Creatine supplementation increases muscle total creatine but not maximal intermittent exercise performance.

This study investigated creatine supplementation (CrS) effects on muscle total creatine (TCr), creatine phosphate (CrP), and intermittent sprinting performance by using a design incorporating the time course of the initial increase and subsequent washout period of muscle TCr. Two groups of seven volunteers ingested either creatine [Cr; 6 x (5 g Cr-H(2)O + 5 g dextrose)/day)] or a placebo (6 x 5 g dextrose/day) over 5 days. Five 10-s maximal cycle ergometer sprints with rest intervals of 180, 50, 20, and 20 s and a resting vastus lateralis biopsy were conducted before and 0, 2, and 4 wk after placebo or CrS. Resting muscle TCr, CrP, and Cr were unchanged after the placebo but were increased (P < 0.05) at 0 [by 22.9 +/- 4.2, 8.9 +/- 1.9, and 14.0 +/- 3.3 (SE) mmol/kg dry mass, respectively] and 2 but not 4 wk after CrS. An apparent placebo main effect of increased peak power and cumulative work was found after placebo and CrS, but no treatment (CrS) main effect was found on either variable. Thus, despite the rise and washout of muscle TCr and CrP, maximal intermittent sprinting performance was unchanged by CrS.     

Muscle metabolites and performance during high-intensity, intermittent exercise

Six men werestudied during four 30-s "all-out" exercise bouts on anair-braked cycle ergometer. The first three exercise bouts wereseparated by 4 min of passive recovery; after the third bout, subjectsrested for 4 min, exercised for 30 min at 30-35% peakO₂ consumption, and rested for afurther 60 min before completing the fourth exercise bout. Peak powerand total work were reduced (P < 0.05) during bout 3 [765 ± 60 (SE) W; 15.8 ± 1.0 kJ] compared withbout 1 (1,168 ± 55 W, 23.8 ± 1.2 kJ), but no difference in exercise performance was observed betweenbouts 1 and4 (1,094 ± 64 W, 23.2 ± 1.4 kJ). Before bout 3, muscle ATP,creatine phosphate (CP), glycogen, pH, and sarcoplasmic reticulum (SR)Ca²⁺ uptake were reduced, whilemuscle lactate and inosine 5'-monophosphate wereincreased. Muscle ATP and glycogen before bout4 remained lower than values beforebout 1 (P < 0.05), but there were no differences in muscle inosine 5'-monophosphate, lactate, pH, and SR Ca²⁺ uptake. Muscle CP levelsbefore bout 4 had increased aboveresting levels. Consistent with the decline in muscle ATP wereincreases in hypoxanthine and inosine before bouts3 and 4. The decline in exercise performance does not appear to be related to a reduction inmuscle glycogen. Instead, it may be caused by reduced CP availability, increased H⁺ concentration,impairment in SR function, or some other fatigue-inducing agent.

     

Effect of creatine supplementation on intermittent sprint running performance in highly trained athletes

This study examined the impact of short-term (7-day), high-dose (0.35 g.kg(-1).d(-1)) oral creatine monohydrate supplementation (CrS) on single sprint running performance (40 m, <6 seconds) and on intermittent sprint performance in highly trained sprinters. Nine subjects completed the double-blind cross-over design with 2 supplementation periods (placebo and creatine) and a 7-week wash-out period. A test protocol consisting of 40-m sprint runs was performed, and running velocity was continuously recorded over the total distance. The maximal sprint performance, the relative degree of fatigue at the end of intermittent sprint exercise (6 x 40 m, 30-second rest interval), as well as the degree of recovery (120-second passive rest) remained unchanged following CrS. There were no significant changes related to CrS in absolute running velocity at any distance between start and finish (40 m). It was concluded that no ergogenic effect on single or repeated 40-m sprint times with varying rest periods was observed in highly trained athletes.     

