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 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.

     

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.

     

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.

     

Effects of emphysema on diaphragm blood flow during exercise

Chronichyperinflation of the lung in emphysema displaces the diaphragmcaudally, thereby placing it in a mechanically disadvantageous positionand contributing to the increased work of breathing. We tested thehypothesis that total and regional diaphragm blood flows are increasedin emphysema, presumably reflecting an increased diaphragm energeticdemand. Male Syrian Golden hamsters were randomly divided intoemphysema (E; intratracheal elastase 25 units/100 g body wt) andcontrol (C; saline) groups, and experiments were performed 16-20wk later. The regional distribution of blood flow withinthe diaphragm was determined by using radiolabeled microspheres inhamsters at rest and during treadmill exercise (walking at 20 feet/min,20% grade). Consistent with pronounced emphysema, lung volume per unitbody weight was greater in E hamsters (C, 59.3 ± 1.8; E, 84.5 ± 5.0 ml/kg; P < 0.001) and arterialPO₂ was lower both at rest (C, 74 ± 3; E, 59 ± 2 Torr; P < 0.001) and during exercise (C, 93 ± 3; E, 69 ± 4 Torr; P < 0.001). At rest, total diaphragm blood flow was not different between C and Ehamsters (C, 47 ± 4; E, 38 ± 4 ml · min¹ · 100 g¹;P = 0.18). In both C and E hamsters,blood flow at rest was lower in the ventral costal region of thediaphragm than in the dorsal and medial costal regions and the cruraldiaphragm. During exercise in both C and E hamsters, blood flowsincreased more in the dorsal and medial costal regions and in thecrural diaphragm than in the ventral costal region. Total diaphragmblood flow was greater in E hamsters during exercise (C, 58 ± 7; E,90 ± 14 ml · min¹ · 100 g¹;P = 0.03), as a consequence ofsignificantly higher blood flows in the medial and ventral costalregions and crural diaphragm. In addition, exercise-induced increasesin intercostal (P < 0.005) andabdominal (P < 0.05) muscle bloodflows were greater in E hamsters. The finding that diaphragm blood flowwas greater in E hamsters during exercise supports the contention thatemphysema increases the energetic requirements of the diaphragm.

     

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.

     

Utilization of glycogen but not plasma glucose is reduced in individuals with NIDDM during mild-intensity exercise

Colberg, Sheri R., James M. Hagberg, Steve D. McCole, JosephM. Zmuda, Paul D. Thompson, and David E. Kelley. Utilization ofglycogen but not plasma glucose is reduced in individuals with NIDDMduring mild-intensity exercise. J. Appl.Physiol. 81(4): 2027-2033, 1996.To test thehypothesis that substrate utilization during mild-intensity exercisediffers in non-insulin-dependent diabetes mellitus (NIDDM) comparedwith nondiabetic subjects, seven lean healthy subjects (L), seven obesehealthy subjects (O), and seven individuals with NIDDM were studiedduring 40 min of mild-intensity cycling (40% of peakO₂ uptake). Systemic utilization of plasma glucose (Glc Rd) was determined by using isotope dilution methods. Gas exchange was measured to determine rates of carbohydrate (CHO) and lipid oxidation. During exercise, when CHOoxidation was greater than Glc Rd, the net oxidation of glycogen wascalculated as the difference: CHO oxidation  Glc Rd. Duringmild-intensity cycling, the respiratory exchange ratio was similaracross groups (0.87 ± 0.02, 0.85 ± 0.02, and 0.86 ± 0.01 inL, O, and NIDDM subjects, respectively), and CHO oxidation accountedfor one-half of total energy expenditure during exercise. Glc Rdincreased during exercise and was greatest in subjects with NIDDM (3.0 ± 0.2, 2.9 ± 0.2, and 4.5 ± 0.4 ml ^· kg^{1 ·} min¹in L, O, and NIDDM subjects, respectively,P < 0.05), yet Glc Rd wasless than CHO oxidation during exercise, indicating net oxidation ofglycogen. Glycogen oxidation was greater in L and O than in NIDDMsubjects (3.4 ± 1.0, 2.5 ± 0.9, and 1.7 ± 0.8 ml ^· kg^{1 ·} min¹;P < 0.05). In summary, duringmild-intensity exercise, NIDDM subjects have an increased Glc Rd and adecreased oxidation of muscle glycogen.

