Creatine supplementation does not affect human skeletal muscle glycogen content in the absence of prior exercise.

Due to the current lack of clarity, we examined whether 5 days of dietary creatine (Cr) supplementation per se can influence the glycogen content of human skeletal muscle. Six healthy male volunteers participated in the study, reporting to the laboratory on four occasions to exercise to the point of volitional exhaustion, each after 3 days of a controlled normal habitual dietary intake. After a familiarization visit, participants cycled to exhaustion in the absence of any supplementation (N), and then 2 wk later again they cycled to exhaustion after 5 days of supplementation with simple sugars (CHO). Finally, after a further 2 wk, they again cycled to exhaustion after 5 days of Cr supplementation. Muscle samples were taken at rest before exercise, at the time point of exhaustion in visit 1, and at subsequent visit time of exhaustion. There was a treatment effect on muscle total Cr content in Cr compared with N and CHO supplementation (P < 0.01). Resting muscle glycogen content was elevated above N following CHO (P < 0.05) but not after Cr. At exhaustion following N, glycogen content was no different from CHO and Cr measured at the same time point during exercise. Cr supplementation under conditions of controlled habitual dietary intake had no effect on muscle glycogen content at rest or after exhaustive exercise. We suggest that any Cr-associated increases in muscle glycogen storage are the result of an interaction between Cr supplementation and other mediators of muscle glycogen storage.     

Creatine supplementation increases muscle total creatine but not maximal intermittent exercise performance.

This study investigated creatine supplementation (CrS) effects on muscle total creatine (TCr), creatine phosphate (CrP), and intermittent sprinting performance by using a design incorporating the time course of the initial increase and subsequent washout period of muscle TCr. Two groups of seven volunteers ingested either creatine [Cr; 6 x (5 g Cr-H(2)O + 5 g dextrose)/day)] or a placebo (6 x 5 g dextrose/day) over 5 days. Five 10-s maximal cycle ergometer sprints with rest intervals of 180, 50, 20, and 20 s and a resting vastus lateralis biopsy were conducted before and 0, 2, and 4 wk after placebo or CrS. Resting muscle TCr, CrP, and Cr were unchanged after the placebo but were increased (P < 0.05) at 0 [by 22.9 +/- 4.2, 8.9 +/- 1.9, and 14.0 +/- 3.3 (SE) mmol/kg dry mass, respectively] and 2 but not 4 wk after CrS. An apparent placebo main effect of increased peak power and cumulative work was found after placebo and CrS, but no treatment (CrS) main effect was found on either variable. Thus, despite the rise and washout of muscle TCr and CrP, maximal intermittent sprinting performance was unchanged by CrS.     

Creatine supplementation and age influence muscle metabolism during exercise

Young[n = 5, 30 ± 5 (SD) yr] andmiddle-aged (n = 4, 58 ± 4 yr) menand women performed single-leg knee-extension exercise inside a wholebody magnetic resonance system. Two trials were performed 7 days apartand consisted of two 2-min bouts and a third bout continued toexhaustion, all separated by 3 min of recovery.³¹P spectra were used to determinepH and relative concentrations ofP_i, phosphocreatine (PCr), and-ATP every 10 s. The subjects consumed 0.3 g · kg¹ · day¹of a placebo (trial 1) or creatine(trial 2) for 5 days before eachtrial. During the placebo trial, the middle-aged group had a lowerresting PCr compared with the young group (35.0 ± 5.2 vs. 39.5 ± 5.1 mmol/kg, P < 0.05) and alower mean initial PCr resynthesis rate (18.1 ± 3.5 vs. 23.2 ± 6.0 mmol · kg¹ · min¹,P < 0.05). After creatinesupplementation, resting PCr increased 15%(P < 0.05) in the young group and30% (P < 0.05) in the middle-aged group to 45.7 ± 7.5 vs. 45.7 ± 5.5 mmol/kg, respectively. Mean initial PCr resynthesis rate also increased in the middle-aged group(P < 0.05) to a level not differentfrom the young group (24.3 ± 3.8 vs. 24.2 ± 3.2 mmol · kg¹ · min¹).Time to exhaustion was increased in both groups combined after creatinesupplementation (118 ± 34 vs. 154 ± 70 s,P < 0.05). In conclusion, creatinesupplementation has a greater effect on PCr availability andresynthesis rate in middle-aged compared with youngerpersons.

