Research Watch

Reference
Øyvind H, Therese FM , Truls R. The Effect of Meal Frequency on Body Composition during 12-Weeks of Strength Training. Annual Congress of the ECSS. Jyväskylä, Finland, 2007.

Abstract
Human trials on the effect of meal frequency on body composition are scarce. Short-term studies show increased rate of protein synthesis immediately after intake of amino acids (1), and frequent meals are shown to aid in the preservation of lean body mass when dieting (2). Consequently it could be hypothesised that in response to strength training, more frequent meals will give larger muscle mass accumulation and lower fat mass (FM) than fewer meals. The purpose of this study was to compare the effects of 3 vs. 6meals per day on changes in body composition in young men and women performing strength training over 12 weeks. Men (n=33) and women (n=15) aged 21 to 35 with at least one year of previous strength training experience were randomly assigned to either a 6 meals a day group or a 3 meals a day group. The prescribed total dietary intake in both groups was equal and calculated to give a positive energy balance of approximately 1200 KJ/day, a protein intake of 1.5-1.7 g/kg/day and a carbohydrate intake of 5-7 g/kg/day. During the training period the dietary intake was controlled by repeated 24-hours recalls. All participants performed the same strength training program, training four times per week, giving each muscle group one heavy session and one light session per week. In the heavy sessions, training intensity varied between 10 and 3 RM sets, and 3-6 sets were performed in each exercise. Determination of body composition was performed with DEXA at the beginning of and immediately after the training period. A total of 16 men and 11 women completed the project. After multiple regression analysis the 3 meal group had a significant greater gain in lean body mass (LBM) than the 6 meal group when adjusted for gender and energy intake (p=0.04), when adjusted for gender and protein intake (p=0.03), and when adjusted for gender, protein intake, carbohydrate intake and fat intake* (p=0.01). (*: Fat intake in g/kg body weight/day showed significance on LBM, p=0.03). No significant differences in regional changes in LBM were observed, although there was a tendency towards a greater gain in the three meal group. There were no significant differences in change in fat mass (FM) between the groups, but a tendency towards a greater gain in the three meal group, 7.33% (-5.23, 19.90), p=0.24. The three meal group had a 2.87%(0.62, 5.12) larger weight gain than the six meal group, p=0.01.The participants had a 2.31% (0.83, 3.79), gain in bone mineral density of the spine during the twelve weeks of strength training, p<0.01, class="blsp-spelling-error" id="SPELLING_ERROR_9">LBM from strength training.

References:
(1). Rennie, MJ., Bohe, J., Wolfe, RR. Latency, duration and dose response relationships of amino acid effects on human muscle protein synthesis. J Nutr 132(10):3225S-7S, 2002.
(2). Iwao, S., Mori, K., Sato, Y. Effects of meal frequency on body composition during weight control in boxers. Scan J Med Sci Sports 6:265-272, 1996

My Thoughts
I don't usually put a lot of effort into abstracts or conference presentations due to the inability to pedantically go through the experimental methodologies. But this abstract was relatively interesting.

Typically the bodybuilding/fitness crowd is told to eat 6x per day to achieve their goals, because you have to provide a constant supply of protein to "feed the machine". Of course, this type of effect has not been studied in the past, but typically we have relied on the research in untrained individuals showing no difference on body composition with meals 3 or 6x per day in untrained subjects.

But this trial produces an interesting response, and while the abstract doesn't show a lot, its quite amusing to see a potential benefit going towards the group consuming their food over three meals, rather than six.

I suspect while the goal was 1200kj extra, the effect may be ultimately due to a small, non-significant, variation in energy intake (Cannot confirm this as there is not enough information in the abstract). Even if this is the ultimate cause, it would just show the style of eating that allows the most food intake will equate to the best gains.

