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Abstract

Water comprises approximately 40% of muscle mass, and intracellular fluid shifts occur in response to osmotic gradients between intracellular and extracellular (e.g., blood) compartments. Fluid also enters injured muscle during inflammation, resulting a temporary increase in muscle cross sectional area (mCSA). Dehydration elevates blood osmolality, and fluid enters damaged tissue. However, it remains unclear if dehydration-induced osmotic stress and swelling from muscle damage can influence fluid dynamics (fluid retention) in non-damaged muscle. PURPOSE: To determine whether hydration status and damage-related swelling alter fluid retention in the contralateral non-damaged leg. METHODS: Six recreationally active men (age: 20±3 yrs, height: 173.6±8.1 cm, weight: 79.9±12.2 kg, lean mass: 58.6±13.0 kg, body fat percent: 28.3±6.5%) completed two identical bouts of unilateral maximal knee extension exercise consisted of 10 sets of 30 repetitions (EXE) in a euhydrated state then underwent a 3-d recovery period either under the EUHY or DEHY conditions. During the 3-d recovery participants consumed >3.7 L/d of fluid in the EUHY condition. For DEHY, participants did not consume any fluid for the first 24 hours and consumed 1.5 L/d of fluid for the subsequent 48 hours. Ultrasound images of the rectus femoris (RF) of the non-damage leg were taken at before (PRE), and 24hr, 48hr, and 72hr after EXE. The mCSA was assessed via ImageJ. RESULTS: No significant differences were observed; however, trends toward the main effects of condition (p=0.083, hp2 = 0.482) and time (p=0.096, hp2 = 0.335) were observed for the mCSA of the non-damaged RF (0.207±0.96; p=0.083, d= 0.482). In DEHY, mCSA was trended towards smaller than EUHY (p=0.083, d=0.482). In addition, mCSA decreased from PRE to 48hr (0.211±0.091; p=0.069, d = 0.335) and from 24hr to 48hr (0.312±0.134; p=0.067, d = 0.335). CONCLUSION: A trend in the data suggests that dehydration may reduce intramuscular fluid in the non-damage leg. Dehydration-induced osmotic stress, combined with inflammatory response, may promote fluid efflux from the contralateral non-damaged leg, reflecting whole-body fluid redistribution rather than a purely local response to muscle damage.

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