Interaction between exercise and food restriction: effects on longevity of male rats

Male rats that exercise in running wheels have a longer average survival than freely eating sedentary controls but, in contrast to food-restricted sedentary controls of the same weight, show no extension of maximal life span (J. Appl. Physiol. 59: 826-831, 1985). To test the possibility that exercise may counteract a life-extending effect of decreased availability of energy for certain biological processes such as cell proliferation, we examined the combined effects of exercise and food restriction on longevity of male rats. As before, wheel running improved average length of life, 978 +/- 172 vs. 875 +/- 175 (SD) days, for the sedentary controls (P less than 0.01) without increasing maximal life span. Paired-weight controls, food restricted (approximately 30% below ad libitum) to weight the same as the runners, showed increases in both average (1,056 +/- 144 days) and maximal life span. Food-restricted runners, with intake restricted to the same extent (approximately 30%), had an increased mortality rate over the first approximately 50% of their survival curve up to approximately 900 days of age; their average life span (995 +/- 226) was similar to that of the control group of runners and shorter than that of their paired-weight food-restricted sedentary controls (1,088 +/- 159 days, P less than 0.05). However, after approximately 900 days of age the food-restricted runners' survival became similar to that of the food-restricted sedentary groups, with a comparable increase in maximal life span. Thus the exercise did not counteract the increase in maximal life span induced by food restriction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of voluntary exercise on longevity of rats

The purpose of this study was to obtain information regarding the effects of exercise on longevity in rats. The exercise used was voluntary activity wheel running. The runners gradually decreased their running from approximately 4 to approximately 1 mile/day as they aged from 9 to 30 mo. The runners lived slightly but significantly longer than sedentary freely eating controls and sedentary pair-fed controls (1,012 +/- 138 vs. 923 +/- 160 and 928 +/- 186 days) but significantly less long than food-restricted paired-weight sedentary controls (1,113 +/- 150 days). Although the exercise improved survival, it did not result in an extension of life-span. In contrast, the food-restricted paired-weight sedentary rats showed a true increase in life-span. The paired-weight rats also had a significantly reduced incidence of malignancies compared with the other three groups. However, there was no significant difference between the runners and the freely eating or pair-fed sedentary controls in the cause of death. These results provide evidence that exercise improves survival but does not result in an extension of life-span in rats.     

Effects of dietary manipulations and glucose infusion on glucagon response during exercise in rats

Tadjoré, Maurice, Raynald Bergeron, Martin Latour,François Désy, Claude Warren, and Jean-Marc Lavoie.Effects of dietary manipulations and glucose infusion on glucagonresponse during exercise in rats. J. Appl.Physiol. 83(1): 148-152, 1997.The purpose of thepresent investigation was to test the hypothesis that blood glucoseconcentration is not always related to glucagon response duringexercise. Three groups of rats were submitted to a prolonged (3-h)swimming exercise. Two groups of rats had their normal food intakerestricted by 50% the night before the experiment. One of these twogroups of rats was intravenously infused with glucose throughoutexercise to maintain euglycemia. The third group of rats swam whileunder normal dietary conditions. Plasma glucose, sampled in arterialblood, was reduced (P < 0.05) at 75, 105, 150, and 170 min of exercise (from ~130 to 110 mg/dl) in thefood-restricted animals without glucose infusion, whereas a significant(P < 0.05) increase was measured inthe two other groups during exercise. A significant(P < 0.01) difference in the meanintegrated areas under the glucose-concentration curve was found onlybetween the fed and the two food-restricted groups. Plasma insulinconcentrations decreased (P < 0.05)similarly in all groups during exercise, whereas plasma epinephrine andnorepinephrine concentrations increased significantly(P < 0.01) in all groups. Despitedifferences between groups in plasma glucose response during exercise,and despite the absence of any decrease in exercising blood glucoselevels in at least two of the three groups, plasma glucagon responseswere increased (P < 0.05) similarlyin all groups (from ~250 to 550 pg/ml) at the end of the exerciseperiod. The increase in glucagon was significant after 90 min ofexercise in the food-restricted groups, with or without glucoseinfusion, but only after 140 min in the fed group. These resultsindicate that the glucagon response during exercise is not alwayslinked to the decrease in plasma glucose.

