Muscle Calcium Regulation from Reducing Hypokinetic and Gravity Effects using Chronic Antiorthostatic Sleeping and Chronic Periodic Fluid Redistribution
Background and Aim: Chronic periodic fluid redistribution (CPFR) and chronic antiorthostatic sleeping (CAOS) counteracting diminished muscular activity (hypokinesia [HK]) and earth gravity effects contribute to vascular volume and electrolyte regulation. We hypothesized that CPFR and CAOS counteracting gravity compression effects and HK could affect muscle calcium (Ca++). We therefore studied the potential clinical benefits of CPFR and CAOS on muscle calcium. Methods: Studies were conducted on 40 male volunteers. They were equally divided into four groups: active control subjects (ACS), hypokinetic subjects (HKS), CAOS control subjects (CAOSCS), and CAOS hypokinetic subjects (CAOSHS). We measured Ca++ in the muscle, plasma, urine, and feces during a preexperimental period of 390 days and an experimental period of 364 days. Results: In the CAOSHS group, muscle Ca++ increased (P < 0.05) and plasma Ca++ and Ca++ losses decreased (P < 0.05) compared to the HKS group. Muscle Ca++ increased more and Ca++ losses decrease more in a higher than a lower degree of CAOS position or higher than lower fluid shift to the head. In the HKS group without treatment of CPFR and CAOS, muscle Ca++ decreased (P < 0.05) and plasma Ca++ and Ca++ losses increased (P < 0.05) compared to the ACS, CAOSHS, and CAOSCS groups and the values at the preexperimental period. In the CAOSCS group, muscle Ca++ and plasma Ca++ and Ca++ losses did not change compared to the ACS group, and muscle Ca++ did not increase and plasma Ca++ and Ca++ losses did not decrease as in the CAOSHS group. Muscle Ca++, plasma Ca++, and Ca++ losses did not alter in the ACS group compared to their values at preexperimental period. All treated participants experience the need to urinate during the early preorthostatic and orthostatic position. Excretion of urine was (P < 0.05) higher in orthostatic position than in CAOS position and (P < 0.05) higher with lower fluid shift to the head than with higher fluid shift to the head. The participants were not experience blood pressure and heart rate changes in orthostatic position. Conclusion: The study provides evidence that muscle Ca++ increases from CPFR and CAOS, suggesting a potential benefit of muscle Ca++ regulation with treatment of CPFR and CAOS via chronically applied periodic and progressive fluid volume expansion.