Effects of recovery beverages on glycogen restoration and endurance exercise performance

The restorative capacities of a high carbohydrate-protein (CHO-PRO) beverage containing electrolytes and a traditional 6% carbohydrate-electrolyte sports beverage (SB) were assessed after glycogen-depleting exercise. Postexercise ingestion of the CHO-PRO beverage, in comparison with the SB, resulted in a 55% greater time to exhaustion during a subsequent exercise bout at 85% maximum oxygen consumption (VO(2)max). The greater recovery after the intake of the CHO-PRO beverage could be because of a greater rate of muscle glycogen storage. Therefore, a second study was designed to investigate the effects of after exercise CHO-PRO and SB supplements on muscle glycogen restoration. Eight endurance-trained cyclists (VO(2)max = 62.1 +/- 2.2 ml.kg(-1) body wt.min(-1)) performed 2 trials consisting of a 2-hour glycogen-depletion ride at 65-75% VO(2)max. Carbohydrate-protein (355 ml; approximately 0.8 g carbohydrate (CHO).kg(-1) body wt and approximately 0.2 g protein.kg(-1) body wt) or SB (355 ml; approximately 0.3 g CHO.kg(-1) body wt) was provided immediately and 2 hours after exercise. Trials were randomized and separated by 7-15 days. Ingestion of the CHO-PRO beverage resulted in a 17% greater plasma glucose response, a 92% greater insulin response, and a 128% greater storage of muscle glycogen (159 +/- 18 and 69 +/- 32 micromol.g(-1) dry weight for CHO-PRO and SB, respectively) compared with the SB (p < 0.05). These findings indicate that the rate of recovery is coupled with the rate of muscle glycogen replenishment and suggest that recovery supplements should be consumed to optimize muscle glycogen synthesis as well as fluid replacement.     

Cellular adaptation to repeated eccentric exercise-induced muscle damage.

Eccentrically biased exercise results in skeletal muscle damage and stimulates adaptations in muscle, whereby indexes of damage are attenuated when the exercise is repeated. We hypothesized that changes in ultrastructural damage, inflammatory cell infiltration, and markers of proteolysis in skeletal muscle would come about as a result of repeated eccentric exercise and that gender may affect this adaptive response. Untrained male (n = 8) and female (n = 8) subjects performed two bouts (bout 1 and bout 2), separated by 5.5 wk, of 36 repetitions of unilateral, eccentric leg press and 100 repetitions of unilateral, eccentric knee extension exercises (at 120% of their concentric single repetition maximum), the subjects' contralateral nonexercised leg served as a control (rest). Biopsies were taken from the vastus lateralis from each leg 24 h postexercise. After bout 2, the postexercise force deficit and the rise in serum creatine kinase (CK) activity were attenuated. Women had lower serum CK activity compared with men at all times (P < 0.05), but there were no gender differences in the relative magnitude of the force deficit. Muscle Z-disk streaming, quantified by using light microscopy, was elevated vs. rest only after bout 1 (P < 0.05), with no gender difference. Muscle neutrophil counts were significantly greater in women 24 h after bout 2 vs. rest and bout 1 (P < 0.05) but were unchanged in men. Muscle macrophages were elevated in men and women after bout 1 and bout 2 (P < 0.05). Muscle protein content of the regulatory calpain subunit remained unchanged whereas ubiquitin-conjugated protein content was increased after both bouts (P < 0.05), with a greater increase after bout 2. We conclude that adaptations to eccentric exercise are associated with attenuated serum CK activity and, potentially, an increase in the activity of the ubiquitin proteosome proteolytic pathway.     

The effects of ibuprofen on delayed muscle soreness and muscular performance after eccentric exercise