     

Exercise training and the glucose transport system in obese SHHF/Mcc-facp rats

Ferrara, Cynthia M., W. Michael Sherman, Nicole Leenders,Sylvia A. McCune, and Karla Roehrig. Exercise training and theglucose transport system in obeseSHHF/Mcc-fa^cprats. J. Appl. Physiol. 81(4):1670-1676, 1996.The effects of a similar exercise trainingstimulus on maximal insulin-stimulated (MIS) plasma membrane glucosetransporter number and glucose transport were determined in lean andobeseSHHF/Mcc-fa^cprats. Six-week-old lean and obese male rats were randomly divided intofour groups: lean sedentary (LSed), obese sedentary (OSed), leanexercise (LEx), and obese exercise (OEx). An 8- to 12-wk treadmillrunning program equalized daily muscular work for LEx and OEx. Plasmamembranes were isolated from control and MIS muscles of mixed fibertypes. MIS significantly increased glucose transport (3.4- and2.8-fold) in LSed and OSed, respectively. MIS significantly increased glucose transporter number (2.5-fold) in LSed, but there wasno increase in glucose transporter number in OSed. Peak oxygen uptakeand citrate synthase activity were increased a similar amount for LExand OEx groups, demonstrating a similar training stimulus. MISsignificantly and similarly increased glucose transport in LEx and OEx(4.4- and 5.1-fold, respectively). The effects of MIS on plasmamembrane glucose transporter number in the exercise-trained rats weresimilar to the responses observed in the sedentary lean and obesegroups. MIS significantly increased glucose transporter number(2.6-fold) in LEx, whereas there was no increase in glucose transporternumber in OEx. The reduction in MIS glucose transport in OSed appearsto be related to a defect in the processes associated with thetranslocation of glucose transporters to the plasma membrane. Exercisetraining of the obese rats apparently did not alter this defect.Similar increases in peak oxygen uptake, citrate synthase, and MISglucose transport in LEx and OEx groups suggest that insulin resistancedoes not limit the ability of the glucose transport system to adapt toexercise training in the obese maleSHHF/Mcc-fa^cprats.

     

Exercise training increases sarcolemmal GLUT-4 protein and mRNA content in diabetic heart

Osborn, Brett A., June T. Daar, Richard A. Laddaga, Fred D. Romano, and Dennis J. Paulson. Exercise training increases sarcolemmal GLUT-4 protein and mRNA content in diabetic heart. J. Appl. Physiol. 82(3): 828-834, 1997.This study determined whether dynamic exercise training ofdiabetic rats would increase the expression of the GLUT-4 glucosetransport protein in prepared cardiac sarcolemmal membranes. Fourgroups were compared: sedentary control, sedentary diabetic, trainedcontrol, and trained diabetic. Diabetes was induced by intravenousstreptozotocin (60 mg/kg). Trained control and diabetic rats were runon a treadmill for 60 min, 27 m/min, 10% grade, 6 days/wk for 10 wk.Sarcolemmal membranes were isolated by using differentialcentrifugation, and the activity of sarcolemmalK⁺-p-nitrophenylphosphatase( pNPPase; an indicator ofNa⁺-K⁺-adenosinetriphosphataseactivity) was quantified. Hearts from the sedentary diabetic groupexhibited a significant depression of sarcolemmal pNPPaseactivity. Exercise training did not significantly alterpNPPase activity. Sedentary diabetic rats exhibited an 84 and 58% decrease in GLUT-4 protein and mRNA, respectively, relative tocontrol rats. In the trained diabetic animals, sarcolemmal GLUT-4protein levels were only reduced by 50% relative to control values,whereas GLUT-4 mRNA were returned to control levels. The increase inmyocardial sarcolemmal GLUT-4 may be beneficial to the diabetic heartby enhancing myocardial glucose oxidation and cardiac performance

