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.

     

Progressive decrease of intramyocellular accumulation of H+ and Pi in human skeletal muscle during repeated isotonic exercise

The purpose of this study was to evaluatethe hypotheses that accumulation of hydrogen ions and/or inorganicphosphate (Pi) in skeletal muscle increases with repeated bouts ofisotonic exercise. ³¹P-Magnetic resonance spectroscopy wasused to examine the gastrocnemius muscle of seven highly aerobicallytrained females during four bouts of isotonic plantar flexion. Theexercise bouts (EX1-4) of 3 min and 18 swere separated by 3 min and 54 s of complete rest. Muscle ATP did notchange during the four bouts. Phosphocreatine (PCr) degradation duringEX1 (13.3 ± 2.4 mmol/kg wet weight) was higher(P < 0.01) compared with EX3-4(9.7 ± 1.6 and 9.6 ± 1.8 mmol/kg wet weight, respectively).The intramyocellular pH at the end of EX1 (6.87 ± 0.05) was significantly lower (P < 0.001) than thoseof EX2 (6.97 ± 0.02), EX3 (7.02 ± 0.01), and EX4 (7.02 ± 0.02). Total Pi anddiprotonated Pi were significantly higher (P < 0.001)at the end of EX1 (17.3 ± 2.7 and 7.8 ± 1.6 mmol/kg wet weight, respectively) compared with the values at the end of EX3 and EX4. The monoprotonated Pi at the endof EX1 (9.5 ± 1.2 mmol/kg wet weight) was alsosignificantly higher (P < 0.001) than that afterEX4 (7.5 ± 1.1 mmol/kg wet weight). Subjects' ratingof perceived exertion increased (P < 0.001) towardexhaustion as the number of exercises progressed (7.1 ± 0.4, EX1; 8.0 ± 0.3, EX2; 8.5 ± 0.3, EX3; and 9.0 ± 0.4, EX4; scale from 0 to10). The present results indicate that human muscle fatigue during repeated intense isotonic exercise is not due to progressive depletion of high energy phosphates nor to intracellular accumulation of hydrogenions, total, mono-, or diprotonated Pi.

     

Human growth hormone response to repeated bouts of aerobic exercise

Kanaley, J. A., J. Y. Weltman, J. D. Veldhuis, A. D. Rogol,M. L. Hartman, and A. Weltman. Human growth hormone response torepeated bouts of aerobic exercise. J. Appl.Physiol. 83(5): 1756-1761, 1997.We examinedwhether repeated bouts of exercise could override growth hormone (GH)auto-negative feedback. Seven moderately trained men were studied onthree occasions: a control day (C), a sequential exercise day (SEB; at1000, 1130, and 1300), and a delayed exercise day (DEB; at 1000, 1400, and 1800). The duration of each exercise bout was 30 min at 70%maximal O₂ consumption (O_{2 max}) on a cycleergometer. Standard meals were provided at 0600 and 2200. GH wasmeasured every 5-10 min for 24 h (0800-0800). Daytime(0800-2200) integrated GH concentrations were ~150-160% greater during SEB and DEB than during C: 1,282 ± 345, 3,192 ± 669, and 3,389 ± 991 min · µg · l¹for C, SEB, and DEB, respectively [SEB > C(P < 0.06), DEB > C(P < 0.03)]. There were nodifferences in GH release during sleep (2300-0700). Deconvolutionanalysis revealed that the increase in 14-h integrated GH concentrationon DEB was accounted for by an increase in the mass of GH secreted perpulse (per liter of distribution volume,l_v): 7.0 ± 2.9 and 15.9 ± 2.6 µg/l_v for C and DEB,respectively (P < 0.01). Comparisonof 1.5-h integrated GH concentrations on the SEB and DEB days (30 minexercise + 60 min recovery) revealed that, with each subsequentexercise bout, GH release apparently increased progressively, with aslightly greater increase on the DEB day [SEB vs. DEB: 497 ± 162 vs. 407 ± 166 (bout 1), 566 ± 152 vs. 854 ± 184 (bout2), and 633 ± 149 vs. 1,030 ± 352 min · µg · l¹(bout 3),P < 0.05]. We conclude thatthe GH response to acute aerobic exercise is augmented with repeatedbouts of exercise.

