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Purpose: The physiological examination of boxing has been limited to systemic response in amateur athletes. The demands of professional boxing have been overlooked, despite the different competition format. We sought to determine the physiological demands placed on skeletal muscle in professional boxing. Methods: Ten male professional boxers (age 26 ± 5 years, height 177 ± 4 cm, weight 71 ± 6 kg) were recruited for this observational study. On different days, the athletes completed 6 × 3 min rounds of pad, bag or spar-based training with 1 min recovery between each round. Prior to each session, participants put on a heart rate monitor and near-infrared spectroscopy attached to the belly of the rectus femoris muscle to record heart rate and muscle oxygenation. Results: There were significantly less punches thrown in sparring compared to other training modalities (p < 0.001). Skeletal muscle oxygenation across training modalities consisted of a delay, fast desaturation and steady state. Across rounds there was a significant increase in time delay for desaturation (p = 0.016), rate of fast desaturation (p < 0.001) and duration of fast desaturation (p = 0.019). There was a significant difference in sparring for the heart rate where skeletal muscle oxygenation changes occurred compared to pads or bag sessions (p < 0.001). Conclusion: The findings highlight differences in the skeletal muscle response to the different training modalities. Practitioners need to be aware of the muscular demands of each session to allow optimal adaptation across a training camp. Training needs to allow the skeletal muscle to achieve a new oxygenation steady state rapidly to promote efficient performance across rounds. [ABSTRACT FROM AUTHOR]

We demonstrated previously that, in healthy young men, 5-aminoimidazole-4-carboxamide 1-[beta]-D-ribofuranoside (AICAR) stimulates human muscle 2-deoxyglucose (2DG) uptake without detectable activation of muscle AMP-activated protein kinase (AMPK) but with extracellular-regulated kinase 1/2 (ERK1/2) activation. We tested whether AICAR stimulates muscle 2DG uptake in healthy older patients with or without type 2 diabetes (T2D). Six healthy young subjects (23 [+ or -] 3 yr, BMI 25 [+ or -] 2 kg/[m.sup.-2]; means [+ or -] SE), eight older subjects (59 [+ or -] 4 yr, BMI 28 [+ or -] 2 kg/[m.sup.-2]), and eight subjects with T2D (62 [+ or -] 4 yr, BMI 27 [+ or -] 2 kg/[m.sup.-2]) received a 6-h 2DG infusion (prime 10 mg/kg, 6 mg x [kg.sup.-1] x [h.sup.-1]) and AICAR (10 or 20 mg x [kg.sup.-1] x [h.sup.-1]) from 3 to 6 h. Quadriceps biopsies were taken at 0, 3, and 6 h. We determined 1) 2DG uptake, 2) total AMPK[alpha] activity, AMPK, acetyl-CoA carboxylase (ACC), and AS 160 phosphorylation, and 3) ERK1/2 phosphorylation. Ten milligrams per kilogram per hour AICAR increased 2DG uptake by 2.9 [+ or -] 0.7-fold in young men (P < 0.001), 1.8 [+ or -] 0.2-fold in older men (P < 0.01), and 1.6 [+ or -] 0.1-fold in men with T2D; 20 mg x [kg.sup.-1] x [h.sup.-1] AICAR increases were 2.5 [+ or -] 0.1-fold (older men, P < 0.001) and 2.2 [+ or -] 0.2-fold (men with T2D, P < 0.00l). At 3-h AMPK activity and AMPK, ACC and AS160 phosphorylation were unchanged, but ERK1/2 phosphorylation increased at both AICAR doses. The fold changes of ERK 1/2 phosphorylation and 2DG uptake closely correlated ([R.sup.2] = 0.55, P = 0.003). AICAR stimulates muscle 2DG uptake in T2D to the same extent as in healthy age-matched controls, but there is an age-related reduction. 5-aminoimidazole-4-carboxamide-l-[beta]-D-ribofuranoside; adenosine 5'-monophosphate-activated protein kinase; extracellular-signal-regulated kinase 1/2

