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Caffeine, Acute Stretching And Maximum Knee Flexion Strength.: 598 Board #13 May 28, 3
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Scientific information about the effects of caffeine intake on combat sport performance is scarce and controversial. The aim of this study was to investigate the effectiveness of caffeine to improve Brazilian Jiu-jitsu (BJJ)-specific muscular performance. Fourteen male and elite BJJ athletes (29.2 ± 3.3 years; 71.3 ± 9.1 kg) participated in a randomized double-blind, placebo-controlled and crossover experiment. In two different sessions, BJJ athletes ingested 3 mg kg(-1) of caffeine or a placebo. After 60 min, they performed a handgrip maximal force test, a countermovement jump, a maximal static lift test and bench-press tests consisting of one-repetition maximum, power-load, and repetitions to failure. In comparison to the placebo, the ingestion of the caffeine increased: hand grip force in both hands (50.9 ± 2.9 vs. 53.3 ± 3.1 kg; respectively p < .05), countermovement jump height (40.6 ± 2.6 vs. 41.7 ± 3.1 cm; p = .02), and time recorded in the maximal static lift test (54.4 ± 13.4 vs. 59.2 ± 11.9 s; p < .01).The caffeine also increased the one-repetition maximum (90.5 ± 7.7 vs. 93.3 ± 7.5 kg; p = .02), maximal power obtained during the power-load test (750.5 ± 154.7 vs. 826.9 ± 163.7 W; p < .01) and mean power during the bench-press exercise test to failure (280.2 ± 52.5 vs. 312.2 ± 78.3 W; p = .04). In conclusion, the pre-exercise ingestion of 3 mg kg(-1) of caffeine increased dynamic and isometric muscular force, power, and endurance strength in elite BJJ athletes. Thus, caffeine might be an effective ergogenic aid to improve physical performance in BJJ.
Recently, there has been a shift from static stretching (SS) or proprioceptive neuromuscular facilitation (PNF) stretching within a warm-up to a greater emphasis on dynamic stretching (DS). The objective of this review was to compare the effects of SS, DS, and PNF on performance, range of motion (ROM), and injury prevention. The data indicated that SS- (–3.7%), DS- (+1.3%), and PNF- (–4.4%) induced performance changes were small to moderate with testing performed immediately after stretching, possibly because of reduced muscle activation after SS and PNF. A dose–response relationship illustrated greater performance deficits with ≥60 s (–4.6%) than with <60 s (–1.1%) SS per muscle group. Conversely, SS demonstrated a moderate (2.2%) performance benefit at longer muscle lengths. Testing was performed on average 3–5 min after stretching, and most studies did not include poststretching dynamic activities; when these activities were included, no clear performance effect was observed. DS produced small-to-moderate performance improvements when completed within minutes of physical activity. SS and PNF stretching had no clear effect on all-cause or overuse injuries; no data are available for DS. All forms of training induced ROM improvements, typically lasting <30 min. Changes may result from acute reductions in muscle and tendon stiffness or from neural adaptations causing an improved stretch tolerance. Considering the small-to-moderate changes immediately after stretching and the study limitations, stretching within a warm-up that includes additional poststretching dynamic activity is recommended for reducing muscle injuries and increasing joint ROM with inconsequential effects on subsequent athletic performance.
To investigate whether caffeine ingestion counteracts the morning reduction in neuromuscular performance associated with the circadian rhythm pattern.
Twelve highly resistance-trained men underwent a battery of neuromuscular tests under three different conditions; i) morning (10:00 a.m.) with caffeine ingestion (i.e., 3 mg kg(-1); AM(CAFF) trial); ii) morning (10:00 a.m.) with placebo ingestion (AM(PLAC) trial); and iii) afternoon (18:00 p.m.) with placebo ingestion (PM(PLAC) trial). A randomized, double-blind, crossover, placebo controlled experimental design was used, with all subjects serving as their own controls. The neuromuscular test battery consisted in the measurement of bar displacement velocity during free-weight full-squat (SQ) and bench press (BP) exercises against loads that elicit maximum strength (75% 1RM load) and muscle power adaptations (1 m s(-1) load). Isometric maximum voluntary contraction (MVC(LEG)) and isometric electrically evoked strength of the right knee (EVOK(LEG)) were measured to identify caffeine's action mechanisms. Steroid hormone levels (serum testosterone, cortisol and growth hormone) were evaluated at the beginning of each trial (PRE). In addition, plasma norepinephrine (NE) and epinephrine were measured PRE and at the end of each trial following a standardized intense (85% 1RM) 6 repetitions bout of SQ (POST).