     

Validity of NIR spectroscopy for quantitatively measuring muscle oxidative metabolic rate in exercise

The purpose of this studywas to examine the validity of the quantitative measurement of muscleoxidative metabolism in exercise by near-infrared continuous-wavespectroscopy (NIRcws). Twelve male subjects performed two bouts ofdynamic handgrip exercise, once for the NIRcws measurement and once forthe ³¹P-magnetic resonance spectroscopy (MRS) measurementas a standard measure. The resting muscle metabolic rate (RMRmus) wasindependently measured by ³¹P-MRS during 15 min of arterialocclusion at rest. During the first exercise bout, the quantitativevalue of muscle oxidative metabolic rate at 30 s postexercisewas evaluated from the ratio of the rate of oxyhemoglobin/myoglobindecline measured by NIRcws during arterial occlusion 30 s afterexercise and the rate at rest. Therefore, the absolute values of muscleoxidative metabolic rate at 30 s after exercise[O_2NIR(30)] wascalculated from this ratio multiplied by RMRmus. During the secondexercise bout, creatine phosphate (PCr) resynthesis rate was measuredby ³¹P-MRS at 30 s postexercise[Q₍₃₀₎] under the same conditions but without arterial occlusion postexercise. To determine the validity ofNIRcws, O_2NIR(30) wascompared with Q₍₃₀₎. There was a significant correlation betweenO_2NIR(30), which rangedbetween 0.018 and 0.187 mM ATP/s, and Q₍₃₀₎,which ranged between 0.041 and 0.209 mM ATP/s (r = 0.965, P < 0.001). This result supports theapplication of NIRcws to quantitatively evaluate muscle oxidativemetabolic rate in exercise.

     

Effect of creatine supplementation on sprint exercise performance and muscle metabolism

The aim of thepresent study was to examine the effect of creatine supplementation(CrS) on sprint exercise performance and skeletal muscle anaerobicmetabolism during and after sprint exercise. Eight active, untrainedmen performed a 20-s maximal sprint on an air-braked cycle ergometerafter 5 days of CrS [30 g creatine (Cr) + 30 g dextrose perday] or placebo (30 g dextrose per day). The trials wereseparated by 4 wk, and a double-blind crossover design was used. Muscleand blood samples were obtained at rest, immediately after exercise,and after 2 min of passive recovery. CrS increased the muscle total Crcontent (9.5 ± 2.0%, P < 0.05, mean ± SE); however, 20-s sprint performance was not improved byCrS. Similarly, the magnitude of the degradation or accumulation ofmuscle (e.g., adenine nucleotides, phosphocreatine, inosine 5'-monophosphate, lactate, and glycogen) and plasma metabolites (e.g., lactate, hypoxanthine, and ammonia/ammonium) were also unaffected by CrS during exercise or recovery. These data demonstrated that CrS increased muscle total Cr content, but the increase did notinduce an improved sprint exercise performance or alterations inanaerobic muscle metabolism.

     

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.

     

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.

     

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.

     

Muscle glycogen recovery after exercise during glucose and fructose intake monitored by 13C-NMR

Van Den Bergh, Adrianus J., Sibrand Houtman, ArendHeerschap, Nancy J. Rehrer, Hendrikus J. Van Den Boogert, BerendOeseburg, and Maria T. E. Hopman. Muscle glycogen recovery afterexercise during glucose and fructose intake monitored by¹³C-NMR. J. Appl.Physiol. 81(4): 1495-1500, 1996.The purpose of this study was to examine muscle glycogen recovery with glucose feeding(GF) compared with fructose feeding (FF) during the first 8 h afterpartial glycogen depletion by using¹³C-nuclear magneticresonance (NMR) on a clinical 1.5-T NMR system. After measurement of the glycogen concentration of the vastus lateralis (VL) muscle in seven male subjects, glycogen stores of the VLwere depleted by bicycle exercise. During 8 h after completion ofexercise, subjects were orally given either GF or FF while the glycogencontent of the VL was monitored by¹³C-NMR spectroscopy every secondhour. The muscular glycogen concentration was expressed as a percentageof the glycogen concentration measured before exercise. The glycogenrecovery rate during GF (4.2 ± 0.2%/h) was significantly higher(P < 0.05) compared withvalues during FF (2.2 ± 0.3%/h). This study shows that1) muscle glycogen levels areperceptible by ¹³C-NMRspectroscopy at 1.5 T and 2) theglycogen restoration rate is higher after GF compared with after FF.