We hypothesized a differential activation of the anabolic signaling proteins protein kinase B (PKB) and p70 S6 kinase ([p70.sup.S6K]) and subsequent differential stimulation of human muscle protein synthesis (MPS) after dynamic shortening or lengthening exercise. Eight healthy men [25 [+ or -] 5 yr, BMI 26 [+ or -] 3 kg/[m.sup.-2] (means [+ or -] SD)] were studied before and alter 12 min of repeated stepping up to knee height, and down again, while carrying 25% of their body weight, i.e., shortening exercise with the ''up' leg and lengthening exercise with contralateral 'down' leg. Quadriceps biopsies were taken before and 3, 6, and 24 h after exercise. After exercise, over 2 h before the biopsies, the subjects ingested 500 ml of water containing 45 g of essential amino acids and 135 g of sucrose. Rates of muscle protein synthesis were determined via incorporation over time of [1-[sup.13]C]leucine ([less than or equal to]6 h after exercise) or [1-[sup.13]C]valine (21-24 h after exercise) and phosphorylation of signaling proteins by Western analysis. PKB and [p70.sup.S6K] phosphorylation increased ~3-fold after 3 h and remained elevated at 6 and 24 h. After exercise, rates of myofibrillar and sarcoplasmic protein synthesis were unchanged over the period including exercise and 3 h of recovery but had increased significantly at 6 (~3.0- and 2.4-fold, respectively) and 24 h (~3.2- and 2.0-fold, respectively), independently of the mode of exercise. Short-term dynamic exercise in either shortening or lengthening mode increases MPS at least as much as resistance exercise and is associated with long-term activation of PKB and [p70.sup.S6K]. exercise-induced anabolism; myofibrillar, sarcoplasmic, and collagen synthesis

We tested the hypothesis that acute exercise would stimulate synthesis of myofibrillar protein and intramuscular collagen in women and that the phase of the menstrual cycle at which the exercise took place would influence the extent of the change. Fifteen young, healthy female subjects were studied in the follicular (FP, n = 8) or the luteal phase (LP, n = 7, n = 1 out of phase) 24 h after an acute bout of one-legged exercise (60 min of kicking at 67% [W.sub.max]), samples being taken from the vastus lateralis in both the exercised and resting legs. Rates of synthesis of myofibrillar and muscle collagen proteins were measured by incorporation of [[.sup.13]C]leucine. Myofibrillar protein synthesis (means [+ or -] SD; rest FP: 0.053 [+ or -] 0.009%/h, LP: 0.055 [+ or -] 0.013%/h) was increased at 24-h postexercise (FP: 0.131 [+ or -] 0.018%/h, P < 0.05, LP: 0.134 [+ or -] 0.018%/h, P < 0.05) with no differences between phases. Similarly, muscle collagen synthesis (rest FP: 0.024 [+ or -] 0.017%/h, LP: 0.021 [+ or -] 0.006%/h) was elevated at 24-h postexercise (FP: 0.073 [+ or -] 0.016%/h, P < 0.05, LP: 0.072 [+ or -] 0.015%/h, P < 0.05), but the responses did not differ between menstrual phases. Therefore, there is no effect of menstrual cycle phase, at rest or in response to an acute bout of exercise, on myofibrillar protein synthesis and muscle collagen synthesis in women. stable isotopes; estrogen; exercise

