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Hydration, Protein Synthesis, BPA, and Performance

The importance of hydration for optimal performance cannot be overstated. The effects of dehydration and hypohydration on aerobic and anaerobic performance have been well documented (Maughn, 2012) and include: accelerated exhaustion times (Walsh et al., 1994), increased perceived exertion (Logan-Sprenger et al., 2012), reduced lactate threshold (Kenefick et al., 2002), and performance of sport specific skills, such as shooting a basketball (Carvalho et al., 2011).

Hydrate or else!

Although the majority of the literature addresses endurance, a growing body of research is demonstrating that dehydration also effects strength and power performance. Judelson et al. (Judelson et al., 2007) reported as little as 2.5% dehydration reduces total work performed during strength training. Hayes and Morse (2010) demonstrated reduced force output with 2.6% dehydration. The effects of dehydration are not just limited to the large muscles of the lower body. Jones et al. reported that 2.9% dehydration reduced upper body power output by 14%. The results of these studies suggest that training in even a mild state of hypohydration will reduce work load and force output, resulting in fewer adaptations over several sessions thus compromising the effectiveness of progressive overload and ultimately costing the athlete gains.

Beyond nutrition and rest, recovering from intense exercise and avoiding over-training is governed by the hormonal milieu. In particular, testosterone and growth hormone stimulate protein synthesis (muscle repair and growth) while cortisol promotes muscle breakdown (Tarpenning et al., 2001) and overtime hinders recovery (Perna & McDowell, 1995). Hypohydration during weight training increases cortisol and maintain this increase for a significant amount of time post workout, and also delays the testosterone response to training (Judelson et al., 2008). Additionally, performing hypohydrated high intensity conditioning (as many athletes do following strength/power training) has a similar negative effect on the testosterone to cortisol ratio (Maresh et al., 2006), furthering the importance of intra-workout hydration to optimize recovery.

Dehydration increases the cortisol response to exercise (adapted from Judelson et al.)

On a cellular level, the mammalian target of rapamycin (mTOR) pathway is a major regulator in the initiation of protein synthesis, and has received a great deal of press in performance and bodybuilding circles over the past 10 years. Athletes use protein/carbohydrate supplements post workout to provide amino acids and stimulate protein synthesis via insulin mediated mTOR signaling; however, cellular dehydration has been shown to inactivate the mTOR pathway even in the presence of insulin, thereby directly inhibiting protein synthesis, glucose uptake, and glycogen synthesis (Schliess et al., 2006). Thus, dehydration compromises muscle tissue repair and the ability to recover from intense workouts, thus diminishing the athlete’s ability to engage in the frequent, intense workouts required to compete at a high level.

Hydration needs have been addressed ad nauseum; however, the mode has often been overlooked. With that said, there’s something very disturbing about the image blow, and unfortunately it cannot be seen by the naked eye.

Contained within that water bottle is bisphenol A (BPA), which has received significant attention in the media as an environmental endocrine-disruptor. In particular, BPA has been causally suggested in the earlier onset of puberty and altered reproductive function in females (Howdeshell et al., 1991). More recently BPA has been linked to adiposity. In mice BPA has been found to enhance adipogenesis and lipogenesis, in part by increasing PPAR-λ and adipose lipoprotein lipase activity (Somm et al., 2009).

In human adipocytes environmentally relevant concentrations of BPA increased lipid storage in both subcutaneous and visceral tissue (Wang et al., 2012). BPA has also been shown to contribute to diet-induced adipocyte differentiation (stem cells forming adipocytes) and visceral adiposity (De Sousa et al., 2008). Perhaps of more concern are the effects of BPA in humans at concentrations similar to what would be consumed by drinking from a typical water bottle. Shankar et al. (2012) demonstrated an association between urinary BPA and measures of obesity independent from the traditional risk factors.

