High intensity interval training does not have compensatory effects on physical activity levels in older adults

Exercise has beneficial effects on older adults, but controversy surrounds the purported "compensatory effects" that training may have on total daily physical activity and energy expenditure in the elderly. We wanted to determine whether 8 weeks of high-intensity interval training (HIIT) induced such effects on physical activity and energy expenditure in healthy, active older adult men

Energetics of running in top-level marathon runners from Kenya

On ten top-level Kenyan marathon runners (KA) plus nine European controls (EC, equivalent to KA), we measured maximal oxygen consumption ( $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ ) and the energy cost of running (C r) on track during training camps at moderate altitude, to better understand the KA dominance in the marathon. At each incremental running speed, steady-state oxygen consumption ( $$\dot{V}{\text{O}}_{ 2}$$ ) was measured by telemetric metabolic cart, and lactate by electro-enzymatic method. The speed requiring $$\dot{V}{\text{O}}_{ 2} = \dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ provided the maximal aerobic velocity (v max). The energy cost of running was calculated by dividing net $$\dot{V}{\text{O}}_{ 2}$$ by the corresponding speed. The speed at lactate threshold (v ΘAN) was computed from individual Lâb versus speed curves. The sustainable $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ fraction (F d) at v ΘAN (F ΘAN) was computed dividing v ΘAN by v max. The F d for the marathon (F mar) was determined as F mar=0.92 F ΘAN. Overall, $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ (64.9±5.8 vs. 63.9±3.7mlkg−1min−1), v max (5.55±0.30 vs. 5.41±0.29ms−1) and C r (3.64±0.28 vs. 3.63±0.31Jkg−1m−1) resulted the same in KA as in EC. In both groups, C r increased linearly with the square of speed. F ΘAN was 0.896±0.054 in KA and 0.909±0.068 in EC; F mar was 0.825±0.050 in KA and 0.836±0.062 in EC (NS). Accounting for altitude, running speed predictions from present data are close to actual running performances, if F ΘAN instead of F mar is taken as index of F d. In conclusion, both KA and EC did not have a very high $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ , but had extremely high F d, and low C r, equal between them. The dominance of KA over EC cannot be explained on energetic ground

Vagal blockade suppresses the phase I heart rate response but not the phase I cardiac output response at exercise onset in humans

Purpose We tested the vagal withdrawal concept for heart rate (HR) and cardiac output (CO) kinetics upon moderate exercise onset, by analysing the effects of vagal blockade on cardiovascular kinetics in humans. We hypothesized that, under atropine, the φ1 amplitude (A1) for HR would reduce to nil, whereas the A1 for CO would still be positive, due to the sudden increase in stroke volume (SV) at exercise onset. Methods On nine young non-smoking men, during 0–80 W exercise transients of 5-min duration on the cycle ergometer, preceded by 5-min rest, we continuously recorded HR, CO, SV and oxygen uptake (˙O2) upright and supine, in control condition and after full vagal blockade with atropine. Kinetics were analysed with the double exponential model, wherein we computed the amplitudes (A) and time constants (τ) of phase 1 (φ1) and phase 2 (φ2). Results In atropine versus control, A1 for HR was strongly reduced and fell to 0 bpm in seven out of nine subjects for HR was practically suppressed by atropine in them. The A1 for CO was lower in atropine, but not reduced to nil. Thus, SV only determined A1 for CO in atropine. A2 did not differ between control and atropine. No effect on τ1 and τ2 was found. These patterns were independent of posture. Conclusion The results are fully compatible with the tested hypothesis. They provide the first direct demonstration that vagal blockade, while suppressing HR φ1, did not affect φ1 of CO

Testing the vagal withdrawal hypothesis during light exercise under autonomic blockade: a heart rate variability study