We aimed to determine whether there were differences in the extent and time course of skeletal muscle myofibrillar protein synthesis (MPS) and muscle collagen protein synthesis (CPS) in human skeletal muscle in an 8.5-h period after bouts of maximal muscle shortening (SC; average peak torque = 225 [+ or -] 7 N*m, means [+ or -] SE) or lengthening contractions (LC; average peak torque = 299 [ + or -] 18 N*m) with equivalent work performed in each mode. Eight healthy young men (21.9 [+ or -] 0.6 yr, body mass index 24.9 [+ or -] 1.3 kg/[m.sup.2]) performed 6 sets of 10 maximal unilateral LC of the knee extensors on an isokinetic dynamometer. With the contralateral leg, they then performed 6 sets of maximal unilateral SC with work matched to the total work performed during LC (10.9 [+ or -] 0.7 vs. 10.9 [+ or -] 0.8 kJ, P = 0.83). After exercise, the participants consumed small intermittent meals to provide 0.1 g*[kg.sup.-1] * [h.sup.-1] of protein and carbohydrate. Prior exercise elevated MPS above rest in both conditions, but there was a more rapid rise after LC (P < 0.01). The increases (P < 0.001) in CPS above rest were identical for both SC and LC and likely represent a remodeling of the myofibrillar basement membrane. Therefore, a more rapid rise in MPS after maximal LC could translate into greater protein accretion and muscle hypertrophy during chronic resistance training utilizing maximal LC. eccentric; concentric; resistance exercise; z-band streaming

Louis, Magali, Jacques R. Poortmans, Marc Francaux, Jacques BerrY, Nathalie Boisseau, Eric Brassine, Daniel J. R. Cuthbertson, Kenneth Smith, John A. Babraj, Tom Waddell, and Michael J. Rennie. No effect of creatine supplementation on human myofibrillar and sarcoplasmic protein synthesis after resistance exercise. Am J Physiol Endocrinol Metab 285: E1089-E1094, 2003. First published June 24, 2003; 10.1152/ajpendo.00195.2003.--Muscle hypertrophy during resistance training is reportedly increased by creatine supplementation. Having previously failed to find an anabolic effect on muscle protein turnover at rest, either fed or fasted, we have now examined the possibility of a stimulatory effect of creatine in conjunction with acute resistance exercise. Seven healthy men (body mass index, 23 [+ or -] 2 kg/[m.sup.2], 21 [+ or -] 1 yr, means [+ or -] SE) performed 20 x 10 repetitions of leg extension-flexion at 75% one-repetition maximum in one leg, on two occasions, 4 wk apart, before and after ingesting 21 g/day creatine for 5 days. The subjects ate ~21 g maltodextrin + 6 g protein/h for 3 h postexercise. We measured incorporation of [[1-.sup.13]C]leucine into quadriceps muscle proteins in the rested and exercised legs. Leg protein breakdown (as dilution of [[2.sup][H.sub.5]]phenylalanine) was also assessed in the exercised and rested leg postexercise. Creatine supplementation increased muscle total creatine by ~21% (P < 0.01). Exercise increased the synthetic rates of myofibrillar and sarcoplasmic proteins by two- to threefold (P < 0.05), and leg phenylalanine balance became more positive, but creatine was without any anabolic effect. skeletal muscle; protein turnover.

Dietary creatine supplementation is associated with increases in muscle mass, but the mechanism is unknown. We tested the hypothesis that creatine supplementation enhanced myofibrillar protein synthesis (MPS) and diminished muscle protein breakdown (MPB) in the fed state. Six healthy men (26 [+ or -] 7 yr, body mass index 22 [+ or -] 4 kg/[m.sup.2]) were studied twice, 2-4 wk apart, before and after ingestion of creatine (21 g/day, 5 days). We carried out two sets of measurements within 5.5 h of both MPS (by incorporation of [[1.sup.-13]C]leucine in quadriceps muscle) and MPB (as dilution of [[1.sup.-13]C]leucine or [sup.2][H.sub.5]]phenylalanine across the forearm); for the first 3 h, the subjects were postabsorptive but thereafter were fed orally (0.3 g maltodextrin and 0.083 g protein*kg body [wt.sup.-1*[h.sup.1]). Creatine supplementation increased muscle total creatine by ~30% (P < 0.01). Feeding had significant effects, doubling MPS (P < 0.001) and depressing MPB by ~40% (P < 0.026), but creatine had no effect on turnover in the postabsorptive or fed states. Thus any increase in muscle mass accompanying creatine supplementation must be associated with increased physical activity. skeletal muscle; protein synthesis; protein breakdown

