Glycogen loading alters muscle glycogen resynthesis after exercise.

This study compared muscle glycogen recovery after depletion of approximately 50 mmol/l (DeltaGly) from normal (Nor) resting levels (63.2 +/- 2.8 mmol/l) with recovery after depletion of approximately 50 mmol/l from a glycogen-loaded (GL) state (99.3 +/- 4.0 mmol/l) in 12 healthy, untrained subjects (5 men, 7 women). To glycogen load, a 7-day carbohydrate-loading protocol increased muscle glycogen 1.6 +/- 0.2-fold (P < or = 0.01). GL subjects then performed plantar flexion (single-leg toe raises) at 50 +/- 3% of maximum voluntary contraction (MVC) to yield DeltaGly = 48.0 +/- 1.3 mmol/l. The Nor trial, performed on a separate occasion, yielded DeltaGly = 47.5 +/- 4.5 mmol/l. Interleaved natural abundance (13)C-(31)P-NMR spectra were acquired and quantified before exercise and during 5 h of recovery immediately after exercise. During the initial 15 min after exercise, glycogen recovery in the GL trial was rapid (32.9 +/- 8.9 mmol. l(-1). h(-1)) compared with the Nor trial (15.9 +/- 6.9 mmol. l(-1). h(-1)). During the next 45 min, GL glycogen synthesis was not as rapid as in the Nor trial (0.9 +/- 2.5 mmol. l(-1). h(-1) for GL; 14.7 +/- 3.0 mmol. l(-1). h(-1) for Nor; P < or = 0.005) despite similar glucose 6-phosphate levels. During extended recovery (60-300 min), reduced GL recovery rates continued (1.3 +/- 0.5 mmol. l(-1). h(-1) for GL; 3.9 +/- 0.3 mmol. l(-1). h(-1) for Nor; P < or = 0.001). We conclude that glycogen recovery from heavy exercise is controlled primarily by the remaining postexercise glycogen concentration, with only a transient synthesis period when glycogen levels are not severely reduced.     

Hypohydration does not impair skeletal muscle glycogen resynthesis after exercise

The purpose of this investigation was to examine the effects of moderate hypohydration (HY) on skeletal muscle glycogen resynthesis after exhaustive exercise. On two occasions, eight males completed 2 h of intermittent cycle ergometer exercise (4 bouts of 17 min at 60% and 3 min at 80% of maximal O2 consumption/10 min rest) to reduce muscle glycogen concentrations (control values 711 +/- 41 mumol/g dry wt). During one trial, cycle exercise was followed by several hours of light upper body exercise in the heat without fluid replacement to induce HY (-5% body wt); in the second trial, sufficient water was ingested during the upper body exercise and heat exposure to maintain euhydration (EU). In both trials, 400 g of carbohydrate were ingested at the completion of exercise and followed by 15 h of rest while the desired hydration level was maintained. Muscle biopsy samples were obtained from the vastus lateralis immediately after intermittent cycle exercise (T1) and after 15 h of rest (T2). During the HY trial, the muscle water content was lower (P less than 0.05) at T1 and T2 (288 +/- 9 and 265 +/- 5 ml/100 g dry wt, respectively; NS) than during EU (313 +/- 8 and 301 +/- 4 ml/100 g dry wt, respectively; NS). Muscle glycogen concentration was not significantly different during EU and HY at T1 (200 +/- 35 vs. 251 +/- 50 mumol/g dry wt) or T2 (452 +/- 34 vs. 491 +/- 35 mumol/g dry wt). These data indicate that, despite reduced water content during the first 15 h after heavy exercise, skeletal muscle glycogen resynthesis is not impaired.     

