Effect of exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoA carboxylase

Rasmussen, B. B., and W. W. Winder. Effectof exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoAcarboxylase. J. Appl. Physiol. 83(4):1104-1109, 1997.Malonyl-CoA is synthesized by acetyl-CoAcarboxylase (ACC) and is an inhibitor of fatty acid oxidation. Exerciseinduces a decline in skeletal muscle malonyl-CoA, which is accompaniedby inactivation of ACC and increased activity of AMP-activated proteinkinase (AMPK). This study was designed to determine the effect ofexercise intensity on the enzyme kinetics of ACC, malonyl-CoA levels,and AMPK activity in skeletal muscle. Male Sprague-Dawley rats werekilled (pentobarbital sodium anesthesia) at rest or after 5 min ofexercise (10, 20, 30, or 40 m/min at 5% grade). The fast-twitch redand white regions of the quadriceps muscle were excised and frozen inliquid nitrogen. A progressive decrease in red quadriceps ACC maximalvelocity (from 28.6 ± 1.5 to 14.3 ± 0.7 nmol · g¹ · min¹,P < 0.05), an increase in activationconstant for citrate, and a decrease in malonyl-CoA (from 1.9 ± 0.2 to 0.9 ± 0.1 nmol/g, P < 0.05) were seen with theincrease in exercise intensity from rest to 40 m/min. AMPK activityincreased more than twofold. White quadriceps ACC activity decreasedonly during intense exercise. We conclude that the extent of ACCinactivation during short-term exercise is dependent on exerciseintensity.

     

Moderate exercise increases postexercise thresholds for vasoconstriction and shivering

The purpose of this study was to evaluate theeffect of exercise on the subsequent postexercise thresholds forvasoconstriction and shivering. On two separate days, with six subjects(3 women), a whole body water-perfused suit slowly decreased mean skintemperature (~7.0°C/h) until thresholds for vasoconstriction andshivering were clearly established. Subjects were then rewarmed byincreasing water temperature until both esophageal and mean skintemperatures returned to near-baseline values. Subjects eitherperformed 15 min of cycle ergometry (65% maximalO₂ consumption) followed by 30 minof recovery (Exercise) or remained seated with no exercise for 45 min(Control). Subjects were then cooled again. We mathematically compensated for changes in skin temperatures by using the established linear cutaneous contribution of skin to the control ofvasoconstriction and shivering (20%). The calculated core temperaturethreshold (at a designated skin temperature of 30.0°C) forvasoconstriction increased significantly from 36.64 ± 0.20 to 36.89 ± 0.22°C postexercise (P < 0.01). Similarly, the shivering threshold increased from 35.73 ± 0.13 to 36.13 ± 0.12°C postexercise(P < 0.01). In contrast, sequentialmeasurements, without exercise, demonstrate a time-dependent decreasein both the vasoconstriction (0.10°C) and shivering (0.12°C) thresholds. These data indicate that exercise has a prolonged effect byincreasing the postexercise thresholds for both cold thermoregulatoryresponses.

     

Effect of epinephrine on muscle glycogenolysis during exercise in trained men

Febbraio, M. A., D. L. Lambert, R. L. Starkie, J. Proietto,and M. Hargreaves. Effect of epinephrine on muscle glycogenolysis during exercise in trained men. J. Appl.Physiol. 84(2): 465-470, 1998.To test thehypothesis that an elevation in circulating epinephrine increasesintramuscular glycogen utilization, six endurance-trained men performedtwo 40-min cycling trials at 71 ± 2% of peak oxygen uptake in20-22°C conditions. On the first occasion, subjects wereinfused with saline throughout exercise (Con). One week later, afterdetermination of plasma epinephrine levels in Con, subjects performedthe second trial (Epi) with an epinephrine infusion, which resulted ina twofold higher (P < 0.01) plasmaepinephrine concentration in Epi compared with Con. Although oxygenuptake was not different when the two trials were compared, respiratoryexchange ratio was higher throughout exercise in Epi compared with Con(0.93 ± 0.01 vs. 0.89 ± 0.01; P < 0.05). Muscle glycogenconcentration was not different when the trials were comparedpreexercise, but the postexercise value was lower(P < 0.01) in Epi compared with Con.Thus net muscle glycogen utilization was greater during exercise withepinephrine infusion (224 ± 37 vs. 303 ± 30 mmol/kg for Con andEpi, respectively; P < 0.01). Inaddition, both muscle and plasma lactate and plasma glucoseconcentrations were higher (P < 0.05) in Epi compared with Con. These data indicate that intramuscularglycogen utilization, glycolysis, and carbohydrate oxidation areaugmented by elevated epinephrine during submaximal exercise in trainedmen.