Abstract Background Traditional high volume aerobic exercise training reduces cardiovascular and metabolic disease risk but involves a substantial time commitment. Extremely low volume high-intensity interval training (HIT) has recently been demonstrated to produce improvements to aerobic function, but it is unknown whether HIT has the capacity to improve insulin action and hence glycemic control. Methods Sixteen young men (age: 21 ± 2 y; BMI: 23.7 ± 3.1 kg·m-2; VO2peak: 48 ± 9 ml·kg-1·min-1) performed 2 weeks of supervised HIT comprising of a total of 15 min of exercise (6 sessions; 4–6 × 30-s cycle sprints per session). Aerobic performance (250-kJ self-paced cycling time trial), and glucose, insulin and NEFA responses to a 75-g oral glucose load (oral glucose tolerance test; OGTT) were determined before and after training. Results Following 2 weeks of HIT, the area under the plasma glucose, insulin and NEFA concentration-time curves were all reduced (12%, 37%, 26% respectively, all P < 0.001). Fasting plasma insulin and glucose concentrations remained unchanged, but there was a tendency for reduced fasting plasma NEFA concentrations post-training (pre: 350 ± 36 v post: 290 ± 39 μmol·l-1, P = 0.058). Insulin sensitivity, as measured by the Cederholm index, was improved by 23% (P < 0.01), while aerobic cycling performance improved by ~6% (P < 0.01). Conclusion The efficacy of a high intensity exercise protocol, involving only ~250 kcal of work each week, to substantially improve insulin action in young sedentary subjects is remarkable. This novel time-efficient training paradigm can be used as a strategy to reduce metabolic risk factors in young and middle aged sedentary populations who otherwise would not adhere to time consuming traditional aerobic exercise regimes.

Vitamin D3 supplementation can affect the strength and power of an athlete, however the effect on endurance performance remains unclear. Twenty-seven recreational male combat athletes with at least 12 months experience within combat sports were recruited (age: 24 ± 4 years, stature: 176 ± 6 cm, weight: 77 ± 14 kg). Participants completed baseline testing for blood haemoglobin and haematocrit, upper and lower body VO2peak and upper and lower body Wingate. Following testing participants were stratified to 50,000IU (D1), 80,000IU (D2) or 110,000IU (D3) of vitamin D3 per week. They then completed a 6-week placebo period followed by a 6-week supplementation period. Retesting was carried out after the placebo and supplementation period. There was a significant effect for time for haemoglobin and haematocrit, upper and lower body VO2peak and upper body Wingate power (P < 0.01) but no effect for dose of vitamin D given. Performance data were normalised to vitamin D intake and there was a moderate effect size between D1 and D2 for lower body VO2peak (d = 0.6), upper body VO2peak (d = 0.13) and upper body average power (d = 0.75), with a large effect size between D1 and D2 for haemoglobin (d = 1.19), haematocrit (d = 0.93) and upper body peak power (d = 0.95). There was a large effect size for D1 compared to D3 for all variables (d > 0.8). Therefore, there is no additional benefit to increasing dose above 50,000IU vitamin D per week. Given the endurance adaptations from vitamin D supplementation and the importance of endurance for combat performance, recreational combat athletes should supplement at 50,000IU per week for six weeks. [ABSTRACT FROM AUTHOR]

In adolescent soccer, 23% of the distance covers happens at speeds above onset of blood lactate accumulation which suggests that lactate kinetics may be important for soccer performance. We sought to determine the effectiveness of sprint interval training (SIT) on changing performance and lactate kinetics in adolescent soccer players. Thirteen elite soccer academy players (age 15 ± 0.5y) underwent baseline testing (0–10 m and 10–20 m sprint performance, Wingate anaerobic Test (WaNT) with blood lactate measurements and incremental VO2 peak test) before being allocated to control or SIT group. The control group maintained training whilst the HIT group carried out twice-weekly all-out effort cycle sprints consisting of 6 × 10 s sprint with 80 s recovery. There were significant time x group interactions for 10–20 m sprint time (Control pre: 1.32 ± 0.07 s post: 1.35 ± 0.08 s; SIT pre: 1.29 ± 0.04 s post: 1.25 ± 0.04 s; p = 0.01), Peak Power (Control pre: 13.1 ± 1.3 W.kg−1 post: 13.2 ± 1.47 W.kg−1; SIT pre: 12.4 ± 1.3 W.kg−1 post: 15.3 ± 0.7 W.kg−1; p = 0.01) and time to exhaustion (Control pre: 596 ± 62 s post: 562 ± 85 s; SIT pre: 655 ± 54 s post: 688 ± 55 s; p = 0.001). The changes in performance were significantly correlated to changes in lactate kinetics (power: r = 0.55; 10–20 m speed: r = −0.54; time to exhaustion: r = 0.55). Therefore, cycle based SIT is an effective training paradigm for elite adolescent soccer players and the improvements in performance are associated with changes in lactate kinetics. [ABSTRACT FROM AUTHOR]