The development of obesity is likely not a major concern of most Jason Cholewa Physical Performance readers; however, chronically elevated cortisol should be. At this point we must note the difference performance effects between chronic and exercise-induced acute cortisol increases. Cortisol without regard for condition (acute vs. chronic) has been unfairly demonized in bodybuilding and strength circles. In fact, West and Phillips (2012) found a positive correlation between acute cortisol and hypertrophy, but not testosterone in a 12 week study. With that out of the way, chronically elevated cortisol contributes to muscle protein breakdown and is a marker of overtraining (Filaire et al., 2012). Inactive dehydrocorticosterone (cortisone) is catalyzed to cortisol (and vice versa) via the enzyme 11β-hydroxysteroid type 1 (11β-HSD1).

This brings forth the issue with drinking out of plastic cups and water bottles. BPA has been shown to not only activate 11β-HSD1, but also to drive 11β-HSD1 toward the reduction of cortisone in environmentally relevant concentrations (Wang et al., 2012). Therefore, by increasing resting cortisol, staying hydrated with BPA bottles may actually compromise recovery. Furthermore, a major site for 11β-HSD1 activation by BPA is in adipose tissue; consequently, drinking from non BPA-free bottles may also compromise an athlete’s ability to decrease body fat. Moreover, BPA itself has been shown to directly bind to glucocorticoid receptors with an affinity similar to cortisol (Prasanth et al., 2010). Although the effects of BPA on myocytes are yet be studied, it is possible that BPA may bind skeletal muscle glucocorticoid receptors and thereby directly inhibit protein synthesis.

Avoid foods and beverages in BPA-containing plastics

To recap: dehydration negatively affects performance by reducing work and force output. Dehydration has compromises recovery and adaptation by negatively influencing the testosterone:cortisol ratio and inhibiting insulin-induced mTOR activation. Although hydration is important, we now see that the vehicle in which we hydrate in is equally important. BPA is found in plastic water bottles, and increases adipogensis, adipocyte differentiation, and the conversion of inert cortisone to the catabolic hormone cortisol. Therefore, investing in a BPA-free water bottle may be an inexpensive mean to promote hydration and improve performance.

References

Carvalho, P., Oliveira, B., Barros, R., Padrão, P., Moreira, P., & Teixeira, V. H. (2011). Impact of fluid restriction and ad libitum water intake or an 8% carbohydrate-electrolyte beverage on skill performance of elite adolescent basketball players.International journal of sport nutrition and exercise metabolism, 21(3), 214–21. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21719902

De Sousa Peixoto, R. A., Turban, S., Battle, J. H., Chapman, K. E., Seckl, J. R., & Morton, N. M. (2008). Preadipocyte 11beta-hydroxysteroid dehydrogenase type 1 is a keto-reductase and contributes to diet-induced visceral obesity in vivo.Endocrinology, 149(4), 1861–8. doi:10.1210/en.2007-1028

Filaire, E., Ferreira, J. P., Oliveira, M., & Massart, A. (2012). Diurnal patterns of salivary alpha-amylase and cortisol secretion in female adolescent tennis players after 16 weeks of training. Psychoneuroendocrinology. doi:10.1016/j.psyneuen.2012.11.001

Hayes, L. D., & Morse, C. I. (2010). The effects of progressive dehydration on strength and power: is there a dose response? European journal of applied physiology, 108(4), 701–7. doi:10.1007/s00421-009-1288-y

Howdeshell, K. L., Hotchkiss, A. K., Thayer, K. A., Vandenbergh, J. G., & Vom Saal, F. S. (1999). Exposure to bisphenol A advances puberty. Nature, 401(6755), 763–4. doi:10.1038/44517

Judelson, D. a, Maresh, C. M., Farrell, M. J., Yamamoto, L. M., Armstrong, L. E., Kraemer, W. J., Volek, J. S., et al. (2007). Effect of hydration state on strength, power, and resistance exercise performance. Medicine and science in sports and exercise, 39(10), 1817–24. doi:10.1249/mss.0b013e3180de5f22

