Effects of 3 days of carbohydrate supplementation on muscle glycogen content and utilisation during a 1-h cycling performance

This study compared the effects of supplementing the normal diets of six trained cyclists [maximal oxygen uptake O_2max) 4.5 (0.36)l · min⁻¹; values are mean (SD)] with additional carbohydrate (CHO) on muscle glycogen utilisation during a 1-h cycle time-trial (TT). Using a randomised crossover design, subjects consumed either their normal diet (NORM) for 3 days, which consisted of 426 (137) g · day⁻¹ CHO [5.9 (1.4) g · kg⁻¹ body mass (BM)], or additional CHO (SUPP) to increase their intake to 661 (76) g · day⁻¹ [9.3 (0.7) g · kg⁻¹ BM]. The SUPP diet elevated muscle glycogen content from 459 (83) to 565 (62) mmol · kg⁻¹ dry weight (d.w.) (P < 0.05). However, despite the increased pre-exercise muscle glycogen stores, there was no difference in the distance cycled during the TT [40.41 (1.44) vs 40.18 (1.76) km for NORM and SUPP, respectively]. With NORM, muscle glycogen declined from 459 (83) to 175 (64) mmol · kg⁻¹ d.w., whereas with SUPP the corresponding values were 565 (62) and 292 (113) mmol · kg⁻¹ d.w. Accordingly, both muscle glycogen utilisation [277 (64) vs 273 (114) mmol · kg⁻¹ d.w.] and total CHO oxidation [169 (20) vs 165 (30) g · h⁻¹ for NORM and SUPP, respectively] were similar. Neither were there any differences in plasma glucose or lactate concentrations during the two experimental trials. Plasma glucose concentration averaged 5.5 (0.5) and 5.6 (0.6) mmol · l⁻¹, while plasma lactate concentration averaged 4.4 (1.9) and 4.4 (2.3) mmol · l⁻¹ for NORM and SUPP, respectively. The results of this study show that when well-trained subjects increase the CHO content of their diet for 3 days from 6 to 9 g · kg⁻¹ BM there is only a modest increase in muscle glycogen content. Since supplementary CHO did not improve TT performance, we conclude that additional CHO provides no benefit to performance for athletes who compete in intense, continuous events lasting 1 h. Furthermore, the substantial muscle CHO reserves observed at the termination of exercise indicate that whole-muscle glycogen depletion does not determine fatigue at this exercise intensity and duration. Accepted: 25 November 1996     

Exercise training induces glycogen sparing during exercise by old rats

Glycogen utilization during exercise appears to be related to muscle respiratory capacity. Since the decline in hindlimb muscle respiratory capacity that occurs in rats during old age is eliminated when young and old rats undergo an identical exercise training protocol, liver and gastrocnemius glycogen concentrations were determined in identically trained young and old Fischer 344 rats at rest and immediately after a 30-min run requiring approximately 75% of maximal O2 consumption. These values were also compared with untrained age-matched control animals. The animals, which were 10 or 24 mo old after 6 mo of training, were fasted for 24 h before they were killed. Resting gastrocnemius glycogen did not differ among the groups. After 30 min of running, gastrocnemius glycogen was lower in the untrained than the trained groups and was not different between the trained groups. Resting liver glycogen was lower in the old trained group than the untrained groups but not statistically different from the young trained group. The postrun liver glycogen did not differ among the groups. Estimated gastrocnemius and liver glycogen utilization during exercise was decreased in both trained groups compared with untrained age-matched controls. These results indicate that the training-induced glycogen sparing during exercise of the same relative intensity was not diminished with age in identically trained young and old rats.     

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats

β-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05 mg · kg⁻¹ +0.05 mg · kg⁻¹ · h⁻¹, n = 24); (2) naloxone (N, bolus 0.8 mg · kg⁻¹ + 0.4 mg · kg⁻¹, n = 24); or (3) volume-matched saline (S, n = 24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22 m · min⁻¹, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60 min [5.93 (0.32) mM] and 90 min [4.16 (0.29) mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26 mM] and N [4.97 (0.38) and 3.44 (0.25) mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU · ml⁻¹] at 60 and 90 min compared to S [24.5 (0.5) and 20.6 (0.6) uIU · ml⁻¹] and N [24.5 (0.4) and 21.6 (0.7) uIU · ml⁻¹] groups. Plasma C-peptide declined to a greater extent at 60 and 90 min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release. Accepted: 26 February 1997     

