
Current literature focuses on maximal apneas to improve apnea duration, whereas in practice, apnea training often involves two distinct forms of timed-repeated submaximal apnea protocols: “O2-tables”, intended to progressively decrease oxygenation and purportedly train O2 conservation, and “CO2-tables”, intended to progressively accumulate carbon dioxide (CO2) and purportedly train hypercapnia tolerance. In apnea novices, O2- and CO2-tables failed to induce strong deoxygenation and CO2 accumulation, respectively. Therefore, the aim of this study was to compare physiological responses to maximal apneas, O2- and CO2-tables in apnea trained individuals. After medical screening, fourteen freedivers performed three apnea protocols: maximal apneas, O2-table and CO2-table. During apnea, heart rate (HR), muscle tissue oxygenation index (mTOI) and peripheral oxygen saturation (SpO2) were measured continuously. End-tidal carbon dioxide (EtCO2) was measured before and after apneas. Capillary partial pressure of CO2 (PCO2) was measured after the fourth and final apnea. Perceived Exertion (RPE) was rated after each protocol. RPE was lower after O2- and CO2-tables than after maximal apneas. Changes in HR and mTOI did not differ between O2- and CO2-tables. CO2-tables elicited greater increases in PCO2 and EtCO2 compared to O2-tables and maximal apneas. Maximal apneas induced greater changes in SpO2 than O2- and CO2-tables. These results suggest that, in freedivers, O2- and CO2-tables offer a less mentally and physically demanding alternative to repeated maximal apneas, allowing greater variation in apnea training while still targeting O2 conservation and CO2 tolerance, respectively.
Exercise is commonly recommended to support stress regulation and mental health, yet it remains unclear whether these benefits translate to conditions characterized by prolonged stress and fatigue. The aims were to examine whether autonomic and hypothalamic–pituitary–adrenal (HPA) axis responses to a single exercise bout differ between individuals with stress-related exhaustion and healthy controls, and whether responses vary by exercise intensity. In a randomized, counterbalanced crossover design, 30 individuals with stress-related exhaustion (93.3
Slow-paced breathing (SPB) improves autonomic balance and increases heart rate variability (HRV). The influence of combat-related traumatic injury (CRTI), baseline respiratory rate (RR), and physical function/activity on the relationship between SPB and HRV has not been examined previously and was the aim of this study. We analysed the first follow-up data from the ongoing ArmeD serVices trAuma rehabilitatioN outComE (ADVANCE) Cohort study. Short-term HRV was measured using a single-lead electrocardiogram during five minutes of spontaneous breathing, followed by five minutes of SPB (six breaths/minute). We examined the effect modification of SPB on HRV by CRTI (yes/no), RR during spontaneous breathing (< 15/≥15 breaths/minute), weekly moderate-to-vigorous physical activity (MVPA) using the International Physical Activity Questionnaire and physical function (6-minute-walk-distance; 6MWD). Linear models for panel data were run, adjusting for age, sampling rank, ethnicity, and cardiovascular and respiratory medication. A total of 962 male participants (median age: 37.6 years; n = 487 injured, n = 495 uninjured; mean 11years post-injury/deployment) with paired spontaneous-SPB HRV data were included. All short-term HRV measures increased during SPB when compared to spontaneous breathing. CRTI, 6MWD and MVPA did not significantly moderate the effect of SPB on HRV, but baseline RR ≥ 15 breaths/minute did, with Root-Mean-Square-Of-Successive-Difference (RMSSD) increasing from 15.57ms to 21.89ms (p < 0.001) during SPB. SPB improves HRV regardless of CRTI status. Those with higher baseline RR are more likely to obtain a significant improvement in HRV during SPB. SPB-based interventions may be introduced for the rehabilitation of military personnel following injury/deployment.
Accurate estimation of total energy expenditure (TEE) in athletes is essential for determining energy requirements to support training, recovery, and performance. Basal metabolic rate (BMR) is one of the key components associated with the accuracy of TEE estimation. However, few studies have evaluated the accuracy of BMR and TEE estimation methods in athletic populations. This study aimed to examine the validity of the Cunningham equation for BMR estimation and the accelerometer-based method (ACCTRI) for TEE estimation in elite female university runners, using the doubly labeled water (DLW) method as the reference criterion. We analyzed data from 16 elite female university runners (mean age 20 ± 1 years). We assessed: (1) the association and agreement between BMR estimated using the Cunningham equation and BMR measured by indirect calorimetry, and (2) the association and agreement between TEE estimated using the ACCTRI method and TEE measured using the DLW method. Correlational analysis revealed significant, positive, and strong associations between estimated and measured BMR (r = 0.728, P = 0.001) and between estimated and measured TEE (r = 0.828, P = 0.001). Bland–Altman analyses showed good agreement between estimated and measured BMR (bias, 1.6
Aging contributes to progressive hepatic dysfunction, characterized by increased oxidative stress, chronic inflammation, and mitochondrial impairment, which collectively exacerbate metabolic decline. This study examined the effects of high-intensity interval training (HIIT) on the SIRT1–P16 axis, oxidative stress, and inflammatory markers in a D-galactose (D-gal )-induced aging model in male Wistar rats. Twenty-eight rats were assigned to four groups: Control (CTL), HIIT, D-gal, and D-gal+HIIT. Aging model was induced via daily subcutaneous injections of D-galactose (150 mg/kg) for eight weeks, while HIIT was performed on a treadmill five times per week over the same period. Gene expression and protein levels were measured by Real-time PCR and Western blot, respectively. Antioxidant and oxidant, and inflammatory markers were determined via colorimetric and ELISA methods. Gene expression analysis showed that D-gal significantly downregulated the expression of AMPK, SIRT1, and PGC-1α, whereas HIIT was associated with increased expression of these markers. Western blot analysis confirmed a reduction and elevation in SIRT1 and P16 protein, respectively, in the D-gal group, which were reversed following HIIT. HIIT also ameliorated the increase in the levels of malondialdehyde, IL-1β, IL-6, and TNF-α and the decrease in the SOD and GPx activities. Concurrent HIIT attenuated D-galactose-induced hepatic molecular and biochemical alterations associated with aging. These effects were accompanied by changes in SIRT1–P16-related markers, improved redox balance, and reduced inflammatory responses, supporting the potential of HIIT as a non-pharmacological strategy for promoting liver health during aging.