     

Influence of treadmill running on femoral bone in young orchidectomized rats

Horcajada, M.-N., V. Coxam, M.-J. Davicco, N. Gaumet, P. Pastoureau, C. Leterrier, J. Culioli, and J.-P. Barlet. Influence of treadmill running on femoral bone in young orchidectomized rats.J. Appl. Physiol. 83(1): 129-133, 1997.Forty 6-wk-old male Wistar rats weighing 308 ± 24 g weredivided into two groups. On day 0, the20 animals in one group were surgically castrated and the other groupwas sham operated. Within each group, 10 rats were selected fortreadmill running (60% maximal O₂consumption, 1 h/day, 6 days/wk for 15 wk). The 20 sedentary rats wereused as controls. At the time the rats were killed(day 105), running had nosignificant effect on femoral mechanical properties either in castratedor in sham-operated rats. Femoral bone density was lowerin orchidectomized than in sham-operated rats. Nevertheless, it washigher in exercised than in sedentary rats. Femoral Ca contentparalleled changes in bone density. Treadmill running had nosignificant effect on plasma osteocalcin concentration but inhibitedthe increase in urinary deoxypyridinoline excretion observed incastrated rats. Image analysis (measured at the distal femoraldiaphysis) revealed that these effects mainly resulted from decreasedtrabecular bone resorption in castrated exercised rats.

     

Effect of endurance training and seasonal fluctuation on coagulation and fibrinolysis in young sedentary men

Van den Burg, P. J. M., J. E. H. Hospers, M. Van Vliet, W. L. Mosterd, B. N. Bouma, and I. A. Huisveld. Effect of endurance training and seasonal fluctuation on coagulation and fibrinolysis inyoung sedentary men. J. Appl. Physiol.82(2): 613-620, 1997.The effect of 12 wk of submaximal trainingon hemostatic variables was studied in 20 young sedentary men (Tr) and19 nontraining matched controls (Con). After training, a morepronounced increase in factor VIII coagulant activity(P < 0.01), reflected in a decrease in activated partial thromboplastin time(P < 0.01) during maximal exercise,was seen. Both basal plasminogen activator inhibitor 1 antigen (PAI-1Ag) and activity (PAI-1 Act; P < 0.05), as well as basal and exercise-induced tissue-type plasminogenactivator antigen (t-PA Ag; P < 0.05), were decreased after training. The overall effect onfibrinolysis was reflected in an increase in the t-PA Act/t-PA Ag ratioin the Tr group. In contrast, during the same period (February-June),the Con group demonstrated an increase in basal PAI-1 Ag and PAI-1 Act(P < 0.05), together with anincrease in basal and exercise-induced t-PA Ag(P < 0.05). Both basal andexercise-induced t-PA Act were unchanged, but t-PA Act/t-PA Ag wasdecreased (P < 0.05) in the Congroup. We conclude that physical training promotes both coagulation andfibrinolytic potential during exercise and may reverse unfavorableseasonal effects on fibrinolysis.

     

Exercise training restores decreased cellular immune functions in obese Zucker rats

Moriguchi, S., M. Kato, K. Sakai, S. Yamamoto, and E. Shimizu. Exercise training restores decreased cellular immune functions in obese Zucker rats. J. Appl.Physiol. 84(1): 311-317, 1998.This studyinvestigated whether exercise training had a beneficial effect on thedecreased mitogen response and improved a decreased expression ofglucose transporter 1 (GLUT-1) in splenocytes from obese Zucker rats.Experimental groups were lean and sedentary and exercise-trained obeseZucker rats. Exercise training, running on a motor-driven treadmill for5 days/wk for 40 wk, did not induce a significant decrease in bodyweight in obese Zucker rats. The plasma insulin concentration, showinga significant increase compared with lean Zucker rats, was unaffectedby exercise training. However, the plasma triglyceride concentration inobese Zucker rats was significantly depressed by exercise training,whereas it was still higher than that in lean Zucker rats. In addition,natural killer cell activity and concanavalin A-induced mitogenesis ofsplenic lymphocytes of obese Zucker rats were significantly restored. In these splenic lymphocytes, glucose uptake was significantly lowercompared with that in lean Zucker rats, which was also improved byexercise training. Although the expression of GLUT-1, the major glucosetransporter in immune cells, was depressed in splenic lymphocytes ofobese Zucker rats, exercise training induced a significant improvement.These results suggest that exercise training has a beneficial effect onthe decreased cellular immune functions in obese Zucker rats, which isassociated, in part, with the improvement in GLUT-1 expression.

