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

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

     

The VO2 slow component for severe exercise depends on type of exercise and is not correlated with time to fatigue

The purpose ofthis study was to examine the influence of the type of exercise(running vs. cycling) on the O₂uptake (O₂) slow component.Ten triathletes performed exhaustive exercise on a treadmill and on acycloergometer at a work rate corresponding to 90% of maximalO₂ (90% work rate maximalO₂). The duration of thetests before exhaustion was superimposable for both type of exercises(10 min 37 s ± 4 min 11 s vs. 10 min 54 s ± 4 min 47 s forrunning and cycling, respectively). TheO₂ slow component (difference between O₂ atthe last minute and minute 3 ofexercise) was significantly lower during running compared with cycling(20.9 ± 2 vs. 268.8 ± 24 ml/min). Consequently, there was norelationship between the magnitude of theO₂ slow component and thetime to fatigue. Finally, because blood lactate levels at the end of the tests were similar for both running (7.2 ± 1.9 mmol/l) and cycling (7.3 ± 2.4 mmol/l), there was a clear dissociation between blood lactate and the O₂slow component during running. These data demonstrate that1) theO₂ slow component dependson the type of exercise in a group of triathletes and2) the time to fatigue isindependent of the magnitude of theO₂ slow component and bloodlactate concentration. It is speculated that the difference in muscularcontraction regimen between running and cycling could account for thedifference in theO₂ slow component.

     

Glucose infusion partially attenuates glucose production and increases uptake during intense exercise

Glucose infusioncan prevent the increase in glucose production (R_a) andincrease glucose uptake (R_d) during exercise of moderate intensity. We postulated that 1)because in postabsorptive intense exercise (>80% maximalO₂ uptake) the eightfold increasein R_a may be mediated by catecholamines rather than byglucagon and insulin, exogenous glucose infusion would not prevent theR_a increment, and 2)such infusion would cause greater R_d. Fit young men were exercised at >85% maximal O₂uptake for 14 min in the postabsorptive state [controls (Con),n = 12] or atminute 210 of a 285-min glucose infusion. In seven subjects, the infusion was constant(CI; 4 mg · kg¹ · min¹),and in seven subjects it was varied (VI) to mimic the exercise R_a response in Con. Although glucose suppressedR_a to zero (with glycemia ~6 mM and insulin ~150 pM),an endogenous R_a response to exercise occurred, to peakincrements two-thirds those in Con, in both CI and VI. Glucagon wasunchanged, and very small increases in the glucagon-to-insulin ratiooccurred in all three groups. Catecholamine responses were similar inall three groups, and correlation coefficients of R_a withplasma norepinephrine and epinephrine were significant in all. In allCI and VI, R_d at rest was 2× Con, increased earlierin exercise, and was higher for the 1 h of recovery with glucoseinfusion. Thus the R_a response was only partly attenuated,and the catecholamines are likely to be the regulators. This suggeststhat an acute endogenous R_a rise is possible even in thepostprandial state. Furthermore, the fact that more circulating glucoseis used by muscle during exercise and early recovery suggests thatmuscle glycogen is spared.

     

Effects of glucose, glucose plus branched-chain amino acids, or placebo on bike performance over 100km

Madsen, Klavs, Dave A. MacLean, Bente Kiens, and DirkChristensen. Effects of glucose, glucose plus branched-chain aminoacids, or placebo on bike performance over 100 km. J. Appl. Physiol. 81(6): 2644-2650, 1996.This studywas undertaken to determine the effects of ingesting either glucose(trial G) or glucose plusbranched-chain amino acids (BCAA; trialB), compared with placebo (trialP), during prolonged exercise. Nine well-trained cyclists with a maximal oxygen uptake of 63.1 ± 1.5 mlO₂ ^· min^{1 ·} kg¹performed three laboratory trials consisting of 100 km of cycling separated by 7 days between each trial. During these trials, the subjects were encouraged to complete the 100 km as fast as possible ontheir own bicycles connected to a magnetic brake. No differences inperformance times were observed between the three trials (160.1 ± 4.1, 157.2 ± 4.5, and 159.8 ± 3.7 min, respectively). Intrial B, plasma BCAA levels increased from339 ± 28 µM at rest to 1,026 ± 62 µM after exercise(P < 0.01). Plasma ammoniaconcentrations increased during the entire exercise period for allthree trials and were significantly higher intrial B compared withtrials G andP (P < 0.05). The respiratory exchange ratio was similar in the threetrials during the first 90 min of exercise; thereafter, it tended todrop more in trial P than intrials G andB. These data suggest that neitherglucose nor glucose plus BCAA ingestion during 100 km of cyclingenhance performance in well-trained cyclists.

