottE. Gordon, Thomas Incledon, Susan M. Puhl, N. Travis Triplett-McBride, Jeffrey M. McBride, Margot Putukian, and Wayne J. Sebastianelli. Physiological adaptations to a weight-loss dietary regimen andexercise programs in women. J. Appl.Physiol. 83(1): 270-279, 1997.Thirty-one women(mean age 35.4 ± 8.5 yr) who were overweight were matched andrandomly placed into either a control group (Con; n = 6), a diet-only group (D;n = 8), a diet+aerobic endurance exercise training group (DE; n = 9),or a diet+aerobic endurance exercise training+strength training group(DES; n = 8). After 12 wk, the threedietary groups demonstrated a significant(P  0.05) reduction in body mass,%body fat, and fat mass. No differences were observed in the magnitudeof loss among groups, in fat-free mass, or in resting metabolic rate.The DE and DES groups increased maximal oxygen consumption, and the DESgroup demonstrated increases in maximal strength. Weight loss resultedin a similar reduction in total serum cholesterol, low-densitylipoprotein cholesterol, and high-density lipoprotein cholesterol amongdietary groups. These data indicate that weight loss during moderatecaloric restriction is not altered by inclusion of aerobic oraerobic+resistance exercise, but diet in conjunction with training caninduce remarkable adaptations in aerobic capacity and muscular strengthdespite significant reductions in body mass.

     

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.

     

Resistance exercise maintains skeletal muscle protein synthesis during bed rest

Ferrando, Arny A., Kevin D. Tipton, Marcas M. Bamman, andRobert R. Wolfe. Resistance exercise maintains skeletal muscle protein synthesis during bed rest. J. Appl.Physiol. 82(3): 807-810, 1997.Spaceflightresults in a loss of lean body mass and muscular strength. Aground-based model for microgravity, bed rest, results in a loss oflean body mass due to a decrease in muscle protein synthesis (MPS).Resistance training is suggested as a proposed countermeasure forspaceflight-induced atrophy because it is known to increase both MPSand skeletal muscle strength. We therefore hypothesized that scheduledresistance training throughout bed rest would ameliorate the decreasein MPS. Two groups of healthy volunteers were studied during 14 days ofsimulated microgravity. One group adhered to strict bed rest (BR;n = 5), whereas a second group engagedin leg resistance exercise every other day throughout bed rest (BREx;n = 6). MPS was determined directly bythe incorporation of infusedL-[ring-¹³C₆]phenylalanineinto vastus lateralis protein. After 14 days of bed rest, MPS in theBREx group did not change and was significantly greater than in the BRgroup. Thus moderate-resistance exercise can counteract the decrease inMPS during bed rest.

     

Respiratory effort sensation during exercise with induced expiratory-flow limitation in healthy humans

Kayser, Bengt, Pawel Sliwinski, Sheng Yan, Mirek Tobiasz,and Peter T. Macklem. Respiratory effort sensation during exercisewith induced expiratory-flow limitation in healthy humans. J. Appl. Physiol. 83(3): 936-947, 1997.Nine healthy subjects (age 31 ± 4 yr) exercised with andwithout expiratory-flow limitation (maximal flow ~1 l/s). Wemonitored flow, end-tidal PCO₂, esophageal (Pes) and gastric pressures, changes in end-expiratory lungvolume, and perception (sensation) of difficulty in breathing. Subjectscycled at increasing intensity (+25 W/30 s) until symptom limitation.During the flow-limited run, exercise performance was limited in allsubjects by maximum sensation. Sensation was equally determined byinspiratory and expiratory pressure changes. In both runs, 90% of thevariance in sensation could be explained by the Pes swings (differencebetween peak inspiratory and peak expiratory Pes). End-tidalPCO₂ did not explain any variance insensation in the control run and added only 3% to the explained variance in the flow-limited run. We conclude that in healthy subjects,during normal as well as expiratory flow-limited exercise, the pleuralpressure generation of the expiratory muscles is equally related to theperception of difficulty in breathing as that of the inspiratorymuscles.

     

Exercise causes blood glutathione oxidation in chronic obstructive pulmonary disease: prevention by O2 therapy

Viña, José, Emilio Servera, Miguel Asensi, JuanSastre, Federico V. Pallardó, José A. Ferrero, JoséGarcía-de-la-Asunción, Vicente Antón, and JulioMarín. Exercise causes blood glutathione oxidation inchronic obstructive pulmonary disease: prevention by O₂therapy. J. Appl. Physiol. 81(5):2199-2202, 1996.The aim of the present study was to determinewhether glutathione oxidation occurs in chronic obstructive pulmonarydisease (COPD) patients who perform exercise and whether this could beprevented. Blood glutathione red-ox ratio [oxidized-to-reducedglutathione (GSSG/GSH)] was significantly increased when patientsperformed exercise for a short period of time until exhaustion. Theirresting blood GSSG/GSH was 0.039 ± 0.008 (SD)(n = 5), whereas after exercise itincreased to 0.085 ± 0.019, P < 0.01. Glutathione oxidation associated with exercise was partiallyprevented by oxygen therapy (resting value: 0.037 ± 0.014, n = 5; after exercise: 0.047 ± 0.016, n = 5, P < 0.01). We conclude that lightexercise causes an oxidation of glutathione in COPD patients, which canbe partially prevented by oxygen therapy.