Muscle performance and enzymatic adaptations to sprint interval training

Our purpose was to examine the effects of sprintinterval training on muscle glycolytic and oxidative enzyme activityand exercise performance. Twelve healthy men (22 ± 2 yr of age)underwent intense interval training on a cycle ergometer for 7 wk.Training consisted of 30-s maximum sprint efforts (Wingate protocol)interspersed by 2-4 min of recovery, performed three times perweek. The program began with four intervals with 4 min of recovery persession in week 1 and progressed to 10 intervals with 2.5 min of recovery per session by week7. Peak power output and total work over repeated maximal 30-s efforts and maximal oxygen consumption(O_{2 max}) weremeasured before and after the training program. Needle biopsies weretaken from vastus lateralis of nine subjects before and after theprogram and assayed for the maximal activity of hexokinase, totalglycogen phosphorylase, phosphofructokinase, lactate dehydrogenase, citrate synthase, succinate dehydrogenase, malate dehydrogenase, and3-hydroxyacyl-CoA dehydrogenase. The training program resulted insignificant increases in peak power output, total work over 30 s, andO_{2 max}. Maximalenzyme activity of hexokinase, phosphofructokinase, citrate synthase,succinate dehydrogenase, and malate dehydrogenase was alsosignificantly (P < 0.05) higherafter training. It was concluded that relatively brief but intensesprint training can result in an increase in both glycolytic andoxidative enzyme activity, maximum short-term power output, andO_{2 max}.

     

Cytokine response to eccentric exercise in young and elderly humans

To examine the plasma interleukin(IL)-6 response in elderly (E) and young (Y) humans, 10 E and 10 Ysubjects completed 60 min of eccentric lower limb exercise at the samerelative oxygen uptake. Plasma IL-6 was measured before, immediatelyafter, and 5 days into recovery from exercise, as were the biochemicalmarkers of muscle damage, creatine kinase (CK), and myoglobin. In both groups, IL-6 increased (P < 0.05) immediately afterexercise and peaked 4 h after exercise at 4.35 ± 1.7 vs.5.05 ± 3.17 pg/ml for E and Y subjects, respectively. However,the increase in IL-6 in both groups was modest relative to theincreases in CK peaking at 539 ± 413 vs. 10,301 ± 5,863 U/lfor E and Y subjects, respectively. In addition, the increase in IL-6was less pronounced (P < 0.05) in E subjects comparedwith Y subjects. These results suggest that IL-6 increasesprogressively after eccentric exercise, suggesting that this increaseis related to muscle damage. However, the modest increase in IL-6,despite large increases in CK, suggests that the IL-6 response tomuscle damage does not make an important contribution to the largeincrease in IL-6 observed during concentric exercise of long duration.Our data also suggest that aging may be associated with impaired repairmechanisms for exercise-induced muscle damage.

     

Effects of 4 weeks of creatine supplementation in junior swimmers on freestyle sprint and swim bench performance

To determine whether 4 weeks of oral creatine (Cr) supplementation could enhance single freestyle sprint and swim bench performance in experienced competitive junior swimmers, 10 young men and 10 young women (x age = 16.4 +/- 1.8 years) participated in a 27-day supplementation period and pre- and posttesting sessions. In session 1 (presupplementation testing), subjects swam one 50-m freestyle and then (after approximately 5 minutes of active recovery) one 100-m freestyle at maximum speed. Blood lactate was measured before and 1 minute after each swim trial. Forty-eight hours later, height, mass, and the sum of 6 skinfolds were recorded, and a Biokinetic Swim Bench total work output test (2 x 30-second trials, with a 10-minute passive recovery in between) was undertaken. After the pretests were completed, participants were divided into 2 groups (n = 10, Cr; and n = 10, placebo) by means of matched pairs on the basis of gender and 50-m swim times. A Cr loading phase of 20 g x d(-1) for 5 days was then instituted, followed by a maintenance phase of 5 g x d(-1) for 22 days. Postsupplementation testing replicated the presupplementation tests. Four weeks of Cr supplementation did not influence single sprint performance in the pool or body mass and composition. However, 30-second swim bench total work scores for trial 1 and trial 2 increased after Cr (p < 0.05) but not placebo ingestion. Postexercise blood lactate values were not different after supplementation for the 50- and 100-m sprint trials either within or between groups. It was concluded that 4 weeks of Cr supplementation did not significantly improve single sprint performance in competitive junior swimmers, but it did enhance swim bench test performance.     