     

Reduced oxidation rates of ingested glucose during prolonged exercise with low endogenous CHO availability

Jeukendrup, Asker E., Lars B. Borghouts, Wim H. M. Saris,and Anton J. M. Wagenmakers. Reduced oxidation rates of ingested glucose during prolonged exercise with low endogenous CHO availability. J. Appl. Physiol. 81(5):1952-1957, 1996.This study investigated the effect of endogenouscarbohydrate (CHO) availability on oxidation rates of ingested glucoseduring moderate-intensity exercise. Seven well-trained cyclistsperformed two trials of 120 min of cycling exercise in random order at57% maximal O₂ consumption. Preexercise glycogen concentrations were manipulated byglycogen-lowering exercise in combination with CHO restriction[low-glycogen (LG) trial] or CHO loading[moderate-to-high-glycogen (HG) trial]. In the LG and HGtrials, subjects ingested 4 ml/kg body wt of an 8% corn-derivedglucose solution of high natural¹³C abundance at the start,followed by boluses of 2 ml/kg every 15 min. The third trial, in whichpotato-derived glucose was ingested, served as a control test forbackground correction. Exogenous glucose oxidation rates werecalculated from the ¹³C enrichmentof the ingested glucose and of the breathCO₂. Total CHO oxidation was lowerin the LG trial than in the HG trial during 60-120 min of exercise[84 ± 7 (SE) vs. 116 ± 8 g;P < 0.05]. Exogenous CHOoxidation in this period was 28% lower in the LG trial compared withthe HG trial. Maximal exogenous oxidation rates were also lower(P < 0.05) in the LG trial (0.64 ± 0.05 g/min) than in the HG trial (0.88 ± 0.04 g/min). Thisdecreased utilization of exogenous glucose was accompanied by increased plasma free fatty acid levels (2-3 times higher) and lower insulin concentrations. It is concluded that glycogen-lowering exercise, performed the evening before an exercise bout, in combination with CHOrestriction leads to a reduction of the oxidation rate of ingestedglucose during moderate-intensity 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.

     

Effect of heat stress on glucose kinetics during exercise

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

     

Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise

Barstow, Thomas J., Andrew M. Jones, Paul H. Nguyen, andRichard Casaburi. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.J. Appl. Physiol. 81(4):1642-1650, 1996.We tested the hypothesis that the amplitude ofthe additional slow component ofO₂ uptake(O₂) during heavy exerciseis correlated with the percentage of type II (fast-twitch) fibers inthe contracting muscles. Ten subjects performed transitions to a workrate calculated to require aO₂ equal to 50% betweenthe estimated lactate (Lac) threshold and maximalO₂ (50%).Nine subjects consented to a muscle biopsy of the vastus lateralis. Toenhance the influence of differences in fiber type among subjects,transitions were made while subjects were pedaling at 45, 60, 75, and90 rpm in different trials. Baseline O₂ was designed to besimilar at the different pedal rates by adjusting baseline work ratewhile the absolute increase in work rate above the baseline was thesame. The O₂ response after the onset of exercise was described by a three-exponential model. Therelative magnitude of the slow component at the end of 8-min exercisewas significantly negatively correlated with %type I fibers at everypedal rate (r = 0.64 to 0.83, P < 0.05-0.01). Furthermore,the gain of the fast component forO₂ (asml ^· min^{1 ·} W¹)was positively correlated with the %type I fibers across pedal rates(r = 0.69-0.83). Increase inpedal rate was associated with decreased relative stress of theexercise but did not affect the relationships between%fiber type and O₂parameters. The relative contribution of the slow component was alsosignificantly negatively correlated with maximalO₂(r = 0.65), whereas the gainfor the fast component was positively associated(r = 0.68-0.71 across rpm). Theamplitude of the slow component was significantly correlated with netend-exercise Lac at all four pedal rates(r = 0.64-0.84), but Lac was notcorrelated with %type I (P > 0.05).We conclude that fiber type distribution significantly affects both thefast and slow components ofO₂ during heavy exerciseand that fiber type and fitness may have both codependent andindependent influences on the metabolic and gas-exchange responses toheavy exercise.