Judelson, D. a, Maresh, C. M., Yamamoto, L. M., Farrell, M. J., Armstrong, L. E., Kraemer, W. J., Volek, J. S., et al. (2008). Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism.Journal of applied physiology (Bethesda, Md. : 1985), 105(3), 816–24. doi:10.1152/japplphysiol.01010.2007

Kenefick, R. W., Mahood, N. V, Mattern, C. O., Kertzer, R., & Quinn, T. J. (2002). Hypohydration adversely affects lactate threshold in endurance athletes. Journal of strength and conditioning research / National Strength & Conditioning Association,16(1), 38–43. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11834105

Logan-Sprenger, H. M., Heigenhauser G, J. F., Jones, G. L., & Spriet, L. L. (2012). Progressive Dehydration during Cycling Increases Skeletal Muscle Glycogenolysis and Perceived Exertion in Hydrated Males. International journal of sport nutrition and exercise metabolism. Retrieved fromhttp://www.ncbi.nlm.nih.gov/pubmed/23114793

Maresh, C. M., Whittlesey, M. J., Armstrong, L. E., Yamamoto, L. M., Judelson, D. a, Fish, K. E., Casa, D. J., et al. (2006). Effect of hydration state on testosterone and cortisol responses to training-intensity exercise in collegiate runners. International journal of sports medicine, 27(10), 765–70. doi:10.1055/s-2005-872932

Maughan, R. J. (2012). Investigating the associations between hydration and exercise performance: methodology and limitations. Nutrition reviews, 70 Suppl 2, S128–31. doi:10.1111/j.1753-4887.2012.00536.x

Perna, F. M., & McDowell, S. L. (1995). Role of psychological stress in cortisol recovery from exhaustive exercise among elite athletes. International journal of behavioral medicine, 2(1), 13–26. doi:10.1207/s15327558ijbm0201_2

Prasanth, G. K., Divya, L. M., & Sadasivan, C. (2010). Bisphenol-A can bind to human glucocorticoid receptor as an agonist: an in silico study. Journal of applied toxicology : JAT, 30(8), 769–74. doi:10.1002/jat.1570

Schliess, F., Richter, L., Vom Dahl, S., & Häussinger, D. (2006). Cell hydration and mTOR-dependent signalling. Acta physiologica (Oxford, England), 187(1-2), 223–9. doi:10.1111/j.1748-1716.2006.01547.x

Somm, E., Schwitzgebel, V. M., Toulotte, A., Cederroth, C. R., Combescure, C., Nef, S., Aubert, M. L., et al. (2009). Perinatal exposure to bisphenol a alters early adipogenesis in the rat. Environmental health perspectives, 117(10), 1549–55. doi:10.1289/ehp.11342

Tarpenning, K. M., Wiswell, R. A., Hawkins, S. A., & Marcell, T. J. (2001). Influence of weight training exercise and modification of hormonal response on skeletal muscle growth. Journal of science and medicine in sport / Sports Medicine Australia, 4(4), 431–46. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11905937

Walsh, R. M., Noakes, T. D., Hawley, J. A., & Dennis, S. C. (1994). Impaired high-intensity cycling performance time at low levels of dehydration. International journal of sports medicine, 15(7), 392–8. doi:10.1055/s-2007-1021076

Wang, J., Sun, B., Hou, M., Pan, X., & Li, X. (2012). The environmental obesogen bisphenol A promotes adipogenesis by increasing the amount of 11β-hydroxysteroid dehydrogenase type 1 in the adipose tissue of children. International journal of obesity (2005), (September), 1–7. doi:10.1038/ijo.2012.173

West, D. W. D., & Phillips, S. M. (2012). Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training.European journal of applied physiology, 112(7), 2693–702. doi:10.1007/s00421-011-2246-z

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