     

Creatine supplementation during college football training does not increase the incidence of cramping or injury

The purpose of this study was to examine the effects of creatine supplementation on the incidence of injury observed during 3-years of NCAA Division IA college football training and competition. In an open label manner, athletes participating in the 1998–2000 football seasons elected to take creatine or non-creatine containing supplements following workouts/practices. Subjects who decided to take creatine were administered 15.75 g of creatine for 5 days followed by ingesting an average of 5 g/day thereafter administered in 5–10 g doses. Creatine intake was monitored and recorded by research assistants throughout the study and ranged between 34–56% of players during the course of the study. Subjects practiced or played in environmental conditions ranging from 8–40°C (mean 24.7 ± 9°C) and 19–98% relative humidity (49.3 ± 17%). Injuries treated by the athletic training staff were recorded and categorized as cramping, heat/dehydration, muscle tightness, muscle strains/pulls, non-contact joint injuries, contact injuries, and illness. The number of missed practices due to injury/illness was also recorded. Data are presented as the total number of treated injuries for creatine users/total injuries observed and percentage occurrence rate of injuries for creatine users for all seasons. The incidence of cramping (37/96, 39%), heat/dehydration (8/28, 36%), muscle tightness (18/42, 43%), muscle pulls/strains (25/51, 49%), non-contact joint injuries (44/132, 33%), contact injuries (39/104, 44%), illness (12/27, 44%), number of missed practices due to injury (19/41, 46%), players lost for the season (3/8, 38%), and total injuries/missed practices (205/529, 39%) were generally lower or proportional to the creatine use rate among players. Creatine supplementation does not appear to increase the incidence of injury or cramping in Division IA college football players.     

Effects of beta-alanine supplementation on muscle function during recovery from resistance exercise in young adults

Amino Acids - β-Alanine supplementation has been shown to increase muscle carnosine levels and exercise performance. However, its effects on muscle recovery from resistance exercise (RE)...     

Creatine supplementation decreases oxidative DNA damage and lipid peroxidation induced by a single bout of resistance exercise

Rahimi, R. Creatine supplementation decreases oxidative DNA damage and lipid peroxidation induced by a single bout of resistance exercise. J Strength Cond Res 25(12): 3448-3455, 2011-Creatine (Cr), or methyl guanidine-acetic acid, can be either ingested from exogenous sources, such as fish or meat, or produced endogenously by the body, primarily in the liver. It is used as an ergogenic aid to improve muscle mass, strength, and endurance. Heretofore, Cr's positive therapeutic benefits in various oxidative stress-associated diseases have been reported in the literature and, recently, Cr has also been shown to exert direct antioxidant effects. Therefore, the purpose of this study was to investigate the effects of an acute bout of resistance exercise (RE) on oxidative stress response and oxidative DNA damage in male athletes and whether supplementation with Cr could negate any observed differences. Twenty-seven resistance-trained men were randomly divided into a Cr supplementation group (the Cr group [21.6 ± 3.6 years], taking 4 × 5 g Cr monohydrate per day) or a placebo (PL) supplementation group (the PL group [21.2 ± 3.2 years], taking 4 × 5 g maltodextrin per day). A double-blind research design was employed for a 7-day supplementation period. Before and after the seventh day of supplementation, the subjects performed an RE protocol (7 sets of 4 exercises using 60-90 1 repetition maximum) in the flat pyramid loading pattern. Blood and urine samples taken before, immediately, and 24-hour postexercise were analyzed for plasma malondialdehyde (MDA) and urinary 8-hydroxy-2-deoxyguanosine (8-OHdG) excretion. Before the supplementation period, a significant increase in the urinary 8-OHdG excretion and plasma MDA levels was observed after RE. The Cr supplementation induces a significant increase in athletics performance, and it attenuated the changes observed in the urinary 8-OHdG excretion and plasma MDA. These results indicate that Cr supplementation reduced oxidative DNA damage and lipid peroxidation induced by a single bout of RE.     

