The Army Combat Fitness Test (ACFT), an updated and newly developed metric to assess combat readiness, may require specialized exercise and nutritional interventions. The purpose of this cross-sect...
17 August 2020 in European Journal of Applied Physiology
Evidence indicates that both vitamin D and the gut microbiome are involved in the process of colon carcinogenesis. However, it is unclear what effects supplemental vitamin D 3 has on the gut microbiome and its metabolites in healthy adults. We conducted a double-blind, randomized, placebo-controlled trial to identify the acute and long-term microbiota structural and metabolite changes that occur in response to a moderate dose (4,000 IU) of vitamin D 3 for 12 weeks in healthy adults. Our results demonstrated a significant increase in serum 25-hydroxy-vitamin D (25(OH)D) in the treatment group compared to placebo ( P < 0.0001). Vitamin D 3 significantly increased compositional similarity ( P < 0.0001) in the treatment group, and enriched members of the Bifidobacteriaceae family. We also identified a significant inverse relationship between the percent change in serum 25(OH)D and microbial stability in the treatment group ( R = −0.52, P < 0.019). Furthermore, vitamin D 3 supplementation resulted in notable metabolic shifts, in addition to resulting in a drastic rewiring of key gut microbial-metabolic associations. In conclusion, we show that a moderate dose of vitamin D 3 among healthy adults has unique acute and persistent effects on the fecal microbiota, and suggest novel mechanisms by which vitamin D may affect the host-microbiota relationship. IMPORTANCE: Preventative measures to reduce the rise in early-onset colorectal cancer are of critical need. Both vitamin D, dietary and serum levels, and the gut microbiome are implicated in the etiology of colorectal cancer. By understanding the intimate relationship between vitamin D, the gut microbiome, and its metabolites, we may be able to identify key mechanisms that can be targeted for intervention, including inflammation and metabolic dysfunction. Furthermore, the similarity of vitamin D to cholesterol, which is metabolized by the gut microbiome, gives precedence to its ability to produce metabolites that can be further studied and leveraged for controlling colorectal cancer incidence and mortality.
25 August 2020 in Research Quarterly for Exercise and Sport
Sleep deprivation in healthy adults has been associated with disrupted autonomic nervous system function, which in turn has been linked to cardiovascular health. High-intensity interval exercise (HIIE) may affect both sleep and cardiac autonomic modulation. Purpose: To investigate the impact of acute partial sleep deprivation on autonomic cardiac regulation before and after an acute bout of HIIE and the length of time for the autonomic system to return to resting levels. Methods: Fifteen healthy males with body mass index (BMI) of 25.8 ± 2.7 kg·m−2 and age 31 ± 5 y participated in a reference sleep (~9.5 hr) with no HIIE (RS), a reference sleep with HIIE (RSX), and an acute partial sleep deprivation (~3.5 hr) with HIIE (SDX). HIIE was performed in 3:2 intervals at 90% and 40% of VO2 reserve. Autonomic regulation through HRV selected time and frequency domain indices were recorded the night before, the morning of the next day, 1 hr-, 2 hr-, 4hr-, and 6-hr post-exercise. Results: HIIE performed in a 3:2 W:R ratio decreased the HRV (p < .05) at 1-hr post exercise and it took up to 4 hr to return to baseline levels. Parasympathetic related HRV indices increased the morning of the next day for SDX (p < .05). Acute partial sleep deprivation and HIIE did not modify the HRV responses compared to reference sleep and HIIE. Conclusion: HRV disturbance typically seen in responses to an acute episode of HIIE is not influenced by acute partial sleep deprivation.
Resistance exercise training (RET) is a common and well-established method to induce hypertrophy and improvement in strength. Interestingly, fish oil supplementation (FOS) may augment RET-induced a...
Chronic kidney disease (CKD) is directly influenced by the deleterious effects of systemic inflammation and oxidative stress. The vascular endothelium may transiently respond to aerobic exercise and improve post-exercise vascular renal function in moderate stages of CKD. Brachial artery flow-mediated dilation (FMD) is a nitric-oxide-dependent measure of endothelial function that is transiently potentiated by exercise. The purpose of the study was to determine the acute influence of a single bout of high-intensity interval exercise (HIIE) or steady-state moderate-intensity exercise (SSE) on endothelial dysfunction in moderate stages of CKD. Twenty participants (n = 6 men; n = 14 women) completed 30 min of SSE (65%) and HIIE (90:20%) of VO2reserve in a randomized crossover design. FMD measurements and blood samples were obtained before, 1 h, and 24 h post-exercise. FMD responses were augmented 1 h post-exercise in both conditions (p < 0.005). Relative to pre-exercise measures, total antioxidant capacity increased by 4.3% 24 h post-exercise (p = 0.012), while paraoxonase-1 was maintained 1 h and elevated by 6.1% 24 h after SSE, but not HIIE (p = 0.035). In summary, FMD can be augmented by a single episode of either HIIE or SSE in moderate stages of CKD. Modest improvements were observed in antioxidant analytes, and markers of oxidative stress were blunted in response to either SSE or HIIE.