     

Hydration effects on physiological strain of horses during exercise-heat stress

This study examined the effects ofhyperhydration, exercise-induced dehydration, and oral fluidreplacement on physiological strain of horses during exercise-heatstress. On three occasions, six horses completed a 90-min exerciseprotocol (50% maximal O₂ uptake,34.5°C, 48% relative humidity) divided into two 45-min periods(exercise I andexercise II) with a 15-min recoverybetween exercise bouts. In random order, horses receivedno fluid (NF), 10 liters of water (W), or a carbohydrate-electrolytesolution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (), stroke volume (SV), corebody temperature, sweating rate (SR), or sweating sensitivity duringexercise I. In contrast, afterexercise II, exercise-induceddehydration in NF (decrease in body mass: NF, 5.6 ± 0.8%; W, 1.1 ± 0.4%; CE, 1.0 ± 0.2%) resulted in greater heat storage,with core body temperature ~1.0°C higher compared with W and CE.In exercise II, the greater thermalstrain in NF was associated with significant(P < 0.05) decreases in (10 ± 2%), SV (9 ± 3%), SR, and sweatingsensitivity. We concluded that 1)preexercise hyperhydration provided no thermoregulatory advantage;2) maintenance of euhydration byoral fluid replacement (~85% of sweat fluid loss) during exercise inthe heat was reflected in higher , SV, and SR withdecreased heat storage; and 3) W oran isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.

     

Increased GLUT-4 translocation mediates enhanced insulin sensitivity of muscle glucose transport after exercise

The purpose of this study was to determinewhether the increase in insulin sensitivity of skeletal muscle glucosetransport induced by a single bout of exercise is mediated by enhancedtranslocation of the GLUT-4 glucose transporter to the cell surface.The rate of3-O-[³H]methyl-D-glucosetransport stimulated by a submaximally effective concentration ofinsulin (30 µU/ml) was approximately twofold greater in the musclesstudied 3.5 h after exercise than in those of the sedentary controls(0.89 ± 0.10 vs. 0.43 ± 0.05 µmol · ml¹ · 10 min¹; means ± SE forn = 6/group). GLUT-4 translocation wasassessed by using theATB-[2-³H]BMPAexofacial photolabeling technique. Prior exercise resulted in greatercell surface GLUT-4 labeling in response to submaximal insulintreatment (5.36 ± 0.45 dpm × 10³/g in exercised vs. 3.00 ± 0.38 dpm × 10³/g insedentary group; n = 10/group) thatclosely mirrored the increase in glucose transport activity. The signalgenerated by the insulin receptor, as reflected in the extent ofinsulin receptor substrate-1 tyrosine phosphorylation, was unchangedafter the exercise. We conclude that the increase in muscle insulinsensitivity of glucose transport after exercise is due to translocationof more GLUT-4 to the cell surface and that this effect is not due topotentiation of insulin-stimulated tyrosine phosphorylation.

     

Muscle power and metabolism in maximal intermittent exercise

Muscle power and the associated metabolic changes in muscle were investigated in eight male human subjects who performed four 30-s bouts of maximal isokinetic cycling at 100 rpm, with 4-min recovery intervals. In the first bout peak power and total work were (mean +/- SE) 1,626 +/- 102 W and 20.83 +/- 1.18 kJ, respectively; muscle glycogen decreased by 18.2 mmol/kg wet wt, lactate increased to 28.9 +/- 2.7 mmol/kg, and there were up to 10-fold increases in glycolytic intermediates. External power and work decreased by 20% in both the second and third exercise periods, but no further change occurred in the fourth bout. Muscle glycogen decreased by an additional 14.8 mmol/kg after the second exercise and thereafter remained constant. Muscle adenosine triphosphate (ATP) was reduced by 40% from resting after each exercise period; creatine phosphate (CP) decreased successively to less than 5% of resting; in the recovery periods ATP and CP increased to 76 and 95% of initial resting levels, respectively. Venous plasma glycerol increased linearly to 485% of resting; free fatty acids did not change. Changes in muscle glycogen, lactate, and glycolytic intermediates suggested rate limitation at phosphofructokinase during the first and second exercise periods, and phosphorylase in the third and fourth exercise periods. Despite minimal glycolytic flux in the third and fourth exercise periods, subjects generated 1,000 W peak power and sustained 400 W for 30 s, 60% of the values recorded in the first exercise period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of high-intensity intermittent swimming on glucose transport in rat epitrochlearis muscle