Branched-chain amino acids do not improve muscle recovery from resistance exercise in untrained young adults

Amino Acids - The purpose of this study was to investigate the effects of BCAA supplementation on muscle recovery from resistance exercise (RE) in untrained young adults. Twenty-four young adults...     

Low muscle glycogen concentration does not suppress the anabolic response to resistance exercise

We determined the effect of muscle glycogen concentration and postexercise nutrition on anabolic signaling and rates of myofibrillar protein synthesis after resistance exercise (REX). Sixteen young, healthy men matched for age, body mass, peak oxygen uptake (Vo(2peak)) and strength (one repetition maximum; 1RM) were randomly assigned to either a nutrient or placebo group. After 48 h diet and exercise control, subjects undertook a glycogen-depletion protocol consisting of one-leg cycling to fatigue (LOW), whereas the other leg rested (NORM). The next morning following an overnight fast, a primed, constant infusion of l-[ring-(13)C(6)] phenylalanine was commenced and subjects completed 8 sets of 5 unilateral leg press repetitions at 80% 1RM. Immediately after REX and 2 h later, subjects consumed a 500 ml bolus of a protein/CHO (20 g whey + 40 g maltodextrin) or placebo beverage. Muscle biopsies from the vastus lateralis of both legs were taken at rest and 1 and 4 h after REX. Muscle glycogen concentration was higher in the NORM than LOW at all time points in both nutrient and placebo groups (P < 0.05). Postexercise Akt-p70S6K-rpS6 phosphorylation increased in both groups with no differences between legs (P < 0.05). mTOR(Ser2448) phosphorylation in placebo increased 1 h after exercise in NORM (P < 0.05), whereas mTOR increased ~4-fold in LOW (P < 0.01) and ~11 fold in NORM with nutrient (P < 0.01; different between legs P < 0.05). Post-exercise rates of MPS were not different between NORM and LOW in nutrient (0.070 ± 0.022 vs. 0.068 ± 0.018 %/h) or placebo (0.045 ± 0.021 vs. 0.049 ± 0.017 %/h). We conclude that commencing high-intensity REX with low muscle glycogen availability does not compromise the anabolic signal and subsequent rates of MPS, at least during the early (4 h) postexercise recovery period.     

Essential amino acids and muscle protein recovery from resistance exercise

This study tests the hypothesis that a dose of 6 g of orally administered essential amino acids (EAAs) stimulates net muscle protein balance in healthy volunteers when consumed 1 and 2 h after resistance exercise. Subjects received a primed constant infusion of L-[(2)H(5)]phenylalanine and L-[1-(13)C]leucine. Samples from femoral artery and vein and biopsies from vastus lateralis were obtained. Arterial EAA concentrations increased severalfold after drinks. Net muscle protein balance (NB) increased proportionally more than arterial AA concentrations in response to drinks, and it returned rapidly to basal values when AA concentrations decreased. Area under the curve for net phenylalanine uptake above basal value was similar for the first hour after each drink (67 +/- 17 vs. 77 +/- 20 mg/leg, respectively). Because the NB response was double the response to two doses of a mixture of 3 g of EAA + 3 g of nonessential AA (NEAA) (14), we conclude that NEAA are not necessary for stimulation of NB and that there is a dose-dependent effect of EAA ingestion on muscle protein synthesis.     

Leucine supplementation does not enhance acute strength or running performance but affects serum amino acid concentration

This study described the effect of leucine supplementation on serum amino acid concentration during two different exercise sessions in competitive male power athletes. The subjects performed a strength exercise session (SES; n = 16; 26 +/- 4 years) or a maximal anaerobic running exercise session (MARE; n = 12; 27 +/- 5 years) until exhaustion twice at a 7-day interval. The randomized subjects consumed drinks containing leucine (100 mg x kg/body weight before and during SES or 200 mg x kg/body weight before MARE) or placebo. Blood specimens taken 10 min before (B) and after (A) the sessions were analyzed for serum amino acids. In SES the concentration of leucine was distinctly higher in the leucine supplemented group than in the placebo group in both B (p < 0.001) and A (p < 0.001) samples. The leucine concentration decreased in placebo but not in the leucine supplemented group following the exercise session. Isoleucine (p = 0.017) and valine (p = 0.006) concentration decreased more in the leucine supplemented group than in placebo in A samples. In MARE the concentration of leucine was higher in the leucine supplemented group than in placebo in both B (p < 0.001) and A (p < 0.001) samples and increased (p < 0.001) in the supplemented group following the session. Isoleucine (p = 0.020) and valine (p = 0.006) concentration decreased in the supplemented group in A samples. There were no differences in a counter movement jump after SES or in the running performance in MARE between the leucine supplemented group and placebo. These findings indicate that consuming leucine before or before and during exercise sessions results in changes in blood amino acid concentration. However, the supplementation does not affect an acute physical performance.     