     

Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712-717, 1997.Ten patients with preserved inotropic function having adual-chamber (right atrium and right ventricle) pacemaker placed forcomplete heart block were studied. They performed static one-leggedknee extension at 20% of their maximal voluntary contraction for 5 minduring three conditions: 1)atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HRfixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and3) HR fixed at peak exercise rate(DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode),mean arterial pressure (MAP) increased by 25 mmHg with no change instroke volume (SV) or systemic vascular resistance. During DOO-Rest andDOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of aSV-dependent increase in cardiac output (+1.3 and +1.8 l/min,respectively). The increase in SV during DOO-Rest utilized acombination of increased contractility and the Frank-Starling mechanism(end-diastolic volume 118-136 ml). However, during DOO-Ex, agreater left ventricular contractility (end-systolic volume 55-38ml) mediated the increase in SV.

     

Acute and chronic effects of exercise on leptin levels in humans

Pérusse, Louis, Gregory Collier, Jacques Gagnon,Arthur S. Leon, D. C. Rao, James S. Skinner, Jack H. Wilmore,André Nadeau, Paul Z. Zimmet, and Claude Bouchard. Acute andchronic effects of exercise on leptin levels in humans.J. Appl. Physiol. 83(1): 5-10, 1997.The acute (single bout of exercise) and chronic (exercisetraining) effects of exercise on plasma leptin were investigated in 97 sedentary adult men (n = 51) and women(n = 46) participating in the HERITAGEFamily Study. Exercise training consisted of a standardized 20-wkendurance training program performed in the laboratory on acomputer-controlled cycle ergometer. Maximal oxygen uptake, bodycomposition assessed by hydrostatic weighing, and fasting insulin levelwere also measured before and after training. Pre- and posttrainingblood samples were obtained before and after completion of a maximalexercise test on the cycle ergometer. Exercise training resulted insignificant changes in maximal oxygen uptake (increase in both genders)and body compostion (reduction of fat mass in men and increase infat-free mass in women). There were considerable interindividualdifferences in the leptin response to acute and chronic effects ofexercise, some individuals showing either increase or reduction inleptin, others showing almost no change. On average, leptin levels werenot acutely affected by exercise. After endurance training wascompleted, leptin levels decreased significantly in men (from 4.6 to3.9 ng/ml; P = 0.004) but not inwomen. However, after the training-induced changes in body fat masswere accounted for, the effects of exercise training were no longersignificant. Most of the variation observed in leptin levels afteracute exercise or endurance training appears to be within theconfidence intervals of the leptin assay. We conclude that there are nomeaningful acute or chronic effects of exercise, independent of theamount of body fat, on leptin levels in humans.

     

Plasma lipids and other factors in the LA/N corpulent rat in the presence of chronic exercise and food restriction