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

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

     

Impaired muscle glycogen resynthesis after a marathon is not caused by decreased muscle GLUT-4 content

Asp, Sven, Thomas Rohde, and Erik A. Richter. Impairedmuscle glycogen resynthesis after a marathon is not caused by decreasedmuscle GLUT-4 content. J. Appl.Physiol. 83(5): 1482-1485, 1997.Our purpose wasto investigate whether the slow rate of muscle glycogen resynthesisafter a competitive marathon is associated with a decrease in the totalmuscle content of the muscle glucose transporter (GLUT-4). Sevenwell-trained marathon runners participated in the study, and musclebiopsies were obtained from the lateral head of the gastrocnemiusmuscle before, immediately after, and 1, 2, and 7 days after themarathon, as were venous blood samples. Muscle GLUT-4 content wasunaltered over the experimental period. Muscle glycogen concentrationwas 758 ± 53 mmol/kg dry weight before the marathon anddecreased to 148 ± 39 mmol/kg dry weight immediately afterward.Despite a carbohydrate-rich diet (containing at least 7 gcarbohydrate · kg bodymass¹ · day¹),the muscle glycogen concentration remained 30% lower than before-race values 2 days after the race, whereas it had returned to before-race levels 7 days after the race. We conclude that the total GLUT-4 proteincontent is unaltered in the lateral gastrocnemius after a competitivemarathon and that the slow recovery of muscle glycogen after the raceapparently involves factors other than changes in the total content ofthis protein.

     

Lactate as substrate for glycogen resynthesis after exercise

Muscle glycogen levels in the perfused rat hemicorpus preparation were reduced two-thirds by electrical stimulation plus exposure to epinephrine (10(-7) M) for 30 min. During the contraction period muscle lactate concentrations increased from a control level of 3.6 +/- 0.6 to a final value of 24.1 +/- 1.6 mumol/g muscle. To determine whether the lactate that had accumulated in muscle during contraction could be used to resynthesize glycogen, glycogen levels were determined after 1-3 h of recovery from the contraction period during which time the perfusion medium (flow-through system) contained low (1.3 mmol/l) or high (10.5 or 18 mmol/l) lactate concentrations but no glucose. With the low perfusate lactate concentration, muscle lactate levels declined to 7.2 +/- 0.8 mumol/g muscle by 3 h after the contraction period and muscle glycogen levels did not increase (1.28 +/- 0.07 at 3 h vs. 1.35 +/- 0.09 mg glucosyl U/g at end of exercise). Lactate disappearance from muscle was accounted for entirely by output into the venous effluent. With the high perfusate lactate concentrations, muscle lactate levels remained high (13.7 +/- 1.7 and 19.3 +/- 2.0 mumol/g) and glycogen levels increased by 1.11 and 0.86 mg glucosyl U/g, respectively, after 1 h of recovery from exercise. No more glycogen was synthesized when the recovery period was extended. Therefore, it appears that limited resynthesis of glycogen from lactate can occur after the contraction period but only when arterial lactate concentrations are high; otherwise the lactate that builds up in muscle during contraction will diffuse into the bloodstream.     

Impaired muscle glycogen storage after muscle biopsy

To assess the effects of repeated needle biopsies on the rate of muscle glycogen repletion, eight male subjects were studied immediately after and 2 days after an exhaustive cycling bout. A single biopsy was obtained from the right vastus lateralis muscle immediately after an exhaustive cycling bout. Two days later, a sample was taken 1 cm lateral or medial to sample A. In four of these subjects, additional biopsies were taken 3 cm distal and proximal. A control specimen was also taken from the left leg 2 days after the exercise. Ten days after the exercise, muscle was again sampled from each leg of these four subjects. Analysis of these samples revealed that the initial biopsy impaired glycogen storage in the muscle taken 1 cm medial or lateral to the previous site. This reduction in glycogen storage was most pronounced in the first 2 days after the exercise. Samples taken distal and proximal to the initial biopsy contained, on the average, less glycogen than the contralateral leg, but these differences were only significantly different in the distal muscle sample. Alteration in muscle glycogen storage was seen to persist for 10 days after the first biopsy, suggesting that care must be taken in selecting the site for repeated biopsies from the same muscle.     

High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine.