     

Phosphorylation of p70S6k correlates with increased skeletal muscle mass following resistance exercise

High-resistance exercise training results in an increase inmuscle wet mass and protein content. To begin to address the acute changes following a single bout of high-resistance exercise, a newmodel has been developed. Training rats twice a week for 6 wk resultedin 13.9 and 14.4% hypertrophy in the extensor digitorum longus (EDL)and tibialis anterior (TA) muscles, respectively. Polysome profilesafter high-resistance lengthening contractions suggest that the rate ofinitiation is increased. The activity of the 70-kDa S6 protein kinase(p70^S6k), a regulator oftranslation initiation, is also increased following high-resistancelengthening contractions (TA, 363 ± 29%; EDL, 353 ± 39%).Furthermore, the increase inp70^S6k activity 6 h after exercisecorrelates with the percent change in muscle mass after 6 wk oftraining (r = 0.998). The tightcorrelation between the activation ofp70^S6k and the long-term increasein muscle mass suggests thatp70^S6k phosphorylation may be agood marker for the phenotypic changes that characterize musclehypertrophy and may play a role in load-induced skeletal muscle growth.

     

Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training

McCall, G. E., W. C. Byrnes, A. Dickinson, P. M. Pattany,and S. J. Fleck. Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training.J. Appl. Physiol. 81(5):2004-2012, 1996.Twelve male subjects with recreationalresistance training backgrounds completed 12 wk of intensifiedresistance training (3 sessions/wk; 8 exercises/session; 3 sets/exercise; 10 repetitions maximum/set). All major muscle groupswere trained, with four exercises emphasizing the forearm flexors.After training, strength (1-repetition maximum preacher curl) increasedby 25% (P < 0.05). Magneticresonance imaging scans revealed an increase in the biceps brachiimuscle cross-sectional area (CSA) (from 11.8 ± 2.7 to 13.3 ± 2.6 cm²;n = 8;P < 0.05). Muscle biopsies of thebiceps brachii revealed increases(P < 0.05) in fiber areas for type I(from 4,196 ± 859 to 4,617 ± 1,116 µm²;n = 11) and II fibers (from 6,378 ± 1,552 to 7,474 ± 2,017 µm²;n = 11). Fiber number estimated fromthe above measurements did not change after training (293.2 ± 61.5 × 10³ pretraining; 297.5 ± 69.5 × 10³ posttraining;n = 8). However, the magnitude ofmuscle fiber hypertrophy may influence this response because thosesubjects with less relative muscle fiber hypertrophy, but similarincreases in muscle CSA, showed evidence of an increase in fibernumber. Capillaries per fiber increased significantly(P < 0.05) for both type I(from 4.9 ± 0.6 to 5.5 ± 0.7;n = 10) and II fibers (from 5.1 ± 0.8 to 6.2 ± 0.7; n = 10). Nochanges occurred in capillaries per fiber area or muscle area. Inconclusion, resistance training resulted in hypertrophy of the totalmuscle CSA and fiber areas with no change in estimated fiber number,whereas capillary changes were proportional to muscle fiber growth.

     

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.

     

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.

     

Exogenous glucose oxidation during exercise in endurance-trained and untrained subjects