The effects of regular exercise and food restriction were studied in the LA/N corpulent rat up to age 9 months. This congenic strain of the Lister and Albany rat is normotensive, corpulent, and hyperlipidemic when homozygous for the corpulent (cp) gene derived from the Koletsky strain. Food restriction of corpulent animals to the intake of matched lean rats caused body weight to be significantly lower, although not as low as that of the lean animals. Plasma total cholesterol in freely eating sedentary corpulent animals was significantly higher (210 mg/100 mL) than in food-restricted rats (165 mg/100 mL), in which plasma cholesterol was considerably elevated compared with lean rats (80 mg/100 mL). Exercise caused a modest but significant increase in both total and high density lipoprotein cholesterol in both corpulent and lean rats. The rise was greater in corpulent rats and, in food-restricted exercising corpulent rats, the cholesterol concentrations were equivalent to those of freely eating corpulent animals. Systolic blood pressure in lean rats fell slowly from 146 mmHg at 8 weeks to 132 mmHg at 36 weeks and was not affected by exercise. Sedentary corpulent rats showed a rapid rise in systolic pressure from 107 mmHg at 7 weeks to 128 mmHg at 11 weeks. This rise was reduced by food restriction and completely prevented by the combination of food restriction and exercise. Thus, in this strain of rats exercise was associated with higher plasma cholesterol concentrations, while food restriction had limited effects.     

Enlargement of glycogen store in rat liver and muscle by fructose-diet intake and exercise training

Murakami, Taro, Yoshiharu Shimomura, Noriaki Fujitsuka,Masahiro Sokabe, Koji Okamura, and Shuichi Sakamoto. Enlargement of glycogen store in rat liver and muscle by fructose-diet intake andexercise training. J. Appl. Physiol.82(3): 772-775, 1997.This study investigated the effect oflong-term intake of a fructose diet and exercise training on glycogencontent in liver and skeletal muscle in female rats. Thirty-six rats (8 wk old) were divided into two dietary groups and were fed with acontrol (chow) diet or fructose diet (containing 20% fructose) for 12 wk. During this period, one-half of the rats in each dietary group weretrained by using a motor-driven treadmill (running speed of 25 m/minand duration of 90 min/day, 5 days/wk). The liver glycogen wasincreased by intake of a fructose diet and exercise training, and thecontent was in the following order: control-diet and sedentary rats < fructose-diet and sedentary rats  control-diet and trained rats < fructose-diet and trained rats in the ratio of 1:3.4:3.6:5.0. Theglycogen content in gastrocnemius muscle showed the same trend as thatin liver; the ratio was 1:1.3:1.3:1.6. These results indicate that bothlong-term intake of the fructose diet and exercise training synergistically increased glycogen in both tissues.

     

Effect of vitamin E deprivation and exercise training on induction of HSP70

Kelly, D. A., P. M. Tiidus, M. E. Houston, and E. G. Noble.Effect of vitamin E deprivation and exercise training on inductionof HSP70. J. Appl. Physiol. 81(6):2379-2385, 1996.To investigate the effects of dietary vitamin Edeprivation and chronic exercise on the relative content of selectedisoforms of the heat-shock protein 70 (HSP70) family in rat hindlimbmuscle, vitamin E was withheld for 16 wk from female rats thatunderwent treadmill run training during the final 8 wk. As indicated byincreased (P < 0.05) content of thestress-inducible isoform (HSP72), training did stress the exercisingmuscles. However, vitamin E deficiency did not alter HSP72 content innontrained rats and was associated with a lesser induction(P < 0.01) in some muscles oftrained animals. The constitutive isoform, which exhibited similarlevels in muscles of varying fiber types, was demonstrated to belargely refractory to exercise, with an equivocal response to vitamin Edeprivation. HSP72 content was correlated to type I myosin heavy chain(MHC-I) content but only in muscles of sedentary normal-diet rats.After training, HSP72 content in a muscle essentially devoid of MHC-I(superficial vastus lateralis) reached levels comparable to those in amuscle high in MHC-I (soleus).

     

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.

