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A paradox of so-called developed countries is that, as the major historical causes of human mortality are eliminated or mitigated by medical progress, life-style related diseases have become major killers. Furthermore, as life-span is extended by the combined effects of modern medicine, health-span is struggling to keep apace because of the burden of non-communicable diseases linked to diet and sedentary life-style. The gut microbiome is now recognized as a plastic environmental risk factor for many of these diseases, the microbiome being defined as the complex community of co-evolved commensal microbes that breaks down components of a complex diet, modulates innate immunity, and produces signalling molecules and metabolites that can impact on diverse regulatory systems in mammals. Aspects of the so-called â Westernâ life-style linked to disease risk such as energy dense diet and antibiotic treatment are known to affect the composition and function of the microbiome. Here we review the detailed mechanisms whereby the gut microbiome may modulate risk of diseases linked to sedentary life-style, and ageing related health loss. We focus on the comparative value of natural animal models such as hibernation for studying metabolic regulation, and the challenge of extrapolating from animal models to processes that occur in human ageing.

Purpose: This cross-sectional study examined the mutual independent associations of sedentary behavior, lower intensity physical activity (LPA) and higher intensity physical activity (HPA) (an approximation of moderate to vigorous physical activity with cardiorespiratory fitness (CRF). Methods: Two thousand twenty-four participants were included from The Maastricht Study (mean +/- SD age, 59.7 +/- 8.1 yr; 49.6% men). With the activPAL3 activity monitor, we assessed sedentary time (ST), sedentary pattern variables (number of sedentary breaks, average sedentary bout duration, and number of prolonged sedentary bouts [>= 30 min]), LPA, and HPA. CRF was calculated as maximum power output per kilogram body mass (W-max.kg(-1)) estimated from a submaximal cycle ergometer test. Linear regression analyses and isotemporal substitution analyses were used to examine associations of ST, sedentary pattern variables, and HPA with CRF. Analyses were stratified by sex. Results: One hour of ST per day was associated with a lower W-max.kg(-1) : B-men = -0.03 (95% confidence interval [CI], -0.05 to -0.01) and B-women = -0.02 (95% CI, -0.04 to 0.00), independent of HPA. No statistically significant associations between sedentary patterns variables and CRF were observed. LPA was associated with a higher W-max.kg(-1): B-men = 0.12 (95% CI, 0.07-0.17) and B-women = -0.12 (95% CI, 0.07-0.18). HPA was associated with a higher W-max.kg(-1) : B-men = 0.48 (95% CI, 0.38-0.58) and B-women = 0.27 (95% CI, 0.18-0.36). Replacing ST with LPA (B-men, 0.08; 95% CI, 0.03-0.14; B-women, 0.10; 95% CI, 0.05-0.16) or with HPA (B-men, 0.49; 95% CI, 0.39-0.59; B-women = 0.28; 95% CI, 0.19-0.36), but not with standing was associated with higher CRF. Conclusions: Modest associations between sedentary behavior and CRF were observed. Replacing ST with LPA was associated with higher CRF, which could be of particular importance for individuals who cannot engage in HPA. Nonetheless, replacing ST with HPA was associated with greatest estimated change in CRF.