The purpose of this study was to examine the effects of ibuprofen on delayed onset muscle soreness (DOMS), indirect markers of muscle damage and muscular performance. Nineteen subjects (their mean [+/- SD] age, height, and weight was 24.6 +/- 3.9 years, 176.2 +/- 11.1 cm, 77.3 +/- 18.7 kg) performed the eccentric leg curl exercise to induce muscle soreness in the hamstrings. Nine subjects took an ibuprofen pill of 400 mg every 8 hours within a period of 48 hours, whereas 10 subjects received a placebo randomly (double blind). White blood cells (WBCs) and creatine kinase (CK) were measured at pre-exercise, 4-6, 24, and 48 hours after exercise and maximal strength (1 repetition maximum). Vertical jump performance and knee flexion range of motion (ROM) were measured at pre-exercise, 24 and 48 hours after exercise. Muscle soreness increased (p < 0.05) in both groups after 24 and 48 hours, although the ibuprofen group yielded a significantly lower value (p < 0.05) after 24 hours. The WBC levels were significantly (p < 0.05) increased 4-6 hours postexercise in both groups with no significant difference (p > 0.05) between the 2 groups. The CK values increased (p < 0.05) in the placebo group at 24 and 48 hours postexercise, whereas no significant differences (p > 0.05) were observed in the ibuprofen group. The CK values of the ibuprofen group were lower (p < 0.05) after 48 hours compared with the placebo group. Maximal strength, vertical jump performance, and knee ROM decreased significantly (p < 0.05) after exercise and at 24 and 48 hours postexercise in both the placebo and the ibuprofen groups with no differences being observed (p > 0.05) between the 2 groups. The results of this study reveal that intake of ibuprofen can decrease muscle soreness induced after eccentric exercise but cannot assist in restoring muscle function.     

Effect of carbohydrate intake on net muscle protein synthesis during recovery from resistance exercise.

The purpose of this study was to determine the effect of ingestion of 100 g of carbohydrates on net muscle protein balance (protein synthesis minus protein breakdown) after resistance exercise. Two groups of eight subjects performed a resistance exercise bout (10 sets of 8 repetitions of leg presses at 80% of 1-repetition maximum) before they rested in bed for 4 h. One group (CHO) received a drink consisting of 100 g of carbohydrates 1 h postexercise. The other group (Pla) received a noncaloric placebo drink. Leg amino acid metabolism was determined by infusion of 2H5- or 13C6-labeled phenylalanine, sampling from femoral artery and vein, and muscle biopsies from vastus lateralis. Drink intake did not affect arterial insulin concentration in Pla, whereas insulin increased several times after the drink in CHO (P < 0.05 vs. Pla). Arterial phenylalanine concentration fell slightly after the drink in CHO. Net muscle protein balance between synthesis and breakdown did not change in Pla, whereas it improved in CHO from -17 +/- 3 nmol.ml(-1).100 ml leg(-1) before drink to an average of -4 +/- 4 and 0 +/- 3 nmol.ml(-1).100 ml leg(-1) during the second and third hour after the drink, respectively (P < 0.05 vs. Pla during last hour). The improved net balance in CHO was due primarily to a progressive decrease in muscle protein breakdown. We conclude that ingestion of carbohydrates improved net leg protein balance after resistance exercise. However, the effect was minor and delayed compared with the previously reported effect of ingestion of amino acids.     

Efficacy of prior eccentric exercise in attenuating impaired exercise performance after muscle injury in resistance trained men

Previous research has demonstrated that prior exercise may reduce the magnitude of muscle soreness and impaired function (i.e., repeated bout effect [RBE]) observed during subsequent eccentric exercise. Previous investigations have predominantly used research designs that include single-joint exercise performed by untrained individuals. It is unknown how resistance trained individuals respond to novel multi-joint eccentric actions of the upper body and whether prior exercise offers protection. Thirty-one resistance trained men (23.4 +/- 3.5 y, 177.2 +/- 5.1 cm, 86.4 +/- 16.5 kg, mean +/- SD) were randomly assigned to repeated bout ([RB] N = 15) or single bout ([CON] N = 16) conditions. Both groups performed 100 eccentric actions of the bench press ([ECC] at 70% concentric 1 repetition maximum) to induce muscle injury. Bilateral maximal isometric force, dynamic exercise performance (e.g., bench press throws), and muscle soreness were measured before, immediately after, and at 24 and 48 hours post-ECC. Total work, percent fatigue, and rating of perceived exertion (ECC) data were collected during ECC. Those assigned to RB condition exhibited less fatigue (9.5 vs. 22.6%) and lower RPE (14.8 vs. 17.1) during ECC. A significant interaction (p < 0.05) was found such that RB individuals experienced less soreness at 24 (6.5 vs. 4.9) and 48 (6.6 vs. 3.9) hours postexercise than the CON condition. No significant group differences (p < 0.05) were found for any measured performance variable. Although soreness, fatigue, and RPE suggest a RBE, this was not found in regards to exercise performance. It appears that in trained men, performing a strenuous high-volume eccentric exercise bout 2 weeks prior to an identical future bout offers no additional amelioration of impaired exercise performance.     