Jeukendrup, A. E., M. Mensink, W. H. M. Saris, and A. J. M. Wagenmakers. Exogenous glucose oxidation during exercise in endurance-trained and untrained subjects. J. Appl.Physiol. 82(3): 835-840, 1997.To investigate theeffect of training status on the fuel mixture used during exercise withglucose ingestion, seven endurance-trained cyclists (Tr; maximumO₂ uptake 67 ± 2.3 ml ^· kg^{1 ·} min¹)and eight untrained subjects (UTr; 48 ± 2 ml ^· kg^{1 ·} min¹)were studied during 120 min of exercise at ~60% maximumO₂ uptake. At the onset of exercise, 8 ml ^· kg^{1 ·} min¹of an 8% naturally enriched[¹³C]glucose solutionwas ingested and 2 ml/kg every 15 min thereafter. Energy expenditurewas higher in Tr subjects compared with UTr subjects (3,404 vs. 2,630 kJ; P < 0.01). During the secondhour, fat oxidation was higher in Tr subjects (37 ± 2 g) comparedwith UTr subjects (23 ± 1 g), whereas carbohydrateoxidation was similar (116 ± 8 g in Tr subjects vs. 114 ± 4 g in UTr subjects). No differences were observed in exogenousglucose oxidation (50 ± 2 g in Tr subjects and 45 ± 3 g in UTr subjects, respectively). Peak exogenous glucose oxidationrates were similar in the two groups (0.95 ± 0.07 g/min in Trsubjects and 0.96 ± 0.03 g/min in UTr subjects). It is concluded that the higher energy expenditure in Tr subjects during exercise atthe same relative exercise intensity is entirely met by a higher rateof fat oxidation without changes in the rates of exogenous andendogenous carbohydrates.

     

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.

     

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.

     

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.

     

Muscle quality. II. Effects of strength training in 65-to 75-yr-old men and women

To determine theeffects of strength training (ST) on muscle quality (MQ,strength/muscle volume of the trained muscle group), 12 healthy oldermen (69 ± 3 yr, range 65-75 yr) and 11 healthy older women (68 ± 3 yr, range 65-73 yr) were studied before and after aunilateral leg ST program. After a warm-up set, four sets ofheavy-resistance knee extensor ST exercise were performed 3 days/wk for9 wk on the Keiser K-300 leg extension machine. The men exhibitedgreater absolute increases in the knee extension one-repetition maximum(1-RM) strength test (75 ± 2 and 94 ± 3 kg before andafter training, respectively) and in quadriceps muscle volume measuredby magnetic resonance imaging (1,753 ± 44 and 1,955 ± 43 cm³) than the women (42 ± 2 and 55 ± 3 kg for the 1-RM test and 1,125 ± 53 vs.1,261 ± 65 cm³ forquadriceps muscle volume before and after training, respectively, inwomen; both P < 0.05). However,percent increases were similar for men and women in the 1-RM test (27 and 29% for men and women, respectively), muscle volume (12% forboth), and MQ (14 and 16% for men and women, respectively).Significant increases in MQ were observed in both groups in the trainedleg (both P < 0.05) and in the 1-RMtest for the untrained leg (both P < 0.05), but no significant differences were observed between groups,suggesting neuromuscular adaptations in both gender groups. Thus,although older men appear to have a greater capacity for absolutestrength and muscle mass gains than older women in response to ST, the relative contribution of neuromuscular and hypertrophic factors to theincrease in strength appears to be similar between genders.

     

Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise

Sinoway, Lawrence, Jeffrey Shenberger, Gretchen Leaman,Robert Zelis, Kristen Gray, Robert Baily, and Urs Leuenberger. Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise. J. Appl.Physiol. 81(4): 1778-1784, 1996.We previouslydemonstrated that nonfatiguing rhythmic forearm exercise at 25%maximal voluntary contraction (12 2-s contractions/min) evokessympathoexcitation without significant engagement ofmetabolite-sensitive muscle afferents (B. A. Batman, J. C. Hardy, U. A. Leuenberger, M. B. Smith, Q. X. Yang, and L. I. Sinoway.J. Appl. Physiol. 76: 1077-1081,1994). This is in contrast to the sympathetic nervous system responsesobserved during fatiguing static forearm exercise wheremetabolite-sensitive afferents are the key determinants of sympatheticactivation. In this report we examined whether forearm exercisetraining would attenuate sympathetic nervous system responses torhythmic forearm exercise. We measured heart rate, mean arterial bloodpressure (MAP), muscle sympathetic nerve activity (microneurography),plasma norepinephrine (NE), and NE spillover and clearance (tritiatedNE kinetics) during nonfatiguing rhythmic forearm exercise before andafter a 4-wk unilateral forearm training paradigm. Training had noeffect on forearm mass, maximal voluntary contraction, or heart ratebut did attenuate the increase in MAP (increase in MAP: from 15.2 ± 1.8 before training to 11.4 ± 1.4 mmHg after training;P < 0.017), muscle sympathetic nerve activity (increase in bursts: from 10.8 ± 1.4 before training to6.2 ± 1.1 bursts/min after training;P < 0.030), and the NE spillover(increase in arterial spillover: from 1.3 ± 0.2 before training to0.6 ± 0.2 nmol ^· min^{1 ·} m²after training, P < 0.014; increasein venous spillover: from 2.0 ± 0.6 beforetraining to 1.0 ± 0.5 nmol ^· min^{1 ·} m²after training, P < 0.037) seen inresponse to exercise performed by the trained forearm. Thus forearmtraining reduces sympathetic responses during a nonfatiguing rhythmichandgrip paradigm that does not engage muscle metaboreceptors. Wespeculate that this effect is due to a conditioning-inducedreduction in mechanically sensitive muscle afferentdischarge.

