939 resultados para blood lactate concentration


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Our aim was to investigate the immediate effects of bilateral, 830 nm, low-level laser therapy (LLLT) on high-intensity exercise and biochemical markers of skeletal muscle recovery, in a randomised, double-blind, placebo-controlled, crossover trial set in a sports physiotherapy clinic. Twenty male athletes (nine professional volleyball players and eleven adolescent soccer players) participated. Active LLLT (830 nm wavelength, 100 mW, spot size 0.0028 cm(2), 3-4 J per point) or an identical placebo LLLT was delivered to five points in the rectus femoris muscle (bilaterally). The main outcome measures were the work performed in the Wingate test: 30 s of maximum cycling with a load of 7.5% of body weight, and the measurement of blood lactate (BL) and creatine kinase (CK) levels before and after exercise. There was no significant difference in the work performed during the Wingate test (P > 0.05) between subjects given active LLLT and those given placebo LLLT. For volleyball athletes, the change in CK levels from before to after the exercise test was significantly lower (P = 0.0133) for those given active LLLT (2.52 U l(-1) +/- 7.04 U l(-1)) than for those given placebo LLLT (28.49 U l(-1) +/- 22.62 U l(-1)). For the soccer athletes, the change in blood lactate levels from before exercise to 15 min after exercise was significantly lower (P < 0.01) in the group subjected to active LLLT (8.55 mmol l(-1) +/- 2.14 mmol l(-1)) than in the group subjected to placebo LLLT (10.52 mmol l(-1) +/- 1.82 mmol l(-1)). LLLT irradiation before the Wingate test seemed to inhibit an expected post-exercise increase in CK level and to accelerate post-exercise lactate removal without affecting test performance. These findings suggest that LLLT may be of benefit in accelerating post-exercise recovery.

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Background and Objectives: There are some indications that low-level laser therapy (LLLT) may delay the development of skeletal muscle fatigue during high-intensity exercise. There have also been claims that LED cluster probes may be effective for this application however there are differences between LED and laser sources like spot size, spectral width, power output, etc. In this study we wanted to test if light emitting diode therapy (LEDT) can alter muscle performance, fatigue development and biochemical markers for skeletal muscle recovery in an experimental model of biceps humeri muscle contractions. Study Design/Materials and Methods: Ten male professional volleyball players (23.6 [SD +/- 5.6] years old) entered a randomized double-blinded placebo-controlled crossover trial. Active cluster LEDT (69 LEDs with wavelengths 660/850 nm, 10/30 mW, 30 seconds total irradiation time, 41.7J of total energy irradiated) or an identical placebo LEDT was delivered under double-blinded conditions to the middle of biceps humeri muscle immediately before exercise. All subjects performed voluntary biceps humeri contractions with a workload of 75% of their maximal voluntary contraction force (MVC) until exhaustion. Results: Active LEDT increased the number of biceps humeri contractions by 12.9% (38.60 [SD +/- 9.03] vs. 34.20 [SD +/- 8.68], P = 0.021) and extended the elapsed time to perform contractions by 11.6% (P = 0.036) versus placebo. In addition, post-exercise levels of biochemical markers decreased significantly with active LEDT: Blood Lactate (P = 0.042), Creatine Kinase (P = 0.035), and C-Reative Protein levels (P = 0.030), when compared to placebo LEDT. Conclusion: We conclude that this particular procedure and dose of LEDT immediately before exhaustive biceps humeri contractions, causes a slight delay in the development of skeletal muscle fatigue, decreases post-exercise blood lactate levels and inhibits the release of Creatine Kinase and C-Reative Protein. Lasers Surg. Med. 41:572-577, 2009. (C) 2009 Wiley-Liss, Inc.

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This study aimed to investigate the effect of 830 nm low-level laser therapy (LLLT) on skeletal muscle fatigue. Ten healthy male professional volleyball players entered a crossover randomized double-blinded placebo-controlled trial. Active LLLT (830 nm wavelength, 100 mW output, spot size 0.0028 cm(2), 200 s total irradiation time) or an identical placebo LLLT was delivered to four points on the biceps humeri muscle immediately before exercises. All subjects performed voluntary biceps humeri contractions with a load of 75% of the maximum voluntary contraction (MVC) force until exhaustion. After active LLLT the mean number of repetitions was significantly higher than after placebo irradiation [mean difference 4.5, standard deviation (SD) +/- 6.0, P = 0.042], the blood lactate levels increased after exercises, but there was no significant difference between the treatments. We concluded that 830 nm LLLT can delay the onset of skeletal muscle fatigue in high-intensity exercises, in spite of increased blood lactate levels.