Quantitative assessment of degenerative changes in soleus muscle after hindlimb suspension and recovery

The aim of this study was to quantify the degenerative and regenerative changes in rat soleus muscle resulting from 3-week hindlimb suspension at 45° tilt (HS group, n = 8) and 4-week normal cage recovery (HS-R group, n = 7). Degenerative changes were quantified by microscope examination of muscle cross sections, and the myosin heavy chain (MHC) composition of soleus muscles was studied by sodium dodecyl sulphate polyacrylamide gel electrophoresis. At the end of 3-week hindlimb suspension, histological signs of muscle degenerative changes were detected in soleus muscles. There was a significant variability in the percentage of fibres referred to as degenerating (%dg) in individual animals in the HS group [%dg = 8.41 (SEM 0.5)%, range 4.66%–14.08%]. Moreover, %dg varied significantly along the length of the soleus muscle. The percentage of fibres with internal nuclei was less than %dg in HS-soleus muscles [4.12 (SEM 0.3)%, range 1.24%–8.86%]. In 4-week recovery rats, the greater part of the fibres that were not referred to as normal, retained central nuclei [15.8 (SEM 2.2)%, range 6.2%–21.1%]. A significant increase in the slow isoform of MHC was recorded in the HS-R rats, compared to muscles from age-matched rats (P < 0.01). These results would suggest that a cycle of myofibre degeneration-regeneration occurred during HS and passive recovery, and that the increased accumulation of slow MHC observed in soleus muscles after recovery from HS could be related to the prevalence of newly formed fibres. Accepted: 14 October 1996     

Treadmill exercise suppresses muscle cell apoptosis by increasing nerve growth factor levels and stimulating p-phosphatidylinositol 3-kinase activation in the soleus of diabetic rats

We investigated the effects of treadmill exercise performed regularly for 6 weeks on the levels of nerve growth factor (NGF), tyrosine kinase A and p75 receptors, phosphatidylinositol 3-kinase (PI3-K), mitogen-activated protein kinase/extracellular signal-regulated kinase (Erk) 1,2, cyclic AMP response element-binding protein (CREB), and caspase-3 in the soleus of rats with streptozotocin (STZ)-induced diabetes. Thirty-two male Sprague–Dawley rats were divided into the following four groups: (1) normal control group (NCG; n = 8), (2) normal exercise group (NEG; n = 8), (3) diabetes control group (DCG; n = 8), and (4) diabetes exercise group (DEG; n = 8). Diabetes was induced by intraperitoneal injection of STZ (55 mg/kg dissolved in 0.05 M citrate buffer, pH 4.5). Rats were subjected to treadmill exercise 5 days a week for 6 weeks. The protein level of NGF significantly increased in the NEG and DEG (p < 0.001), whereas the levels of tyrosine kinase A and p75 receptors significantly increased in the NEG (p < 0.001). The levels of t-PI3-K, p-PI3-K, and p-CREB, and the p-CREB/t-CREB ratio significantly increased in the NEG (p < 0.001, respectively). The p-PI3-K/t-PI3-K ratio significantly increased in the DEG (p < 0.001). The p-Erk1/t-Erk1 ratio significantly increased in the NEG (p < 0.001), whereas the p-Erk2/t-Erk2 ratio significantly decreased in the DCG and DEG (p < 0.001). The caspase-3 level significantly increased in the DCG compared with that in the DEG (p < 0.001). These results suggest that treadmill exercise increases NGF levels and accelerates p-PI3-K activation in order to suppress apoptotic cell death in the soleus muscle of diabetic rats.     

Endurance exercise training reduces lactate production

In situ muscle stimulation in trained and untrained rats was used to reevaluate whether adaptations induced by endurance exercise training result in decreased lactate production by contracting muscles. The gastrocnemius-plantaris-soleus muscle group was stimulated to perform isotonic contractions. After 3 min of stimulation with 100-ms trains at 50 Hz at 60/min, the increases in lactate concentration in the plantaris, soleus, and fast-twitch red muscle (deep portion of lateral head of gastrocnemius) were only approximately 50% as great in trained as in sedentary rats. In the predominantly fast-twitch white superficial portion of the medial head of the gastrocnemius the increase in lactate concentration was 28% less in the trained than in the sedentary group. The decreases in muscle glycogen concentration seen after 3 min of stimulation at 60 trains/min were smaller in the trained than in the untrained group. The reduction in lactate accumulation that occurred in the different muscles in response to training was roughly proportional to the degree of glycogen sparing. These results show that endurance training induces adaptations that result in a slower production of lactate by muscle during contractile activity.     