Recently (K. Kawanaka, I. Tabata, and M. Higuchi. J. Appl. Physiol. 83:429-433, 1997), we demonstrated that glucose transport activity after repeated 10-s-long in vitro tetani in rat epitrochlearis (Epi) muscle was negatively correlated with the postcontraction muscleglycogen concentration. Therefore, we examined whether high-intensityintermittent swimming, which depletes muscle glycogen to a lower levelthan that observed after ten 10-s-long in vitro tetani, elicits higherglucose transport than that observed after ten 10-s-long in vitrotetani, which has been regarded as the exercise-induced maximalstimulus for glucose transport. In male rats,2-deoxy-D-glucose transport rate in Epi muscle after eight bouts of high-intensity intermittent swimming with a weight equal to18% of body mass (exercise duration: 20 s, rest duration between exercise bouts: 40 s) was higher than that observed after the ten10-s-long tetani (2.25 ± 0.08 vs. 1.02 ± 0.16µmol · ml intracellular water¹ · 20 min¹). Muscleglycogen concentration in Epi after eight bouts of high-intensity intermittent swimming was significantly lower than that observed afterten 10-s-long in vitro tetani (7.6 ± 0.5 vs. 14.8 ± 1.4 µmolglucose/g muscle). These observations show that the high-intensity intermittent swimming increases glucose transport in rat Epi to a muchhigher level than that induced by ten 10-s-long in vitro tetani, whichhas been regarded as the exercise-related maximal stimulus for glucosetransport. Furthermore, this finding suggests that the lower muscleglycogen level after high-intensity intermittent swimming than after invitro tetani may play a role, because there was a significant negativecorrelation between glucose transport and muscle glycogen concentrationin Epi after high-intensity swimming and in vitro tetani.

     

Muscle use during dynamic knee extension: implication for perfusion and metabolism

Dynamic one-legged knee extension (DKE) iscommonly used to examine physiological responses to "aerobic"exercise. Muscle blood flow during DKE is often expressed relative toquadriceps femoris muscle mass irrespective of work rate.This is contrary to the notion that increased force is achieved byrecruitment in large muscles. The purpose of this study, therefore, wasto determine muscle use during DKE. Six subjects had magnetic resonance images taken of their quadriceps femoris before and after 4 min of DKEat 20 and 40 W. Muscle use was determined by shifts in T2. Thecross-sectional area of quadriceps femoris that had an elevated T2 was16 ± 1% (mean ± SE) preexercise, and 54 ± 5 and 94 ± 4% after 20- and 40-W DKE, respectively. Volume of quadriceps femorisincreased 11.4 ± 0.2% (P = 0.006), from 2,230 ± 233 cm³before exercise to 2,473 ± 232 cm³ after 40-W DKE. Extrapolationof these data indicates that 1,301 ± 111 cm³ of quadriceps femoris wereengaged during 20-W DKE compared with 2,292 ± 154 cm³ during 40-W DKE. By usingmuscle blood flow data for submaximal DKE at 20 W [P. Andersenand B. Saltin. J. Physiol. (Lond.)366: 233-249, 1985; and L. B. Rowell, B. Saltin, B. Kiens, and N. J. Christensen. Am. J. Physiol. 251 (Heart Circ.Physiol. 20): H1038-H1044, 1986] andestimating muscle use in those studies from our data (total muscle mass × 0.54), extrapolated blood flow to active muscle (263 and 278 ml · min¹ · 100 g¹, respectively) iscomparable to that obtained during peak aerobic DKE when expressedrelative to total muscle mass (243 and 250 ml · min¹ · 100 g¹,respectively). These findings indicate that increasedpower during aerobic DKE is achieved by recruitment.Additionally, they suggest that blood flow to the active quadricepsfemoris muscle does not increase with increases in submaximal work ratebut instead is maximal to support aerobic metabolism. Thus increases inmuscle blood flow are directed to newly recruited muscle, not toincreased perfusion of muscle already engaged.