Introduction. We performed the first analysis of heart rate variability (HRV) at rest and exercise under full autonomic blockade on the same subjects, to test the conjecture that vagal tone withdrawal occurs at exercise onset. We hypothesized that, between rest and exercise: i) no differences in total power (PTOT) under parasympathetic blockade; ii) a PTOT fall under β1-sympathetic blockade; iii) no differences in PTOT under blockade of both ANS branches. Methods. 7 males (24±3 years) performed 5-min cycling (80W) supine, preceded by 5-min rest during control and with administration of atropine, metoprolol and atropine+metoprolol (double blockade). Heart rate and arterial blood pressure were continuously recorded. HRV and blood pressure variability were determined by power spectral analysis, and baroreflex sensitivity (BRS) by the sequence method. Results. At rest, PTOT and the powers of low (LF) and high (HF) frequency components of HRV were dramatically decreased in atropine and double blockade compared to control and metoprolol, with no effects on LF/HF ratio and on the normalised LF (LFnu) and HF (HFnu). At exercise, patterns were the same as at rest. Comparing exercise to rest, PTOT varied as hypothesized. For SAP and DAP, resting PTOT was the same in all conditions. At exercise, in all conditions, PTOT was lower than in control. BRS decreased under atropine and double blockade at rest, under control and metoprolol during exercise. Conclusions. The results support the hypothesis that vagal suppression determined disappearance of HRV during exercise

An overview of grid-edge control with the digital transformation

Distribution networks are evolving to become more responsive with increasing integration of distributed energy resources (DERs) and digital transformation at the grid edges. This evolution imposes many challenges to the operation of the network, which then calls for new control and operation paradigms. Among others, a so-called grid-edge control is emerging to harmonise the coexistence of the grid control system and DER’s autonomous control. This paper provides a comprehensive overview of the grid-edge control with various control architectures, layers, and strategies. The challenges and opportunities for such an approach at the grid edge with the integration of DERs and digital transformation are summarised. The potential solutions to support the network operation by using the inherent controllability of DER and the availability of the digital transformation at the grid edges are discussed

Tropical Cyclones and Climate Change

Trabajo presentado en: 10th International Worskshop Cyclones Tropicales, celebrado del 5 al 9 de diciembre de 2022 en Bali, Indonesia.A substantial number of studies have been published since the IWTC-9 in 2018, improving our understanding of the effect of climate change on tropical cyclones (TCs) and associated hazards and risks. They reinforced the robustness of increases in TC intensity and associated TC hazards and risks due to anthropogenic climate change. New modeling and observational studies suggested the potential influence of anthropogenic climate forcings, including greenhouse gases and aerosols, on global and regional TC activity at the decadal and century time scale. However, there is still substantial uncertainty owing to model uncertainty in simulating historical TC decadal variability in the Atlantic and owing to limitations of observed TC records. The projected future change in the global number of TCs has become more uncertain since IWTC-9 due to projected increases in TC frequency by a few climate models. A new paradigm, TC seeds, has been proposed, and there is currently a debate on whether seeds can help explain the physical mechanism behind the projected changes in global TC frequency. New studies also highlighted the importance of large-scale environmental fields on TC activity, such as snow cover and air-sea interactions. Future projections on TC translation speed and Medicanes are new additional focus topics in our report. Recommendations and future research are proposed relevant to the remaining scientific questions and assisting policymakers

Effects of eight weeks of aerobic interval training and of isoinertial resistance training on risk factors of cardiometabolic diseases and exercise capacity in healthy elderly subjects

We investigated the effect of 8 weeks of high intensity interval training (HIT) and isoinertial resistance training (IRT) on cardiovascular fitness, muscle mass-strength and risk factors of metabolic syndrome in 12 healthy older adults (68 yy \ub1 4). HIT consisted in 7 two-minute repetitions at 80%-90% of V\ucb\u99O2max, 3 times/w. After 4 months of recovery, subjects were treated with IRT, which included 4 sets of 7 maximal, bilateral knee extensions/flexions 3 times/w on a leg-press flywheel ergometer. HIT elicited significant: i) modifications of selected anthropometrical features; ii) improvements of cardiovascular fitness and; iii) decrease of systolic pressure. HIT and IRT induced hypertrophy of the quadriceps muscle, which, however, was paralleled by significant increases in strength only after IRT. Neither HIT nor IRT induced relevant changes in blood lipid profile, with the exception of a decrease of LDL and CHO after IRT. Physiological parameters related with aerobic fitness and selected body composition values predicting cardiovascular risk remained stable during detraining and, after IRT, they were complemented by substantial increase of muscle strength, leading to further improvements of quality of life of the subjects

Substrate Stiffness Modulates Gene Expression and Phenotype in Neonatal Cardiomyocytes In Vitro