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In the last years, phototherapy has becoming a promising tool to improve skeletal muscle recovery after exercise, however, it was not compared with other modalities commonly used with this aim. In the present study we compared the short-term effects of cold water immersion therapy (CWIT) and light emitting diode therapy (LEDT) with placebo LEDT on biochemical markers related to skeletal muscle recovery after high-intensity exercise. A randomized double-blind placebo-controlled crossover trial was performed with six male young futsal athletes. They were treated with CWIT (5A degrees C of temperature [SD +/- 1A degrees]), active LEDT (69 LEDs with wavelengths 660/850 nm, 10/30 mW of output power, 30 s of irradiation time per point, and 41.7 J of total energy irradiated per point, total of ten points irradiated) or an identical placebo LEDT 5 min after each of three Wingate cycle tests. Pre-exercise, post-exercise, and post-treatment measurements were taken of blood lactate levels, creatine kinase (CK) activity, and C-reactive protein (CRP) levels. There were no significant differences in the work performed during the three Wingate tests (p > 0.05). All biochemical parameters increased from baseline values (p < 0.05) after the three exercise tests, but only active LEDT decreased blood lactate levels (p = 0.0065) and CK activity (p = 0.0044) significantly after treatment. There were no significant differences in CRP values after treatments. We concluded that treating the leg muscles with LEDT 5 min after the Wingate cycle test seemed to inhibit the expected post-exercise increase in blood lactate levels and CK activity. This suggests that LEDT has better potential than 5 min of CWIT for improving short-term post-exercise recovery.

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OBJECTIVE: To investigate whether skeletal muscle gene expression of calpain 3 is related to obesity and insulin resistance.

DESIGN: Cross-sectional studies in 27 non-diabetic human subjects and in Psammomys obesus, a polygenic animal model of obesity and type 2 diabetes.

MEASUREMENTS: Expression of CAPN3 in skeletal muscle was measured using Taqman fluorogenic PCR. In the human subjects, body composition was assessed by DEXA and insulin sensitivity was measured by euglycemic-hyperinsulinemic clamp. In Psammomys obesus, body composition was determined by carcass analysis, and substrate oxidation rates, physical activity and energy expenditure were measured by whole-body indirect calorimetry.

RESULTS: In human subjects, calpain 3 gene expression was negatively correlated with total (P=0.022) and central abdominal fat mass (P=0.034), and with blood glucose concentration in non-obese subjects (P=0.017). In Psammomys obesus, calpain 3 gene expression was negatively correlated with circulating glucose (P=0.013) and insulin (P=0.034), and with body fat mass (P=0.049). Indirect calorimetry revealed associations between calpain 3 gene expression and carbohydrate oxidation (P=0.009) and energy expenditure (P=0.013).

CONCLUSION/INTERPRETATION: Lower levels of expression of calpain 3 in skeletal muscle were associated with reduced carbohydrate oxidation and elevated circulating glucose and insulin concentrations, and also with increased body fat and in particular abdominal fat. Therefore, reduced expression of calpain 3 in both humans and Psammomys obesus was associated with phenotypes related to obesity and insulin resistance.

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Introduction: Sodium bicarbonate (NaHCO3) ingestion has been shown to increase both muscle glycogenolysis and glycolysis during brief submaximal exercise. These changes may be detrimental to performance during more prolonged, exhaustive exercise. This study examined the effect of NaHCO3 ingestion on muscle metabolism and performance during intense endurance exercise of ~60 min in seven endurance-trained men. Methods: Subjects ingested 0.3 g·kg-1 body mass of either NaHCO3 or CaCO3 (CON) 2 h before performing 30 min of cycling exercise at 77 ± 1% [latin capital V with dot above]O2peak followed by completion of 469 ± 21 kJ as quickly as possible (~30 min, ~80% [latin capital V with dot above]O2peak). Results: Immediately before, and throughout exercise, arterialized-venous plasma HCO3- concentrations were higher (P < 0.05) whereas plasma and muscle H+ concentrations were lower (P < 0.05) in NaHCO3 compared with CON. Blood lactate concentrations were higher (P < 0.05) during exercise in NaHCO3, but there was no difference between trials in muscle glycogen utilization or muscle lactate content during exercise. Reductions in PCr and ATP and increases in muscle Cr during exercise were also unaffected by NaHCO3 ingestion. Accordingly, exercise performance time was not different between treatments. Conclusion: NaHCO3 ingestion resulted in a small muscle alkalosis but had no effect on muscle metabolism or intense endurance exercise performance in well-trained men.