Effect of two different intense training regimens on skeletal muscle ion transport proteins and fatigue development

This study examined the effect of two different intense exercise training regimens on skeletal muscle ion transport systems, performance, and metabolic response to exercise. Thirteen subjects performed either sprint training [ST; 6-s sprints (n = 6)], or speed endurance training [SET; 30-s runs approximately 130% Vo(2 max), n = 7]. Training in the SET group provoked higher (P < 0.05) plasma K(+) levels and muscle lactate/H(+) accumulation. Only in the SET group was the amount of the Na(+)/H(+) exchanger isoform 1 (31%) and Na(+)-K(+)-ATPase isoform alpha(2) (68%) elevated (P < 0.05) after training. Both groups had higher (P < 0.05) levels of Na(+)-K(+)-ATPase beta(1)-isoform and monocarboxylate transporter 1 (MCT1), but no change in MCT4 and Na(+)-K(+)-ATPase alpha(1)-isoform. Both groups had greater (P < 0.05) accumulation of lactate during exhaustive exercise and higher (P < 0.05) rates of muscle lactate decrease after exercise. The ST group improved (P < 0.05) sprint performance, whereas the SET group elevated (P < 0.05) performance during exhaustive continuous treadmill running. Improvement in the Yo-Yo intermittent recovery test was larger (P < 0.05) in the SET than ST group (29% vs. 10%). Only the SET group had a decrease (P < 0.05) in fatigue index during a repeated sprint test. In conclusion, turnover of lactate/H(+) and K(+) in muscle during exercise does affect the adaptations of some but not all related muscle ion transport proteins with training. Adaptations with training do have an effect on the metabolic response to exercise and specific improvement in work capacity.     

Effect of ingested sodium bicarbonate on muscle force, fatigue, and recovery

Verbitsky, O., J. Mizrahi, M. Levin, and E. Isakov.Effect of ingested sodium bicarbonate on muscle force, fatigue, and recovery. J. Appl. Physiol. 83(2):333-337, 1997.The influence of acute ingestion ofNaHCO₃ on fatigue and recovery ofthe quadriceps femoris muscle after exercise was studied in six healthymale subjects. A bicycle ergometer was used for exercising under three loading conditions: test A, loadcorresponding to maximal oxygen consumption; testB, load in test A + 17%; test C, load intest B but performed 1 h after acuteingestion of NaHCO₃.Functional electrical stimulation (FES) was applied to provokeisometric contraction of the quadriceps femoris. The resulting kneetorque was monitored during fatigue (2-min chronic FES) and recovery (10-s FES every 10 min, for 40 min). Quadriceps torques were higher inthe presence of NaHCO₃(P < 0.05): withNaHCO₃ the peak, residual, andrecovery (after 40 min) normalized torques were, respectively, 0.68 ± 0.05 (SD), 0.58 ± 0.05, and 0.73 ± 0.05; withoutNaHCO₃ the values were 0.45 ± 0.04, 0.30 ± 0.06, and 0.63 ± 0.06. The increasedtorques obtained after acute ingestion ofNaHCO₃ indicate the possibleexistence of improved nonoxidative glycolysis in isometric contraction,resulting in reduced fatigue and enhanced recovery.

     

Normal forces and myofibrillar disruption after repeated eccentric exercise

Hortobágyi, Tibor, Joseph Houmard, David Fraser,Ronald Dudek, Jean Lambert, and James Tracy. Normalforces and myofibrillar disruption after repeated eccentric exercise.J. Appl. Physiol. 84(2): 492-498, 1998.To investigate the "rapid-adaptation" phenomenon, weexamined force, neural, and morphological adaptations in 12 subjectswho performed 100 eccentric contractions with the quadriceps muscle(bout 1) and repeated the sameexercise after a 2-wk hiatus (bout2). Two days after bout1, quadriceps muscle strength and surfaceelectromyographic (EMG) activity declined ~37 and 28%, respectively,in the control group (n = 6). Atday 2 after bout 1, significant increases occurred in patellar tendonreflex amplitude (~25%), muscle soreness (fivefold), and serumcreatine kinase (220%), and 65 ± 12% of the total number of pixelsin the EMG indicated myofibrillar disruption. At day7 after bout 1, all variables returned to normal. At day 2 after bout 2, no significant changesoccurred in force, EMG, creatine kinase, or soreness, but reflexamplitude increased, and 23 ± 4% of the total number of pixels inthe EMG still indicated myofibrillar disruption. The results suggestthat the rapid force recovery following eccentric exercise is mediatedat least in part by neural factors and that this recovery may occurindependently of cell disruption.