     

Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise

We used anexercise paradigm with repeated bouts of heavy forearm exercise to testthe hypothesis that alterations in local acid-base environment thatremain after the first exercise result in greater blood flow andO₂ delivery at the onset of the second bout of exercise.Two bouts of handgrip exercise at 75% peak workload were performed for5 min, separated by 5 min of recovery. We continuously measured bloodflow using Doppler ultrasound and sampled venous blood forO₂ content, PCO₂, pH, and lactateand potassium concentrations, and we calculated muscle O₂uptake (O₂). Forearm blood flow waselevated before the second exercise compared with the first andremained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was notdifferent at 5 min. Arteriovenous O₂ content difference waslower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 mlO₂/dl) and higher by 30 s of exercise(11.2 ± 0.7 vs. 10.8 ± 0.7 ml O₂/dl,P < 0.05). Muscle O₂was unchanged before the start of exercise but was elevated during thefirst 30 s of the transition to the second exercise bout(26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood PCO₂, pH, andlactate concentration were consistent with reduced reliance onanaerobic glycolysis at the onset of the second exercise bout. Thesedata show that limitations of muscle blood flow can restrict theadaptation of oxidative metabolism at the onset of heavy muscular exertion.

     

Effect of prolonged, heavy exercise on pulmonary gas exchange in athletes

During maximalexercise, ventilation-perfusion inequality increases, especially inathletes. The mechanism remains speculative. Wehypothesized that, if interstitial pulmonary edema is involved, prolonged exercise would result in increasing ventilation-perfusion inequality over time by exposing the pulmonary vascular bed to highpressures for a long duration. The response to short-term exercise wasfirst characterized in six male athletes [maximal O₂ uptake(O_{2 max}) = 63 ml · kg¹ · min¹] by using 5 minof cycling exercise at 30, 65, and 90%O_{2 max}. Multiple inert-gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained. Resting log SD of the perfusion distribution (logSD) was normal [0.50 ± 0.03 (SE)] and increased with exercise (logSD = 0.65 ± 0.04, P < 0.005), alveolar-arterialO₂ difference increased (to 24 ± 3 Torr), and end-capillary pulmonary diffusion limitation occurred at 90%O_{2 max}. The subjectsrecovered for 30 min, then, after resting measurements were taken,exercised for 60 min at ~65%O_{2 max}.O₂ uptake, ventilation, cardiacoutput, and alveolar-arterial O₂difference were unchanged after the first 5 min of this test, but logSD increased from0.59 ± 0.03 at 5 min to 0.66 ± 0.05 at 60 min(P < 0.05), without pulmonary diffusion limitation. LogSD was negativelyrelated to total lung capacity normalized for body surface area(r = 0.97,P < 0.005 at 60 min). These data are compatible with interstitial edema as a mechanism and suggest that lungsize is an important determinant of the efficiency of gas exchangeduring exercise.

     

Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion

Hinchcliff, K. W., K. H. McKeever, W. W. Muir, and R. A. Sams. Furosemide reduces accumulated oxygen deficit inhorses during brief intense exertion. J. Appl.Physiol. 81(4): 1550-1554, 1996.We theorizedthat furosemide-induced weight reduction would reduce the contributionof anaerobic metabolism to energy expenditure of horses during intenseexertion. The effects of furosemide on accumulatedO₂ deficit and plasma lactateconcentration of horses during high-intensity exercise were examined ina three-way balance randomized crossover study. Nine horses completedeach of three trials: 1) a control(C) trial, 2) a furosemide-unloaded(FU) trial in which the horse received furosemide 4 h before running, and 3) a furosemide weight-loaded(FL) trial during which the horse received furosemide and carriedweight equal to the weight lost after furosemide administration. Horsesran for 2 min at ~120% maximalO₂ consumption. Furosemide (FU)increased O₂ consumption (ml ^· 2 min^{1 ·} kg¹)compared with C (268 ± 9 and 257 ± 9, P < 0.05), whereas FL was notdifferent from C (252 ± 8). AccumulatedO₂ deficit (ml O₂ equivalents/kg) wassignificantly (P < 0.05) lowerduring FU (81.2 ± 12.5), but not during FL (96.9 ± 12.4), thanduring C (91.4 ± 11.5). Rate of increase in blood lactateconcentration (mmol ^· 2 min^{1 ·} kg¹)after FU (0.058 ± 0.001), but not after FL (0.061 ± 0.001), was significantly (P < 0.05) lower than after C (0.061 ± 0.001). Furosemide decreased theaccumulated O₂ deficit and rate ofincrease in blood lactate concentration of horses during briefhigh-intensity exertion. The reduction in accumulatedO₂ deficit in FU-treated horseswas attributable to an increase in the mass-specific rate ofO₂ consumption during thehigh-intensity exercise test.