Creatine but not betaine supplementation increases muscle phosphorylcreatine content and strength performance

We aimed to investigate the role of betaine supplementation on muscle phosphorylcreatine (PCr) content and strength performance in untrained subjects. Additionally, we compared the ergogenic and physiological responses to betaine versus creatine supplementation. Finally, we also tested the possible additive effects of creatine and betaine supplementation. This was a double-blind, randomized, placebo-controlled study. Subjects were assigned to receive betaine (BET; 2?g/day), creatine (CR; 20?g/day), betaine plus creatine (BET?+?CR; 2?+?20?g/day, respectively) or placebo (PL). At baseline and after 10?days of supplementation, we assessed muscle strength and power, muscle PCr content, and body composition. The CR and BET?+?CR groups presented greater increase in muscle PCr content than PL (p?=?0.004 and p?=?0.006, respectively). PCr content was comparable between BET versus PL (p?=?0.78) and CR versus BET?+?CR (p?=?0.99). CR and BET?+?CR presented greater muscle power output than PL in the squat exercise following supplementation (p?=?0.003 and p?=?0.041, respectively). Similarly, bench press average power was significantly greater for the CR-supplemented groups. CR and BET?+?CR groups also showed significant pre- to post-test increase in 1-RM squat and bench press (CR: p?=?0.027 and p?<?0.0001; BET?+?CR: p?=?0.03 and p?<?0.0001 for upper- and lower-body assessments, respectively) No significant differences for 1-RM strength and power were observed between BET versus PL and CR versus BET?+?CR. Body composition did not differ between the groups. In conclusion, we reported that betaine supplementation does not augment muscle PCr content. Furthermore, we showed that betaine supplementation combined or not with creatine supplementation does not affect strength and power performance in untrained subjects.     

Seven days of oral taurine supplementation does not increase muscle taurine content or alter substrate metabolism during prolonged exercise in humans

This study examined 1) the plasma taurine response to acute oral taurine supplementation (T), and 2) the effects of 7 days of T on muscle amino acid content and substrate metabolism during 2 h of cycling at approximately 60% peak oxygen consumption (VO2peak). In the first part of the study, after an overnight fast, 7 volunteers (28+/-3 yr, 184+/-2 cm, 88.0+/-6.6 kg) ingested 1.66 g oral taurine doses with breakfast (8 AM) and lunch (12 noon), and blood samples were taken throughout the day. In the second part of the study, eight men (22+/-1 yr, 181+/-1 cm, 80.9+/-3.8 kg, 4.21+/-0.16 l/min VO2peak) cycled for 2 h after 7 days of placebo (P) ingestion (6 g glucose/day) and again following 7 days of T (5 g/day). In the first part of the study, plasma taurine was 64+/-4 microM before T and rose rapidly to 778+/-139 microM by 10 AM and remained elevated at noon (359+/-56 microM). Plasma taurine reached 973+/-181 microM at 1 PM and was 161+/-31 microM at 4 PM. In the second part of the study, seven days of T had no effect on muscle taurine content (mmol/kg dry muscle) at rest (P, 44+/-15 vs. T, 42+/-15) or after exercise (P, 43+/-12 vs. T, 43+/-11). There was no difference in muscle glycogen or other muscle metabolites between conditions, but there were notable interaction effects for muscle valine, isoleucine, leucine, cystine, glutamate, alanine, and arginine amino acid content following exercise after T. These data indicate that 1) acute T produces a 13-fold increase in plasma taurine concentration; 2) despite the ability to significantly elevate plasma taurine for extended periods throughout the day, 7 days of T does not alter skeletal muscle taurine content or carbohydrate and fat oxidation during exercise; and 3) T appears to have some impact on muscle amino acid response to exercise.     

