Background Exercise and heat trigger dehydration and an increase in extracellular fluid osmolality, leading to deficits in exercise performance and thermoregulation. Evidence from previous studies supports the potential for deep-ocean mineral water to improve recovery of exercise performance post-exercise. We therefore wished to determine whether acute rehydration and muscle strength recovery was enhanced by deep-ocean mineral water following a dehydrating exercise, compared to a sports drink or mountain spring water. We hypothesized that muscle strength would decrease as a result of dehydrating exercise, and that recovery of muscle strength and hydration would depend on the type of rehydrating fluid. Methods Using a counterbalanced, crossover study design, female ( n = 8) and male ( n = 9) participants performed a dehydrating exercise protocol under heat stress until achieving 3% body mass loss. Participants rehydrated with either deep-ocean mineral water ( Deep ), mountain spring water ( Spring ), or a carbohydrate-based sports drink ( Sports ) at a volume equal to the volume of fluid loss. We measured relative hydration using salivary osmolality (S osm ) and muscle strength using peak torque from a leg extension maneuver. Results S osm significantly increased ( p < 0.0001) with loss of body mass during the dehydrating exercise protocol. Males took less time (90.0 ± 18.3 min; P < 0.0034) to reach 3% body mass loss when compared to females (127.1 ± 20.0 min). We used a mono-exponential model to fit the return of S osm to baseline values during the rehydrating phase. Whether fitting stimulated or unstimulated S osm , male and female participants receiving Deep as the hydrating fluid exhibited the most rapid return to baseline S osm (p < 0.0001) regardless of the fit parameter. Males compared to females generated more peak torque ( p = 0.0005) at baseline (308.3 ± 56.7 Nm vs 172.8 ± 40.8 Nm, respectively) and immediately following 3% body mass loss (276.3 ± 39.5 Nm vs 153.5 ± 35.9 Nm). Participants experienced a loss. We also identified a significant effect of rehydrating fluid and sex on post-rehydration peak torque ( p < 0.0117). Conclusion We conclude that deep-ocean mineral water positively affected hydration recovery after dehydrating exercise, and that it may also be beneficial for muscle strength recovery, although this, as well as the influence of sex, needs to be further examined by future research. Trial registration clincialtrials.gov PRS, NCT02486224 ...

We demonstrated that daily delivery of Lactobacillus reuteri to wild-type and hypercholesterolemic lipoprotein receptor knockout mice attenuated cardiac injury following ischemia-reperfusion without lowering total serum cholesterol in the short term. In addition, we validated protection against cardiac injury using histology and immunohistochemistry techniques. L. reuteri offers promise as a probiotic to mitigate ischemic cardiac injury.

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Prior to menopause, women are protected against cardiovascular disease (CVD) compared to age-matched men; this protection is gradually lost after menopause. Mechanisms responsible for loss of CVD protection are unknown. We previously demonstrated that menopause and CVD suppress the AMP-activated protein kinase (AMPK) signaling pathway in mice. We also validated the cellular mechanism by which estrogen (E2) potentiates AMPK activity through a direct interaction of estrogen receptors (ER) with members of the AMPK kinase complex. Because AMPK signaling is down in CVD and menopause, we hypothesized that activation of AMPK will prevent pathological cardiac remodeling in menopausal female mice. First, we demonstrated that E2 potentiates AMPK activity in neonatal rat cardiomyocytes (NRCMs) subjected to energy stress. NRCMs, cultured in estrogen-free media, were treated (10-30 minutes at 100nm) with the electron transport chain uncoupler carbonyl cyanide 4-(trifluoromethoxy)phenyphydrazone (FCCP). As expected, AMPK activity determined by phosphorylation of threonine 172 (p-AMPK172) was increased over controls. Adding 1-100nm of E2 potentiated p-AMPK172 over control-treated NRCMs by 5-fold. Next, we used our novel model of menopause with 4-vinylcyclohexene diepoxide (VCD), which induces gradual ovarian failure, preserving the perimenopause transitional period and androgen secreting capacity of residual ovarian tissue. Starting at 2 months, females received daily (i.p.) injections of VCD (160mg/kg, 20 consecutive days) or sesame oil as vehicle. Peri/menopause were confirmed by vaginal cytology. Menopausal females receiving angiotensin II (Ang II, 800 ng/kg/min via alzet s.c. mini-pump, 14 days) demonstrated exacerbation of hypertension and pathological cardiac remodeling compared to pre- and peri-menopausal mice. Female mice treated with Ang II following surgical removal of ovaries (OVX) experienced a similar exacerbation of cardiac remodeling. Daily adminstration of the AMPK activator (A-769662, s.c. 30mg/kg) prevented pathological remodeling in menopausal and OVX female mice subjected to Ang II. We conclude that AMPK represents a non-canonical target for the mitigation of menopausal susceptibly to CVD.