     

Comparative effects of a low-carbohydrate diet and exercise plus a low-carbohydrate diet on muscle sarcoplasmic reticulum responses in males

We employed a glycogen-depleting session of exercise followed by a low-carbohydrate (CHO) diet to investigate modifications that occur in muscle sarcoplasmic reticulum (SR) Ca²⁺-cycling properties compared with low-CHO diet alone. SR properties were assessed in nine untrained males [peak aerobic power (O_{2 peak}) = 43.6 ± 2.6 (SE) ml·kg^–1·min^–1] during prolonged cycle exercise to fatigue performed at 58% O_{2 peak} after 4 days of low-CHO diet (Lo CHO) and after glycogen-depleting exercise plus 4 days of low-CHO (Ex+Lo CHO). Compared with Lo CHO, Ex+Lo CHO resulted in 12% lower (P < 0.05) resting maximal Ca²⁺-ATPase activity (V_max = 174 ± 12 vs. 153 ± 10 µmol·g protein^–1·min^–1) and smaller reduction in V_max induced during exercise. A similar effect was observed for Ca²⁺ uptake. The Hill coefficient, defined as slope of the relationship between cytosolic free Ca²⁺ concentration and Ca²⁺-ATPase activity, was higher (P < 0.05) at rest (2.07 ± 0.15 vs. 1.90 ± 0.10) with Ex+Lo CHO, an effect that persisted throughout the exercise. The coupling ratio, defined as the ratio of Ca²⁺ uptake to V_max, was 23–30% elevated (P < 0.05) at rest and during the first 60 min of exercise with Ex+Lo CHO. The 27 and 34% reductions (P < 0.05) in phase 1 and phase 2 Ca²⁺ release, respectively, observed during exercise with Lo CHO were not altered by Ex+Lo CHO. These results indicate that when prolonged exercise precedes a short-term Lo CHO diet, Ca²⁺ sequestration properties and efficiency are improved compared with those during Lo CHO alone. calcium cycling; vastus lateralis; contractile activity; glycogen; phosphorylation potential     

Skeletal muscle chemoreflex and pHi in exercise ventilatory control

Oelberg, David A., Allison B. Evans, Mirko I. Hrovat, PaulP. Pappagianopoulos, Samuel Patz, and David M. Systrom. Skeletal muscle chemoreflex and pH_i inexercise ventilatory control. J. Appl.Physiol. 84(2): 676-682, 1998.To determinewhether skeletal muscle hydrogen ion mediates ventilatory drive inhumans during exercise, 12 healthy subjects performed three bouts ofisotonic submaximal quadriceps exercise on each of 2 days in a 1.5-Tmagnet for ³¹P-magnetic resonancespectroscopy(³¹P-MRS). Bilaterallower extremity positive pressure cuffs were inflated to 45 Torr duringexercise (BLPP_ex) or recovery(BLPP_rec) in a randomized orderto accentuate a muscle chemoreflex. Simultaneous measurements were madeof breath-by-breath expired gases and minute ventilation, arterializedvenous blood, and by ³¹P-MRS ofthe vastus medialis, acquired from the average of 12 radio-frequencypulses at a repetition time of 2.5 s. WithBLPP_ex, end-exercise minuteventilation was higher (53.3 ± 3.8 vs. 37.3 ± 2.2 l/min;P < 0.0001), arterializedPCO₂ lower (33 ± 1 vs. 36 ± 1 Torr; P = 0.0009), and quadricepsintracellular pH (pH_i) more acid (6.44 ± 0.07 vs. 6.62 ± 0.07; P = 0.004), compared withBLPP_rec. Bloodlactate was modestly increased withBLPP_ex but without a change inarterialized pH. For each subject, pH_i was linearly relatedto minute ventilation during exercise but not to arterialized pH. Thesedata suggest that skeletal muscle hydrogen ion contributes to theexercise ventilatory response.

     

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.

     

Persistence of supercompensated muscle glycogen in trained subjects after carbohydrate loading