Comparison between voluntary and stimulated contractions of the quadriceps femoris for growth hormone response and muscle damage.

This study aimed to compare voluntary and stimulated exercise for changes in muscle strength, growth hormone (GH), blood lactate, and markers of muscle damage. Nine healthy men had two leg press exercise bouts separated by 2 wk. In the first bout, the quadriceps muscles were stimulated by biphasic rectangular pulses (75 Hz, duration 400 mus, on-off ratio 6.25-20 s) with current amplitude being consistently increased throughout 40 contractions at maximal tolerable level. In the second bout, 40 voluntary isometric contractions were performed at the same leg press force output as the first bout. Maximal voluntary isometric strength was measured before and after the bouts, and serum GH and blood lactate concentrations were measured before, during, and after exercise. Serum creatine kinase (CK) activity and muscle soreness were assessed before, immediately after, and 24, 48, and 72 h after exercise. Maximal voluntary strength decreased significantly (P < 0.05) after both bouts, but the magnitude of the decrease was significantly (P < 0.05) greater for the stimulated contractions (-22%) compared with the voluntary contractions (-9%). Increases in serum GH and lactate concentrations were significantly (P < 0.05) larger after the stimulation compared with the voluntary exercise. Increases in serum CK activity and muscle soreness were also significantly (P < 0.05) greater for the stimulation than voluntary exercise. It was concluded that a single bout of electrical stimulation exercise resulted in greater GH response and muscle damage than voluntary exercise.     

Muscle sympathetic nerve responses to physiological changes in prostaglandin production in humans.

Previous studies suggest that prostaglandins may contribute to exercise-induced increases in muscle sympathetic nerve activity (MSNA). To test this hypothesis, MSNA was measured at rest and during exercise before and after oral administration of ketoprofen, a cyclooxygenase inhibitor, or placebo. Twenty-one subjects completed two bouts of graded dynamic and isometric handgrip to fatigue. Each exercise bout was followed by 2 min of postexercise muscle ischemia. The second exercise bouts were performed after 60 min of rest in which 11 subjects were given ketoprofen (300 mg) and 10 subjects received a placebo. Ketoprofen significantly lowered plasma thromboxane B(2) in the drug group (from 36 +/- 6 to 22 +/- 3 pg/ml, P < 0.04), whereas thromboxane B(2) in the placebo group increased from 40 +/- 5 to 61 +/- 9 pg/ml from trial 1 to trial 2 (P < 0.008). Ketoprofen and placebo did not change sympathetic and cardiovascular responses to dynamic handgrip, isometric handgrip, and postexercise muscle ischemia. There was no relationship between thromboxane B(2) concentrations and MSNA or arterial pressure responses during both exercise modes. The data indicate that physiological increases or decreases in prostaglandins do not alter exercise-induced increases in MSNA and arterial pressure in humans. These findings suggest that contraction-induced metabolites other than prostaglandins mediate MSNA responses to exercise in humans.     

Resistance training alters the response of fed state mixed muscle protein synthesis in young men

Ten healthy young men (21.0 +/- 1.5 yr, 1.79 +/- 0.1 m, 82.7 +/- 14.7 kg, means +/- SD) participated in 8 wk of intense unilateral resistance training (knee extension exercise) such that one leg was trained (T) and the other acted as an untrained (UT) control. After the 8 wk of unilateral training, infusions of L-[ring-d(5)]phenylalanine, L-[ring-(13)C(6)]phenylalanine, and d(3)-alpha-ketoisocaproic acid were used to measure mixed muscle protein synthesis in the T and UT legs by the direct incorporation method [fractional synthetic rate (FSR)]. Protein synthesis was determined at rest as well as 4 h and 28 h after an acute bout of resistance exercise performed at the same intensity relative to the gain in single repetition maximum before and after training. Training increased mean muscle fiber cross-sectional area only in the T leg (type I: 16 +/- 10%; type II: 20 +/- 19%, P < 0.05). Acute resistance exercise increased muscle protein FSR in both legs at 4 h (T: 162 +/- 76%; UT: 108 +/- 62%, P < 0.01 vs. rest) with the increase in the T leg being significantly higher than in the UT leg at this time (P < 0.01). At 28 h postexercise, FSR in the T leg had returned to resting levels; however, the rate of protein synthesis in the UT leg remained elevated above resting (70 +/- 49%, P < 0.01). We conclude that resistance training attenuates the protein synthetic response to acute resistance exercise, despite higher initial increases in FSR, by shortening the duration for which protein synthesis is elevated.     