This study sought to determine effects of recovery intensity on endurance adaptations during sprint interval training (SIT). Fourteen healthy young adults (male: 9 and female: 5) were allocated to 1 of 2 training groups: active recovery group (ARG, male: 4 and female: 3) or passive recovery group (PRG, male: 5 and female: 2). After having completed a 2-week control period, both groups performed 6 sessions of 4- to 6 30-second sprints interspersed with 4-minute recovery over 2 weeks. However, only ARG cycled at 40% ... during the 4-minute recovery periods, while PRG rested on the bike or cycled unloaded. After the 2-week training intervention, both groups improved 10-km time-trial performance to a similar extent (ARG: 8.6%, d = 1.60, p = 0.006; PRG: 6.7%, d = 0.96, p = 0.048) without gains in .... However, critical power was increased by ARG only (7.9%, d = 1.75, p = 0.015) with a tendency of increased maximal incremental power output (5.3%, d = 0.88, p = 0.063). During the training, active recovery maintained ... and heart rate at a higher level compared with passive recovery ... p = 0.005, HR: p = 0.018), suggesting greater cardiorespiratory demands with the active recovery. This study demonstrated that greater endurance performance adaptations are induced with active recovery when performing SIT over a short time frame. The findings of the current study indicate that, with active recovery, individuals can gain greater training benefits without increasing total training commitment time. Further studies are required to determine whether differences are seen with recovery intensity over a longer period [ABSTRACT FROM AUTHOR]

Objectives:Exercise is an important part of disease management in patients with non-alcoholic fatty liver disease (NAFLD), but adherence to current exercise recommendations is poor. Novel low-volume sprint interval training (SIT) protocols with total training time commitments of ≤30 min per week have been shown to improve cardiometabolic risk and functional capacity in healthy sedentary participants, but the efficacy of such protocols in the management of NAFLD remains unknown. The aim of the present study was to examine whether a low-volume SIT protocol can be used to improve liver function, insulin resistance, body composition, physical fitness, cognitive function and general well-being in patients with NAFLD. Methods: In the present study, 7 men and 2 women with NAFLD (age: 45 ± 8 y, BMI: 28.7 ± 4.1 kg·m−2) completed a 6-week control period followed by 6 weeks of twice-weekly SIT sessions (5–10 × 6-s ‘all-out’ cycle sprints). Body composition, blood pressure, liver function, metabolic function, functional capacity, cognitive function and quality of life were assessed at baseline, following the control period, and following the SIT intervention. Results: Walking speed during the walk test (+12%), estimated V̇O2max (+8%), verbal fluency (+44%), and blood platelet count (+12%; all p < 0.05) significantly increased during the control period. These measures remained significantly raised compared to baseline following the SIT intervention, but did not significantly change any further compared to the post-control time-point. Diastolic blood pressure decreased from 87 ± 10 to 77 ± 8 mm Hg from the end of the control period to the end of the SIT intervention (p < 0.05). Conclusion: This study does not support the use of 6 weeks of a low volume SIT protocol involving twice-weekly sessions with 5–10 × 6-s ‘all-out’ cycle sprints as an intervention for NAFLD disease management. [ABSTRACT FROM PUBLISHER]