Whey protein plus bicarbonate supplement has little effects on structural atrophy and proteolysis marker immunopatterns in skeletal muscle disuse during 21 days of bed rest

Objectives: To investigate the effect of whey protein plus potassium bicarbonate supplement on disused skeletal muscle structure and proteolysis after bed rest (BR). Methods: Soleus (SOL) and vastus lateralis (VL) biopsies were sampled from ten (n=10) healthy male subjects (aged 31±6 years) who did BR once with and once without protein supplement as a dietary countermeasure (cross-over study design). The structural changes (myofibre size and type distribution) were analysed by histological sections, and muscle protein breakdown indirectly via the proteolysis markers, calpain 1 and 3, calpastatin, MuRF1 and 2, both in muscle homogenates and by immunohistochemistry. Results: BR caused size-changes in myofiber cross-sectional area (FCSA, SOL, p=0,004; VL, p=0.03), and myofiber slow-to-fast type transition with increased hybrids (SOL, p=0.043; VL, p=0.037) however with campaign differences in SOL (p<0.033). No significant effect of BR and supplement was found by any of the key proteolysis markers. Conclusions: Campaign differences in structural muscle adaptation may be an issue in cross-over design BR studies. The whey protein plus potassium bicarbonate supplement did not attenuate atrophy and fibre type transition during medium term bed rest. Alkaline whey protein supplements may however be beneficial as adjuncts to exercise countermeasures in disuse

Markers of bone metabolism during 14 days of bed rest in young and older men

OBJECTIVE: We aimed at comparing markers of bone metabolism during unloading in young and older men, and to assess countermeasure effectiveness. METHODS: 16 older (60\ub12 years) and 8 younger men (23\ub13 years) underwent bed rest (BR) for 14 days. A subgroup of the Older performed cognitive training during BR and supplemented protein and potassium bicarbonate afterwards. Biochemical markers of bone and calcium/phosphate metabolism were assessed. RESULTS: At baseline urinary NTX and CTX were greater in younger than in older subjects (P0.17). P1NP was greater in young than in older subjects (P<0.001) and decreased during BR in the Young (P<0.001). Sclerostin increased during BR across groups (P=0.016). No systematic effects of the countermeasure were observed. CONCLUSION: In men, older age did not affect control of bone metabolism, but bone turnover was reduced. During BR formation markers were reduced only in younger men whereas resorption markers increased to a comparable extent. Thus, we assume that older men are not at an elevated, and possibly even at a reduced risk to lose bone when immobilize

The importance of timing potassium bicarbonate supplementation to affect acid-base balance

In dealing with the negative consequences of a low-grade-metabolic acidosis, induced partially by the western industrialized world’s nutrient composition, alkaline salts such as potassium bicarbonate (KHCO3) have shown to serve as an effective countermeasure. We have recently shown that high sodium chloride (NaCl) intake also induces a low-grade metabolic acidosis. However, timing of the alkaline salt’s application relative to a meal might lead to different responses. Therefore, the main aim of the present study was to determine the ideal time for the intake of KHCO3 relative to a sodium chloride abundant meal. 10 subjects (6 male, 4 female) completed 4 identically scheduled days of the experiment, with 1 day for the control experiment (no supplementation) and 3 days for the different interventions (supplementation of 45mmol KHCO3 before, with or after lunch, respectively). Meals and bloodgas analyses (measured parameters: pH, HCO3-, base excess (BE)) were appointed at definite times. Additionally, a questionnaire monitored any side effects of the supplementation, possibly gastrointestinal disturbances (e.g. flatulence, nausea, diarrhea). Supplementing KHCO3 results in a more alkaline status within the normal range compared to the control (control/different times of supplementation: HCO3- 24mmol/L/ 26mmol/L (p=0.02); BE 0mmol/L/ 1mmol/L (p=0.002)) (before meal: HCO3- /BE: p=0.02/p=0.002; with the meal: p=0.02/p=0.002; after meal: p=0.003/p<=0.001). In this context pH showed significant effects in only two different times of supplementation (during meal (p=0.007), after lunch (p<=0.001)). Except for pH (p=0.01, originating from the supplementation after lunch) timing of the supplements did not lead to different results (HCO3-: p=0.24; BE (p=0.24). Regarding the side effects, subjects were most comfortable in the supplementation with the meal. With the present study, the positive effects of a KHCO3´s administration on the acid-base balance in combination to a sodium chloride abundant meal were confirmed. In aiming to advise an ideal time of KHCO3`s- intake with the focus on all three main descriptive parameters the results make no allowance for setting an advisable time of intake. When taking into account the side effects supplementation of KHCO3 with the meal is highly appreciated