     

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.

     

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.

     

Effects of hindlimb contraction on pressor and muscle interstitial metabolite responses in the cat

We used the microdialysis technique to measurethe interstitial concentration of several putative metabolic stimulantsof the exercise pressor reflex during 3- and 5-Hz twitch contractions in the decerebrate cat. The peak increases in heart rate and mean arterial pressure during contraction were 20 ± 5 beats/min and 21 ± 8 mmHg and 27 ± 9 beats/min and 37 ± 12 mmHg for the 3- and 5-Hz stimulation protocols, respectively. All variables returned tobaseline after 10 min of recovery. Interstitial lactate rose (P < 0.05) by 0.41 ± 0.15 and0.56 ± 0.16 mM for the 3- and 5-Hz stimulation protocols,respectively, and were not statistically different from one another.Interstitial lactate levels remained above(P < 0.05) baseline during recoveryin the 5-Hz group. Dialysate phosphate concentrations (corrected forshifts in probe recovery) rose with stimulation(P < 0.05) by 0.19 ± 0.08 and0.11 ± 0.03 mM for the 3- and 5-Hz protocols. There were nodifferences between groups. The resting dialysateK⁺ concentrations for the 3- and5-Hz conditions were 4.0 ± 0.1 and 3.9 ± 0.1 meq/l,respectively. During stimulation the dialysate K⁺ concentrations rose steadilyfor both conditions, and the increase from rest to stimulation(P < 0.05) was 0.57 ± 0.19 and0.81 ± 0.06 meq/l for the 3- and 5-Hz conditions, respectively,with no differences between groups. Resting dialysate pH was6.915 ± 0.055 and 6.981 ± 0.032 and rose to 7.013 (P < 0.05) and 7.053 (P < 0.05) for the 3- and 5-Hzconditions, respectively, and then became acidotic (6.905, P < 0.05) during recovery (5 Hzonly). This study represents the first time simultaneous measurements of multiple skeletal muscle interstitial metabolites and pressor responses to twitch contractions have been made in the cat. These datasuggest that interstitial K⁺ andphosphate, but not lactate and H⁺,may contribute to the stimulation of thin fiber muscle afferents duringcontraction.

     

Role of muscular factors in cardiorespiratory responses to static exercise: contribution of reflex mechanisms

We investigated the effects of muscle mass and contractionintensity on the cardiorespiratory responses to static exercise and onthe contribution afforded by muscle metaboreflex and arterial baroreflex mechanisms. Ten subjects performed static handgrip at 30%maximal voluntary contraction (MVC) (SHG-30) and one-leg extension at15% (SLE-15) and 30% (SLE-30) MVC, followed by postexercise circulatory occlusion (PECO). Mean arterial pressure (MAP) and heartrate (HR) responses were greater during SLE-30 than during SHG-30. Thedifference in MAP was maintained by PECO, and the part of the pressorresponse maintained by PECO was greater after SLE-30 than after SHG-30(88.3 ± 10.6 and 67.8 ± 12.7%, respectively, P = 0.02). There were no differences in MAP and HR responses between SHG-30and SLE-15 trials. Baroreflex sensitivity was maintained during SHG-30and SLE-15, whereas it was significantly reduced during SLE-30 andrecovered back to the resting level during PECO. Minute ventilation andoxygen uptake increased more during SLE-30 than during both SHG-30 andSLE-15 trials. Minute ventilation remained significantly elevated aboverest only during PECO following SLE-30. These data suggest that duringstatic exercise the muscle mass and contraction intensity affect1) the magnitude of the cardiorespiratory responses,2) the contribution of muscle metaboreflex to thecardiorespiratory responses, and 3) the arterialbaroreflex contribution to HR control.