Research Watch

Reference
Bray GA, Most M, Rood J, Redmann S, Smith SR. Hormonal Responses to a Fast-Food Meal Compared with Nutritionally Comparable Meals of Different Composition. Ann Nutr Metab 2007;51:163-171

Abstract
Background: Fast food is consumed in large quantities each day. Whether there are differences in the acute metabolic response to these meals as compared to 'healthy' meals with similar composition is unknown. Design: Three-way crossover. Methods: Six overweight men were given a standard breakfast at 8:00 a.m. on each of 3 occasions, followed by 1 of 3 lunches at noon. The 3 lunches included: (1) a fast-food meal consisting of a burger, French fries and root beer sweetened with high fructose corn syrup; (2) an organic beef meal prepared with organic foods and a root beer containing sucrose, and (3) a turkey meal consisting of a turkey sandwich and granola made with organic foods and an organic orange juice. Glucose, insulin, free fatty acids, ghrelin, leptin, triglycerides, LDL-cholesterol and HDL-cholesterol were measured at 30-min intervals over 6 h. Salivary cortisol was measured after lunch. Results: Total fat, protein and energy content were similar in the 3 meals, but the fatty acid content differed. The fast-food meal had more myristic (C14:0), palmitic (C16:0), stearic (C18:0) and trans fatty acids (C18:1) than the other 2 meals. The pattern of nutrient and hormonal response was similar for a given subject to each of the 3 meals. The only statistically significant acute difference observed was a decrease in the AUC of LDL cholesterol after the organic beef meal relative to that for the other two meals. Other metabolic responses were not different. Conclusion: LDL-cholesterol decreased more with the organic beef meal which had lesser amounts of saturated and trans fatty acids than in the fast-food beef meal.

My Thoughts
The clean crowd typically shouts that 'unclean' foods are bad because of physiological changes that result in fat gain. A lot of the time they are focussing on one nutrient, insulin, as the be all/end all focus on fat metabolism.
This trial examines the effects of similar foods that are either fast food burger (Big Mac, fries and a root beer), organic burger (organic burger, organic french fries and organic root beer) or a organic turkey sandwich (turkey sandwich, granola and orange juice), on a variety of biological measures. After a standard breakfast, the subjects waited until lunch where they consumed one of the three meals (randomly assigned) and then for the 6hours following the meal they were sampled for insulin, glucose, Free fatty acid, triglycerides, LDL, HDL, leptin and ghrelin.
The study was reasonably controlled, however, due to the lack of any measureable effect, the authors cut the trial off at six subjects rather that recruiting all of the 20 orgionally proposed subjects. Based on the observed changes in insulin, they would have required >50 subjects to power the study suitably to detect the observed differences.
The meals were not identical for nutrient composition or the energy they provided. The McMeal provided the lowest fat, carbs and calories, the organic beef provided the greatest fat and the turkey meal contained the most protein, most carbs and highest calories.
The major difference between the meals is the fatty acid composition, with the McMeal containing the highest level of saturated and trans-unsaturated fatty acids, with the turkey meal providing the lowest. A point for the clean people to note, all meals contained eladic acid, the dominant trans-unsaturated fatty acid in our diets.
After consuming the meal, and for the six hours afterwards, there was no significant differences for insulin, glucose, FFA, TAG, HDL, Ghrelin or Leptin. The only statistically significant effect of the meal was that the organic beef meal resulted in a significantly smaller Area Under the Curve (AUC) for LDL, which the authors presumed was because of the lower trans-unsaturated or saturated fatty acids. The turkey meal was lower in saturates, but did not produce a lower LDL AUC, possibly due to it containing the highest level of fat, which can also influence LDL response.
This trial does not perfectly identify, but aids in the support that whether a food is 'clean' or not, the metabolic responses to macronutrients are similar. The inclusion of a food inside of your diet that fits with your macronutrient and caloric requirements will not result in massive blood glucose changes or similar.
It doesn't, however, take account of the differences in other nutrients, such as the micronutrients, and the levels of fibre etc within the meal.

Research watch

Reference
Duffery, MJ and Challis, JH. Fatigue Effects on Bar Kinematics During the Bench Press. J Strength Cond Res 2007;21:556-560

Abstract
The bench press is one of the most popular weight training exercises. Although most training regimens incorporate multiple repetition sets, there are few data describing how the kinematics of a lift change during a set to failure. To examine these changes, recreational lifters (10 men and 8 women) were recruited. The maximum weight each subject could bench press (1RM) was determined. Subjects then performed as many repetitions as possible at 75% of the 1RM load. Three-dimensional kinematic data were recorded and analyzed for all lifts. Statistical analysis revealed that differences between maximal and submaximal lifts and the kinematics of a submaximal lift change as a subject approaches failure in a set. The time to lift the bar more than doubled from the first to the last repetition, causing a decrease in both mean and peak upward velocity. Furthermore, the peak upward velocity occurred much earlier in the lift phase in these later repetitions. The path the bar followed also changed, with subjects keeping the bar more directly over the shoulder during the lift. In general, most of the kinematic variables analyzed became more similar to those of the maximal lift as the subjects progressed through the set, but there was considerable variation between subjects as to which repetition was most like the maximal lift. This study shows that there are definite changes in the lifting kinematics in recreational lifters during a set to failure and suggests it may be particularly important for coaches and less-skilled lifters to focus on developing the proper bar path, rather than reaching momentary muscular failure, in the early part of a training program.