Acute effect of physical exercise on glycogen content and lipoprotein lipase activity in untrained diabetic rats

The effect of acute physical exercise on skeletal muscle glycogen content and on lipoprotein lipase activity of muscle, adipose and lung tissues was studied in streptozotocin diabetic and control rats. Rats were accustomed to treadmill running for two weeks after streptozotocin treatment. For an exercise bout of moderate intensity rats were randomly divided into two groups: one was sacrificed immediately after exercise and the other 24 hours afterwards. In addition there was a nonexercised sedentary group. No depletion of glycogen was observed after exercise in the vastus lateralis muscle of control (nondiabetic) rats. No difference in glycogen utilization was found in soleus muscle between diabetic and control rats. In diabetic rats a slight decrease occurred in the lipoprotein lipase activity in adipose tissue immediately after exercise, while in control rats there was a significant decline 24 hours after exercise. In soleus muscle a slight but significant increase of lipoprotein lipase activity occurred 24 hours after exercise in diabetic rats but not in control rats. The results suggest that nonketotic streptozotocin diabetes of short duration does not influence muscle glycogen in the resting state, but glycogen utilization is disturbed in white muscle during moderate treadmill running in untrained diabetic rats. The increase in lipoprotein lipase activity after physical exercise in red muscle of diabetic rats occurs during the recovery phase.     

Muscle damage induced by running training during recovery from hindlimb suspension: the effect of dantrolene sodium

We examined the extent of morphological alterations and the myosin heavy chain (MHC) distribution in the rat soleus muscle after a 4-week period of spontaneous recovery or retraining after hindlimb suspension (HS). Moreover, we tested the hypothesis that dantrolene sodium, which affects the flux of calcium over the sarcoplasmic reticulum membrane, was able to attenuate muscle damage. Three groups of rats were submitted to 3 weeks of HS, followed by either 4 weeks of unrestricted cage activity (HC, n = 7), or running training for the same period and were compared to age-matched animals (C, n = 8). Trained rats were treated with either placebo or dantrolene sodium (HTP, HTD, n = 8 each, respectively). Four weeks after HS recovery, the percentage of myofibres with internal nuclei (%in) was determined by histological staining with hematoxylin and eosin. %in was affected by the individual rat (P < 0.001), and was higher in the mid-belly region of the muscle (P < 0.05). Muscle damage, as estimated by %in, was more extensive in trained rats (i.e. HTP and HTD) than in HC animals (23% and 12%, respectively). Moreover, dantrolene sodium tended to exert a protective effect on training-induced muscle injury. A 12% increase in type I MHC was observed in both HTP and HTD rats, in comparison with group C animals (P < 0.001). The relative proportion of type-I MHC was inversely correlated with %in (r = −0.65, P < 0.001). Running recovery led to an increased citrate synthase activity in comparison with that of C or HC rats. In conclusion, the present findings demonstrate that running recovery from HS increases the incidence of muscle damage, and that dantrolene sodium administration has only limited protective effects against exercise-induced muscle injury. Accepted: 29 April 1997     

Exercise-induced muscle glycogen depletion and repletion in diabetic rats.

The purpose of this experiment was to examine glycogen depletion in muscles of chronic diabetic rats during treadmill running of moderate intensity and glycogen repletion following the exercise bouts. Diabetes was induced with a single intravenous injection of streptozotocin (70 mg × kg^?1). Glycogen concentrations in muscles from diabetic and normal animals were determined at rest, after running either 10 or 30 min at 23 m × min^?1 (5% incline), or 2, 4, or 8 hr following 30 min of running at the same speed and incline. With the exception of soleus muscle after 30 min of running, there were no differences in muscle glycogen contents between normal and diabetic rats before exercise, immediately after exercise, or during the recovery period. All muscles showed a significant loss of glycogen during exercise, and most muscles had completely restored their glycogen by 2 hr following exercise. Blood lactate concentrations were also similar for normal and diabetic rats at rest and after exercise. It is concluded that the diabetic condition studied in this experiment did not significantly alter muscle glycogen metabolism during exercise of moderate intensity or during recovery from the activity.     