     

Resistance training and human cervical muscle recruitment plasticity

Conley, Michael S., Michael H. Stone, Michael Nimmons, andGary A. Dudley. Resistance training and human cervical muscle recruitment plasticity. J. Appl.Physiol. 83(6): 2105-2111, 1997.This studyexamined cervical neuromuscular adaptations to resistance training. TheResX group performed conventional resistance training plushead-extension exercise. Another group performed only conventional resistance training, and the control group performed no resistance exercise. Muscle use during head extension was determinedby quantifying shifts in T2 in serial-transaxial magnetic resonanceimages of the neck. ResX was the only group that showed a trainingeffect. Training decreased (P < 0.05) the cross-sectional area (CSA) of cervical muscle used to performsubmaximal head extension by 31%. This reflected a decrease(P < 0.05) in relative use of thesplenius capitis, semispinalis capitis, and semispinalis cervicis andmultifidus muscles by about one-third; their percentage of CSA showingcontrast shift was reduced from 60 to 40% on average. This sameexercise evoked no contrast shift in the levator scapulae, longissimus capitis and cervicis, and scalenus medius and anterior muscles posttraining, yet 20% or more of their CSA was engaged pretraining. The relative CSA of cervical musculature that was used to perform maximal head extension was increased(P < 0.05) 16% bytraining. The findings suggest functional redundancy ofneck musculature that can be modified by training; submaximal tasks canbe performed despite cessation of recruitment of individual muscles,yet recruitment can be increased for maximal efforts. These resultsalso suggest that neuromuscular adaptations to training require aspecific cervical exercise

     

Comparison of leucine kinetics in endurance-trained and sedentary humans

Whole body leucine kinetics was compared inendurance-trained athletes and sedentary controls matched for age,gender, and body weight. Kinetic studies were performed during 3 h ofrest, 1 h of exercise (50% maximal oxygen consumption), and 2 h ofrecovery. When leucine kinetics were expressed both per unit of bodyweight and per unit of fat-free mass, both groups demonstrated anincrease in leucine oxidation during exercise(P < 0.01). Trained athletes had agreater leucine rate of appearance during exercise and recovery compared with their sedentary counterparts(P < 0.05) and an increased leucineoxidation at all times on the basis of body weight(P < 0.05). However, all of thesebetween-group differences were eliminated when leucine kinetics werecorrected for fat-free tissue mass. Therefore, correctionof leucine kinetics for fat-free mass may be important whencross-sectional investigations on humans are performed. Furthermore,leucine oxidation, when expressed relative to whole-body oxygenconsumption during exercise, was similar between groups. It isconcluded that there was no difference between endurance-trained andsedentary humans in whole body leucine kinetics during rest, exercise,or recovery when expressed per unit of fat-free tissue mass.

     

Time- and order-dependent changes in functional and NO-mediated dilation during exercise training

Lash, Julia M., and H. Glenn Bohlen. Time- andorder-dependent changes in functional and NO-mediated dilation during exercise training. J. Appl. Physiol.82(2): 460-468, 1997.Arterial vessel responses to sodiumnitroprusside (SNP) and acetylcholine (ACh) were measured in thespinotrapezius muscle of sedentary (Sed) and treadmill-trained (Tr)rats to determine whether these endothelium-dependent (ACh) and-independent (SNP) mechanisms contribute to thetraining-induced increase in functional vasodilation previouslyobserved. Control and maximal vessel diameters were similar between Sedand Tr. After 8 wk of training, functional dilation (2-, 4-, and 8-Hzcontractions) was enhanced in all orders of vessels studied[terminal feed artery (FA), largest arterioles (1A), andintermediate-sized arterioles (2A)], but responses to SNP wereincreased only in FA. Responses to ACh were not significantly increasedin any vessel order. After 16 wk of training, functional dilation hadregressed in Tr such that only the FA response to 4 Hz wassignificantly elevated relative to Sed. However, the FA and 1Aresponses to SNP were significantly greater in Tr than in Sed, as werethe 1A and 2A responses to ACh. These results show a dissociation offunctional dilation and SNP- or ACh-mediated responses, as well asage-dependent interactions, a time-dependent progression, and vesselorder specificity in the adaptations to training.