The effect of acute resistance exercise on serum malondialdehyde in resistance-trained and untrained collegiate men

The purposes of this study were to determine whether acute resistance exercise increases serum malondialdehyde (MDA) levels postexercise, and if so, whether resistance exercise training status influences the magnitude of the exercise-induced lipid peroxidation response. Twelve recreationally resistance-trained (RT) and 12 untrained (UT) men who did not have resistance exercise experience in the past year participated in this study. All subjects completed an 8-exercise circuit resistance exercise protocol consisting of 3 sets of 10 repetitions at 10 repetitions maximum for each exercise. Blood samples were obtained pre-exercise, at 5 minutes postexercise, and at 6, 24, and 48 hours postexercise. At pre-exercise, MDA (nmol.ml(-1)) averaged 3.41 +/- 0.25 (RT) and 3.20 +/- 0.25 (UT) and did not differ (p > 0.05) either between groups or over time. Creatine kinase (IU.L(-1)) was significantly (p < 0.05) elevated 5 minutes postexercise (170.6 +/- 25.8), 6 hours postexercise (290.3 +/- 34.4), 24 hours postexercise (365.5 +/- 49.9), and 48 hours postexercise (247.5 +/- 38.5) as compared with pre-exercise (126.4 +/- 20.2) for both groups. There was no difference (p > 0.05) in CK activity between groups. This study indicated that moderate-intensity whole-body resistance exercise had no effect on serum MDA concentration in RT and UT subjects.     

Resistance exercise alters MRF and IGF-I mRNA content in human skeletal muscle.

Increasing evidence suggests that the myogenic regulatory factors (MRFs) and IGF-I have important roles in the hypertrophy response observed after mechanical loading. We, therefore, hypothesized that a bout of heavy-resistance training would affect the MRF and IGF-I mRNA levels in human skeletal muscle. Six male subjects completed four sets of 6-12 repetitions on a leg press and knee extensor machine separated by 3 min. Myogenin, MRF4, MyoD, IGF-IEabc (isoforms a, b, and c) and IGF-IEbc (isoform b and c) mRNA levels were determined in the vastus lateralis muscle by RT-PCR before exercise, immediately after, and 1, 2, 6, 24, and 48 h postexercise. Myogenin, MyoD, and MRF4 mRNA levels were elevated (P < 0.005) by 100-400% 0-24 h postexercise. IGF-IEabc mRNA content decreased (P < 0.005) by approximately 44% after 1 and 6 h of recovery. The IGF-IEbc mRNA level was unaffected. The present study shows that myogenin, MyoD, and MRF4 mRNA levels are transiently elevated in human skeletal muscle after a single bout of heavy-resistance training, supporting the idea that the MRFs may be involved in regulating hypertrophy and/or fiber-type transitions. The results also suggest that IGF-IEa expression may be downregulated at the mRNA level during the initial part of recovery from resistance exercise.     

Enhanced plasma IL-6 and IL-1ra responses to repeated vs. single bouts of prolonged cycling in elite athletes.

The impact of repeated bouts of exercise on plasma levels of interleukin (IL)-6 and IL-1 receptor antagonist (IL-1ra) was examined. Nine well-trained men participated in four different 24-h trials: Long [two bouts of exercise, at 0800-0915 and afternoon exercise (Ex-A), separated by 6 h]; Short (two bouts, at 1100-1215 and Ex-A, separated by 3 h); One (single bout performed at the same Ex-A as second bout in prior trials); and Rest (no exercise). All exercise bouts were performed on a cycle ergometer at 75% of maximal O(2) uptake and lasted 75 min. Peak IL-6 observed at the end of Ex-A was significantly higher in Short (8.8 +/- 1.3 pg/ml) than One (5.2 +/- 0.7 pg/ml) but not compared with Long (5.9 +/- 1.2 pg/ml). Peak IL-1ra observed 1 h postexercise was significantly higher in Short (1,774 +/- 373 pg/ml) than One (302 +/- 53 pg/ml) but not compared with Long (1,276 +/- 451 pg/ml). We conclude that, when a second bout of endurance exercise is performed after only 3 h of recovery, IL-6 and IL-1ra responses are elevated. This may be linked to muscle glycogen depletion.     

Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20-31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery VO2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, VO2 was increased by 11 +/- 2%, leg blood flow was increased by 51 +/- 18%, leg vascular conductance was increased by 56 +/- 19%, and mean arterial pressure was decreased by 2.2 +/- 1.0 mmHg (all P <0.05 vs. preexercise). At the end of the protocol, VO2 remained elevated by 4 +/- 2% (P <0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P >0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.     

Leg glucose and protein metabolism during an acute bout of resistance exercise in humans.

The present study investigated the responses of leg glucose and protein metabolism during an acute bout of resistance exercise. Seven subjects (5 men, 2 women) were studied at rest and during a strenuous lower body resistance exercise regimen consisting of approximately 8 sets of 10 repetitions of leg press at approximately 75% 1 repetition maximum and 8 sets of 8 repetitions of knee extensions at approximately 80% 1 repetition maximum. L-[ring-2H5]phenylalanine was infused throughout the study for measurement of phenylalanine rates of appearance, disappearance, protein synthesis, and protein breakdown across the leg. Femoral arterial and venous blood samples were collected at rest and during exercise for determination of leg blood flow, concentrations of glucose, lactate, alanine, glutamine, glutamate, leucine, and phenylalanine, and phenylalanine enrichments. Muscle biopsies were obtained at rest and immediately after exercise. Leg blood flow was nearly three times (P <0.009) higher and glucose uptake more than five times higher (P=0.009) during exercise than at rest. Leg lactate release was 86 times higher than rest during the exercise bout. Although whole body phenylalanine rate of appearance, an indicator of whole body protein breakdown, was reduced during exercise; leg phenylalanine rate of appearance, rate of disappearance, protein synthesis, and protein breakdown did not change. Arterial and venous alanine concentrations and glutamate uptake were significantly higher during exercise than at rest. We conclude that lower body resistance exercise potently stimulates leg glucose uptake and lactate release. In addition, muscle protein synthesis is not elevated during a bout of resistance exercise.     

Effects of postexercise carbohydrate-protein feedings on muscle glycogen restoration.

The purpose of this investigation was to determine the effects of postexercise eucaloric carbohydrate-protein feedings on muscle glycogen restoration after an exhaustive cycle ergometer exercise bout. Seven male collegiate cyclists [age = 25.6 +/- 1.3 yr, height = 180.9 +/- 3.2 cm, wt = 75.4 +/- 4.0 kg, peak oxygen uptake (VO(2 peak)) = 4.20 +/- 0.2 l/min] performed three trials, each separated by 1 wk: 1) 100% alpha-D-glucose [carbohydrate (CHO)], 2) 70% carbohydrate-20% protein (PRO)-10% fat, and 3) 86% carbohydrate-14% amino acid (AA). All feedings were eucaloric, based on 1.0 g. kg body wt(-1). h(-1) of CHO, and administered every 30 min during a 4-h muscle glycogen restoration period in an 18% wt/vol solution. Muscle biopsies were obtained immediately and 4 h after exercise. Blood samples were drawn immediately after the exercise bout and every 0.5 h for 4 h during the restoration period. Increases in muscle glycogen concentrations for the three feedings (CHO, CHO-PRO, CHO-AA) were 118 mmol/kg dry wt; however, no differences among the feedings were apparent. The serum glucose and insulin responses did not differ throughout the restoration period among the three feedings. These results suggest that muscle glycogen restoration does not appear to be enhanced with the addition of proteins or amino acids to an eucaloric CHO feeding after exhaustive cycle exercise.     

Regional hemodynamics during postexercise hypotension. I. Splanchnic and renal circulations.

Moderate exercise elicits a relative postexercise hypotension that is caused by an increase in systemic vascular conductance. Previous studies have shown that skeletal muscle vascular conductance is increased postexercise. It is unclear whether these hemodynamic changes are limited to skeletal muscle vascular beds. The aim of this study was to determine whether the splanchnic and/or renal vascular beds also contribute to the rise in systemic vascular conductance during postexercise hypotension. A companion study aims to determine whether the cutaneous vascular bed is involved in postexercise hypotension (Wilkins BW, Minson CT, and Halliwill JR. J Appl Physiol 97: 2071-2076, 2004). Heart rate, arterial pressure, cardiac output, leg blood flow, splanchnic blood flow, and renal blood flow were measured in 13 men and 3 women before and through 120 min after a 60-min bout of exercise at 60% of peak oxygen uptake. Vascular conductances of leg, splanchnic, and renal vascular beds were calculated. One hour postexercise, mean arterial pressure was reduced (79.1 +/- 1.7 vs. 83.4 +/- 1.8 mmHg; P < 0.05), systemic vascular conductance was increased by approximately 10%, leg vascular conductance was increased by approximately 65%, whereas splanchnic (16.0 +/- 1.8 vs. 18.5 +/- 2.4 ml.min(-1).mmHg(-1); P = 0.13) and renal (20.4 +/- 3.3 vs. 17.6 +/- 2.6 ml.min(-1).mmHg(-1); P = 0.14) vascular conductances were unchanged compared with preexercise. This suggests there is neither vasoconstriction nor vasodilation in the splanchnic and renal vasculature during postexercise hypotension. Thus the splanchnic and renal vascular beds neither directly contribute to nor attenuate postexercise hypotension.     