Noninvasive skeletal muscle lactate detection between periods of intense exercise in humans

We investigated whether localized ¹H nuclear magnetic resonance spectroscopy (NMRS) using stimulated echoes (STEAM) with a long mixing time (t _m) allowed the suppression of the fat signal and detection of lactate in skeletal muscle. The ¹H NMRS sequence was first validated in three isolated and perfused rabbit biceps brachii muscles. Spectra were obtained on a wide-bore spectrometer using a dual-tuned probe (¹H and ³¹P). Death was simulated by ceasing the muscle perfusion, which allowed post-mortem changes to be followed. During and after the simulated death, changes in levels of pH and in content of energy-rich compounds were observed with ³¹P NMRS. Our results showed an inverse linear relationship between pH and lactate in each of the three rabbits (r = 0.93, P < 0.001; r = 0.92, P < 0.01; r = 0.89, P < 0.01) and a decrease in phosphocreatine and concomitant increase in lactate. We then investigated whether this sequence allowed repeated detection of lactate in human soleus muscle during the recovery between periods of intense exercise (force-velocity test, F-v test). Seven subjects mean age 25.1 (SEM 0.8) years participated in this study. Soleus muscle lactate was detected at rest and for 3 min 30 s of the 5-min recovery between periods using a 2.35-T 40-cm bore magnet spectrometer. Arm venous plasma lactate concentration was measured at rest, during the F-v test when the subject stopped pedalling (S₁), and at the end of each 5-min recovery between periods (S₂). Results showed that the venous plasma lactate concentration at S₁ and S₂ increased significantly from the beginning of the F-v test to peak anaerobic power (W _an,peak) (P < 0.001). The spectra showed that muscle lactate resonance intensity rose markedly when W _an,peak was achieved. The muscle lactate resonance intensity plotted as a percentage of the resting value increased significantly at W _an,peak compared with submaximal braking forces (P < 0.05). We concluded from these results that localized ¹H NMRS using STEAM with a long t _m allows suppression of the fat signal and repeated detection of lactate on isolated perfused skeletal muscle in animals and between periods of intense exercise in humans. Accepted: 19 January 1998     

More tetanic contractions are required for activating glucose transport maximally in trained muscle

Kawanaka, Kentaro, Izumi Tabata, and MitsuruHiguchi. More tetanic contractions are requiredfor activating glucose transport maximally in trained muscle.J. Appl. Physiol. 83(2): 429-433, 1997.Exercise training increases contraction-stimulated maximalglucose transport and muscle glycogen level in skeletal muscle.However, there is a possibility that more muscle contractions arerequired to maximally activate glucose transport in trained than inuntrained muscle, because increased glycogen level after training mayinhibit glucose transport. Therefore, the purpose of this study was toinvestigate the relationship between the increase in glucose transportand the number of tetanic contractions in trained and untrained muscle.Male rats swam 2 h/day for 15 days. In untrained epitrochlearis muscle,resting glycogen was 26.6 µmol glucose/g muscle. Ten, 10-s-longtetani at a rate of 1 contraction/min decreased glycogen level to 15.4 µmol glucose/g muscle and maximally increased2-deoxy-D-glucose(2-DG) transport. Training increasedcontraction-stimulated maximal 2-DG transport (+71%;P < 0.01), GLUT-4 protein content(+78%; P < 0.01), and restingglycogen level (to 39.3 µmol glucose/g muscle;P < 0.01) on the next day after thetraining ended, although this training effect might be due, at least inpart, to last bout of exercise. In trained muscle, 20 tetani werenecessary to maximally activate glucose transport. Twenty tetanidecreased muscle glycogen to a lower level than 10 tetani (18.9 vs.24.0 µmol glucose/g muscle; P < 0.01). Contraction-stimulated 2-DG transport was negatively correlatedwith postcontraction muscle glycogen level in trained (r = 0.60;P < 0.01) and untrained muscle(r = 0.57;P < 0.01).