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AMP-activated protein kinase (AMPK) has recently emerged as a key signaling protein in skeletal muscle, coordinating the activation of both glucose and fatty acid metabolism in response to increased cellular energy demand. To determine whether AMPK signaling may also regulate gene transcription in muscle, rats were given a single subcutaneous injection (1 mg/g) of the AMP analog 5-aminoimidazole-4-carboxamide-1-ß-D-ribonucleoside (AICAR). AICAR injection activated (P < 0.05) AMPK-α2 (~2.5-fold) and transcription of the uncoupling protein-3 (UCP3, ~4-fold) and hexokinase II (HKII, ~10-fold) genes in both red and white skeletal muscle. However, AICAR injection also elicited (P < 0.05) an acute drop (60%) in blood glucose and a sustained (2-h) increase in blood lactate, prompting concern regarding the specificity of AICAR on transcription. To maximize AMPK activation in muscle while minimizing potential systemic counterregulatory responses, a single-leg arterial infusion technique was employed in fully conscious rats. Relative to saline-infused controls, single-leg arterial infusion of AICAR (0.125, 0.5, and 2.5 µg · g-1 · min-1 for 60 min) induced a dose-dependent increase (2- to 4-fold, P < 0.05) in UCP3 and HKII transcription in both red and white skeletal muscle. Importantly, AICAR infusion activated transcription only in muscle from the infused leg and had no effect on blood glucose or lactate levels. These data provide evidence that AMPK signaling is linked to the transcriptional regulation of select metabolic genes in skeletal muscle.

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AMP-activated protein kinase (AMPK) is proposed to stimulate fat and carbohydrate catabolism to maintain cellular energy status. Recent studies demonstrate that pharmacologic activation of AMPK and mutations in the enzyme are associated with elevated muscle glycogen content in vivo. Our purpose was to determine the mechanism for increased muscle glycogen associated with AMPK activity in vivo. AMPK activity and glycogen metabolism were studied in red and white gastrocnemius muscles from rats treated with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) in vivo, and also in muscles incubated with AICAR in vitro. In vivo AICAR treatment reduced blood glucose and increased blood lactate compared with basal values. AICAR increased muscle α2 AMPK activity, glycogen, and glucose-6-phosphate concentrations. Glycogen synthase activity was increased in the red gastrocnemius but was decreased in the white gastrocnemius. Glycogen phosphorylase activity increased in both muscles, with an inhibition initially observed in the red gastrocnemius. In vitro incubation with AICAR activated α2 AMPK but had no effect on either glycogen synthase or glycogen phosphorylase. These results suggest that AICAR treatment does not promote glycogen accumulation in skeletal muscle in vivo by altering glycogen synthase and glycogen phosphorylase. Rather, the increased glycogen is due to the well-known effects of AICAR to increase glucose uptake.

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The prevalence of type 2 diabetes has reached to an epidemic proportion in Sri Lanka. The need for achieving better control of blood glucose level has been evident in diabetes management. However it is not easy to achieve this goal in a large proportion of patients. This is partly due to limitations of currently available pharmacological agents which stimulate research on novel anti-diabetic agents with different mechanisms. Digestive enzymes have been targeted as potential avenues for modulation of blood glucose concentration through inhibition of the enzymatic breakdown of complex carbohydrates to meal derived glucose absorption. Acarbose is a widely used oral anti-diabetic drug which inhibits the α-glucosidase, enzyme responsible for breaking down of disaccharides and polysaccharides into glucose. Many herbal extracts have been found to posses similar inhibitory effects. Ginger (Zingiber officinale Roscoe) has developed a reputation in treatment of several diseases. In vitro enzymic inhibitory effect of ginger was investigated in this study. Enzymes α -amylase and α -glucosidase treated with either Acarbose or ginger extract were allowed to react with cooked rice and percentages of glucose content were measured. The glucosidase and amylase activities on the rice were inhibited by addition of ginger cause significant reduction in glucose percentages (36.86± 1.05 to 26.87± 2.17, P<0.05 and 49.04±0.65 to 35.35±2.22, P<0.05) which showed comparable results with Acarbose on glucosidase activity (36.86± 1.05 to, 27.8±1.32 P<0.05). Results of the study indicates ginger as a potential plant based amylase and glucosidase inhibitor in carbohydrate digestion but usage in glycaemic control in human has to be investigated further.