We determined the effect of coingestion of caffeine (Caff) with carbohydrate (CHO) on rates of muscle glycogen resynthesis during recovery from exhaustive exercise in seven trained subjects who completed two experimental trials in a randomized, double-blind crossover design. The evening before an experiment subjects performed intermittent exhaustive cycling and then consumed a low-CHO meal. The next morning subjects rode until volitional fatigue. On completion of this ride subjects consumed either CHO [4 g/kg body mass (BM)] or the same amount of CHO + Caff (8 mg/kg BM) during 4 h of passive recovery. Muscle biopsies and blood samples were taken at regular intervals throughout recovery. Muscle glycogen levels were similar at exhaustion [ approximately 75 mmol/kg dry wt (dw)] and increased by a similar amount ( approximately 80%) after 1 h of recovery (133 +/- 37.8 vs. 149 +/- 48 mmol/kg dw for CHO and Caff, respectively). After 4 h of recovery Caff resulted in higher glycogen accumulation (313 +/- 69 vs. 234 +/- 50 mmol/kg dw, P < 0.001). Accordingly, the overall rate of resynthesis for the 4-h recovery period was 66% higher in Caff compared with CHO (57.7 +/- 18.5 vs. 38.0 +/- 7.7 mmol x kg dw(-1) x h(-1), P < 0.05). After 1 h of recovery plasma Caff levels had increased to 31 +/- 11 microM (P < 0.001) and at the end of the recovery reached 77 +/- 11 microM (P < 0.001) with Caff. Phosphorylation of CaMK(Thr286) was similar after exercise and after 1 h of recovery, but after 4 h CaMK(Thr286) phosphorylation was higher in Caff than CHO (P < 0.05). Phosphorylation of AMP-activated protein kinase (AMPK)(Thr172) and Akt(Ser473) was similar for both treatments at all time points. We provide the first evidence that in trained subjects coingestion of large amounts of Caff (8 mg/kg BM) with CHO has an additive effect on rates of postexercise muscle glycogen accumulation compared with consumption of CHO alone.     

Time course of glycogen accumulation after eccentric exercise.

This study examined the time course of glycogen accumulation in skeletal muscle depleted by concentric work and subsequently subjected to eccentric exercise. Eight men exercised to exhaustion on a cycle ergometer [70% of maximal O2 consumption (VO2max)] and were placed on a carbohydrate-restricted diet. Approximately 12 h later they exercised one leg to subjective failure by repeated eccentric action of the knee extensors against a resistance equal to 120% of their one-repetition maximum concentric knee extension force (ECC leg). The contralateral leg was not exercised and served as a control (CON leg). During the 72-h recovery period, subjects consumed 7 g carbohydrate.kg body wt-1.day-1. Moderate soreness was experienced in the ECC leg 24-72 h after eccentric exercise. Muscle biopsies from the vastus lateralis of the ECC and CON legs revealed similar glycogen levels immediately after eccentric exercise (40.2 +/- 5.2 and 47.6 +/- 6.4 mmol/kg wet wt, respectively; P greater than 0.05). There was no difference in the glycogen content of ECC and CON legs after 6 h of recovery (77.7 +/- 7.9 and 85.1 +/- 4.9 mmol/kg wet wt, respectively; P greater than 0.05), but 18 h later, the ECC leg contained 15% less glycogen than the CON leg (90.2 +/- 8.2 vs. 105.8 +/- 8.9 mmol/kg wet wt; P less than 0.05). After 72 h of recovery, this difference had increased to 24% (115.8 +/- 8.0 vs. 153.0 +/- 12.2 mmol/kg wet wt; P less than 0.05). These data confirm that glycogen accumulation is impaired in eccentrically exercised muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of gluconeogenic precursor flux alterations on glycogen resynthesis after prolonged exercise