     

Ventilatory response to exercise in subjects breathing CO2 or HeO2

Babb, T. G. Ventilatory response to exercise insubjects breathing CO₂ orHeO₂.J. Appl. Physiol. 82(3): 746-754, 1997.To investigate the effects of mechanical ventilatory limitationon the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycleergometry to exhaustion once while breathing room air; once whilebreathing 3% CO₂-21%O₂-balanceN₂; and once while breathing HeO₂ (79% He and 21%O₂). Minute ventilation(E) and respiratory mechanics weremeasured continuously during each 1-min increment in work rate (10 or20 W). Data were analyzed at rest, at ventilatory threshold (VTh),and at maximal exercise. When the subjects were breathing 3%CO₂, there was an increase(P < 0.001) inE at rest and at VTh but not duringmaximal exercise. When the subjects were breathingHeO₂,E was increased(P < 0.05) only during maximalexercise (24 ± 11%). The ventilatory response to exercise belowVTh was greater only when the subjects were breathing 3% CO₂(P < 0.05). Above VTh, theventilatory response when the subjects were breathingHeO₂ was greater than whenbreathing 3% CO₂(P < 0.01). Flow limitation, aspercent of tidal volume, during maximal exercise was greater(P < 0.01) when the subjects werebreathing CO₂ (22 ± 12%) thanwhen breathing room air (12 ± 9%) or when breathingHeO₂ (10 ± 7%)(n = 7). End-expiratory lung volumeduring maximal exercise was lower when the subjects were breathingHeO₂ than when breathing room airor when breathing CO₂(P < 0.01). These data indicate thatolder subjects have little reserve for accommodating an increase inventilatory demand and suggest that mechanical ventilatory constraintsinfluence both the magnitude of Eduring maximal exercise and the regulation ofE and respiratory mechanics duringheavy-to-maximal exercise.

     

Effects of N2O narcosis on breathing and effort sensations during exercise and inspiratory resistive loading

Fothergill, D. M., and N. A. Carlson. Effects ofN₂O narcosis on breathing andeffort sensations during exercise and inspiratory resistive loading.J. Appl. Physiol. 81(4):1562-1571, 1996.The influence of nitrous oxide(N₂O) narcosis on the responses toexercise and inspiratory resistive loading was studied in thirteen maleUS Navy divers. Each diver performed an incremental bicycle exercisetest at 1 ATA to volitional exhaustion while breathing a 23%N₂O gas mixture and a nonnarcoticgas of the same PO₂, density, andviscosity. The same gas mixtures were used during four subsequent30-min steady-state submaximal exercise trials in which the subjectsbreathed the mixtures both with and without an inspiratory resistance(5.5 vs. 1.1 cmH₂O ^· s ^· l¹at 1 l/s). Throughout each test, subjective ratings of respiratory effort (RE), leg exertion, and narcosis were obtained with acategory-ratio scale. The level of narcosis was rated between slightand moderate for the N₂O mixturebut showed great individual variation. Perceived leg exertion and thetime to exhaustion were not significantly different with the twobreathing mixtures. Heart rate was unaffected by the gas mixture andinspiratory resistance at rest and during steady-state exercise but wassignificantly lower with the N₂O mixture during incremental exercise (P < 0.05). Despite significant increases in inspiratory occlusionpressure (13%; P < 0.05),esophageal pressure (12%; P < 0.001), expired minute ventilation (4%;P < 0.01), and the work rate ofbreathing (15%; P < 0.001) when the subjects breathed the N₂O mixture,RE during both steady-state and incremental exercise was 25% lowerwith the narcotic gas than with the nonnarcotic mixture(P < 0.05). We conclude that the narcotic-mediated changes in ventilation, heart rate, and RE induced by23% N₂O are not of sufficientmagnitude to influence exercise tolerance at surface pressure.Furthermore, the load-compensating respiratory reflexes responsible formaintaining ventilation during resistive breathing are not depressed byN₂O narcosis.