     

The addition of fenugreek extract (Trigonella foenum-graecum) to glucose feeding increases muscle glycogen resynthesis after exercise

Summary. The purpose of this study was to determine the effects of ingesting an oral supplement containing 4-Hydroxyisoleucine (4-OH-Ile, isolated from fenugreek seeds [Trigonella foenum-graecum]) with a glucose beverage on rates of post-exercise muscle glycogen resynthesis in trained male cyclists. Following an overnight fast (12hr), subjects completed a 90-minute glycogen depletion ride after which a muscle biopsy was obtained from the vastus lateralis. Immediately and 2 hours after the muscle biopsy, subjects ingested either an oral dose of dextrose (Glu) (1.8g·kg BW^–1) or 4-OH-Ile supplement (Glu+4-OH-Ile, including 2.0mg·kg^–1 4-OH-Ile with the same oral dose of dextrose) with a second muscle biopsy 4 hours after exercise. Post exercise muscle glycogen concentration was similar for both trials. Overall, there was a significant increase in glucose and insulin concentrations from time 0 throughout the majority of the 4-hour recovery period, with no significant differences between the two trials at any time point. Although muscle glycogen concentration significantly increased from immediately post exercise to 4hr of recovery for both trials, the net rate of muscle glycogen resynthesis was 63% greater during Glu+4-OH-Ile (10.6±3.3 vs. 6.5±2.6g·kg wet wt.^–1·hr.^–1 for the Glu+4-OH-Ile and Glu trials, respectively). These data demonstrate that when the fenugreek extract supplement (4-OH-Ile) is added to a high oral dose of dextrose, rates of post-exercise glycogen resynthesis are enhanced above dextrose alone.     

Influence of light physical activity on cardiac responses during recovery from exercise in humans

To examine the influence of light exercise on cardiac responses during recovery from exercise, we measured heart rate (HR), stroke volume (SV), and cardiac output (Q˙ _c) in five healthy untrained male subjects in an upright position before, during, and after 10-min steady-state cycle exercise at an exercise intensity of 170 W, corresponding to a mean of 68 (SD 4)% of maximal oxygen uptake. The recovery phase was evaluated separately for three different conditions: 10 min of complete rest (passive recovery), 7 min of pedalling at 20-W exercise intensity followed by 3 min of rest (partially active recovery), and 7 min of pedalling at 40-W exercise intensity followed by 3 min of rest (partially active recovery), on an upright cycle ergometer. The time courses of decreases in HR in the two active recovery phases at different exercise intensities were almost identical to those in the passive recovery phase. However, the subsequent HR reductions during the rest after active recovery at 20 W and at 40 W were mean 7.5 (SD 4.4) and mean 10.0 (SD 3.1) beats · min⁻¹, respectively, both of which were significantly larger (P<0.05 and P<0.005) than the corresponding reduction [1.4 (SD 2.5) beats · min⁻¹] for passive recovery. The SV values at the two exercise intensities during the active recovery periods were maintained at levels similar to that during 170-W steady-state exercise. In contrast, the SV during passive recovery decreased gradually to a level significantly below the initial baseline level at rest before exercise (P<0.05). The resultant time courses of CO values during active recovery were significantly higher (each P<0.05) than that during passive recovery. It was concluded from these findings that light post-exercise physical activity plays an important role in facilitating the venous return from the muscles and in restoring the elevated HR to the pre-exercise resting level. Accepted: 17 September 1997     

Effect of endurance exercise training on muscle glycogen supercompensation in rats

Nakatani, Akira, Dong-Ho Han, Polly A. Hansen, Lorraine A. Nolte, Helen H. Host, Robert C. Hickner, and John O. Holloszy. Effect of endurance exercise training on muscle glycogensupercompensation in rats. J. Appl.Physiol. 82(2): 711-715, 1997.The purpose of this study was to test the hypothesis that the rate and extent ofglycogen supercompensation in skeletal muscle are increased byendurance exercise training. Rats were trained by using a 5-wk-long swimming program in which the duration of swimming was gradually increased to 6 h/day over 3 wk and then maintained at 6 h/day for anadditional 2 wk. Glycogen repletion was measured in trained anduntrained rats after a glycogen-depleting bout of exercise. The ratswere given a rodent chow diet plus 5% sucrose in their drinking waterad libitum during the recovery period. There were remarkabledifferences in both the rates of glycogen accumulation and the glycogenconcentrations attained in the two groups. The concentration ofglycogen in epitrochlearis muscle averaged 13.1 ± 0.9 mg/g wet wtin the untrained group and 31.7 ± 2.7 mg/g in the trained group(P < 0.001) 24 h after the exercise.This difference could not be explained by a training effect on glycogensynthase. The training induced ~50% increases in muscle GLUT-4glucose transporter protein and in hexokinase activity inepitrochlearis muscles. We conclude that endurance exercise trainingresults in increases in both the rate and magnitude of muscle glycogensupercompensation in rats.