Goforth, Jr., Harold W., David A. Arnall, Brad L. Bennett,and Patricia G. Law. Persistence of supercompensated muscle glycogen in trained subjects after carbohydrate loading.J. Appl. Physiol. 82(1): 342-347, 1997.Several carbohydrate (CHO)-loading protocols have been used toachieve muscle glycogen supercompensation and prolong enduranceperformance. This study assessed the persistence of muscle glycogensupercompensation over the 3 days after the supercompensation protocol.Trained male athletes completed a 6-day CHO-loading protocol thatincluded cycle ergometer exercise and dietary manipulations. The 3-daydepletion phase began with 115 min of cycling at 75% peak oxygenuptake followed by 3 × 60-s sprints and included the subjectsconsuming a low-CHO/high-protein/high-fat (10:41:49%) diet. Subjectscycled 40 min at the same intensity for the next 2 days. During the3-day repletion phase, subjects rested and consumed ahigh-CHO/low-protein/low-fat (85:08:07%) diet, including aglucose-polymer beverage. A 3-day postloading phase followed, whichinvolved a moderately high CHO diet (60%) and no exercise. Glycogenvalues for vastus lateralis biopsies at baseline and postloadingdays 1-3 were 408 ± 168 (SD),729 ± 222, 648 ± 186, and 714 ± 196 mmol/kg dry wt,respectively. The CHO-loading protocol increased muscle glycogen by1.79 times baseline, and muscle glycogen remained near this levelduring the 3-day postloading period. Results indicate thatsupercompensated muscle glycogen levels can be maintained for at least3 days in a resting athlete when a moderate-CHO diet is consumed.

     

Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heart failure

Isnard, Richard, Philippe Lechat, Hanna Kalotka, HafidaChikr, Serge Fitoussi, Joseph Salloum, Jean-Louis Golmard, Daniel Thomas, and Michel Komajda. Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heartfailure. J. Appl. Physiol. 81(6):2571-2579, 1996.Blood flow to working skeletal muscle is usuallyreduced during exercise in patients with congestive heart failure. Anintrinsic impairment of skeletal muscle vasodilatory capacity has beensuspected as a mechanism of this muscle underperfusion during maximalexercise, but its role during submaximal exercise remains unclear.Therefore, we studied by transcutaneous Doppler ultrasonography thearterial blood flow in the common femoral artery at rest and during asubmaximal bicycle exercise in 12 normal subjects and in 30 patientswith heart failure. Leg blood flow was lower in patientsthan in control subjects at rest [0.29 ± 0.14 (SD) vs. 0.45 ± 0.14 l/min, P < 0.01], at absolute powers and at the same relative power (2.17 ± 1.06 vs. 4.39 ± 1.4 l/min, P < 0.001). Because mean arterial pressure was maintained, leg vascularresistance was higher in patients than in control subjects at rest (407 ± 187 vs. 247 ± 71 mmHg ^· l^{1 ·} min,P < 0.01) and at thesame relative power (73 ± 49 vs. 31 ± 13 mmHg ^· l^{1 ·} min,P < 0.01) but not at absolutepowers. Although the magnitude of increase in leg blood flow correctedfor power was similar in both groups (31 ± 10 vs. 34 ± 10 ml ^· min^{1 ·} W¹),the magnitude of decrease of leg vascular resistance corrected forpower was higher in patients than in control subjects (5.9 ± 3.3 vs. 1.9 ± 0.94 mmHg ^· l^{1 ·} min ^· W¹,P < 0.001). These results suggestthat the ability of skeletal muscle vascular resistance to decrease isnot impaired and that intrinsic vascular abnormalities do not limitvasodilator response to submaximal exercise in patients with heartfailure.

     

Muscle glycogen accumulation after a marathon: roles of fiber type and pro- and macroglycogen

Muscle glycogen remains subnormal several days after muscledamaging exercise. The aims of this study were toinvestigate how muscle acid-soluble macroglycogen (MG) andacid-insoluble proglycogen (PG) pools are restored after a competitivemarathon and also to determine whether glycogen accumulates differently in the various muscle fiber types. Six well-trained marathon runners participated in the study, and muscle biopsies were obtained from thevastus lateralis of the quadriceps muscle before, immediately after,and 1, 2, and 7 days (days 1, 2, and7, respectively) after the marathon.During the race, 56 ± 3.8% of muscle glycogen was utilized, and agreater fraction of MG (72 ± 3.7%) was utilized compared with PG(34 ± 6.5%). On day 2, muscleglycogen and MG values remained lower than preracevalues, despite a carbohydrate-rich diet, but they hadboth returned to prerace levels on day7. The PG concentration was lower onday 1 compared with before the race, whereas there were no significant differences between the prerace PGconcentration and the concentrations on days2 and 7. Onday 2 the glycogen concentration wasparticularly low in the type I fibers, indicating that local processesare important for the accumulation pattern. We conclude that a greaterfraction of human muscle MG than of PG is utilized during a marathonand that accumulation of MG is particularly delayed after the prolongedexercise bout. Furthermore, factors produced locally appear importantfor the glycogen accumulation pattern.