     

Exercise training reduces skeletal muscle membrane arachidonate in the obese (fa/fa) Zucker rat

Compared with the lean(Fa/) genotype, obese(fa/fa) Zucker rats have arelative deficiency of muscle phospholipid arachidonate, and skeletalmuscle arachidonate in humans is positively correlated with insulinsensitivity. To assess the hypothesis that the positive effects ofexercise training on insulin sensitivity are mediated by increasedmuscle arachidonate, we randomized 20 lean and 20 obese weanling maleZucker rats to sedentary or treadmill exercise groups. After 9 wk,fasting serum, three skeletal muscles (white gastrocnemius, soleus, andextensor digitorum longus), and heart were obtained. Fasting insulinwas halved by exercise training in the obese rat. In whitegastrocnemius and extensor digitorum longus (fast-twitch muscles), butnot in soleus (a slow-twitch muscle) or heart, phospholipidarachidonate was lower in obese than in lean rats(P < 0.001). In all muscles,exercise in the obese rats reduced arachidonate(P < 0.03, by ANOVA contrast). Weconclude that improved insulin sensitivity with exercise in the obesegenotype is not mediated by increased muscle arachidonate and thatreduced muscle arachidonate in obese Zucker rats is unique tofast-twitch muscles.

     

Prior eccentric contractions impair maximal insulin action on muscle glucose uptake in the conscious rat

Asp, Sven, Allan Watkinson, Nicholas D. Oakes, and Edward W. Kraegen. Prior eccentric contractions impair maximal insulin action on muscle glucose uptake in the conscious rat.J. Appl. Physiol. 82(4):1327-1332, 1997.Our aim was to examine the effect of prioreccentric contractions on insulin action locally in muscle in theintact conscious rat. Anesthetized rats performed one-leg eccentriccontractions through the use of calf muscle electrical stimulationfollowed by stretch of the active muscles. Two days later, basal andeuglycemic clamp studies were conducted with the rats in the awakefasted state. Muscle glucose metabolism was estimated from2-[¹⁴C(U)]deoxy-D-glucoseandD-[3-³H]glucose administration, and comparisons were made between the eccentrically stimulated and nonstimulated (control) calfmuscles. At midphysiological insulin levels, effects ofprior eccentric exercise on muscle glucose uptake were notstatistically significant. Maximal insulin stimulation revealed reducedincremental glucose uptake above basal(P < 0.05 in the red gastrocnemius;P < 0.1 in the white gastrocnemiusand soleus) and impaired net glycogen synthesis in all eccentricallystimulated muscles (P < 0.05). Weconclude that prior eccentric contractions impair maximal insulin action (responsiveness) on local muscle glucose uptake and glycogen synthesis in the conscious rat.

     

Physiological adaptations to a weight-loss dietary regimen and exercise programs in women

Kraemer, William J., Jeff S. Volek, Kristine L. Clark, ScottE. Gordon, Thomas Incledon, Susan M. Puhl, N. Travis Triplett-McBride, Jeffrey M. McBride, Margot Putukian, and Wayne J. Sebastianelli. Physiological adaptations to a weight-loss dietary regimen andexercise programs in women. J. Appl.Physiol. 83(1): 270-279, 1997.Thirty-one women(mean age 35.4 ± 8.5 yr) who were overweight were matched andrandomly placed into either a control group (Con; n = 6), a diet-only group (D;n = 8), a diet+aerobic endurance exercise training group (DE; n = 9),or a diet+aerobic endurance exercise training+strength training group(DES; n = 8). After 12 wk, the threedietary groups demonstrated a significant(P  0.05) reduction in body mass,%body fat, and fat mass. No differences were observed in the magnitudeof loss among groups, in fat-free mass, or in resting metabolic rate.The DE and DES groups increased maximal oxygen consumption, and the DESgroup demonstrated increases in maximal strength. Weight loss resultedin a similar reduction in total serum cholesterol, low-densitylipoprotein cholesterol, and high-density lipoprotein cholesterol amongdietary groups. These data indicate that weight loss during moderatecaloric restriction is not altered by inclusion of aerobic oraerobic+resistance exercise, but diet in conjunction with training caninduce remarkable adaptations in aerobic capacity and muscular strengthdespite significant reductions in body mass.