The importance of gluconeogenic substrates (i.e., lactate, glycerol, and alanine) in the glycogen resynthesis observed in fasting rats after exhausting submaximal exercise [R.D. Fell et al. Am. J. Physiol. 238 (Regulatory Integrative Comp. Physiol. 7): R328-R332, 1980] was examined in muscles and liver in response to pharmacological alterations of gluconeogenic precursor flux. The minor role of lactate for glycogen resynthesis after prolonged submaximal exercise was confirmed by the insignificant accumulation of lactate neither in muscles nor in plasma. When the rate of lipolysis is reduced either by beta-blockade or by nicotinic acid injection, the replenishment of muscle glycogen persisted, suggesting that glycerol released by triglycerides hydrolysis did not play an important role in glycogen resynthesis. On the other hand, when pyruvate oxidation is enhanced by dichloroacetate (DCA), thus reducing plasma levels of lactate and alanine, glycogen resynthesis was completely blocked in liver and partly in some but not all muscles. This failure in total inhibition of glycogen resynthesis associated with the significant reduction of the plasma alanine level could be attributed to the possible stimulation of gluconeogenesis from alanine by DCA (R.A. Harris and D.W. Crabb. Arch. Biochem. Biophys. 189: 364-371, 1978). The results could point out alanine as the major gluconeogenic substrate during recovery from exhaustive exercise in fasting conditions.     

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.     

Potential biomarkers of muscle injury after eccentric exercise

Proteomics was utilized to identify novel potential plasma biomarkers of exercise-induced muscle injury. Muscle injury was induced in nine human volunteers by eccentric upper extremity exercise. Liquid chromatography–mass spectrometry identified 30 peptides derived from nine proteins which showed significant change in abundance post-exercise. Four of these proteins, haemoglobin α chain, haemoglobin β chain, α1-antichymotrypsin (ACT) and plasma C-1 protease inhibitor (C1 Inh), met the criterion for inclusion based on changes in at least two distinct peptides. ACT and C1 Inh peptides peaked earlier post-exercise than creatine kinase, and thus appear to provide new information on muscle response to injury.     

Impaired substrate oxidation in healthy elderly men after eccentric exercise.

The metabolic response to eccentric exercise in healthy older adults is unknown. Therefore, substrate metabolism was examined in the basal state and after sustained hyperglycemia (180 min, 10 mM) in eight healthy, sedentary older [66 +/- 2 yr; body mass index (BMI) of 25.5 +/- 1.2 kg/m] and nine younger (23 +/- 1 yr; BMI of 23.6 +/- 1.7 kg/m) men, under control conditions and 48 h after eccentric exercise. Indirect calorimetry was performed to evaluate carbohydrate and lipid oxidation (C(ox) and L(ox), respectively). Eccentric exercise caused muscle soreness and increased plasma creatine kinase in both groups of men (P < 0.02). Although a similar level of hyperglycemia was maintained in the two groups, glucose infusion rates were lower (P < 0.001) in the older men. Compared with basal levels, hyperglycemia stimulated an increase in C(ox) and a decrease in L(ox) during the control and exercise trials in the younger group (P < 0.03), but only during the control trial in the older subjects (P < 0.007). C(ox) was unchanged after eccentric exercise in the younger men [4.00 +/- 0.30 vs. 3.54 +/- 0.44 mg x kg fat-free mass (FFM)(-1) x min(-1); exercise vs. control] but was suppressed by 20% in the older group (3.37 +/- 0.37 vs. 4.21 +/- 0.23 mg x kg FFM(-1) x min(-1); P < 0.04). Moreover, L(ox) was reduced by 38% in the younger subjects (0.47 +/- 0.09 vs. 0.76 +/- 0.10 mg x kg FFM(-1) x min(-1); P< 0.03) but was augmented by 89% in the older group (0.68 +/- 0.11 vs. 0.36 +/- 0.08 mg x kg FFM(-1) x min(-1); P < 0.04). In addition, hyperglycemia-stimulated C(ox), L(ox), and respiratory exchange ratio responses to eccentric exercise were related to abdominal adiposity (r = -0.57, P < 0.04, r = 0.68, P < 0.02 and r = -0.60, P < 0.02, respectively). Despite normal glucose tolerance and the absence of obesity per se, older men experience a reduction in carbohydrate oxidation in response to hyperglycemia after eccentric exercise.     