LH secretion and testosterone concentrations are blunted after resistance exercise in men.

This study examined the hypothesis that exercise-induced changes in circulating testosterone would be centrally mediated via hypothalamic-pituitary release of luteinizing hormone (LH). We tested this hypothesis by examining overnight LH, total and free testosterone (TT and FT), and cortisol (C) concentrations in 10 young healthy men (21 +/- 1 yr) during two experimental sessions: a control and an acute heavy-resistance exercise bout (50 total sets consisting of squats, bench press, leg press, and latissimus dorsi pull-down). Exercise was performed from 1500 to 1700, and blood sampling began at 1700 and continued until 0600 the next morning. Blood was sampled every 10 min for LH and every hour for TT, FT, and C. Hormonal concentrations were determined via RIA, and the secretion characteristics of LH were analyzed with deconvolution analysis. When overnight postexercise concentrations were compared with control concentrations, no statistically significant (P < or = 0.05) differences were observed for LH half-life, LH pulse frequency, interpulse interval, pulse amplitude, or pulse mass. Significant differences were observed for LH production rate (13.6 +/- 4 and 17.9 +/- 5 IU. l distribution volume(-1) x day(-1) for exercise and control, respectively, a 24% reduction). For the ANOVA marginal main effect means due to condition, C was significantly elevated (5.9 +/- 0.7 vs. 4.0 +/- 0.4 microg/dl), while TT (464 +/- 23 vs. 529 +/- 32 ng/dl) and FT (15.6 +/- 0.7 vs. 18.3 +/- 0.9 pg/ml) were significantly decreased for the exercise condition. These data demonstrate that the decline in overnight testosterone concentrations after acute heavy-resistance exercise is accompanied by a blunted LH production rate and elevated C concentrations.     

Time course of endothelial adaptation after acute and chronic exercise in patients with metabolic syndrome

Clustering of cardiovascular risk factors may lead to endothelial dysfunction. Physical exercise is an important factor in prevention and treatment of endothelial dysfunction. We wanted to determine the time course of adaptation to a single bout of exercise at either high or moderate intensity upon endothelial function both before and after a 16-week fitness program in patients with metabolic syndrome. Twenty-eight patients with metabolic syndrome participated in the study and were randomized and stratified (according to age and sex) into an aerobic interval exercise training group (AIT, n = 11), a continuously moderate-intensity exercise training group (CME, n = 8) or to a control group (n = 9). Flow-mediated dilatation (FMD) was determined at baseline, immediately, 24, 48, and 72 hours after 1 bout of exercise and repeated after 16 weeks of exercise. In the untrained state, FMD improved from 5 to 11% (p = 0.003) immediately after a single bout of aerobic interval training (AIT), an effect lasting 72 hours postexercise. In comparison, continuous moderate exercise (CME) improved FMD immediately after a single bout of exercise from 5 to 8% (p = 0.02), an effect lasting 24 hours postexercise (group difference, p < 0.001). In the trained state, a single bout of AIT resulted in a 2% (p = 0.007) acute increase of FMD lasting 48 hours postexercise. The CME increased FMD by 3% (p < 0.01), an effect lasting 24 hours postexercise (group difference p = 0.0012). Blood glucose level decreased after 1 single bout of AIT in the untrained state (p < 0.05), and the effect lasted at least 72 hours postexercise (p < 0.01). Acute CME decreased blood glucose with normalization of the values 24 hours postexercise (p < 0.01). A single bout of exercise in the trained state reduced fasting blood glucose by 10% (p < 0.05) after both AIT and CME. Exercise training, especially high intensity, thus appears to be highly beneficial in reducing blood glucose and improving endothelial function.