     

The post-exercise glycogen recovery in tissues of trained rats.

The post-exercise glycogen recovery in myocardium, liver, diaphragm muscle and musculus biceps femoris was compared in untrained and trained rats. The glycogen level in myocardium of the trained rats was significantly higher than that in the untrained ones only immediately after the exercise-test and on the second day after the exercise. The liver glycogen levels on each of the examined post-exercise days were similar in both groups and did not differ from the control values. The post-exercise glycogen recovery in the diapraghm muscle of the untrained rats was also similar to that in the trained animals. In musculus bicpes femoris similar post-exercise supercompensation was found in both groups except on the second day when the glycogen level in the trained animals was significantly higher than that in the untrained ones. The results suggest that it is necessary to separate the effects of training from those of the last bout of exercise in the training program when the effect of training is examined.     

Changes in protein synthesis in rats in response to endurance training

Experiments were conducted to investigate the influence of endurance exercise training on protein synthesis in skeletal muscle, heart, and liver. Training decreased incorporation of [¹⁴C]-leucine into proteins of the stromal fraction of muscle but there was no change in amino acid incorporation into proteins of the sarcoplasmic and myofibrillar fractions. Incorporation of [¹⁴C]-leucine into the protein of heart, liver, and plasma was depressed in trained rats compared to untrained rats. The specific radioactivity of [¹⁴C]-leucine was similar in tissues of trained and untrained rats and thus the depressed amino acid incorporation represents a decrease in the rate of protein synthesis. These observations demonstrate that the adaptation of muscle protein metabolism to endurance training is quite different than the alterations during work-induced hypertrophy of muscle. The difference in adaptation probably relates to the functional differences between the types of exercise. However depression of protein synthesis in trained rats is a general effect in several tissues and not an effect localized in muscle tissue.     

Glucose uptake is increased in trained vs. untrained muscle during heavy exercise.

Endurance training increases muscle content of glucose transporter proteins (GLUT-4) but decreases glucose utilization during exercise at a given absolute submaximal intensity. We hypothesized that glucose uptake might be higher in trained vs. untrained muscle during heavy exercise in the glycogen-depleted state. Eight untrained subjects endurance trained one thigh for 3 wk using a knee-extensor ergometer. The subjects then performed two-legged glycogen-depleting exercise and consumed a carbohydrate-free meal thereafter to keep muscle glycogen concentration low. The next morning, subjects performed dynamic knee extensions with both thighs simultaneously at 60, 80, and until exhaustion at 100% of each thigh's peak workload. Glucose uptake was similar in both thighs during exercise at 60% of thigh peak workload. At the end of 80 and at 100% of peak workload, glucose uptake was on average 33 and 22% higher, respectively, in trained compared with untrained muscle (P < 0.05). Training increased the muscle content of GLUT-4 by 66% (P < 0. 05). At exhaustion, glucose extraction correlated significantly (r = 0.61) with total muscle GLUT-4 protein. Thus, when working at a high load with low glycogen concentrations, muscle glucose uptake is significantly higher in trained than in untrained muscle. This may be due to the higher GLUT-4 protein concentration in trained muscle.     

The effect of severe eccentric exercise-induced muscle damage on plasma elastase, glutamine and zinc concentrations

The aim of this study was to determine if severe exercise-induced muscle damage alters the plasma concentrations of glutamine and zinc. Changes in plasma concentrations of glutamine, zinc and polymorphonuclear elastase (an index of phagocytic cell activation) were examined for up to 10 days following eccentric exercise of the knee extensors of one leg in eight untrained subjects. The exercise bout consisted of 20 repetitions of electrically stimulated eccentric muscle actions on an isokinetic dynamometer. Subjects experienced severe muscle soreness and large increases in plasma creatine kinase activity indicative of muscle fibre damage. Peak soreness occurred at 2 days post-exercise and peak creatine kinase activity [21714 (6416) U · l⁻¹, mean (SEM)] occurred at 3 days post-exercise (P < 0.01 compared with pre-exercise). Plasma elastase concentration was increased at 3 days post-exercise compared with pre-exercise (P < 0.05), and is presumably indicative of ongoing phagocytic leucocyte infiltration and activation in the damaged muscles. There were no significant changes in plasma zinc and glutamine concentrations in the days following eccentric exercise. We conclude that exercise-induced muscle damage does not produce changes in plasma glutamine or zinc concentrations despite evidence of phagocytic neutrophil activation. Accepted: 3 November 1997     