Impaired action potential conduction at high force levels after eccentric exercise

High-density surface electromyography was used to examine whether gross sarcolemmal function is impaired in m. biceps brachii after intensive eccentric elbow flexor exercise, when measured at wide range of isometric contraction levels.Root mean square (RMS), mean power frequency (MNF) and mean muscle fibre conduction velocity (CV) were calculated before and up to four days post-exercise.Maximal isometric voluntary (MVC) force decreased by 21.3 ± 5.6% two hours after exercise, and by 12.6 ± 11.1% two days post-exercise. CV and MNF decreased both during MVC (CV from 4.1 ± 0.3 m/s to 3.8 ± 0.4 m/s and MNF from 92.6 ± 10 Hz to 85.2 ± 11 Hz) and during electrically evoked maximal M-wave (CV from 4.1 ± 0.3 m/s to 3.0 ± 0.5 m/s and MNF from 97.1 ± 27.2 Hz to 78.0 ± 24.4 Hz) two hours post-exercise. Furthermore, at submaximal isometric force levels, CV and MNF decreased only at higher contraction levels (40%, 50% and 75% of MVC) two hour post-exercise.It can be concluded that intensive exercise can temporarily impair gross sarcolemmal function. In addition, since this only occurred at high force levels, based on Henneman’s size principle, it seems that higher threshold motor units were predominantly affected.     

Gender differences in muscle inflammation after eccentric exercise.

Unaccustomed exercise is followed by delayed-onset muscle soreness and morphological changes in skeletal muscle. Animal studies have demonstrated that women have an attenuated response to muscle damage. We studied the effect of eccentric exercise in untrained male (n = 8) and female (n = 8) subjects using a unilateral exercise design [exercise (Ex) and control (Con) legs]. Plasma granulocyte counts [before (Pre) and 48 h after exercise (+48h)] and creatine kinase activity [Pre, 24 h after exercise (+24h), +48h, and 6 days after exercise (+6d)] were determined before (Pre) and after (+24h, +48h, +6d) exercise, with biopsies taken from the vastus lateralis of each leg at +48h for determination of muscle damage and/or inflammation. Plasma granulocyte counts increased for men and decreased for women at +48h (P < 0.05), and creatine kinase activity increased for both genders at +48h and +6d (P < 0.01). There were significantly greater areas of both focal (P < 0.001) and extensive (P < 0.01) damage in the Ex vs. Con leg for both genders, which was assessed by using toluidine blue staining. The number of leukocyte common antigen-positive cells/mm(2) tissue increased with exercise (P < 0.05), and men tended to show more in their Ex vs. Con leg compared with women (P = 0.052). Men had a greater total (Ex and Con legs) number of bcl-2-positive cells/mm(2) tissue vs. women (P < 0.05). Atrophic fibers with homogeneous bcl-2-positive staining were seen only in men (n = 3). We conclude that muscle damage is similar between genders, yet the inflammatory response is attenuated in women vs. men. Finally, exercise may stimulate the expression of proteins involved in apoptosis in skeletal muscle.     

Postexercise muscle glycogen resynthesis in obese insulin-resistant Zucker rats.

We determined the effect of an acute bout of swimming (8 x 30 min) followed by either carbohydrate administration (0.5 mg/g glucose ip and ad libitum access to chow; CHO) or fasting (Fast) on postexercise glycogen resynthesis in soleus muscle and liver from female lean (ZL) and obese insulin-resistant (ZO) Zucker rats. Resting soleus muscle glycogen concentration ([glycogen]) was similar between genotypes and was reduced by 73 (ZL) and 63% (ZO) after exercise (P < 0.05). Liver [glycogen] at rest was greater in ZO than ZL (334 +/- 31 vs. 247 +/- 16 micromol/g wet wt; P < 0.01) and fell by 44 and 94% after exercise (P < 0.05). The fractional activity of glycogen synthase (active/total) increased immediately after exercise (from 0.22 +/- 0.05 and 0.32 +/- 0.04 to 0.63 +/- 0.08 vs. 0.57 +/- 0.05; P < 0.01 for ZL and ZO rats, respectively) and remained elevated above resting values after 30 min of recovery. During this time, muscle [glycogen] in ZO increased 68% with CHO (P < 0.05) but did not change in Fast. Muscle [glycogen] was unchanged in ZL from postexercise values after both treatments. After 6 h recovery, GLUT-4 protein concentration was increased above resting levels by a similar extent for both genotypes in both fasted (approximately 45%) and CHO-supplemented (approximately 115%) rats. Accordingly, during this time CHO refeeding resulted in supercompensation in both genotypes (68% vs. 44% for ZL and ZO). With CHO, liver [glycogen] was restored to resting levels in ZL but remained at postexercise values for ZO after both treatments. We conclude that the increased glucose availability with carbohydrate refeeding after glycogen-depleting exercise resulted in glycogen supercompensation, even in the face of muscle insulin-resistance.     

