Measurements in potassium-supplemented athletes during and after hypokinetic and ambulatory conditions.

Hypokinesia (diminished movement) induces significant potassium (K) changes; however, little is known about K deposition and deficiency during hypokinesia (HK). Using K supplements during and after HK, the aim was to establish body K deposition and K deficiency during HK. Studies were done during the pre-HK period of 30 d, HK period of 364 d, and post-HK period of 30 d. Forty male trained athletes aged 24.9 +/- 8.0 y were chosen as subjects. They were equally divided into four groups: unsupplemented active control subjects (UACS), unsupplemented hypokinetic subjects (UHKS), supplemented active control subjects (SACS), and supplemented hypokinetic subjects (SHKS). Hypokinetic subjects were limited to an average walking distance of 0.7 km/d. Control subjects ran an average distance of 11.6 km/d. The SHKS and SACS groups took 95.0 mg elemental K/kg body weight daily. Fecal K excretion, urinary sodium (Na) and K excretion, plasma K and Na levels, plasma renin activity (PRA), plasma aldosterone (PA), food and fluid intake, and physical characteristics were measured. During HK, fecal K loss, urinary K and Na loss, and plasma K, Na, PRA, and PA levels increased significantly (p < or = 0.05), whereas during the initial days of post-HK, the levels of the measured parameters decreased significantly (p < or = 0.05) in the SHKS and UHKS groups as compared with the SACS and UACS groups, respectively. During HK, body weight, body fat, peak oxygen uptake, food and fluid intake decreased significantly (p < or = 0.05), whereas during the initial days of post-HK period remained significantly (p < or = 0.05) depressed and fluid intake increased in SHKS and UHKS groups when compared with the SACS and UACS groups, respectively. However, during HK and post-HK plasma, urinary, and fecal K changed significantly (p < or = 0.05) more in the SHKS group than in the UHKS group. The deposition of K was significantly (p < or = 0.05) lower and K deficiency much higher in the SHKS group than in the UHKS group. Fecal K loss, urinary K and Na loss, plasma K, Na, PRA, and PA levels, body weight, body fat, peak oxygen uptake, and food and fluid intake did not change significantly in the SACS and UACS when compared with their baseline control values. It was shown that plasma K concentration and urinary and fecal K excretion increased during HK and decreased significantly (p < or = 0.05) during post-HK. Oral K supplements did not influence plasma or fecal and urinary K either during HK or post-HK. It was concluded that the low plasma K level and fecal and urinary K loss during post-HK may indicate the presence of K deficiency, and increased K in plasma, urine, and feces during HK and in the presence of K deficiency may suggest the body's inability to retain K during HK.