Background and objectives: Physical load causes structural changes in the heart that vary depending on the type of training and may affect the function of the heart. Aim of the study: To determine, using the applied co-integration method on algebraic data, the impact of sprinting and of endurance adaptation on the dynamic interactions of cardiovascular functional indices while participants were performing under an increasing workload, up to their inability to continue. Materials and Methods: Healthy athletes were chosen to take part in this study and were separated into two groups: Sprinters (n = 11) and endurance athletes (n = 13). The bicycle ergometric method of incremental increase in a provocative workload (graded stress) was used. The heart rate, stroke volume, and cardiac output were determined using the tetrapolar rheography method. Results: Individuals who are adapted to endurance while carrying physical loads, in contrast to well adapted sprinters, are characterized with a lower rate of changing the pace of interactions between stroke volume and cardiac output while performing at an increasing workload up to their inability to continue. Also, endurance athletes displayed a long and relatively stable phase as well as a greater decrease of interaction between indices at the end of the workload. At the beginning of the exercise, the interaction between the stroke volume and the cardiac output was reduced. However, as the physical load continued, this interaction became significantly stronger. The comparison of the stroke volume and the cardiac output’s dynamic interaction revealed that the endurance group had a greater working capacity. Conclusions: Typical dynamics of interactions during the testing with an increasing physical load can be differentiated into separate phases: The decrease of interaction at the onset of the load, the increase during the continuation of an increased workload, and the decrease at the last stages of the load.

The recently defined and yet rather new topic of healthy aging is attracting more attention worldwide. As the world population is getting older, it is rapidly becoming essential to develop and maintain functional abilities at older age and develop mechanisms to protect the senior population from chronic diseases. One of the most effective components, as well as processes associated with aging, is the recently discovered and Nobel prize-awarded—nitric oxide (NO) (as a signaling molecule), which, followed by later discoveries, showed to have a positive metabolic, immunological, and anti-inflammatory effect. Nitrates are one of the most debated topics of the last decade in the scientific community due to their pathways involved in the production of nitric oxide. Thus, the objective of this study is to evaluate the effect of different potassium nitrate concentrate supplementation on Drosophila melanogaster longevity imitating a human carbohydrate-based diet with relationship to possible cause of oxidative stress. Influence of 0.5–3% potassium nitrate medium on the lifespan and motor function in different groups consisting of 100 fruit fly females in each was analyzed. In this assay, female fly species supplemented with potassium nitrate diet showed life span increase by 18.6% and 5.1% with 1% and 2% KNO₃, respectively, with a positive impact on locomotor function. In conclusion, we found that low concentration of potassium nitrate medium increased lifespan and locomotor function in Drosophila melanogaster.

Many short-term studies with dietary nitrate supplementation in humans and animal models reported positive effects on the cardiovascular system, exercise efficiency, and immune function. However, there has been long-standing concern related to cancer and adverse hormonal effects. We studied the long-term effects of different potassium nitrate (KNO₃) concentrations on laboratory mice longevity and structural changes in their organs. Four groups of male mice were treated with 0 mg (0%), 45 mg (1%), 90 mg (2%), and 140 mg (3%) KNO₃ in the drinking water. The groups were monitored for agility and health status daily. The lifespan of mice and organ pathological changes were analyzed. We found no detrimental effects of life-long supplementation of KNO₃ on the survival of mice in treatment groups. Nitrate supplementation was associated with a lower level of pathological changes (p = 0.002). We conclude that KNO₃ supplementation had no carcinogenic effect on mice and possibly prevented the organs from aging.

Adding potassium nitrate (KNO₃) to the diet improves the physiological properties of mammalian muscles (rebuilds weakened muscle, improves structure and functionality). The aim of this study was to investigate the effect of KNO₃ supplementation in a mouse model. BALB/c mice were fed a KNO₃ diet for three weeks, followed by a normal diet without nitrates. After the feeding period, the Extensor digitorum longus (EDL) muscle was evaluated ex vivo for contraction force and fatigue. To evaluate the possible pathological changes, the histology of EDL tissues was performed in control and KNO₃-fed groups after 21 days. The histological analysis showed an absence of negative effects in EDL muscles. We also analyzed 15 biochemical blood parameters. After 21 days of KNO₃ supplementation, the EDL mass was, on average, 13% larger in the experimental group compared to the controls (p < 0.05). The muscle-specific force increased by 38% in comparison with the control group (p < 0.05). The results indicate that KNO₃ has effects in an experimental mouse model, showing nitrate-diet-induced muscle strength. This study contributes to a better understanding of the molecular changes in muscles following nutritional intervention and may help develop strategies and products designated to treat muscle-related issues.

The aim of this study was to find out the characteristics of cardiovascular changes when performing Bosco repeated jumps anaerobic test depending on the duration of jumping in a nonathletes cohort.

Background and Objectives: Controlled breathing can influence autonomic regulation and haemodynamics; however, the role of its timing relative to exercise remains unclear. Materials and Methods: Fourteen healthy, physically active men (mean age 21.8 ± 0.7 years; body mass index within the normal range) participated in this randomised crossover study. Each session consisted of five 5 min cycling bouts at 50% of heart-rate reserve, interspersed with 3 min passive recovery periods. The three conditions were: control (no structured breathing), 30 s hyperventilation (approximately 30 breaths·min⁻¹) performed before each bout, and the same hyperventilation performed after each bout. Resting heart rate variability spectra (low-frequency [LF], high-frequency [HF]) were assessed pre- and post-session; arterial blood pressure was measured stage-wise; quadriceps muscle oxygen saturation (StO₂) was monitored using near-infrared spectroscopy; and a discriminant co-integration index (Dsk) was calculated to integrate multisystem responses. Results: Compared with baseline, LF power increased and HF power decreased after exercise in the control and post-exercise hyperventilation conditions (p < 0.05), whereas pre-exercise hyperventilation attenuated these shifts. Post-exercise hyperventilation blunted the rise in systolic blood pressure and reduced diastolic blood pressure compared with control (p < 0.05). Both breathing interventions accelerated StO₂ recovery, with higher early recovery StO₂ following pre-exercise hyperventilation and sustained advantages after post-exercise hyperventilation (moderate-to-extensive effects). Dsk values were consistently highest after exercise, indicating stronger and more coherent multisystem coupling. Conclusions: In this acute crossover study of healthy young men, hyperventilation performed before or after exercise induced distinct short-term cardiovascular and muscular responses, reflecting respiratory-driven modulation of haemodynamic and autonomic processes. The timing of hyperventilation influenced these responses, suggesting that deliberate hyperventilation may acutely modify exercise-related regulatory mechanisms.