     

Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients

Grassi, Bruno, Claudio Marconi, Michael Meyer, Michel Rieu,and Paolo Cerretelli. Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients. J. Appl. Physiol. 82(6): 1952-1962, 1997.Metabolicand cardiovascular adjustments to various submaximal exercises wereevaluated in 82 heart transplant recipients (HTR) and in 35 controlsubjects (C). HTR were tested 21.5 ± 25.3 (SD) mo (range1.0-137.1 mo) posttransplantation. Three protocols were used:protocol A consisted of 5 min of rectangular 50-W load repeatedtwice, 5 min apart [5 min rest, 5 min 50 W (Ex 1), 5 minrecovery, 5 min 50 W (Ex 2)]; protocol B consistedof 5 min of rectangular load at 25, 50, or 75 W; protocol Cconsisted of 15 min of rectangular load at 25 W. Breath-by-breathpulmonary ventilation (E),O₂ uptake (O₂),and CO₂ output(CO₂) were determined.During protocol A, beat-by-beat cardiacoutput () was estimated by impedance cardiography. The half times (t_1/2) of the on- andoff-kinetics of the variables were calculated. In all protocols,t_1/2 values forO₂ on-,E on-, andCO₂ on-kinetics were higher(i.e., the kinetics were slower) in HTR than in C, independently ofworkload and of the time posttransplantation. Also,t_1/2 on- was higher in HTRthan in C. In protocol A, no significant difference of t_1/2 O₂on- was observed in HTR between Ex 1 (48 ± 9 s) and Ex2 (46 ± 8 s), whereas t_1/2 on- was higher during Ex 1 (55 ± 24 s)than during Ex 2 (47 ± 15 s). In all protocols and for all variables, the t_1/2 off-values were higher in HTRthan in C. In protocol C, no differences of steady-stateE,O₂, andCO₂ were observed in bothgroups between 5, 10, and 15 min of exercise. We conclude that1) in HTR, a "priming" exercise, while effective inspeeding up the adjustment of convective O₂ flow to muscle fibers during a second on-transition, did not affect theO₂ on-kinetics, suggestingthat the slower O₂ on- inHTR was attributable to peripheral (muscular) factors; 2) thedissociation between on- andO₂ on-kinetics in HTRindicates that an inertia of muscle metabolic machinery is the mainfactor dictating theO₂ on-kinetics; and 3) theO₂ off-kinetics was slowerin HTR than in C, indicating a greater alactic O₂ deficitin HTR and, therefore, a sluggish muscleO₂ adjustment.

     

Effect of increased blood glucose availability on glucose kinetics during exercise

This studyexamined the effect of increased blood glucose availability on glucosekinetics during exercise. Five trained men cycled for 40 min at 77 ± 1% peak oxygen uptake on two occasions. During the second trial(Glu), glucose was infused at a rate equal to the average hepaticglucose production (HGP) measured during exercise in the control trial(Con). Glucose kinetics were measured by a primed continuous infusionofD-[3-³H]glucose.Plasma glucose increased during exercise in both trials and wassignificantly higher in Glu. HGP was similar at rest (Con, 11.4 ± 1.2; Glu, 10.6 ± 0.6µmol · kg¹ · min¹).After 40 min of exercise, HGP reached a peak of 40.2 ± 5.5 µmol · kg¹ · min¹in Con; however, in Glu, there was complete inhibition of the increasein HGP during exercise that never rose above the preexercise level. Therate of glucose disappearance was greater(P < 0.05) during the last 15 min ofexercise in Glu. These results indicate that an increase in glucoseavailability inhibits the rise in HGP during exercise, suggesting thatmetabolic feedback signals can override feed-forward activation of HGPduring strenuous exercise.