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This thesis found that light exercise between repeated sprints improved performance in a subsequent bout. This was attributed to a reduction in potentially fatiguing by-products within the muscle and an increased aerobic metabolism in the second sprint.

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The importance of pacing for middle-distance performance is well recognized, yet previous research has produced equivocal results. Twenty-six trained male cyclists ( V O2peak 62.8+5.9 ml ·kg-1 · min-1· maximal aerobic power output 340+43 W; mean+s) performed three cycling time-trials where the total external work (102.7+13.7 kJ) for each trial was identical to the best of two 5-min habituation trials. Markers of aerobic and anaerobic metabolism were assessed in 12 participants. Power output during the first quarter of the time-trials was fixed to control external mechanical work done (25.7+3.4 kJ) and induce fast-, even-, and slow-starting strategies (60, 75, and 90 s, respectively). Finishing times for the fast-start time-trial (4:53+0:11 min:s) were shorter than for the even-start (5:04+0:11 min:s; 95% CI=5 to 18 s, effect size=0.65, P 50.001) and slow-start time-trial (5:09+0:11 min:s; 95% CI=7 to 24 s, effect size=1.00, P 50.001). Mean VO2 during the fast-start trials (4.31+0.51 litres · min-1) was 0.18+0.19 litres · min-1 (95% CI=0.07 to 0.30 litres · min-1, effect size=0.94, P =0.003) higher than the even- and 0.18+0.20 litres · min-1 (95% CI=0.5 to 0.30 litres · min-1, effect size=0.86, P =0.007) higher than the slow-start time-trial. Oxygen deficit was greatest during the first quarter of the fast-start trial but was lower than the even- and slow-start trials during the second quarter of the trial. Blood lactate and pH were similar between the three trials. In conclusion, performance during a 5-min cycling time-trial was improved with the adoption of a fast- rather than an even- or slow-starting strategy.

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Purpose: Given the widespread use of water immersion during recovery from exercise, we aimed to investigate the effect of contrast water immersion on recovery of sprint cycling performance, HR and, blood lactate.

Methods: Two groups completed high-intensity sprint exercise before and after a 30-min randomized recovery. The Wingate group (n = 8) performed 3 x 30-s Wingate tests (4-min rest periods). The repeated intermittent sprint group (n = 8) cycled for alternating 30-s periods at 40% of predetermined maximum power and 120% maximum power, until exhaustion. Both groups completed three trials using a different recovery treatment for each trial (balanced randomized application). Recovery treatments were passive rest, 1:1 contrast water immersion (2.5 min of cold (8-C) to 2.5 min of hot (40-C)), and 1:4 contrast water immersion (1 min of cold to 4 min of hot). Blood lactate and HR were recorded throughout, and peak power and total work for pre- and postrecovery Wingate performance and exercise time and total work for repeated sprinting were recorded.

Results: Recovery of Wingate peak power was 8% greater after 1:4 contrast water immersion than after passive rest, whereas both contrast water immersion ratios provided a greater recovery of exercise time (È10%) and total work (È14%) for repeated sprinting than for passive rest. Blood lactate was similar between trials. Compared with passive rest, HR initially declined more slowly during contrast water immersion but increased with each transition to a cold immersion phase.

Conclusions: These data support contrast water immersion being effective in maintaining performance during a short-term recovery from sprint exercise. This effect needs further investigation but is likely explained by cardiovascular mechanisms, shown here by an elevation in HR upon each cold immersion.