Effect of leucine supplementation on indices of muscle damage following drop jumps and resistance exercise

The purpose of this study was to determine the effect of leucine supplementation on indices of muscle damage following eccentric-based resistance exercise. In vitro, the amino acid leucine has been shown to reduce proteolysis and stimulate protein synthesis. Twenty-seven untrained males (height 178.6 ± 5.5 cm; body mass 77.7 ± 13.5 kg; age 21.3 ± 1.6 years) were randomly divided into three groups; leucine (L) (n = 10), placebo (P) (n = 9) and control (C) (n = 8). The two experimental groups (L and P) performed 100 depth jumps from 60 cm and six sets of ten repetitions of eccentric-only leg presses. Either leucine (250 mg/kg bm) or placebo was ingested 30 min before, during and immediately post-exercise and the morning of each recovery day following exercise. Muscle function was determined by peak force during an isometric squat and by jump height during a static jump at pre-exercise (PRE) and 24, 48, 72, and 96 h post-exercise (24, 48, 72, 96 h). Additionally, at these time points each group’s serum levels of creatine kinase (CK) and myoglobin (Mb) along with perceived feelings of muscle soreness were determined. None of the C group dependent variables was altered by the recurring testing procedures. Peak force was significantly decreased across all time points for both experimental groups. The L group experienced an attenuated drop in mean peak force across all post-exercise time points compared to the P group. Jump height significantly decreased from PRE for both the L and P group at 24 h and 48 h. CK and Mb was significantly elevated from PRE for both experimental groups at 24 h. Muscle soreness increased across all time points for the both the L and P group, and the L group experienced a significantly higher increase in mean muscle soreness post-exercise. Following exercise-induced muscle damage, high-dose leucine supplementation may help maintain force output during isometric contractions, however, not force output required for complex physical tasks thereby possibly limiting its ergogenic effectiveness.     

Effects of vitamin E supplementation on recovery from repeated bouts of resistance exercise

The purpose of this study was to examine the effects of vitamin E (VE) supplementation (1200 IU/day) on recovery responses to repeated bouts of resistance exercise. Non-resistance trained men were assigned to supplement with VE (n = 9) or placebo (PL; n = 9) for 3 weeks and then perform 3 resistance exercise sessions separated by 3 days of recovery (EX-1, EX-2, and EX-3). Performance was assessed at EX-1, EX-2, and EX-3. Fasting morning blood samples and perceived muscle soreness were obtained before EX-1 and for 10 consecutive days. Muscle soreness peaked after EX-1 and gradually returned to baseline values by day 6. Lower and upper body maximal strength and explosive power were significantly (p < or = 0.05) decreased at EX-2 and EX-3 (approximately 10%). Plasma malondialdehyde (MDA) was significantly elevated on days 7 and 8. There were no significant differences between VE and PL in muscle soreness, performance measures, or plasma MDA. Creatine kinase (CK) area under the curve from day 1 to day 10 was significantly greater for VE because of a nearly 2-fold greater increase in CK after EX-1 in VE, compared with PL (404 +/- 146 and 214 +/- 179 U/L, respectively). VE supplementation was not effective at attenuating putative markers of membrane damage, oxidative stress, and performance decrements after repeated bouts of whole-body concentric/eccentric resistance exercise.     

Creatine supplementation attenuates corticosteroid-induced muscle wasting and impairment of exercise performance in rats.