     

Phosphocreatine hydrolysis during submaximal exercise: the effect of FIO2

There isevidence that the concentration of the high-energy phosphatemetabolites may be altered during steady-state submaximal exerciseby the breathing of different fractions of inspiredO₂ (FI_O2). Whereasit has been suggested that these changes may be the result ofdifferences in time taken to achieve steady-state O₂ uptake(O₂) at differentFI_O2 values, we postulated that they are due to a direct effect ofO₂ tension. We used³¹P-magnetic resonancespectroscopy during constant-load, steady-state submaximal exercise todetermine 1) whether changes inhigh-energy phosphates do occur at the sameO₂ with variedFI_O2 and2) that these changes are not due todifferences in O₂onset kinetics. Six male subjects performed steady-state submaximal plantar flexion exercise [7.2 ± 0.6 (SE) W] for 10 minwhile lying supine in a 1.5-T clinical scanner. Magnetic resonancespectroscopy data were collected continuously for 2 min beforeexercise, 10 min during exercise, and 6 min during recovery. Subjectsperformed three different exercise bouts at constant load with theFI_O2 switched after 5 min ofthe 10-min exercise bout. The three exercise treatments were1)FI_O2 of 0.1 switched to0.21, 2)FI_O2 of 0.1 switched to1.00, and 3)FI_O2 of 1.00 switched to0.1. For all three treatments, theFI_O2 switch significantly (P  0.05) altered phosphocreatine:1) 55.5 ± 4.8 to 67.8 ± 4.9% (%rest); 2) 59.0 ± 4.3 to72.3 ± 5.1%; and 3) 72.6 ± 3.1 to 64.2 ± 3.4%, respectively. There were no significantdifferences in intracellular pH for the three treatments. The resultsdemonstrate that the differences in phosphocreatine concentration withvaried FI_O2 are not theresult of different O₂onset kinetics, as this was eliminated by the experimental design.These data also demonstrate that changes in intracellular oxygenation,at the same work intensity, result in significant changes in cell homeostasis and thereby suggest a role for metabolic control by O₂ even during submaximalexercise.

     

Fluid regulatory hormone response to exercise after coca-induced body fluid shifts

Favier, R., E. Caceres, B. Sempore, J. M. Cottet-Emard, G. Gauquelin, C. Gharib, and H. Spielvogel. Fluidregulatory hormone response to exercise after coca-induced body fluidshifts. J. Appl. Physiol. 83(2):376-382, 1997.To determine the effect of coca chewing on heartrate (HR), mean arterial blood pressure (MAP), and plasma volume andtheir relationship with the hormones regulating cardiovascular and bodyfluid homeostasis, 16 male volunteers were examined at rest and during1 h of cycle exercise at ~75% of their peak oxygen uptake in twotrials separated by 1 mo. One trial was performed after the subjectschewed a sugar-free chewing gum(Coca trial), whereas theother was done after the subjects chewed 15 g of coca leaves(Coca⁺), with the order of theCoca andCoca⁺ trials being randomized.Blood samples were taken at rest, before (R₁) and after 1-h chewing(R₂), and during the 5th, 15th,30th, and 60th min of exercise. They were analyzed for hematocrit,hemoglobin concentration, red blood cell count, plasma proteins, andfor the fluid regulatory hormones, including plasma catecholamines [norepinephrine (NE) and epinephrine], renin, argininevasopressin, and the atrial natriuretic peptide (ANP). During thecontrol trial (Coca),from R₁ toR₂, there was no significantchange in hematologic, hormonal, and cardiovascular status except for asmall increase in plasma NE. In contrast, it can be calculated thatcoca chewing at rest induced a significant hemoconcentration(3.8 ± 1.3% in blood and 7.0 ± 0.7% in plasmavolume), increased NE and MAP, and reduced plasma ANP. Chewing cocabefore exercise reduced the body fluid shifts but enhanced HR responseduring exercise. These effects were not accompanied by changes in NE,epinephrine, renin, and arginine vasopressin plasma levels. Incontrast, plasma ANP response to exercise was lower during theCoca⁺ trial, suggesting thatcentral cardiac filling was reduced by coca use. It is likely that thereduction in body fluid volumes is a major contributing factor to thehigher HR at any given time of exercise after coca chewing.