In the PM(PLAC) trial, dynamic muscle strength and power output were significantly enhanced compared with AM(PLAC) treatment (3.0%-7.5%; p≤0.05). During AM(CAFF) trial, muscle strength and power output increased above AM(PLAC) levels (4.6%-5.7%; p≤0.05) except for BP velocity with 1 m s(-1) load (p = 0.06). During AM(CAFF), EVOK(LEG) and NE (a surrogate of maximal muscle sympathetic nerve activation) were increased above AM(PLAC) trial (14.6% and 96.8% respectively; p≤0.05).
These results indicate that caffeine ingestion reverses the morning neuromuscular declines in highly resistance-trained men, raising performance to the levels of the afternoon trial. Our electrical stimulation data, along with the NE values, suggest that caffeine increases neuromuscular performance having a direct effect in the muscle.
An objective of a warm-up prior to an athletic event is to optimize performance. Warm-ups are typically composed of a submaximal aerobic activity, stretching and a sport-specific activity. The stretching portion traditionally incorporated static stretching. However, there are a myriad of studies demonstrating static stretch-induced performance impairments. More recently, there are a substantial number of articles with no detrimental effects associated with prior static stretching. The lack of impairment may be related to a number of factors. These include static stretching that is of short duration (<90 s total) with a stretch intensity less than the point of discomfort. Other factors include the type of performance test measured and implemented on an elite athletic or trained middle aged population. Static stretching may actually provide benefits in some cases such as slower velocity eccentric contractions, and contractions of a more prolonged duration or stretch-shortening cycle. Dynamic stretching has been shown to either have no effect or may augment subsequent performance, especially if the duration of the dynamic stretching is prolonged. Static stretching used in a separate training session can provide health related range of motion benefits. Generally, a warm-up to minimize impairments and enhance performance should be composed of a submaximal intensity aerobic activity followed by large amplitude dynamic stretching and then completed with sport-specific dynamic activities. Sports that necessitate a high degree of static flexibility should use short duration static stretches with lower intensity stretches in a trained population to minimize the possibilities of impairments.
Therapeutic muscle stretch is a commonly used procedure despite little evidence in support of efficacy or information about the mechanisms underlying the various methods. The purpose of this work was to compare the sequential application of static and ballistic muscle stretch with static muscle stretch alone, using the electrically elicited Hoffmann reflex (H-reflex) as a measure of excitability of homonymous motoneurons. The foot was passively dorsiflexed and either maintained in this position or rapidly and repeatedly dorsiflexed at a velocity of 1.0 radian/sec. Hoffmann reflexes were taken using established criteria under control conditions and during stretch conditions. An analysis of variance indicated a significant difference (p < 0.05) between condition means, with H-reflex amplitude reducing to 60 and 15% of the control value during static and ballistic stretch, respectively. Since reductions in alpha-motoneuron pool excitability correlate with increased flexibility, ballistic stretch applied following static stretch appears more effective than static stretch alone.