Specificity of resistance training responses in neck muscle size and strength

This study examined hypertrophy after head extension resistance training to assess which muscles of the complicated cervical neuromuscular system were used in this activity. We also determined if conventional resistance exercises, which are likely to evoke isometric action of the neck, induce generalized hypertrophy of the cervical muscle. Twenty-two active college students were studied. [mean (SE) age, weight and height: 21 (1) years, 71 (4) kg and 173 (3) cm, respectively]. Subjects were assigned to one of three groups: RESX (head extension exercise and other resistance exercises), RES (resistance exercises without specific neck exercise), or CON (no training). Groups RESX (n = 8) and RES (n = 6) trained 3 days/week for 12 weeks with large-muscle mass exercises (squat, deadlift, push press, bent row and mid-thigh pull). Group RESX also performed three sets of ten repetitions of a head extension exercise 3 days/week with a load equal to the 3 × 10 repetition maximum (RM). Group CON (n = 8) was a control group. The cross-sectional area (CSA) of nine individual muscles or muscle groups was determined by magnetic resonance imaging (MRI) of the cervical region. The CSA data were averaged over four contiguous transaxial slices in which all muscles of interest were visible. The 3 × 10 RM for the head extension exercise increased for RESX after training [from 17.9 (1.0) to 23.9 (1.4) kg, P < 0.05] but not for RES [from 17.6 (1.4) to 17.7 (1.9)␣kg] or CON [from 10.1 (2.2) to 10.3 (2.1) kg]. RESX showed an increase in total neck muscle CSA after training [from 19.5 (3.0) to 22.0 (3.6) cm², P < 0.05], but RES and CON did not [from 19.6 (2.9) to 19.7 (2.9)␣cm² and 17.0 (2.5) to 17.0 (2.4) cm², respectively]. This hypertrophy for RESX was due mainly to increases in CSA of 23.9 (3.2), 24.0 (5.8), and 24.9 (5.3)% for the splenius capitis, and semispinalis capitis and cervicis muscles, respectively. The lack of generalized neck muscle hypertrophy in RES was not due to insufficient training. For example, the CSA of their quadriceps femoris muscle group, as assessed by MRI, increased by 7 (1)% after this short-term training (P < 0.05). The results suggest that: (1) the splenius capitis, and semispinalis capitis and cervicis muscles are mainly responsible for head extension; (2) short-term resistance training does not provide a sufficient stimulus to evoke neck muscle hypertrophy unless specific neck exercises are performed; and (3) the postural role of head extensors provides modest loading in bipeds. Accepted: 15 October 1996     

Post-exercise glycogen resynthesis in trained high-protein or high-fat-fed rats after glucose feeding

This study examined the effect on glycogen resynthesis during recovery from exercise of feeding glucose orally to physically trained rats which had been fed for 5 weeks on high-protein low fat (HP), high-protein/long-chain triglyceride (LCT) or high carbohydrate (CHO) diets. Muscle glycogen remained low and hepatic gluconeogenesis was stimulated by long-term fat or high-protein diets. The trained rats received, via a stomach tube, 3 ml of a 34% glucose solution immediately after exercise (2 h at 20 m.min-1), followed by 1-ml portions at hourly intervals until the end of the experiments. When fed glucose soleus muscle glycogen overcompensation occurred rapidly in the rats fed all three diets following prolonged exercise. In LCT- and CHO-fed rats, glucose feeding appeared more effective for soleus muscle repletion than in HP-fed rats. The liver demonstrated no appreciable glycogen overcompensation. A complete restoration of liver glycogen occurred within a 2- to 4-h recovery period in the rats fed HP-diet, while the liver glycogen store had been restored by only 67% in CHO-fed rats and 84% in LCT-fed rats within a 6-h recovery period. This coincides with low gluconeogenesis efficiency in these animals.