Nutritional Strategies and Muscle Recovery: Part 2

Before discussing the latest cutting-edge supplements that may be effective or have sufficient supporting evidence to accelerate muscle-recovery processes in athletes—which we will leave for the third part of this article—we will address a key factor that is often overlooked: (eu)hydration status, loved by some and disliked by others.

We know that recovery is also influenced by the degree of exercise-induced muscle damage (EIMD) caused when the structural and functional properties of skeletal muscle are altered, especially when multiple sessions or numerous competitive events occur within a short period.

Dehydration primarily refers to the loss of intracellular fluid. Because sweat is hypotonic relative to blood, sweat losses increase plasma osmolality and reduce blood volume, producing hyperosmotic and hypovolemic stress.

EIMD is strongly associated with loss of strength, perceived soreness, and elevated circulating muscle enzymes or proteins (e.g., CK and myoglobin).

Although the optimal stimulus for maximizing performance adaptations and optimizing recovery remains unknown, the proposed mechanisms could explain the reduction in performance associated with reduced plasma volume, cardiac filling and stroke volume. These factors in turn reduce blood flow, which ultimately alters muscle metabolism and impairs proper thermoregulation, especially in hot environments. All these factors could intensify EIMD and prolong recovery.

Although the precise role of acute dehydration in EIMD is unclear, rehydration plays an important role in exercise recovery. Adequate hydration may help mitigate all these potential processes that can influence EIMD, such as the independent and combined effects of osmotic stress, cellular swelling (muscle swelling and metabolite accumulation) and hyperthermia.

At higher levels of dehydration (4-5% loss of body mass), increased blood viscosity raises ROS production through increased vascular strain and red-blood-cell rigidity.

Increased ROS generation in skeletal muscle can damage the sarcolemma, cytoskeleton and DNA, as well as the contractile units of skeletal muscle, making muscle contraction more difficult. Importantly, ROS production is necessary to generate adaptations to stressors such as exercise itself; the problem arises when there is an excess—as with anything—of these free radicals and reactive oxygen species, which is when a maladaptive response occurs.

Dehydration may predominantly affect fast-twitch fibers, which are also preferentially damaged by eccentric exercise, potentially creating an additive effect on muscle damage.

Regardless of hydration status, rodent models suggest that hyperthermia has a strong influence on skeletal-muscle damage. Muscle temperatures reaching > 40 ° C (104 ° F) during intense exercise have been shown to increase passive tension. This also leads to greater muscle damage.

A secondary mechanism operates through proteases and phospholipases, as these can impair calcium-mediated calcium release in the sarcoplasmic reticulum, further challenging muscle contraction.

Some studies report that dehydrated athletes showed higher levels of blood biomarkers related to muscle damage and delayed recovery (aspartate aminotransferase, nitrogen, blood urea, LDH and CK) than euhydrated groups.

In conclusion, it is important to recognize the limitations: the independent effects of exercise may obscure interpretation of the results because exercise itself can cause greater heat production, fluid shifts and ROS production.

Despite major methodological problems in current human studies, it is possible that dehydration increases the severity of muscle damage and prolongs recovery, especially when combined with hyperthermia. Therefore, staying hydrated may be one of the most powerful ergogenic aids.

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Bibliography

King, M. A., & Baker, L. B. DEHYDRATION AND EXERCISE-INDUCED MUSCLE DAMAGE: IMPLICATIONS FOR RECOVERY.