My Thoughts
An interesting little piece of research that provides a little more evidence supporting the differences that load and fatigue can create to the bench press. Basically the researchers collected a bunch of trained people, got them to perform a 1rm test in front of a camera, then wait 5minutes and perform a set to failure at 75% of that 1rm.
During this time, the researchers videoed the movement to enable the examination of bar speed and position in the horizontal movement plane. They then compared the figures for the 1rm to all of the reps achieved in the set to failure.
The first rep of the set to failure was relatively dissimilar to the 1rm attempt. The major differences was the bar position at the bottom, the groove it followed on the way up, as well as the obvious overall movement speed. Looking at a chart of the bar velocity during the first and last sets of the set to failure, as well as the 1rm test shows an interesting, but relatively known concept.
At 75%, a rep is completely different to the 1rm. A 75% rep is performed fast, with no apparent sticking point, and one peak in bar velocity that occurs at the end of the movement with lockout. Both the final rep, and the 1rm test appear similar, except the initial peak of velocity is higher in the 75% set. There are two peaks, one during the initial drive off the chest, and the other at lockout. Bar speed is slower on the 75% sticking point, but since the load is lower the lifter can struggle throught. The slowest point of the entire upwards movement occurs at 30-50% of the lift phase, which matches older research showing the sticking point is 25-40% of the lift.

While this research does not provide any actual intervention knowledge, it allows us to look at a little bit of specificity of training. If you want to learn the best groove for a move, a 1rm will be the best teacher for a 1rm. However, training near 1RM's is difficult. Performing reps at 75-85% will result in a groove that is different to the 1rm, however, do more reps and the ultimate movement looks a lot more like a 1rm. This effect can start as early as in the first 10% of a set, or typically occurs at 70-85% of the sets progression. So within a set of 10 to failure, the 7th, 8th and 9th rep would be the most like a 1rm test.
Maybe this is why a sets of three/five are great building points for strength. Most of these sets are close to failure, but not quite there. So a lot of the reps would be performed in a moderately fatigued state, matching the groove for a 1rm test. Same as performing high volume training, where the last sets are done in a relatively fatigued state, or providing a training environment that is more representative of 1rm lifting, without the maximal loading. Proving that this is more efficacious for improving strength is a different story.

Research Watch

The paper I want to comment on today, I haven't completely absorbed, but its more of a commentary about the media rather than anything else.

On TVOne's Breakfast Show, they have a Health Correspondent, Lorelei Mason. As can be seen from TVNZ's profile of Lorelei, she is a reporter, which is fine, but not medically, or more specifically research trained.

This became totally apparent when she reported (video available here) on the paper below.

References
Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Mortality in Randomized Trials of Antioxidant Supplements for Primary and Secondary Prevention: Systematic Review and Meta-analysis. JAMA. 2007;297(8):842-857