     

Impaired calcium pump function does not slow relaxation in human skeletal muscle after prolonged exercise

Booth, John, Michael J. McKenna, Patricia A. Ruell, Tom H. Gwinn, Glen M. Davis, Martin W. Thompson, Alison R. Harmer, Sandra K. Hunter, and John R. Sutton. Impaired calcium pump function doesnot slow relaxation in human skeletal muscle after prolonged exercise.J. Appl. Physiol. 83(2): 511-521, 1997.This study examined the effects of prolonged exercise on humanquadriceps muscle contractile function and homogenate sarcoplasmicreticulum Ca²⁺ uptake andCa²⁺-adenosinetriphosphataseactivity. Ten untrained men cycled at 75 ± 2% (SE) peak oxygenconsumption until exhaustion. Biopsies were taken from theright vastus lateralis muscle at rest, exhaustion, and 20 and 60 minpostexercise. Peak tension and half relaxation time of the leftquadriceps muscle were measured during electrically evoked twitch andtetanic contractions and a maximal voluntary isometric contraction atrest, exhaustion, and 10, 20, and 60 min postexercise. At exhaustion,homogenate Ca²⁺ uptake andCa²⁺ adenosinetriphosphataseactivity were reduced by 17 ± 4 and 21 ± 5%, respectively, andremained depressed after 60 min recovery (P  0.01). Muscle ATP, creatinephosphate, and glycogen were all depressed at exhaustion(P  0.01). Peak tension during a maximal voluntary contraction, a twitch, and a 10-Hz stimulation werereduced after exercise by 28 ± 3, 45 ± 6, 65 ± 5%,respectively (P  0.01), but noslowing of half relaxation times were found. Thus fatigue induced byprolonged exercise reduced muscleCa²⁺ uptake, but this did notcause a slower relaxation of evoked contractions.

     

Endurance training attenuates the decrease in skeletal muscle malonyl-CoA with exercise

Hutber, C. Adrian, B. B. Rasmussen, and W. W. Winder.Endurance training attenuates the decrease in skeletal muscle malonyl-CoA with exercise. J. Appl.Physiol. 83(6): 1917-1922, 1997.Musclemalonyl-CoA has been postulated to regulate fatty acid metabolism byinhibiting carnitine palmitoyltransferase 1. In nontrained rats,malonyl-CoA decreases in working muscle during exercise. Endurancetraining is known to increase a muscle's reliance on fatty acids as asubstrate. This study was designed to investigate whether the declinein malonyl-CoA with exercise would be greater in trained than innontrained muscle, thereby allowing increased fatty acid oxidation.After 6-10 wk of endurance training (2 h/day) or treadmillhabituation (5-10 min/day), rats were killed at rest or afterrunning up a 15% grade at 21 m/min for 5, 20, or 60 min. Trainingattenuated the exercise-induced drop in malonyl-CoA and prevented theexercise-induced increase in the constant for citrate activation ofacetyl-CoA carboxylase in the red quadriceps muscle of rats run for 20 and 60 min. Hence, contrary to expectations, the decrease inmalonyl-CoA was less in trained than in nontrained muscle during asingle bout of prolonged submaximal exercise.

     

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.

     

Effect of caffeinated drinks on substrate metabolism, caffeine excretion, and performance

The effect ofaddition of different dosages of caffeine (Caf) to acarbohydrate-electrolyte solution (CES) on metabolism, Caf excretion,and performance was examined. Subjects(n = 15) ingested 8 ml/kg of waterplacebo (Pla-W), 7% CES (Pla-CES), or 7% CES with 150, 225, and 320 mg/l Caf (CES-150, CES-225, and CES-320, respectively) during a warm-upprotocol (20 min) and 3 ml/kg at one-third and two-thirds of a 1-h timetrial. Performance was improved with Caf supplementation: 62.5 ± 1.3, 61.5 ± 1.1, 60.4 ± 1.0, 58.9 ± 1.0, and 58.9 ± 1.2 min for Pla-W, Pla-CES, CES-150, CES-225, and CES-320, respectively.The postexercise urinary Caf concentration (range 1.3-2.5 µg/ml)was dose dependent and always far below the doping level of theInternational Olympic Committee (12 µg/ml) in all subjects. Sweat Cafexcretion during exercise exceeded postexercise early-void urinary Cafexcretion. Caffeinated CES did not enhance free fatty acidavailability, ruling out the fact that performance improvement resultedfrom enhanced fat oxidation. It is concluded that addition ofrelatively low amounts of Caf to CES improves performance and thatpostexercise urinary Caf concentration remained low.