As muscles are stretched, blood flow and oxygen delivery are compromised, and consequently muscle function is impaired. We tested the hypothesis that the structural microvascular sequellae associated with muscle extension in vivo would impair capillary red blood cell hemodynamics. We developed an intravital spinotrapezius preparation that facilitated direct on-line measurement and alteration of sarcomere length simultaneously with determination of capillary geometry and red blood cell flow dynamics. The range of spinotrapezius sarcomere lengths achievable in vivo was 2.17 ± 0.05 to 3.13 ± 0.11 μm. Capillary tortuosity decreased systematically with increases of sarcomere length up to 2.6 μm, at which point most capillaries appeared to be highly oriented along the fiber longitudinal axis. Further increases in sarcomere length above this value reduced mean capillary diameter from 5.61 ± 0.03 μm at 2.4-2.6 μm sarcomere length to 4.12 ± 0.05 μm at 3.2-3.4 μm sarcomere length. Over the range of physiological sarcomere lengths, bulk blood flow (radioactive microspheres) decreased ~40% from 24.3 ± 7.5 to 14.5 ± 4.6 ml·100 g-1·min-1 . The proportion of continuously perfused capillaries, i.e., those with continuous flow throughout the 60-s observation period, decreased from 95.9 ± 0.6% at the shortest sarcomere lengths to 56.5 ± 0.7% at the longest sarcomere lengths and was correlated significantly with the reduced capillary diameter (r = 0.711, P < 0.01; n = 18). We conclude that alterations in capillary geometry and luminal diameter consequent to increased muscle sarcomere length are associated with a reduction in mean capillary red blood cell velocity and a greater proportion of capillaries in which red blood cell flow is stopped or intermittent. Thus not only does muscle stretching reduce bulk blood (and oxygen) delivery, it also alters capillary red blood cell flow dynamics, which may further impair blood-tissue oxygen exchange.
The purpose of this study was to investigate the factors underlying the force loss occurring after prolonged, static, passive stretching. Subjects were tested before and 5-10 min following 20 min of static, passive stretching of the quadriceps (N=12) or a similar period of no stretch (control, N=6). Measurements included isometric maximal voluntary contraction (MVC) force, surface integrated electromyographic (iEMG) activity of the quadriceps and hamstrings, evoked contractile properties (twitch and tetanic force), and quadriceps inactivation as measured by the interpolated twitch technique (ITT). Following stretching, there was a significant 12% decrement in MVC with no significant changes in the control group. Muscle inactivation as measured by the ITT and iEMG increased by 2.8% and 20.2%, respectively. While twitch forces significantly decreased 11.7%, there was no change in tetanic force post-stretch. Although possible increases in muscle compliance affected twitch force, a lack of tetanic force change would suggest that post-stretch force decrements are more affected by muscle inactivation than changes in muscle elasticity.
Caffeine is probably the most frequently ingested pharmacologically active substance in the world. It is found in common beverages (coffee, tea, soft drinks), in products containing cocoa or chocolate, and in medications. Because of its wide consumption at different levels by most segments of the population, the public and the scientific community have expressed interest in the potential for caffeine to produce adverse effects on human health. The possibility that caffeine ingestion adversely affects human health was investigated based on reviews of (primarily) published human studies obtained through a comprehensive literature search. Based on the data reviewed, it is concluded that for the healthy adult population, moderate daily caffeine intake at a dose level up to 400 mg day(-1) (equivalent to 6 mg kg(-1) body weight day(-1) in a 65-kg person) is not associated with adverse effects such as general toxicity, cardiovascular effects, effects on bone status and calcium balance (with consumption of adequate calcium), changes in adult behaviour, increased incidence of cancer and effects on male fertility. The data also show that reproductive-aged women and children are 'at risk' subgroups who may require specific advice on moderating their caffeine intake. Based on available evidence, it is suggested that reproductive-aged women should consume </=300 mg caffeine per day (equivalent to 4.6 mg kg(-1) bw day(-1) for a 65-kg person) while children should consume </=2.5 mg kg(-1) bw day(-1).
Investigators, who are increasingly implored to present and discuss effect size statistics, might comply more often if they understood more clearly what is required. When investigators wish to report effect sizes derived from analyses of variance that include repeated measures, past advice has been problematic. Only recently has a generally useful effect size statistic been proposed for such designs: generalized eta squared (η
G2; Olejnik & Algina, 2003). Here, we present this method, explain that η
G2 is preferred to eta squared and partial eta squared because it provides comparability across between-subjects and within-subjects designs, show that it can easily be computed from information provided by standard statistical packages, and recommend that investigators provide it routinely in their research reports when appropriate.