Abstract
CONTEXT: Antioxidant supplements are used for prevention of several diseases. OBJECTIVE: To assess the effect of antioxidant supplements on mortality in randomized primary and secondary prevention trials. Data Sources and Trial Selection We searched electronic databases and bibliographies published by October 2005. All randomized trials involving adults comparing beta carotene, vitamin A, vitamin C (ascorbic acid), vitamin E, and selenium either singly or combined vs placebo or vs no intervention were included in our analysis. Randomization, blinding, and follow-up were considered markers of bias in the included trials. The effect of antioxidant supplements on all-cause mortality was analyzed with random-effects meta-analyses and reported as relative risk (RR) with 95% confidence intervals (CIs). Meta-regression was used to assess the effect of covariates across the trials. DATA EXTRACTION: We included 68 randomized trials with 232 606 participants (385 publications). DATA SYNTHESIS: When all low- and high-bias risk trials of antioxidant supplements were pooled together there was no significant effect on mortality (RR, 1.02; 95% CI, 0.98-1.06). Multivariate meta-regression analyses showed that low-bias risk trials (RR, 1.16; 95% CI, 1.05-1.29) and selenium (RR, 0.998; 95% CI, 0.997-0.9995) were significantly associated with mortality. In 47 low-bias trials with 180 938 participants, the antioxidant supplements significantly increased mortality (RR, 1.05; 95% CI, 1.02-1.08). In low-bias risk trials, after exclusion of selenium trials, beta carotene (RR, 1.07; 95% CI, 1.02-1.11), vitamin A (RR, 1.16; 95% CI, 1.10-1.24), and vitamin E (RR, 1.04; 95% CI, 1.01-1.07), singly or combined, significantly increased mortality. Vitamin C and selenium had no significant effect on mortality. CONCLUSIONS: Treatment with beta carotene, vitamin A, and vitamin E may increase mortality. The potential roles of vitamin C and selenium on mortality need further study.

My Thoughts
In the news piece, Lorelei comments "As always with these studies, the devil is in the detail. Uhh, what they did, it's called an epidemiological study. Which is a big word for saying what these researchers did is not look at a whole lot of new people in new trials, they took 68 trials, which involved 230 thousand people, and they looked at those people's, uhh, data that hadn't perhaps been exposed, umm, in those trials... ...and worked out the vitamin intake of these people, um, who later went on to die and from that they extrapolated, if you like, the data they got, to show if you take Vitamin A, you got a 16% higher death risk, um, if you take too much of it of course, and this is what I am saying about the detail, um, vitamin Beta-carotene 7% and Vitamin E, which surprised some, a 4% increase..."

She went on to attempt to pick apart the trial due to the inclusion of asbestosis sufferers (One trial, Lorelei made it sound like a large number).

The trial was a meta-analysis of randomised controlled trials, not epidemiology. While Meta-analyses have been termed the epidemiology of controlled research, this is not the same as the common usage of the term epidemiology, which is usually limited to large scale observational trials, case-control, cohorts, surveys etc.

The meta-analysis collected 16'111 references from five research databases, Central, Medline, Embase, Web of Science and the very basic - reading bibliographies. Due to a very specific selection process, this number was reduced to a total of 68 trials that met the requirements, with 14,003 references removed due to reference duplication (multiple databases will find the same reference and this added up to a large, but not unreasonable number).

These trials involved supplementation with single or combined antioxidant supplementation, at different doses from each other.

The researchers performed multiple statistical regression analysis, but this is not "extrapolated", but the use of this term was an interesting way of weakening the results of this trial to the audience, which is a recurrent theme through the presentation.

When looking at the low biased (high quality) studies the researchers found a small, significant increase in risk of death with three of the antioxidants, Vitamin A, E and Beta-Carotene, as mentioned above.

Performing a meta-regression, there was an extremely small, significant, effect of dose on risk from beta-carotene (RR,1.004 ;95%CI,1.001-1.007; P=.012), an even smaller effect of dose on risk from Vitamin A (RR,1.000006;95%CI, 1.000002-1.000009; P=.003), no effect of dose on Vitamin E risk, and a small reduced risk of dose of selenium (RR,0.998;95%CI,0.997-0.999;P=.002).

Interestingly, in the news reports that are presented on the Breakfast show every half hour, Professor Jim Mann of Otago University presented a more favourable view of the meta-analysis than Lorelei. Maybe because he has more of a background understanding research in this area?

Sure, meta-analyses are not perfect, but they are currently the best tool we have to pick out an effect of diet/treatment on disease risk. The overall analysis is ultimately only as good as the research under the covers, and a large proportion of these trials are performed on older or sick individuals.

Ultimately it points to couple of things. Large supplemental (and in reality food based) doses of Vitamin A may not be the best thing for your mortality risk. Beta-Carotene is an interesting one, but the increase in risk is small, 7% (range 2-11%). Vitamin E is the most interesting one, with a number of the trials pointing towards supplemental Vitamin E increasing risk of death, where observational trails generally show a reduced risk from (food sourced) Vitamin E.