     

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.

     

Enhanced muscle glucose uptake facilitates nitrogen efflux from exercised muscle

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

     

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.

     

Hormonal responses to consecutive days of heavy-resistance exercise with or without nutritional supplementation

Nineresistance-trained men consumed either a protein-carbohydratesupplement or placebo for 1 wk in a crossover design separated by 7 days. The last 3 days of each treatment, subjects performed resistanceexercise. The supplement was consumed 2 h before and immediately afterthe workout, and blood was obtained before and after exercise (0, 15, 30, 45, and 60 min postexercise). Lactate, growth hormone, andtestosterone were significantly (P  0.05) elevated immediately postexercise. The lactate response wassignificantly lower during supplementation on days2 and 3. Growthhormone and prolactin responses on day1 were significantly higher during supplementation.After exercise, testosterone declined below resting values duringsupplementation. Cortisol decreased immediately postexercise onday 1; the response was diminished ondays 2 and 3. Glucose and insulin weresignificantly elevated by 30 min during supplementation and remainedstable during placebo. Insulin-like growth factor-I was higher duringsupplementatiom on days 2 and 3. These data indicate thatprotein-carbohydrate supplementation before and after training canalter the metabolic and hormonal responses to consecutive days ofheavy-resistance 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.

     

Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise

The provision of additional protein (Pro)to a carbohydrate (CHO) supplement resulted in an enhanced rate ofmuscle glycogen resynthesis after endurance exercise (Zawadzki et al.,J. Appl. Physiol. 72: 1854-1859,1992). A comparison of isoenergetic CHO and CHO/Pro formula drinks onmuscle glycogen resynthesis has not been examined after eitherendurance or resistance exercise. We studied the effect of isoenergeticCHO (1 g/kg) and CHO/Pro/fat (66% CHO, 23% Pro, 11% fat) definedformula drinks and placebo (Pl) given immediately(t = 0 h) and 1 h(t = +1 h) after resistance exercisein 10 healthy young men. They performed a whole body workout (9 exercises/3 sets at 80% 1 repetition maximum) with unilateral kneeextension exercise [exercise (Ex) and control (Con) leg].The CHO/Pro/fat and CHO trials resulted in significantly greater(P < 0.05) plasma insulin andglucose concentration compared with Pl. Muscle glycogen wassignificantly lower (P < 0.05) for the Ex vs. Con leg immediately postexercise for all three conditions. The rate of glycogen resynthesis was significantly greater(P < 0.05) for both CHO/Pro/fat andCHO (23.0 ± 4.5 and 19.3 ± 6.1 mmol · kg drymuscle¹ · h¹,respectively) vs. Pl (Ex = 2.8 ± 2.3 and Con = 1.4 ± 3.6 mmol · kg drymuscle¹ · h¹).These results demonstrated that a bout of resistance exercise resultedin a significant decrease in muscle glycogen and that consumption of anisoenergetic CHO or CHO/Pro/fat formula drink resulted in similar ratesof muscle glycogen resynthesis after resistance exercise. This suggeststhat total energy content and CHO content are important in theresynthesis of muscle glycogen.

     

Muscle glycogen accumulation after endurance exercise in trained and untrained individuals