The objective of the present study was to investigate whether creatine (Cr) could attenuate the deleterious effects of high doses of dexamethasone (Dexa) on body mass, exercise performance, and respiratory variables of rodents. Forty-four Wistar rats performed incremental maximal exercise tests. They were then assigned to four groups: G1: subcutaneous (s.c.) and intraperitoneal (i.p.) saline; G2: s.c. saline and i.p. Cr (250 mg x kg(-1) x day(-1)); G3: s.c. Dexa (7.5 mg x kg(-1) x day(-1)) and i.p. saline; G4: s.c. Dexa and i.p. Cr. New exercise tests and analysis of the respiratory pattern under resting conditions and after stimulation with doxapram (2 mg/kg i.p.) were performed after 18 days. Post- minus pretreatment differences were compared between groups. G3 and G4 showed a significant impairment in body mass gain compared with G1 and G2 (P < 0.05) (G1: 65.3 +/- 26.1, G2: 93.1 +/- 27.4, G3: -18.4 +/- 20.1, G4: 9.8 +/- 23.1 kg x 10(-3)). Similar results were observed for maximal oxygen consumption (G1: 9.5 +/- 8.5, G2: 25.8 +/- 14.5, G3: -25.5 +/- 6.0, G4: -4.8 +/- 9.5 ml x kg(-1) x min(-1)) and test duration (G1: 43.0 +/- 45.0, G2: 72.0 +/- 59.5, G3: -165.0 +/- 60.6, G4: -48.0 +/- 48.5 s). Simultaneous use of Cr significantly attenuated the Dexa-induced impairment of the last two variables. Cr attenuated Dexa-induced gastrocnemius and diaphragm muscle weight losses and the atrophy of gastrocnemius type IIb fibers. Cr supplementation had only small effects on Dexa-induced respiratory changes. These results suggest that Cr may play a role in the prophylaxis or treatment of steroid-induced myopathy.     

Acute pantothenic acid and cysteine supplementation does not affect muscle coenzyme A content, fuel selection, or exercise performance in healthy humans

Reduced skeletal muscle free coenzyme A (CoASH) availability may decrease the contribution of fat oxidation to ATP production during high-intensity, submaximal exercise or, alternatively, limit pyruvate dehydrogenase complex (PDC) flux and thereby carbohydrate oxidation. Here we attempted to increase the muscle CoASH pool in humans, via pantothenic acid and cysteine feeding, in order to elucidate the role of CoASH availability on muscle fuel metabolism during exercise. On three occasions, eight healthy male volunteers (age 22.9 ± 1.4 yr, body mass index 24.2 ± 1.5 kg/m(2)) cycled at 75% maximal oxygen uptake (Vo(2max)) to exhaustion, followed by a 15-min work output performance test. Muscle biopsies were obtained at rest, and after 60 min and 91.3 ± 3.1 min of exercise (time to exhaustion on baseline visit) on each occasion. Two weeks following the first visit (baseline), 1 wk of oral supplementation with either 3 g/day of a placebo control (glucose polymer; CON) or 1.5 g/day each of d-pantothenic acid and l-cysteine (CP) was carried out prior to the second and third visits in a randomized, counterbalanced, double-blind manner, leaving a 3-wk gap in total between each visit. Resting muscle CoASH content was not altered by supplementation in any visit. Following 60 min of exercise, muscle CoASH content was reduced by 13% from rest in all three visits (P < 0.05), and similar changes in the respiratory exchange ratio, glycogenolysis (～235 mmol/kg dry muscle), PCr degradation (～57 mmol/kg dry muscle), and lactate (～25 mmol/kg dry muscle) and acetylcarnitine (～12 mmol(.)kg/dry muscle) accumulation was observed during exercise when comparing visits. Furthermore, no difference in work output was observed when comparing CON and CP. Acute feeding with pantothenic acid and cysteine does not alter muscle CoASH content and consequently does not impact on muscle fuel metabolism or performance during exercise in humans.     

Paired immunoglobulin-like receptor B knockout does not enhance axonal regeneration or locomotor recovery after spinal cord injury

Myelin components that inhibit axonal regeneration are believed to contribute significantly to the lack of axonal regeneration noted in the adult central nervous system. Three proteins found in myelin, Nogo, myelin-associated glycoprotein, and oligodendrocyte-myelin glycoprotein, inhibit neurite outgrowth in vitro. All of these proteins interact with the same receptors, namely, the Nogo receptor (NgR) and paired immunoglobulin-like receptor B (PIR-B). As per previous reports, corticospinal tract (CST) regeneration is not enhanced in NgR-knock-out mice after spinal cord injury. Therefore, we assessed CST regeneration in PIR-B-knock-out mice. We found that hindlimb motor function, as assessed using the Basso mouse scale, footprint test, inclined plane test, and beam walking test, did not differ between the PIR-B-knock-out and wild-type mice after dorsal hemisection of the spinal cord. Further, tracing of the CST fibers after injury did not reveal enhanced axonal regeneration or sprouting in the CST of the PIR-B-knock-out mice. Systemic administration of NEP1-40, a NgR antagonist, to PIR-B knock-out mice did not enhance the regenerative response. These results indicate that PIR-B knock-out is not sufficient to induce extensive axonal regeneration after spinal cord injury.     