The Vitamin manufacturers were quick to point out that the type of Vitamin E used in these trials is alpha-tocopherol, which is only one of the eight isomers found in food, and they typically questioned the natural/synthetic concept. But strangely, a lot of the supplement industry keep selling products containing these exact mixtures, and making claims with these.

Research Watch

Reference
Stallknecht B, Dela F, Helge JW. Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions in adjacent muscles in humans? Am J Physiol Endocrinol Metab. 2007;292:E394-E399

Abstract
Aerobic exercise increases whole body adipose tissue lipolysis, but is lipolysis higher in subcutaneous adipose tissue (SCAT) adjacent to contracting muscles than in SCAT adjacent to resting muscles? Ten healthy, overnight-fasted males performed one-legged knee extension exercise at 25% of maximal workload (W(max)) for 30 min followed by exercise at 55% W(max) for 120 min with the other leg and finally exercised at 85% W(max) for 30 min with the first leg. Subjects rested for 30 min between exercise periods. Femoral SCAT blood flow was estimated from washout of (133)Xe, and lipolysis was calculated from femoral SCAT interstitial and arterial glycerol concentrations and blood flow. In general, blood flow and lipolysis were higher in femoral SCAT adjacent to contracting than adjacent to resting muscle (time 15-30 min; blood flow: 25% W(max) 6.6 +/- 1.0 vs. 3.9 +/- 0.8 ml.100 g(-1).min(-1), P <> 0.05; lipolysis: 25% W(max) 102 +/- 19 vs. 55 +/- 14 nmol.100 g(-1).min(-1), P = 0.06; 55% W(max) 86 +/- 11 vs. 50 +/- 20 nmol.100 g(-1).min(-1), P > 0.05; 85% W(max) 88 +/- 31 vs. -9 +/- 25 nmol.100 g(-1).min(-1), P < class="blsp-spelling-error" id="SPELLING_ERROR_11" onclick="BLOG_clickHandler(this)">lipolysis are generally higher in SCAT adjacent to contracting than adjacent to resting muscle irrespective of exercise intensity. Thus specific exercises can induce "spot lipolysis" in adipose tissue.

My Thoughts
This piece of research was pre-published a few months back, and on the surface appears to support the concept of spot reduction. However, taking a slightly deeper look into the paper reveals the difference between statistical and clinical significance.

At the end of the discussion, the authors translate the difference in lipolysis to

"Assuming a molecular weight of 860 g/mol for TG, this corresponds to an extra breakdown of 0.6 –2.1 mg of TG in 30 min/100 g of adipose tissue adjacent to contracting muscles.."

So to lyse 1gram of additional fatty acid per 100gram of adipose would take

0.6mg/30mins = 1.2mg/hour
1000mg/1.2mg/hour = 833 hours of relatively intense activity

or

2.1mg/30mis = 4.2mg/hours
1000mg/4.2mg/hour = 238 hours of relatively intense activity

Sure we can measure it and show a significance difference, but what point is the difference of 1.2-4.2mg/hour/100g fat?

Research Watch

Reference
Lunden ND, Saunders MJ and Todd MK. Postexercise Carbohydrate-Protein- Antioxidant Ingestion Decreases Plasma Creatine Kinase and Muscle Soreness. Int J Sports Nutr Exerc Metab 2007;1:109-123

Abstract
The authors investigated the effects of postexercise carbohydrate-protein-antioxidant (CHO+P+A) ingestion on plasma creatine kinase (CK), muscle soreness, and subsequent cross-country race performance. Twenty-three runners consumed 10 mL/kg body weight of CHO or CHO+P+A beverage immediately after each training session for 6 d before a cross-country race. After a 21-d washout period, subjects repeated the protocol with the alternate beverage. Postintervention CK (223.21 ± 160.71 U/L; 307.3 ± 312.9 U/L) and soreness (medians = 1.0, 2.0) were significantly lower after CHO+P+A intervention than after CHO, despite no differences in baseline measures. There were no overall differences in running performance after CHO and CHO+P+A interventions. There were, however, significant correlations between treatment differences and running mileage, with higher mileage runners having trends toward improved attenuations in CK and race performance after CHO+P+A intervention than lower mileage runners. We conclude that muscle damage incurred during training was attenuated with postexercise CHO+P+A ingestion, which could lead to performance improvements in high-mileage runners.