Stretching long has been commonplace in the training programs of recreational and competitive athletes. Its role in performance enhancement has been debated. This review discusses the literature concerning the effects of static, dynamic, and proprioceptive neuromuscular facilitation stretching on performance in three categories of sporting activity: strength- and power-dominant, speed- and agility-dominant, and endurance-dominant activities.
Introduction:
We examined the effect of caffeine ingestion on muscle torque production and muscle activity at different contraction speeds in trained men.
Methods:
10 men (mean age ± SD=22 ± 1.1 years) volunteered to participate. A double-blind, randomized cross-over design was used. Sixty minutes postingestion of caffeine (6 mg kg(-1) ) or placebo, participants completed 6 repetitions of isokientic knee extension at 3 angular velocities (30°s(-1) , 150°s(-1) , 300°s(-1) ) from which peak torque was determined. Electromyographic activity of the vastus medialis was also collected.
Results:
Repeated measures analysis of variance indicated that muscle torque production was significantly higher (P=0.02) with caffeine compared with placebo. A significant (P=0.02) substance by velocity interaction for muscle activity indicated significantly higher vastus medialis muscle activity in the presence of caffeine versus placebo, and this difference was amplified as angular velocity increased.
Conclusions:
Acute caffeine ingestion improves muscle performance and increases muscle activity during short-duration maximal dynamic contractions.
The relative contributions of central versus peripheral factors to the force loss induced by acute continuous and intermittent plantarflexor stretches were studied.
Eighteen healthy young men with no apparent tissue stiffness limitations randomly performed 1) one 5-min stretch (continuous stretch; CS); 2) five 1-min stretches (intermittent stretch; IS); and 3) a control condition, on three separate days. The stretches were constant-torque ankle stretches performed on an isokinetic dynamometer. Gastrocnemius medialis oxygenation status was quantified during stretch using near infra-red spectroscopy. Measures of isometric plantarflexor peak torque (Tpeak), voluntary activation (%VA; interpolated twitch technique), EMG amplitude normalized by Mmax (EMG:M), V-wave amplitude and excitation-contraction (E-C) coupling efficiency (torque ratio between 20 and 80 Hz tetanic stimulations [20:80]) were taken before, immediately, and 15 and 30 minutes after each condition.
IS caused substantial cyclic variations in tissue oxygenation, but CS resulted in a greater decrease in oxyhemoglobin concentration. Voluntary Tpeak decreased more after IS (-23.8%) than CS (-14.3%), and remained significantly depressed until 30 min after IS only (-5.6%). EMG:M (-27.7%) and %VA (-15.9%) were reduced only after IS. After CS and IS, the magnitude of decrease in Tpeak was correlated with decreases in EMG:M (r=0.81 and 0.89, respectively), %VA (r=0.78 and 0.93) and V-wave (r=0.51, only after IS). 20 Hz and 80 Hz tetanic torque were decreased after IS (-13.1% and -6.4%, respectively) and CS (-10.9% and -6.7%), but 20:80 was not different from the control group.
These results suggest that IS reduced Tpeak more than CS, and these reductions were strongly associated with a depression in central drive.
The effect of pre- versus postsynaptic mechanisms in the decrease in spinal reflex response during passive muscle stretching was studied. The change in the electromyographic (EMG) responses of two reflex pathways sharing a common pool of motoneurones, with (Hoffmann or H reflex) or without (exteroceptive or E reflex) a presynaptic inhibitory mechanism, was compared. The EMG activities were recorded in the soleus muscle in response to the electrical stimulation of the tibial nerve at the popliteal fossa (H reflex), and at the ankle (E reflex) for different dorsiflexion angles of the ankle. The compound muscle action potential (M wave) in the soleus and the abductor hallucis was recorded in order to control the stability of the electrical stimulation during stretching. The results indicate that in the case of small-amplitude muscle stretching (10 degrees of dorsiflexion), a significant reduction (-25%; P < 0.05) in the Hmax/Mmax ratio was present without any significant change in the Emax/Mmax ratio. At a greater stretching amplitude (20 degrees of dorsiflexion), the E reflex was found to be reduced (-54.6%; P < 0.001) to a similar extent as the H reflex (-54.2%). As soon as the ankle joint returned to the neutral position (ankle at 90 degrees), the two reflex responses recovered their initial values. In additional experiments, motor-evoked potential (MEP) induced by the magnetic stimulation of the motor cortex was recorded and showed a similar type of behaviour to that observed in the E reflex. These results indicate that reduced motoneurone excitation during stretching is caused by pre- and postsynaptic mechanisms. Whereas premotoneuronal mechanisms are mainly involved in the case of small stretching amplitude, postsynaptic ones play a dominant role in the reflex inhibition when larger stretching amplitude is performed.