Smoking impairs muscle recovery from exercise

Cigarette smoking is a leading cause of many adverse health consequences. Chronic nicotine exposure leads to insulin resistance and may increase the risk of developing non-insulin-dependent diabetes mellitus in young otherwise healthy smokers. To evaluate smoking-induced effects on carbohydrate metabolism, we studied muscle glycogen recovery from exercise in a young healthy population of smokers. The study used 31P-13C NMR spectroscopy to compare muscle glycogen and glucose 6-phosphate levels during recovery in exercised gastrocnemius muscles of randomized cohorts of healthy male smokers (S) and controls (C). Data for the two groups were as follows: S, > or =20 cigarettes/day (n = 8), 24 +/- 2 yr, 173 +/- 3 cm, 70 +/- 4 kg and age- and weight-matched nonsmoking C (n = 10), 23 +/- 1 yr, 175 +/- 3 cm, 67 +/- 3 kg. Subjects performed single-leg toe raises to deplete glycogen to approximately 20 mmol/l, and glycogen resynthesis was measured during the first 4 h of recovery. Plasma samples were assayed for glucose and insulin at rest and during recovery. Test subjects were recruited from the general community surrounding Yale University. Glycogen was depleted to similar levels in the two groups [23.5 +/- 1.2 (S) and 19.1 +/- 1.3 (C) mmol/l]. During the 1st h of recovery, glycogen synthesis rates were similar [13.8 +/- 1.1 (S) and 15.3 +/- 1.3 (C) mmol x l-1 x h-1]. Between hours 1 and 4, glycogen synthesis was impaired in smokers [0.8 +/- 0.2 (S) and 4.5 +/- 0.5 (C) mmol x l-1 x h-1, P = 0.0002] compared with controls. Glucose 6-phosphate was reduced in smokers during hours 1-4 [0.105 +/- 0.006 (S) and 0.217 +/- 0.019 (C) mmol/l, P = 0.0212]. We conclude that cigarette smoking impairs the insulin-dependent portion of muscle recovery from glycogen-depleting exercise. This impairment likely results from a reduction in glucose uptake.     

Glucose ingestion before and during exercise does not enhance performance of daily repeated endurance exercise

The effect of glucose (Glc) ingestion before and during daily, repeated, prolonged exercise on metabolism and performance was tested. Seven young, healthy males performed cycling exercise in two series, with 1 month interval. Each exercise series consisted of 1 h/day on 3 successive days. On the 3rd day, exercise was continued until exhaustion. The intensity was 73.4 (7.7) % [mean (SD)] of maximal oxygen uptake ( ). Glucose (Glc) or placebo (P) drink was ingested 15 min before the start, and at 15 and 45 min of each daily exercise. The total amount of Glc ingested was 43.1 (4.2) g. During exercise, blood Glc concentrations were significantly higher (P<0.05) when Glc was ingested than when P was ingested [Glc 5.14 (0.32) and P 4.12 (4.17) mmol · 1^–1 at exhaustion]. However, Glc ingestion did not improve performance time to exhaustion [Glc 92.05 (29.55) and P 98.07 (27.33) min]. Free fatty acid concentrations were significantly lower when Glc was ingested than when P was ingested [Glc 0.63 (0.21) and P 1.39 (0.46) mmol · l^–1 at exhaustion]. There were no significant differences in exercise heart rate, , respiratory exchange ratio, blood lactate concentrations or rating of perceived exertion between the conditions nor were there any significant differences in these parameters on different days of exercise. It seems that ingestion of small amounts of Glc does not increase the metabolism of carbohydrate or improve the performance of intensive endurance exercise of poorly trained subjects, even when the exercise is repeated daily.     

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.