Measurements in Potassium-Supplemented Athletes During and After Hypokinetic and Ambulatory Conditions

Abstract

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.

Measurement of potassium absorption during hypokinesia in potassium supplemented and unsupplemented healthy subjects

“…During a normal muscular activity, K + depletion develops because of the decreased K + consumption, excessive K + losses through gastrointestinal tract and kidney, and a redistribution of K + within the body due to insulin intake, and magnesium depletion. However, K + depletion during prolonged HK is much more complicated, because K + depletion is present with and without K + supplementation, and K + depletion is accompanied by a significant increase of plasma K + level [5][6][7][8][9] and K + losses [5][6][7][8][9]. Using K + supplementation to normalize K + depletion during prolonged HK had shown that K + is neither entering nor being retained by muscles, where most K + is normally deposited.…”

“…Using K + supplementation to normalize K + depletion during prolonged HK had shown that K + is neither entering nor being retained by muscles, where most K + is normally deposited. This shows the presence of another mechanisms and primarily the presence of decreased K + deposition, that may lead to significant increase of K + losses with K + imbalance and consequently may contribute to the development of K + depletion in healthy subjects during prolonged HK [5][6][7][8][9].…”

“…The continued search to establish the reasons for decreased K + deposition during prolonged HK, led to the conclusion that K + imbalance is not so much a matter of K + shortage in the diet as the decreased K + deposition; this was demonstrated by the fact that a daily K + supplementation failed to prevent K + imbalance during prolonged HK [5][6][7][8][9]. The main effect of decreased K + deposition during HK is that contributes to the significant K + losses with K + depletion [5][6][7][8][9].…”

“…The main effect of decreased K + deposition during HK is that contributes to the significant K + losses with K + depletion [5][6][7][8][9]. Furthermore, it has been shown that during HK the physiological systems that regulate the level of each mineral in blood and other endogenous fluids and the balance between consumption and K + loss and thus total K + content in the body, are significantly affected.…”

“…Furthermore, it has been shown that during HK the physiological systems that regulate the level of each mineral in blood and other endogenous fluids and the balance between consumption and K + loss and thus total K + content in the body, are significantly affected. Meanwhile data have been accumulated about the effect of HK on decreased K + deposition [5][6][7][8][9]; concluding therefore that during HK K + depletion development due to the decreased K + deposition is possible. For this the hypothesis has been put forward that prolonged HK may be one of the mechanisms at the basis of development of decreased K + deposition that may contribute to the significant K + loss from the body and thus to K + depletion [5][6][7][8][9].…”