Coffee is often perceived as producing greater pharmacological effects than cola. The present study compared the magnitude and rapidity of peak caffeine levels and subjective effects between coffee and cola. Thirteen users of both coffee and cola (mean daily caffeine consumption = 456 mg) ingested 400 mg caffeine via 12 oz unsweetened coffee, 24 oz sugar-free cola or 2 capsules in a random, double-blind, placebo-controlled, within-subjects design. Subjects provided a saliva sample and completed subjective effect scales 15 min before and 30, 60, 90, 120, 180 and 240 min after ingestion. Mean peak saliva caffeine levels did not differ between coffee (9.7 ± 1.2 μg/ml) and cola (9.8 ± 0.9 μg/ml) and appeared to be greater with these beverages than with the capsule (7.8 ± 0.6 μg/ml; p = NS). Saliva caffeine levels peaked at similar times for coffee (42 ± 5 min) and cola (39 ± 5 min) but later for capsule (67 ± 7 min; p = 0.004). There was no main effect of vehicle or interaction of vehicle and drug on magnitude of peak effect or time to peak increase on self-report scales. In summary, peak caffeine absorption, time to peak absorption, and subjective effects do not appear to be influenced by cola vs. coffee vehicle. Perceived differences in the effects of coffee vs. cola may be due to differences in dose, time of day, added sweetener, environmental setting or contingencies.
The benefits of preexercise muscle stretching have been recently questioned after reports of significant poststretch reductions in force and power production. However, methodological issues and equivocal findings have prevented a clear consensus being reached. As no detailed systematic review exists, the literature describing responses to acute static muscle stretch was comprehensively examined.
MEDLINE, ScienceDirect, SPORTDiscus, and Zetoc were searched with recursive reference checking. Selection criteria included randomized or quasi-randomized controlled trials and intervention-based trials published in peer-reviewed scientific journals examining the effect of an acute static stretch intervention on maximal muscular performance.
Searches revealed 4559 possible articles; 106 met the inclusion criteria. Study design was often poor because 30% of studies failed to provide appropriate reliability statistics. Clear evidence exists indicating that short-duration acute static stretch (<30 s) has no detrimental effect (pooled estimate = -1.1%), with overwhelming evidence that stretch durations of 30-45 s also imparted no significant effect (pooled estimate = -1.9%). A sigmoidal dose-response effect was evident between stretch duration and both the likelihood and magnitude of significant decrements, with a significant reduction likely to occur with stretches ≥ 60 s. This strong evidence for a dose-response effect was independent of performance task, contraction mode, or muscle group. Studies have only examined changes in eccentric strength when the stretch durations were >60 s, with limited evidence for an effect on eccentric strength.
The detrimental effects of static stretch are mainly limited to longer durations (≥ 60 s), which may not be typically used during preexercise routines in clinical, healthy, or athletic populations. Shorter durations of stretch (<60 s) can be performed in a preexercise routine without compromising maximal muscle performance.
