The aim of this study was to investigate the effects of oral branched-chain amino acids (BCAAs) intake on muscular (creatine kinase and myoglobin) and central (serotonin) fatigue during an incremental exercise protocol and to determine the time to exhaustion. Sixteen male long-distance runners (25.7 ± 2.0 yrs) performed two trials, 14 days apart. Using a double-blind, placebo-controlled, randomised crossover design, participants ingested either 20 g of BCAAs (BCAA trial) or a placebo 1 hour prior to performing an incremental exercise session on a treadmill. The starting speed was 8 km/h and this was increased by 1 km/h every 5 minutes until volitional exhaustion. Blood analysis indicated that plasma levels of serotonin were lower in the BCAA trial (259.3 ± 13.5 ng/ml) than the placebo trial (289.1 ± 14.5 ng/ml) (p < 0.05). There was a similar pattern of results for free fatty acid (p < 0.05). The creatine kinase level was higher in the BCAA trial (346.1 ± 33.7 U/L) than the placebo trial (307.3 ± 30.2 U/L). No significant difference between trials was observed regarding the level of myoglobin (p = 0.139). Time to exhaustion was longer in the BCAA trial (50.4 ± 2.3 min) than the placebo trial (46.6 ± 3.2 min). In conclusion, oral intake of 20 g of BCAAs 1 hour prior to an incremental treadmill exercise session increased time to exhaustion, probably due to the reduction in serotonin concentration. As myoglobin levels were within the normal range in both trials, we conclude that the participants did not reach muscular fatigue.
This study was designed to determine the effect of oral supplementation with L-carnitine on the performance time in a 5000 m race. In addition, free fatty acid, blood carnitine, lactate, and glucose responses to the race following the supplementation period were measured. Twenty male trained-endurance athletes were randomly divided into two groups (L-carnitine, n = 10 (22.13 ± 2.66 yrs) or placebo, n = 10 (21.63 ± 2.23 yrs)). The study was performed with a randomized, double-blind, placebo-controlled parallel-group, in which participants ingested an L-carnitine supplement or a placebo 2 × 1.5 g/day for 3 weeks. Athletes completed a 5000 m race before and after the supplementation period. Blood samples were collected from each athlete before and after the race, preand post-supplementation to measure the physiological responses. Data showed that there were no differences in performance time before (p=0.624) and after (p=0.407) supplementation period between groups and within a group (p>0.05). No differences existed in physiological responses between groups after supplementation before beginning the race (p>0.05), except for the blood carnitine level, which was significantly higher in the L-carnitine than the placebo (P=0.001) group. After the finish of the race, however, data showed better physiological responses in response to L-carnitine supplementation compared to the placebo group (p<0.05). In conclusion, although L-carnitine supplementation increases blood carnitine concentration, it has no beneficial effect on performance time of 5000 m race probably due to the short duration of the race; it might also have no ergogenic effect.
The present study was designed to investigate the acute effect of caffeine on muscle damage biomarkers (creatine kinase, lactate dehydrogenase, creatine kinase MB, and myoglobin) measured before, immediately after, and 24 h after a single session of resistance exercises followed by exhaustive incremental test. In addition, the effect of caffeine intake on time to exhaustion during exhaustive incremental test was determined. Fifteen male long-distance runners (30.67 ± 3.40 yrs.) performed two consecutive trials (7 days apart). Athletes were assigned randomly either to ingest caffeine (6 mg/kg) 1 h prior to exercise or placebo using a double-blind crossover design. Each trial consisted of 5 resistance exercises followed by exhaustive incremental test. Blood samples were collected before, immediately, and 24 h after each trial. The independent t test of data showed no significant differences in biomarkers of muscle damage at all time points between trials (p > .05). Using paired sample t test, data revealed that caffeine increased the time to exhaustion (45.78 ± 2.42 min) during exhaustive incremental test compared to the placebo (43.83 ± 2.21 min) (p = .001). In conclusion, 6 mg/kg of caffeine 1 hour prior to resistance exercises followed by exhaustive incremental test had no effect on muscle damage biomarkers in long-distance runners probably due to mechanical stress precisely affected fast twitch fibres rather than slow twitch fibres. However, the increased time to exhaustion due to caffeine consume may attributed to dampened pain sensation.
This case is unique in which the patient had two previous lumbar spinal surgeries, recurrent herniated discs, and new bulged and herniated discs were developed. We aimed to investigate whether implementing the McKenzie method would reduce the symptoms of a long history of Low Back Pain (LBP) with multiple surgeries. A 2-months of McKenzie-type exercise program was performed at a rate of 5 days/week. Disability index, pain intensity, lumbar Range of Motion (ROM), and lower limb strength were tested before and after the exercise treatment intervention. Disability and pain were also measured at 3-months follow-up. The Oswestry disability index and pain visual analogue scale score reduced immediately after the treatment intervention and remained reduced at 3-months follow-up from 44% to 22%, and from 8 to 4, respectively. Lumbar ROM improved about 1.5 cm during standing flexion and 3 cm during extension. Unilateral leg extension of the affected leg and bilateral leg press increased by 16.5 kg and 70 kg, respectively. The current protocol has shown that Mckenzie-type exercise treatment can improve the physical functions and reduce pain in a patient with a history of lumbar spine surgeries and prolonged LBP. In addition, despite no additional exercise, McKenzie method increased the lower limb strength, possibly through nerve root decompression.
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