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Australian Football (AF) is Australia's major football code. Despite research in other football codes, to date, no data has been published on the physiological responses of AF players during match play. Fifteen athletes (17.28 ± 0.76 yrs) participated in four pre-season matches, sanctioned by Australian Football League (AFL) Victoria, investigating Heart Rate (HR), Blood Lactate (BLa), Core Temperature (Tcore), and Hydration status. Match HR was measured continuously using HR monitors. BLa was measured via finger prick lancet at the end of each quarter of play. Tcore was measured by use of ingestible temperature sensor and measured wirelessly at the end of each quarter of play. Hydration status was measured using refractometry, measuring urine specific gravity, and body weight pre and post-match. Environmental conditions were measured continuously during matches. Results of HR responses showed a high exertion of players in the 85-95% maximum HR range. Elevated mean BLa levels, compared to rest, were observed in all players over the duration of the matches (p = 0.007). Mean Tcore rose 0.68 °C between start and end of matches. Mean USG increased between 0.008 g/ml (p = 0.001) with mean body weight decreasing 1.88 kg (p = 0.001). This study illustrates physiological responses in junior AF players playing in the heat as well as providing physiological data for consideration by AF coaching staff when developing specific training programs. Continued research should consider physiological measurements under varying environments, and at all playing levels of AF, to ascertain full physiological responses during AF matches.

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1. The role of adrenaline in regulating muscle glycogenolysis and hormonesensitive lipase (HSL) activity during exercise was examined in six adrenalinedeficient bilaterally adrenalectomised, adrenocorticohormonalsubstituted humans (Adr) and in six healthy control individuals (Con).

2. Subjects cycled for 45 min at •70% maximal pulmonary Oμ uptake (ýO2,max) followed by 15 min at •86% ýO2,max either without (−Adr and Con) or with (+Adr) adrenaline infusion that elevated plasma adrenaline levels (45 min, 4·49 ± 0·69 nmol l¢; 60 min, 12·41 ± 1·80 nmol l¢). Muscle samples were obtained at 0, 45 and 60 min of exercise.

3. In −Adr and Con, muscle glycogen was similar at rest (−Adr, 409 ± 19 mmol (kg dry wt)¢; Con, 453 ± 24 mmol (kg dry wt)¢) and following exercise (−Adr, 237 ± 52 mmol (kg dry wt)¢; Con, 227 ± 50 mmol (kg dry wt)¢). Muscle lactate, glucose6phosphate and glucose were similar in −Adr and Con, whereas glycogen phosphorylase (aÏa + b ² 100 %) and HSL (% phosphorylated) activities increased during exercise in Con only. Adrenaline infusion increased activities of phosphorylase and HSL as well as blood lactate concentrations compared with those in −Adr, but did not enhance glycogen breakdown (+Adr, glycogen following exercise: 274 ± 55 mmol (kg dry wt)¢) in contracting muscle.

4. The present findings demonstrate that during exercise muscle glycogenolysis can occur in the absence of adrenaline, and that adrenaline does not enhance muscle glycogenolysis in exercising adrenalectomised subjects. Although adrenaline increases the glycogen phosphorylase activity it is not essential for glycogen breakdown in contracting muscle. Finally, a novel finding is that the activity of HSL in human muscle is increased in exercising man and this is due, at least partly, to stimulation by adrenaline.

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Achieving an appropriate balance between training and competition stresses and recovery is important in maximising the performance of athletes. A wide range of recovery modalities are now used as integral parts of the training programmes of elite athletes to help attain this balance. This review examined the evidence available as to the efficacy of these recovery modalities in enhancing between-training session recovery in elite athletes. Recovery modalities have largely been investigated with regard to their ability to enhance the rate of blood lactate removal following high-intensity exercise or to reduce the severity and duration of exercise-induced muscle injury and delayed onset muscle soreness (DOMS). Neither of these reflects the circumstances of between-training session recovery in elite athletes. After high-intensity exercise, rest alone will return blood lactate to baseline levels well within the normal time period between the training sessions of athletes. The majority of studies examining exercise-induced muscle injury and DOMS have used untrained subjects undertaking large amounts of unfamiliar eccentric exercise. This model is unlikely to closely reflect the circumstances of elite athletes. Even without considering the above limitations, there is no substantial scientific evidence to support the use of the recovery modalities reviewed to enhance the between-training session recovery of elite athletes. Modalities reviewed were massage, active recovery, cryotherapy, contrast temperature water immersion therapy, hyperbaric oxygen therapy, nonsteroidal anti-inflammatory drugs, compression garments, stretching, electromyostimulation and combination modalities. Experimental models designed to reflect the circumstances of elite athletes are needed to further investigate the efficacy of various recovery modalities for elite athletes. Other potentially important factors associated with recovery, such as the rate of post-exercise glycogen synthesis and the role of inflammation in the recovery and adaptation process, also need to be considered in this future assessment.