Hickner, R. C., J. S. Fisher, P. A. Hansen, S. B. Racette,C. M. Mier, M. J. Turner, and J. O. Holloszy. Muscle glycogen accumulation after endurance exercise in trained and untrained individuals. J. Appl. Physiol. 83(3):897-903, 1997.Muscle glycogen accumulation was determined in sixtrained cyclists (Trn) and six untrained subjects (UT) at 6 and either48 or 72 h after 2 h of cycling exercise at ~75% peakO₂ uptake(O_{2 peak}), which terminated with five 1-min sprints. Subjects ate 10 gcarbohydrate · kg¹ · day¹for 48-72 h postexercise. Muscle glycogen accumulation averaged 71 ± 9 (SE) mmol/kg (Trn) and 31 ± 9 mmol/kg (UT) during the first 6 h postexercise (P < 0.01) and 79 ± 22 mmol/kg (Trn) and 60 ± 9 mmol/kg (UT) between 6 and 48 or 72 h postexercise (not significant). Muscle glycogenconcentration was 164 ± 21 mmol/kg (Trn) and 99 ± 16 mmol/kg(UT) 48-72 h postexercise (P < 0.05). Muscle GLUT-4 content immediately postexercise was threefoldhigher in Trn than in UT (P < 0.05)and correlated with glycogen accumulation rates (r = 0.66, P < 0.05). Glycogen synthase in theactive I form was 2.5 ± 0.5, 3.3 ± 0.5, and 1.0 ± 0.3 µmol · g¹ · min¹in Trn at 0, 6, and 48 or 72 h postexercise, respectively;corresponding values were 1.2 ± 0.3, 2.7 ± 0.5, and 1.6 ± 0.3 µmol · g¹ · min¹in UT (P < 0.05 at 0 h). Plasmainsulin and plasma C-peptide area under the curve were lower in Trnthan in UT over the first 6 h postexercise(P < 0.05). Plasma creatine kinaseconcentrations were 125 ± 25 IU/l (Trn) and 91 ± 9 IU/l (UT)preexercise and 112 ± 14 IU/l (Trn) and 144 ± 22 IU/l(UT; P < 0.05 vs.preexercise) at 48-72 h postexercise (normal: 30-200 IU/l).We conclude that endurance exercise training results in an increasedability to accumulate muscle glycogen after exercise.

     

Fibrinolytic responses to acute physical activity in older hypertensive men

DeSouza, Christopher A., Donald R. Dengel, Marc A. Rogers,Kim Cox, and Richard F. Macko. Fibrinolytic responsesto acute physical activity in older hypertensive men.J. Appl. Physiol. 82(6):1765-1770, 1997.We tested the hypothesis that the fibrinolytic response to acute physical activity is impaired in sedentary older hypertensive men, which may contribute to the risk ofexertion-triggered acute myocardial infarction in this population.Tissue-type plasminogen activator (t-PA) antigen and activity andplasminogen activator inhibitor-1 (PAI-1) antigen and activity weremeasured in 12 hypertensive (69 ± 1 yr) and 11 normotensive (64 ± 1 yr) men before and after an acute bout of submaximal exercise.Contrary to our hypothesis, there were no differences between the twogroups in the fibrinolytic response to exercise. t-PA antigen andactivity were significantly elevated in both the hypertensive (38 and172%, respectively) and normotensive (45 and 130%, respectively)groups immediately after exercise but they returned to resting levelswithin 30 min. There was no change in PAI-1 antigen levels immediatelyafter exercise in either group; however, PAI-1 antigen wassignificantly lower at 30 and 60 min postexercise in both thehypertensive (31 and 16%, respectively) and normotensive (35 and 20%,respectively) groups. PAI-1 activity was significantly lowerimmediately after exercise in both the hypertensive (25%) andnormotensive (22%) groups and remained lower than preexercise levelsat 30 min (23 and 26%, respectively) and 60 min (16 and 12%,respectively) postexercise in both groups. The results of this studydemonstrate that the fibrinolytic response to an acute bout of moderatephysical activity is not impaired in sedentary older hypertensive men.

     

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

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

     

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.

     

Muscle malonyl-CoA decreases during exercise

Malonyl-CoA, the inhibitor of carnitine acyltransferase I, is an important regulator of fatty acid oxidation and ketogenesis in the liver. Muscle carnitine acyltransferase I has previously been reported to be more sensitive to malonyl-CoA inhibition than is liver carnitine acyltransferase I. Fluctuations in malonyl-CoA concentration may therefore be important in regulating the rate of fatty acid oxidation in muscle during exercise. Male rats were anesthetized (pentobarbital via venous catheters) at rest or after 30 min of treadmill exercise (21 m/min, 15% grade). The gastrocnemius/plantaris muscles were frozen at liquid N2 temperature. Muscle malonyl-CoA decreased from 1.66 +/- 0.17 to 0.60 +/- 0.05 nmol/g during the exercise. This change was accompanied by a 31% increase in cAMP in the muscle. The decline in malonyl-CoA occurred before muscle glycogen depletion and before onset of hypoglycemia. Plasma catecholamines, corticosterone, and free fatty acids were all significantly increased during the exercise. This exercise-induced decrease in malonyl-CoA may be important for allowing the increase in muscle fatty acid oxidation during exercise.     

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.

     

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.