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Hydration Levels and Resistance Training
 
 
 

It is fairly common knowledge that the endocrine system plays an integral role in the response to exercise. A majority of these responses are regulated with assistance from the sympathetic nervous system (SNS). Some fundamental examples of SNS regulation during exercise include an increase in heart rate and contractility of the heart, an increase in the depth and rate of respiration, changes in macronutrient metabolism dynamics, and an increase in the reabsorption rate of fluids and electrolytes within the glomerulus. The central nervous system (CNS) harbors many of the master endocrine glands that allow for various acute reactions and potential long-term adaptations to exercise-induced stressors or homeostatic disturbances. However, many of these processes are not fully understood as CNS dynamics are complex; and in many cases exercise physiologists can only study the actions and reactions involved in the biological control systems executed to maintain a disease free and homeostatic condition. Recent research published in the Journal of Applied Physiology attempts to elucidate the endocrine and metabolic responses due to resistance training in differing hydration states. Previous research notes that hypohydration (decreased total body water) enhances catabolic hormonal responses to endurance exercise, but limited research has evaluated the effects of hypohydration on endocrine responses to resistance exercise. As the acute post-exercise systemic hormonal environment ultimately dictates long-term adaptations, examining variables such as hydration during this crucial period is important to potentially maximizing performance increases.

 

Seven healthy, resistance trained men (23 +/- 4 years of age) engaged in three identical exercise bouts in diverse hydration states: euhydrated (EU), moderately hypohydrated by ~2.5% body mass (HY25), and significantly hypohydrated by ~5.0% body mass (HY50). Such severe hypohydration was assessed due to the incidence in sports such as wrestling. Hydration status was manipulated via controlled water deprivation and exercise-heat stress the day before the exercise session. Humoral (bodily fluid) and urinary levels of various hormones and metabolic indicators including cortisol, epinephrine and norepinephrine, testosterone, growth hormone, insulin-like growth factor-I (IGF-I), insulin, glucose, lactate, glycerol, and free fatty acids were measured during euhydrated rest, immediately preceding and following the resistance training session, and at 60 minutes of recovery. Post-exercise body mass decreased by 0.2% +/- 0.4%, 2.4% +/- 0.4%, and 4.8% +/- 0.4% during EU, HY25, and HY50 respectively, indicating that the subjects did truly engage in the training sessions in three distinct hydration states. The results indicated that a hypohydrated state can have a profound effect on the hormonal and metabolic responses to resistance exercise and the post-exercise systemic environment for adaptation. It appears that this effect occurred through multiple dynamics.

 

Firstly, hypohydration appeared to increase circulating stress hormones such as cortisol, epinephrine, and norepinephrine. This results in an enhanced catabolic response with the potential undesirable effect of lean mass utilization for energy. These catabolic hormones were thought to be stimulated by increased core temperature and amplified cardiovascular demand due to lower blood plasma volume. A secondary effect of catabolic hormone release examined within the study was modified concentrations of insulin and other metabolic markers. This would be due to a massive substrate release initiated by the catabolic hormones to help deal with the physiological demands imposed by the training session in a non-optimal, hypohydrated state. Secondly, it appeared to diminish anabolic responses to exercise. Testosterone responses in particular were reduced which can result in potential attenuation of lean mass hypertrophy and other growth-oriented adaptations. Growth hormone (GH) responses did remain unaltered, but this was most likely due to the balanced negating effects of GH stimulators (catecholamines) and inhibitors (glucose and free fatty acids) present in the hypohydrated state.

 

These findings were further supported by a very recent study published in the European Journal of Applied Physiology (Jan 2010) which looked at resistance training performance in males exposed to heat but supplementing with a carbohydrate electrolyte drink (100% replenishment) and males dehydrated to the 3% level by means of pre-exercise hot bath. Male participants performed three sets to failure on the bench press, lat pulldown, overhead press, barbell curl, triceps press and leg press with 2 minutes recovery used between sets. In comparison, those men exposed to training stress but remaining hydrated using an electrolyte replenishment drink outperformed those men who exercised in a hypohydrated state. Similar to the previous article the group exercising in a hypohydrated condition experienced elevated heart rates, higher rates of perceived exertion and reduced performance common of low blood plasma and SNS detriments at the same relative intensities.

 

Overall, it appears that a dehydrated state significantly alters metabolic and endocrine dynamics before and after intense resistance exercise. Of even greater importance is how even limited dehydration can negatively affect performance. Most of these effects are at the detriment of adaptations associated with structured resistance training. These findings suggest that proper hydration may be more important than previously thought; particularly related to the endocrine response to resistance training. As in most cases a homeostatic environment can be more conducive to promoting performance improvements when training for one given parameter. The physiological demands and stress of being in a hypohydrated state may draw from the potential adaptations to the stress of resistance exercise when compared to training with proper hydration as well as compromise the function of the tissue thereby limiting the overload needed for anabolic response and recovery.