Caffeine ingestion (3-9 mg/kg body weight) prior to exercise increases performance during prolonged endurance exercise and short-term intense exercise lasting approximately 5 min in the laboratory. These results are generally reported in well-trained elite or recreational subjects. However, there is a lack of well-controlled field studies to determine the applicability of laboratory results to the athletic world. Caffeine does not appear to enhance performance during incremental exercise tests lasting 8-20 min and during sprinting lasting less than 90 s, although research examining sprinting is rare. In addition, the mechanisms responsible for any improvement in endurance and short-term exercise have not been clearly established. The ergogenic effects of caffeine are present with urinary caffeine levels that are below the limit of 12 micrograms/ml allowed by the International Olympic Committee, which raises serious ethical issues regarding the use of caffeine to improve athletic performance. One solution would be to add caffeine to the list of banned substances, thereby requiring athletes to abstain from caffeine ingestion 48-72 hr prior to competition.
It is well established that altering O2 delivery to contracting skeletal muscle affects human performance. In this respect, a reduced O2 supply (e.g., hypoxia) increases the rate of muscle fatigue, whereas increasing O2 supply (e.g., hyperoxia) reduces the rate of fatigue. Interestingly, the faster onset of fatigue in moderate hypoxia does not appear to be a consequence of mitochondrial O2 limitation because these effects occur at submaximal rates of O2 consumption for these conditions and at O2 tensions well above that which impairs mitochondrial O2 uptake in vitro. Alterations in O2 supply modulate the regulation of cellular respiration and may affect the onset of impaired Ca2+ handling with fatigue. Specifically, changes in O2 supply alter the coupling between phosphocreatine hydrolysis and O2 uptake in contracting muscles, which by determining the rate of inorganic phosphate (Pi) accumulation may affect Ca2+ release. Partial ischemia differs somewhat in that the reduction in force could be due to reduced O2 supply and/or impaired removal of metabolic by-products secondary to insufficient blood flow. Nonetheless, recent evidence shows a parallel decline and restoration of force with alterations in O2 supply but not blood flow alone during submaximal contractions. Furthermore, the causes of fatigue are similar when O2 is plentiful and when it is reduced.
This review focuses on caffeine's effects on the central modulation of muscle activation in humans. The drug's effects on voluntary muscle activation, the Hoffman reflex, motor-evoked potentials, self-sustained firing, pain, and sensation are discussed, and the possibility that caffeine maybe useful in the study of central fatigue is explored.
To determine the effect of water, carbohydrate, and caffeine ingestion on fatigue during prolonged exercise in the heat.
Seven endurance-trained cyclists (V O2max = 61 +/- 8 mL.kg.min) pedaled for 120 min at 63% V O2max in a hot-dry environment (36 degrees C; 29% humidity), ingesting either no fluid (NF), water (WAT) to replace 97% fluid losses, the same volume of a 6% carbohydrate-electrolyte solution (CES), or each of these treatments along with ingestion of 6 mg of caffeine per kilogram of body weight (NF + CAFF, WAT + CAFF, and CES + CAFF). At regular intervals during exercise, maximal cycling power (PMAX) was measured. Before and after exercise, maximal voluntary contraction (MVC), voluntary activation (VA), and electrically evoked contractile properties of the quadriceps were determined.
Without fluid replacement (NF and NF + CAFF), subjects were dehydrated by 3.8 +/- 0.3%, and rectal temperature reached 39.4 +/- 0.3 degrees C, while it was maintained at 38.7 +/- 0.3 degrees C in trials with rehydration (P < 0.05). Trials with caffeine ingestion increased PMAX by 3% above trials without caffeine (P < 0.05). MVC reductions after exercise were larger with NF (-11 +/- 5%) than for the rest of the trials (P < 0.05). MVC was reduced in WAT compared with CES + CAFF (-6 +/- 4 vs 2 +/- 4%; P < 0.05). However, NF + CAFF maintained MVC at the level of the CES trial. VA showed the same treatment response pattern as MVC. There were no differences in electrically evoked contractile properties among trials.
During prolonged exercise in the heat, caffeine ingestion (6 mg.kg body weight) maintains MVC and increases PMAX despite dehydration and hyperthermia. When combined with water and carbohydrate, caffeine ingestion increases maximal leg force by increasing VA (i.e., reducing central fatigue).
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