My thoughts
This is another in a line of Pacfic Health Laboratories research from the Saunders group. Pacific Health Laboratories produce the Endurox and Accelerade product ranges, as well as Satiatrim (a weight management product).
This was a randomised cross over trial, which looked at the effect of a carbohydrate supplement, compared to a carbohydrate-protein-antioxidant supplement, on muscle soreness and creatine kinase (a marker of muscle damage) levels in 24 cross country runners.
It is worthy to note that while there were 24 subjects included in the final analysis, this was only 67% of the initial study group, with 5 failing to complete data recording and 8 did not comply with the external exercise requirements.
The results show similar trends to earlier reports in different study groups and different exercise situations. Cross country running tends to provide an interesting model, as the downhill segments increase eccentric loading on the athletes, creating larger levels of delayed onset muscle soreness.
The final conclusion seems somewhat extrapolated from the results, which showed no differences in running performance, but perhaps points the way to a larger longer term training trial that allows a large group of athletes to be selected into a randomised controlled trial, that follows their total mileage, tracks feelings of muscle pain and ultimately attempts to measure a performance gain at the end of the trial. These longer term trials are important because if there is a performance benefit of using these products, it is likely to be small in the acute setting, but if the benefits are somewhat additive over time, it may produce an attractive performance benefit to the athlete.
But even though the use of protein in endurance sports is still a novel approach, this provides further evidence for the use of a carbohydrate-protein (and antioxidant) beverage following training sessions.

Research watch

Reference
Folland JP and Williams AG. The Adaptations to Strength Training: Morphological and Neurological Contributions to Increased Strength. Sports Med 2007;2:145-168

Abstract
High-resistance strength training (HRST) is one of the most widely practiced forms of physical activity, which is used to enhance athletic performance, augment musculo-skeletal health and alter body aesthetics. Chronic exposure to this type of activity produces marked increases in muscular strength, which are attributed to a range of neurological and morphological adaptations. This review assesses the evidence for these adaptations, their interplay and contribution to enhanced strength and the methodologies employed.The primary morphological adaptations involve an increase in the cross-sectional area of the whole muscle and individual muscle fibres, which is due to an increase in myofibrillar size and number. Satellite cells are activated in the very early stages of training; their proliferation and later fusion with existing fibres appears to be intimately involved in the hypertrophy response. Other possible morphological adaptations include hyperplasia, changes in fibre type, muscle architecture, myofilament density and the structure of connective tissue and tendons.Indirect evidence for neurological adaptations, which encompasses learning and coordination, comes from the specificity of the training adaptation, transfer of unilateral training to the contralateral limb and imagined contractions. The apparent rise in whole-muscle specific tension has been primarily used as evidence for neurological adaptations; however, morphological factors (e.g. preferential hypertrophy of type 2 fibres, increased angle of fibre pennation, increase in radiological density) are also likely to contribute to this phenomenon. Changes in inter-muscular coordination appear critical. Adaptations in agonist muscle activation, as assessed by electromyography, tetanic stimulation and the twitch interpolation technique, suggest small, but significant increases. Enhanced firing frequency and spinal reflexes most likely explain this improvement, although there is contrary evidence suggesting no change in cortical or corticospinal excitability.The gains in strength with HRST are undoubtedly due to a wide combination of neurological and morphological factors. Whilst the neurological factors may make their greatest contribution during the early stages of a training programme, hypertrophic processes also commence at the onset of training.

My Thoughts
While I try to maintain a somewhat up to date coverage of most published peer-reviewed research surrounding strength training, it is difficult. Review papers such as this one by Folland and Williams provide a nice coverage of the concepts underlying the development of strength.

I especially liked the section entitled "Indirect Evidence of Neural Adaptations, Learning and Coordination"

The authors comment on the observation that increases in dynamic strength (1 Rep max) are disproportionately greater than the gains in isometric strength. This indicates that performing a 1RM is more than just strength, but the ability to display the muscles maximal force potential, in a coordinated effort of the agonist and antagonist muscle groups. This effect can even been seen on relatively simple single joint movements. These neural adaptations are highlighted in a section highlighting Imagined Contractions and their ability to increase strength gains. Going through a lift in the mind has long been a method, for good or bad, used by lifters to help with the big lift. I generally perform the desired movement pattern during the day (bench), it started with the "Grease the Groove" concept by Pavel Tsatsouline, but now its just a habit.