Time course of muscle adaptation after high force eccentric exercise

The repeated bout effect on changes in muscle damage indicators was examined in two groups of subjects following two bouts of 70 maximal eccentric actions of the forearm flexors. Fourteen college age female subjects were placed into two groups. The two bouts were separated by 6 weeks (n = 6), and 10 weeks (n = 8). The subjects performed the same amount of work for the bouts. The muscle damage indicators were isometric strength (STR), relaxed elbow joint angle (RANG), flexed elbow joint angle (FANG), perceived muscle soreness ratings (SOR), and plasma creatine kinase activity (CK). These measures were obtained pre-exercise and 5 days following each bout. The first bout showed significant changes in all measures over time for both groups (P less than 0.01). For the 6-week group, significantly smaller changes in RANG (P less than 0.01), SOR (P less than 0.05), and CK (P less than 0.01), as well as significantly faster recoveries (P less than 0.05) for STR and FANG were produced in the second bout. For the 10-week group, significantly smaller changes in RANG (P less than 0.05) and CK (P less than 0.01) were demonstrated by the second bout, but not significant difference was found for STR, FANG, and SOR between bouts 1 and 2. Changes in CK were still significantly smaller than that of the first bout when 6 subjects (3 subjects from each group) performed the same exercise 6 months after the second bout, but no difference in other measures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of streptozotocin-induced diabetes on glycogen resynthesis in fasted rats post-high-intensity exercise

It has recently been shown that food intake is not essential for the resynthesis of the stores of muscle glycogen in fasted animals recovering from high-intensity exercise. Because the effect of diabetes on this process has never been examined before, we undertook to explore this issue. To this end, groups of rats were treated with streptozotocin (60 mg/kg body mass ip) to induce mild diabetes. After 11 days, each animal was fasted for 24 h before swimming with a lead weight equivalent to 9% body mass attached to the tail. After exercise, the rate and the extent of glycogen repletion in muscles were not affected by diabetes, irrespective of muscle fiber composition. Consistent with these findings, the effect of exercise on the phosphorylation state of glycogen synthase in muscles was only minimally affected by diabetes. In contrast to its effects on nondiabetic animals, exercise in fasted diabetic rats was accompanied by a marked fall in hepatic glycogen levels, which, surprisingly, increased to preexercise levels during recovery despite the absence of food intake.     

Effect of antioxidant vitamin supplementation on muscle function after eccentric exercise

This study investigated the effects of antioxidant vitamin supplementation upon muscle contractile function following eccentric exercise and was performed double blind. Twenty-four physically active young subjects ingested either placebo (400 mg; n = 8), vitamin E (400 mg; n=8) or vitamin C (400 mg; n = 8) for 21 days prior to and for 7 days after performing 60 min of box-stepping exercise. Contractile function of the triceps surae was assessed by the measurement of maximal voluntary contraction (MVC) and the ratio of the force generated at 20 Hz and 50 Hz tetanic stimulation before and after eccentric exercise and for 7 days during recovery. Following eccentric exercise, MVC decreased to 75 (4) % [mean (SE); n = 24; P < 0.05] of the preexercise values and the 20/50 Hz ratio of tetanic tension from 0.76 (0.01) to 0.49 (0.03) [mean (SE); n = 24; P<0.05). Compared to the placebo group no significant changes in MVC were observed immediately post-exercise, though recovery of MVC in the first 24 h post-exercise was greater in the group supplemented with vitamin C. The decrease in 20/50 Hz ratio of tetanic tension was significantly less (P < 0.05) post-exercise and in the initial phase of recovery in subjects supplemented with vitamin C but not with vitamin E. These data suggest that prior vitamin C supplementation may exert a protective effect against eccentric exercise-induced muscle damage.