Markers of bone matebolism during 14 days of bed rest in young and older men

Objective: We aimed at comparing markers of bone metabolism during unloading in young and older men, and toassess countermeasure effectiveness. Methods: 16 older (60±2 years) and 8 younger men (23±3 years) underwentbed rest (BR) for 14 days. A subgroup of the Older performed cognitive training during BR and supplemented proteinand potassium bicarbonate afterwards. Biochemical markers of bone and calcium/phosphate metabolism were assessed.Results: At baseline urinary NTX and CTX were greater in younger than in older subjects (P0.17). P1NP was greater in young than in older subjects (P<0.001) and decreasedduring BR in the Young (P<0.001). Sclerostin increased during BR across groups (P=0.016). No systematic effects ofthe countermeasure were observed. Conclusion: In men, older age did not affect control of bone metabolism, but boneturnover was reduced. During BR formation markers were reduced only in younger men whereas resorption markersincreased to a comparable extent. Thus, we assume that older men are not at an elevated, and possibly even at a reducedrisk to lose bone when immobilized.Fil: Buehlmeier, J.. Institute of Aerospace Medicine; Alemania. Universitat Bonn; AlemaniaFil: Frings Meuthen, P.. Institute of Aerospace Medicine; AlemaniaFil: Mohorko, N.. University of Primorska; EsloveniaFil: Lau, P.. Institute of Aerospace Medicine; AlemaniaFil: Mazzucco, S.. University Trieste; ItaliaFil: Ferretti, Jose Luis. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; ArgentinaFil: Biolo, G.. University Trieste; ItaliaFil: Pisot, R.. University of Primorska; EsloveniaFil: Simunic, B.. University of Primorska; EsloveniaFil: Rittweger, J.. Institute of Aerospace Medicine; Alemani

Serum sclerostin and DKK1 in relation to exercise against bone loss in experimental bed rest

The impact of effective exercise against bone loss during experimental bed rest appears to be associated with increases in bone formation rather than reductions of bone resorption. Sclerostin and dickkopf-1 are important inhibitors of osteoblast activity. We hypothesized that exercise in bed rest would prevent increases in sclerostin and dickkopf-1. Twenty-four male subjects performed resistive vibration exercise (RVE; n&nbsp;=&nbsp;7), resistive exercise only (RE; n&nbsp;=&nbsp;8), or no exercise (control n&nbsp;=&nbsp;9) during 60 days of bed rest (2nd Berlin BedRest Study). We measured serum levels of BAP, CTX-I, iPTH, calcium, sclerostin, and dickkopf-1 at 16 time-points during and up to 1&nbsp;year after bed rest. In inactive control, after an initial increase in both BAP and CTX-I, sclerostin increased. BAP then returned to baseline levels, and CTX-I continued to increase. In RVE and RE, BAP increased more than control in bed rest (p&nbsp;&le;&nbsp;0.029). Increases of CTX-I in RE and RVE did not differ significantly to inactive control. RE may have attenuated increases in sclerostin and dickkopf-1, but this was not statistically significant. In RVE there was no evidence for any impact on sclerostin and dickkopf-1 changes. Long-term recovery of bone was also measured and 6-24 months after bed rest, and proximal femur bone mineral content was still greater in RVE than control (p&nbsp;=&nbsp;0.01). The results, while showing that exercise against bone loss in experimental bed rest results in greater bone formation, could not provide evidence that exercise impeded the rise in serum sclerostin and dickkopf-1 levels