     

Phosphocreatine kinetics at the onset of contractions in skeletal muscle of MM creatine kinase knockout mice

Phosphocreatine (PCr) depletion duringisometric twitch stimulation at 5 Hz was measured by³¹P-NMR spectroscopy in gastrocnemius muscles ofpentobarbital-anesthetized MM creatine kinase knockout (MMKO) vs.wild-type C57B (WT) mice. PCr depletion after 2 s of stimulation,estimated from the difference between spectra gated to times 200 ms and140 s after 2-s bursts of contractions, was 2.2 ± 0.6% ofinitial PCr in MMKO muscle vs. 9.7 ± 1.6% in WT muscles(mean ± SE, n = 7, P < 0.001).Initial PCr/ATP ratio and intracellular pH were not significantlydifferent between groups, and there was no detectable change inintracellular pH or ATP in either group after 2 s. The initialdifference in net PCr depletion was maintained during the first minuteof continuous 5-Hz stimulation. However, there was no significantdifference in the quasi-steady-state PCr level approached after 80 s (MMKO 36.1 ± 3.5 vs. WT 35.5 ± 4.4% of initial PCr;n = 5-6). A kinetic model of ATPase, creatinekinase, and adenylate kinase fluxes during stimulation was consistentwith the observed PCr depletion in MMKO muscle after 2 s only ifADP-stimulated oxidative phosphorylation was included in the model.Taken together, the results suggest that cytoplasmic ADP more rapidlyincreases and oxidative phosphorylation is more rapidly activated atthe onset of contractions in MMKO compared with WT muscles.

     

Effects of intensity of acute-resistance exercise on rates of protein synthesis in moderately diabetic rats

Thesestudies determined whether increases in rates of protein synthesisobserved in skeletal muscle after moderate or severe acute-resistanceexercise were blunted by insulinopenia. Rats (n = 6-9 per group) were madeinsulin deficient by partial pancreatectomy or remained nondiabetic.Groups either remained sedentary or performed acute-resistance exercise16 h before rates of protein synthesis were measured in vivo. Exerciserequired 50 repetitions of standing on the hindlimbs with either 0.6 gbackpack wt/g body wt (moderate exercise) or 1.0 g backpack wt/g bodywt (severe exercise). Insulin-deficient rats had a mean blood glucoseconcentration >15 mM and reduced insulin concentrations in theplasma. Rates of protein synthesis in gastrocnemius muscle were notdifferent in all sedentary groups. The moderate-exercised nondiabeticgroup (192 ± 12 nmol phenylalanine incorporated · gmuscle¹ · h¹)and moderate-exercised diabetic group (215 ± 18) had significantly (P < 0.05, ANOVA) higher rates ofprotein synthesis than did respective sedentary groups. In contrast,diabetic rats that performed severe-resistance exercise had rates ofprotein synthesis (176 ± 12) that were not different(P > 0.05) from diabetic sedentaryrats (170 ± 9), whereas nondiabetic rats that performed severeexercise had higher (212 ± 24) rates compared withnondiabetic sedentary rats (178 ± 10) P < 0.05. The present data in combination with previous studies [J. D. Fluckey, T. C. Vary, L. S. Jefferson, and P. A. Farrell. Am. J. Physiol. 270 (Endocrinol. Metab. 33): E313-E319,1996] show that the amount of insulin required for an invivo permissive effect of insulin on rates of protein synthesis can bequite low after moderate-intensity resistance exercise. However, severe exercise in combination with low insulin concentrations can ablate ananabolic response.

     

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

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

     

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.

     

Almitrine and doxapram decrease fatigue and increase subsequent recovery in isolated rat diaphragm

