Examination of subjective measures of soreness and fatigue resulted in no significant differences between the groups throughout the study (see Figures 6 and 7, respectively). However, comparison of the Δ scores of fatigue revealed a significant reduction (Figure 8) in subjective measures of fatigue in BET compared to PL. No difference between the groups was observed in Δ soreness scores.
The results of this study indicated that 15 days of betaine ingestion did not increase isokinetic force output during CON and ECC movements in the chest press exercise. In addition, the quality of the workout (as determined by the mean peak and average force outputs per workout) was not significantly affected by the BET. Although subjective soreness ratings were not changed by betaine ingestion, supplementation did appear to reduce subjective feelings of fatigue.
The results of this study do not support the ergogenic benefits reported by previous studies (11,13). It is likely that differences related to the mode of exercise (isokinetic vs. dynamic constant resistance) or study protocol used contributed to the contrasting results. In the investigations reporting a significant ergogenic benefit from betaine ingestion, investigators employed a dynamic constant resistance exercise protocol that required subjects to lift a specific percentage of their 1RM. As a result, performance improvements were relative to the baseline strength measures performed before the supplementation protocol. In this study, peak CON and ECC force outputs were determined before each workout, and the subsequent training loads were relative to that outcome. Thus, previous studies examined workout quality relative to the initial assessment, whereas this study investigated workout quality relative to the daily change in force output. Regardless, no significant changes were noted in peak CON or ECC force outputs during the BET protocol.
There have been several mechanisms attributed to the ergogenic potential of betaine ingestion. One potential mechanism involves the role of betaine as an osmolyte. Under stressful conditions, such as from perturbing electrolytes, urea or ammonia, cells may accumulate betaine to maintain normal function (7,14). This has been demonstrated in a variety of tissues including muscle (1), where it may have an important role in maintaining skeletal muscle myosin ATPase activity (18). Betaine acts by redistributing water in cells leading to more effective biopolymer hydration and increased cytoplasmic osmolality (6). The role of betaine as an osmolyte has been suggested to be related its role in the synthesis of creatine (1). However, this is only speculative considering that muscle creatine concentrations have not been demonstrated to be increased from betaine intake in humans. Betaine supplementation has previously been shown to increase muscle creatine concentrations, albeit in chickens (18). There have been no studies known to date that have examined changes in muscle creatine concentrations in humans supplementing with betaine. The donation of methyl groups from betaine is thought to occur via a series of enzymatic reactions in the mitochondria of liver and kidney cells (6). Betaine donates a methyl group to homocysteine to form methionine. This transfer is controlled by the enzyme betaine homocysteine methyl transferase that results in betaine being converted to dimethylglycine. Methionine is converted to SAM, which acts as a methyl donor contributing to the synthesis of creatine, and a number of other proteins (5). Dietary betaine has been shown to increase serum methionine, transmethylation rate, and methionine oxidation in healthy men (16), and animals injected with betaine have shown a dose-response increase in red blood cell SAM (17). However, the relationship of betaine ingestion and muscle creatine synthesis in humans is yet to be established. It is possible that longer ingestion periods may be necessary to result in significant elevations in muscle creatine concentrations or that creatine synthesis is not the primary benefactor from the increase in the methyl pool from betaine ingestion. Recent reports have indicated that creatine synthesis from methyl donation may be overestimated and that phosphatidylcholine synthesis may be a greater consumer of the increase in endogenous methyl groups (15).
An elevation in phosphatidylcholine concentration may have potential ergogenic implications for athletic performance. Considering that choline intake is important for enhancing neurotransmitter concentration, the ability to enhance strength, power, or ability to react to external stimuli could be enhanced with greater neurotransmitter formation. However, there is only limited research conducted examining the ergogenic potential of choline. Although improvements in memory and cognition have been reported from choline ingestion (1,3,4,7), there have been only limited investigations regarding choline and athletic performance and no studies known to have examined choline ingestion and resistance exercise. A recent study showed that phosphatidylcholine intake contributed to enhanced reactive ability to both visual and auditory stimulus after exhaustive exercise (10). In addition, subjects consuming the Bet also reported significantly lower subjective measures of fatigue. This is consistent with the results reported in this study and suggests, although speculative, that betaine ingestion may have contributed to increases in phosphatidylcholine concentrations.
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