ABSTRACT
BACKGROUND: The exact causes of skeletal muscle weakness in chronic kidney disease (CKD) remain unknown with uremic toxicity and redox imbalances being implicated. To understand whether uremic muscle has acquired any sensitivity to acute redox changes we examined the effects of redox disturbances on force generation capacity. METHODS: Permeabilized single psoas fibers (N =37) from surgically induced CKD (UREM) and sham-operated (CON) rabbits were exposed to an oxidizing (10 mM Hydrogen Peroxide, H2O2) and/or a reducing [10 mM Dithiothreitol (DTT)] agent, in a blind design, in two sets of experiments examining: A) the acute effect of the addition of H2O2 on maximal (pCa 4.4) isometric force of actively contracting fibers and the effect of incubation in DTT on subsequent re-activation and force recovery (N =9 CON; N =9 UREM fibers); B) the effect of incubation in H2O2 on both submaximal (pCa 6.2) and maximal (pCa 4.4) calcium activated isometric force generation (N =9 CON; N =10 UREM fibers). RESULTS: Based on cross-sectional area (CSA) calculations, a 14 % atrophy in UREM fibers was revealed; thus forces were evaluated in absolute values and corrected for CSA (specific force) values. A) Addition of H2O2 during activation did not significantly affect force generation in any group or the pool of fibers. Incubation in DTT did not affect the CON fibers but caused a 12 % maximal isometric force decrease in UREM fibers (both in absolute force p =0.024, and specific force, p =0.027). B) Incubation in H2O2 during relaxation lowered subsequent maximal (but not submaximal) isometric forces in the Pool of fibers by 3.5 % (for absolute force p =0.033, for specific force p =0.019) but not in the fiber groups separately. CONCLUSIONS: Force generation capacity of CON and UREM fibers is affected by oxidation similarly. However, DTT significantly lowered force in UREM muscle fibers. This may indicate that at baseline UREM muscle could have already been at a more reduced redox state than physiological. This observation warrants further investigation as it could be linked to disease-induced effects. HIPPOKRATIA 2017, 21(1): 3-7.
ABSTRACT
AIM: Exercise induced arterial hypoxemia (EIAH) is a reduction in arterial oxygenation, which may result from a drop in arterial oxygen pressure and therefore in oxygen saturation. We examined EIAH in swimmers, while till now it was known to occur in cyclists and runners. METHODS: We studied 8 male highly trained swimmers (age: 23+/-1.7; (.-)VO(2peak), 5.3+/-0.1 l/min and 8 male ex-swimmers (age: 21.5+/-0.6; (.-)VO(2peak), 3.4+/-0.3 l/min). All subjects performed 200-meter freestyle at maximum effort. Hemoglobin saturation (SaO(2)%) was measured using a finger pulse oximeter before exercise in the water in an upright position and immediately after exercise, within 5 seconds. RESULTS: Highly trained swimmers developed a statistically significant decrease in SaO(2)% (from 98.3+/-0.3 to 94+/-0.9, p= or <0.01) after exercise, while ex-swimmers did not (from 98.4+/-0.3 to 96.8+/-0.3 ns). The 4% decrease in SaO(2)% observed in highly trained swimmers can be characterized as mild EIAH. CONCLUSIONS: Our study suggests that highly trained swimmers but not ex-swimmers may develop mild EIAH after 200 meters freestyle swimming at maximum effort.