McGuire, Michelle, Michael F. Carey, and John J. O'Connor.Almitrine and doxapram decrease fatigue and increase subsequent recovery in isolated rat diaphragm. J. Appl.Physiol. 83(1): 52-58, 1997.The effects ofalmitrine bimesylate and doxapram HCl on isometric force produced by invitro rat diaphragm were studied during direct muscle activation at37°C. Doxapram and almitrine ameliorate respiratory failureclinically by indirectly increasing phrenic nerve activity. This studywas carried out to investigate possible direct actions of these agentson the diaphragm before and after fatigue of the fibers. Two age groupsof animals were chosen [6-14 wk (group1) and 50-55 wk (group2)] because it is known that increasing agedecreases a muscle fiber's resistance to fatigue. Muscle strips wereisolated from both group 1 and group 2 and directly stimulated (2-mspulse duration, 5-15 V) to produce twitch tensions of 1.3 and 2.1 N/cm², respectively. At lowconcentrations, doxapram (20 µg/ml) and almitrine (12 µg/ml)had no effect on twitch contraction or 100-Hz tetanic tension. However,40 µg/ml doxapram and 30 µg/ml almitrine increased twitch tensionby 9.0 ± 1.4 and 11.6 ± 1.9%, respectively, in animals ofgroup 2 (n = 5). A fatigue protocol consistingof low-frequency stimulation (30-Hz trains, 250-ms duration every 2 sfor 5 min) caused a reduction of twitch tension in animals ofgroup 1 (48 ± 4% ofcontrol) and group 2 (28 ± 4% ofcontrol). At 90 min postfatigue, the twitch tension recovered to 72 ± 3 and 42 ± 2% of control values ingroup 1 and group2, respectively. In the presence of doxapram (20 µg/ml), there was a significant increase in the recovery of twitchtension at 90 min in group 1 andgroup 2 (84.5 ± 3.2 and 80.1 ± 2.8%, respectively) compared with controls at 90 min postfatigue. Inthe presence of almitrine (12 µg/ml), there was a full recovery fromfatigue in group 1 animals (100% ofcontrol) and a recovery to 95.6 ± 2.1% of control ingroup 2 animals at 90 min. Theseresults demonstrate a significant improvement in the rapidity andmagnitude of recovery from fatigue in the rat diaphragm muscle in thepresence of both doxapram and, especially, almitrine. These effects maybe due to changes in intracellular calcium, ADP/ATP ratios, or oxygenfree radical scavenging.

     

A moderate glycemic meal before endurance exercise can enhance performance

Kirwan, John P., Donal O'Gorman, and William J. Evans.A moderate glycemic meal before endurance exercise can enhance performance. J. Appl. Physiol. 84(1):53-59, 1998.The purpose of this study was to determine whetherpresweetened breakfast cereals with various fiber contents and amoderate glycemic index optimize glucose availability and improveendurance exercise performance. Six recreationally active women ate 75 g of available carbohydrate in the form of breakfast cereals: sweetenedwhole-grain rolled oats (SRO, 7 g of dietary fiber) or sweetenedwhole-oat flour (SOF, 3 g of dietary fiber) and 300 ml of water orwater alone (Con). The meals were provided 45 min before semirecumbentcycle ergometer exercise to exhaustion at 60% of peakO₂ consumption (O_{2 peak}). Diet andphysical activity were controlled by having the subjects reside in theGeneral Clinical Research Center for 2 days before each trial. Bloodsamples were drawn from an antecubital vein for glucose, free fattyacid (FFA), glycerol, insulin, epinephrine, and norepinephrinedetermination. Breath samples were obtained at 15-min intervals aftermeal ingestion and at 30-min intervals during exercise. Muscle glycogenconcentration was determined from biopsies taken from the vastuslateralis muscle before the meal and immediately after exercise. PlasmaFFA concentrations were lower (P < 0.05) during the SRO and SOF trials for the first 60 and 90 min ofexercise, respectively, than during the Con trial. Respiratory exchangeratios were higher (P < 0.05) at 90 and 120 min of exercise for the SRO and SOF trials, respectively, than for the Con trial. At exhaustion, glucose, insulin, FFA, glycerol, epinephrine, and norepinephrine concentrations, respiratory exchange ratio, and muscle glycogen use in the vastus lateralis muscle weresimilar for all trials. Exercise time to exhaustion was 16% longer(P < 0.05) during the SRO thanduring the Con trial: 266.5 ± 13 and 225.1 ± 8 min,respectively. There was no difference in exercise time for the SOF(250.8 ± 12) and Con trials. We conclude that eating ameal with a high dietary fiber content and moderate glycemic index 45 min before prolonged moderately intense exercise significantly enhancesexercise capacity.

     

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.