     

Muscle capillarization, O2 diffusion distance, and VO2 kinetics in old and young individuals

Chilibeck, P. D., D. H. Paterson, D. A. Cunningham, A. W. Taylor, and E. G. Noble. Muscle capillarization,O₂ diffusion distance, andO₂ kinetics in old andyoung individuals. J. Appl. Physiol.82(1): 63-69, 1997.The relationships between muscle capillarization, estimated O₂diffusion distance from capillary to mitochondria, andO₂ uptake(O₂) kineticswere studied in 11 young (mean age, 25.9 yr) and 9 old (mean age, 66.0 yr) adults. O₂kinetics were determined by calculating the time constants () forthe phase 2 O₂ adjustment to andrecovery from the average of 12 repeats of a 6-min, moderate-intensityplantar flexion exercise. Muscle capillarization was determined fromcross sections of biopsy material taken from lateral gastrocnemius.Young and old groups had similarO₂ kinetics(O₂-on = 44 vs. 48 s;O₂-off = 33 vs. 44 s, for young and old, respectively), muscle capillarization, andestimated O₂ diffusion distances.Muscle capillarization, expressed as capillary density or averagenumber of capillary contacts per fiber/average fiber area, and theestimates of diffusion distance were significantly correlated toO₂-off kinetics in theyoung (r = 0.68 to 0.83;P < 0.05). We conclude that1) capillarization andO₂ kinetics during exerciseof a muscle group accustomed to everyday activity (e.g., walking) arewell maintained in old individuals, and2) in the young, recovery of O₂ after exercise isfaster, with a greater capillary supply over a given muscle fiber areaor shorter O₂ diffusion distances.

     

Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training

It is welldocumented that endurance exercise training results in a bluntednorepinephrine (NE) response to exercise of a given absolute exerciseintensity. However, it is not clear what effect traininghas on the catecholamine response to exercise of the same relativeintensity because previous studies have provided conflicting results.The purpose of the present study was, therefore, to determine thecatecholamine response to exercise of the same relative exerciseintensity before and after endurance exercise training. Six women andthree men [age 28 ± 8 (SD) yr] performed 10 wk oftraining. Maximal O₂ uptake(O_{2 max}) wasdetermined during treadmill exercise. Fifteen-minute treadmill exercisebouts were performed at 60, 65, 70, 75, 80, and 85% ofO_{2 max} before andafter training.O_{2 max} was increasedby 20% (from 39.2 ± 7.7 to 46.9 ± 8.1 ml · kg¹ · min¹;P < 0.05) in response to training.Plasma NE concentrations were higher(P < 0.05) during exercise at thesame relative intensity after, compared with before, training at65-85% ofO_{2 max.}Differences between heart rates and plasma epinephrine concentrationsafter, compared with before, training were not statisticallysignificant. These results provide evidence that the NE response toexercise is dependent on the absolute as well as the relative intensity of the exercise.     

Reduced blood flow in abdominal viscera measured by Doppler ultrasound during one-legged knee extension

The redistributionof blood flow (BF) in the abdominal viscera during right-legged kneeextension-flexion exercise at very low intensity [peak heart rate(HR), 76 beats/min] was examined by using Doppler ultrasound.While sitting, subjects performed a right-legged knee extension-flexionexercise every 6 s for 20 min. BF was measured in the upper abdominalaorta (Ao), right common femoral artery (RCFA), and left common femoralartery (LCFA). Visceral BF(BF_Vis) was determined by theequation [BF_Ao  (BF_RCFA + BF_LCFA)]. A comparisonwith the change in BF (BF) preexercise showed a greater increase inBF_RCFA than inBF_Ao during exercise. Thisresulted in a reduction of BF_Visto 56% of its preexercise value or a decrease in flow by 1,147 ± 293 (±SE) ml/min at the peak workload. Oxygen consumptioncorrelated positively withBF_Ao, BF_RCFA, andBF_LCFA but inversely withBF_Vis during exercise andrecovery. Furthermore, BF_Vis (% of preexercise value) correlated inversely with both an increase in HR(r = 0.89), and percent peakoxygen consumption (r = 0.99).This study demonstrated that, even during very-low-intensity exercise(HR <90 beats/min), there was a significant shift in BF from theviscera to the exercising muscles.