Biomaterials to be used as cell delivery systems for cardiac tissue engineering should be able to comply with cardiac muscle contractile activity, while favoring cell survival and neo-angiogenesis in a hostile environment. Biocompatible synthetic materials can be tailored to mimic cardiac tissue three-dimensional organization in the micro- and nanoscales. Nonetheless, they usually display mechanical properties that are far from those of the native myocardium and thus could affect host cell survival and activity. In the present investigation, inert poly-ɛ-caprolactone planar layers were manufactured to change the surface stiffness (with Young's modulus ranging from 1 to 133 MPa) without changing matrix chemistry. These substrates were challenged with neonatal murine cardiomyocytes to study the possible effect of substrate stiffness on such cell behavior without changing biological cues. Interestingly, softer substrates (0.91±0.08 and 1.53±0.16 MPa) were found to harbor mostly mature cardiomyocytes having assembled sarcomeres, as shown by the expression of alpha actinin and myosin heavy chain in typical striations and the upregulation of sarcomeric actin mRNA. On the other hand, a preferential expression of immature cardiac cell genes (Nkx-2.5) and proteins (GATA-4) in cardiac cells grown onto stiffer materials (49.67±2.56 and 133.23±8.67 MPa) was detected. This result could not be ascribed to significant differences in cell adhesion or proliferation induced by the substrates, but to the stabilization of cardiomyocyte differentiated phenotype induced by softer layers. In fact, cardiac cell electromechanical coupling was shown to be more organized on softer surfaces, as highlighted by connexin 43 distribution. Moreover, a differential regulation of genes involved in extracellular matrix remodeling was detected on soft films (0.91±0.08 MPa) as compared with the stiffest (133.23±8.67 MPa). Finally, the upregulation of a number of genes involved in inflammatory processes was detected when the stiffest polymer is used. These events highlight the differences in cell mechanosensitivity in a heterogeneous cell preparation and are likely to contribute to the differences encountered in cardiac cell phenotype induced by substrate stiffness.Peer reviewe

Remodeling of the chromatin structure of the facioscapulohumeral muscular dystrophy (FSHD) locus and upregulation of FSHD-related gene 1 (FRG1) expression during human myogenic differentiation

<p>Abstract</p> <p>Background</p> <p>Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant neuromuscular disorder associated with the partial deletion of integral numbers of 3.3 kb D4Z4 DNA repeats within the subtelomere of chromosome 4q. A number of candidate FSHD genes, adenine nucleotide translocator 1 gene (<it>ANT1</it>), FSHD-related gene 1 (<it>FRG1</it>), <it>FRG2 </it>and <it>DUX4c</it>, upstream of the D4Z4 array (FSHD locus), and double homeobox chromosome 4 (<it>DUX4</it>) within the repeat itself, are upregulated in some patients, thus suggesting an underlying perturbation of the chromatin structure. Furthermore, a mouse model overexpressing <it>FRG1 </it>has been generated, displaying skeletal muscle defects.</p> <p>Results</p> <p>In the context of myogenic differentiation, we compared the chromatin structure and tridimensional interaction of the D4Z4 array and <it>FRG1 </it>gene promoter, and <it>FRG1 </it>expression, in control and FSHD cells. The <it>FRG1 </it>gene was prematurely expressed during FSHD myoblast differentiation, thus suggesting that the number of D4Z4 repeats in the array may affect the correct timing of <it>FRG1 </it>expression. Using chromosome conformation capture (3C) technology, we revealed that the <it>FRG1 </it>promoter and D4Z4 array physically interacted. Furthermore, this chromatin structure underwent dynamic changes during myogenic differentiation that led to the loosening of the <it>FRG1</it>/4q-D4Z4 array loop in myotubes. The <it>FRG1 </it>promoter in both normal and FSHD myoblasts was characterized by H3K27 trimethylation and Polycomb repressor complex binding, but these repression signs were replaced by H3K4 trimethylation during differentiation. The D4Z4 sequences behaved similarly, with H3K27 trimethylation and Polycomb binding being lost upon myogenic differentiation.</p> <p>Conclusion</p> <p>We propose a model in which the D4Z4 array may play a critical chromatin function as an orchestrator of <it>in cis </it>chromatin loops, thus suggesting that this repeat may play a role in coordinating gene expression.</p