Purpose: Dehydration is hypothesized to cause exercise-associated muscle cramps. The theory states that dehydration contracts the interstitial space, thereby increasing the pressure on nerve terminals and cramps ensue. Research supporting this theory is often observational, and fatigue is rarely controlled. Inducing cramps with electrical stimulation minimizes many of the confounding factors associated with exercise-induced cramps (e.g., fatigue, metabolites). Thus, our goal was to minimize fatigue and determine whether hypohydration decreases the electrical stimuli required to elicit cramping (termed "threshold frequency").
Methods: Ten males cycled for 30-min bouts with their nondominant leg at 41°C and 15% relative humidity until they lost ~3% of their body mass (~2 h). Dominant leg flexor hallucis brevis muscle cramps were induced before and after hypohydration, and threshold frequency was recorded. Plasma osmolality (OSMp) characterized hydration status. Total sweat electrolytes (Na+, K+, Mg2+, and Ca2+) lost during exercise was calculated. Subjects repeated the protocol 1 wk later.
Results: Subjects were hypohydrated after exercise (preexercise OSMp = 282.5 T 1 mOsm·kg−¹ H2O, postexercise OSMp = 295.1 ± 1 mOsm·kg−¹ H2O, P < 0.001). Subjects lost 3.0% ± 0.1% of their body mass, 144.9 ± 9.8 mmol of Na+, 11.2 ± 0.4 mmol of K+, 3.3 ± 0.3 mmol of Mg2+, and 3.1 ± 0.1 mmol of Ca2+. Mild hypohydration with minimal neuromuscular fatigue did not affect threshold frequency (euhydrated = 23.7 ± 1.5 Hz, hypohydrated = 21.3 ± 1.4 Hz; F1,9 = 2.81, P = 0.12).
Conclusions: Mild hypohydration with minimal neuromuscular fatigue does not seem to predispose individuals to cramping. Thus, cramps may be more associated with neuromuscular fatigue than dehydration/electrolyte losses. Health care professionals may have more success preventing exercise-associated muscle cramp by focusing on strategies that minimize neuromuscular fatigue rather than dehydration. However, the effect of greater fluid losses on cramp threshold frequency is unknown and merits further research.
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http://dx.doi.org/10.1249/MSS.0b013e3181dd5e3a | DOI Listing |
Ann Neurol
January 2025
Department of Neurology, Boston Medical Center and Boston University Chobanian and Avedisian School of Medicine, Boston, MA, USA.
Objective: This study assesses whether longitudinal quantitative pupillometry predicts neurological deterioration after large middle cerebral artery (MCA) stroke and determines how early changes are detectable.
Methods: This prospective, single-center observational cohort study included patients with large MCA stroke admitted to Boston Medical Center's intensive care unit (2019-2024). Associations between time-to-neurologic deterioration and quantitative pupillometry, including Neurological Pupil Index (NPi), were assessed using Cox proportional hazards models with time-dependent covariates adjusted for age, sex, and Alberta Stroke Program Early CT Score.
J Coll Physicians Surg Pak
January 2025
Department of Rheumatology and Immunology, The Second Affiliated Hospital of Anhui Medical University, Anhui, China.
Objective: To investigate the characteristics of Adult-onset Still's disease (AOSD) patients with macrophage activation syndrome (MAS) and explore the risk factors for the development of MAS.
Study Design: A case-control study. Place and Duration of the Study: Department of Rheumatology and Immunology, the Second Hospital of Anhui Medical University, Anhui, China, from January 2008 to June 2024.
Eur Arch Otorhinolaryngol
January 2025
ENT Institute and Department of Otorhinolaryngology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China.
Objective: To evaluate the diagnostic potential of spontaneous otoacoustic emissions (SOAE), distortion product otoacoustic emissions (DPOAE), and pure-tone audiometry (PTA) in patients with pulsatile tinnitus (PT) caused by sigmoid sinus wall anomalies (SSWA).
Methods: This study included 20 PT patients and 20 matched healthy controls. SOAE, DPOAE, and PTA were assessed before and after compression of the internal jugular vein.
J Am Acad Dermatol
January 2025
Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania, Philadelphia PA; Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania, Philadelphia PA.
J Affect Disord
January 2025
Department of Orthopaedics, Xiangya Hospital, Central South University, Changsha, Hunan Province, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan Province, China. Electronic address:
Background: Studies have demonstrated that the gut microbiome-immune system-brain axis plays an important role in neurological disorders. Furthermore, recent studies have shown that the gut microbiota influences the occurrence and progression of anxiety disorders, with potential involvement of immune cells. We aimed to investigate the causal impact of gut microbiota on anxiety disorders and identify potential immune cell mediators.
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