     

Training, muscle volume, and energy expenditure in nonobese American girls

Little is known about the relationship among training,energy expenditure, muscle volume, and fitness in prepubertalgirls. Because physical activity is high in prepubertalchildren, we hypothesized that there would be no effect of training.Forty pre- and early pubertal (mean age 9.1 ± 0.1 yr) nonobesegirls enrolled in a 5 day/wk summer school program for 5 wk and were randomized to control (n = 20) or training groups(n = 20; 1.5 h/day, endurance-type exercise). Totalenergy expenditure (TEE) was measured using doubly labeled water, thighmuscle volume using magnetic resonance imaging, and peak O₂uptake (O_2 peak) using cycle ergometry.TEE was significantly greater (17%, P < 0.02) in thetraining girls. Training increased thigh muscle volume (+4.3 ± 0.9%, P < 0.005) andO_2 peak (+9.5 ± 6%,P < 0.05), effects surprisingly similar to thoseobserved in adolescent girls using the same protocol (Eliakim A,Barstow TJ, Brasel JA, Ajie H, Lee W-NP, Renslo R, Berman N, and CooperDM, J Pediatr 129: 537-543, 1996). We furthercompared these two sample populations: thigh muscle volume per weightwas much lower in adolescent compared with prepubertal girls (17.0 ± 0.3 vs. 27.8 ± 0.6 ml/kg body mass; P < 0.001), and allometric analysis revealed remarkably low scaling factorsrelating muscle volume (0.34 ± 0.05, P < 0.0001), TEE (0.24 ± 0.06, P < 0.0004), andO_2 peak (0.28 ± 0.07, P < 0.0001) to body mass in all subjects. Muscle andcardiorespiratory functions were quite responsive to brief training inprepubertal girls. Moreover, a retrospective, cross-sectional analysissuggests that increases in muscle mass andO_2 peak may be depressed in nonobeseAmerican girls as they mature.

     

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

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

     

Effects of the ovarian cycle on sympathetic neural outflow during static exercise

We comparedreflex responses to static handgrip at 30% maximal voluntarycontraction (MVC) in 10 women (mean age 24.1 ± 1.7 yr) during twophases of their ovarian cycle: the menstrual phase (days 1-4) and the follicularphase (days10-12). Changes in muscle sympathetic nerve activity (MSNA; microneurography) in response tostatic exercise were greater during the menstrual compared withfollicular phase (phase effect P = 0.01). Levels of estrogen were less during the menstrual phase(75 ± 5.5 vs. 116 ± 9.6 pg/ml, days 1-4 vs.days 10-12;P = 0.002). Generated tension did not explain differences in MSNA responses (MVC: 29.3 ± 1.3 vs. 28.2 ± 1.5 kg, days 1-4 vs.days 10-12;P = 0.13). In a group of experiments with the use of ³¹P-NMRspectroscopy, no phase effect was observed forH⁺ andH₂PO₄ concentrations(n = 5). During an ischemicrhythmic handgrip paradigm (20% MVC), a phase effect was notobserved for MSNA or H⁺ orH₂PO₄ concentrations,suggesting that blood flow was necessary for the expression of thecycle-related effect. The present studies suggest that, during statichandgrip exercise, MSNA is increased during the menstrual compared withthe follicular phase of the ovarian cycle.