Alzheimer’s disease (AD) is a progressive degenerative disorder and a leading cause of dementia in the elderly. The etiology of AD is multifactorial, including an increased oxidative state, deposition of amyloid plaques, and neurofibrillary tangles of the tau protein. The formation of amyloid plaques is considered one of the first signs of the illness, but only in the central nervous system (CNS). Interestingly, results indicate that AD is not just localized in the brain but is also found in organs distant from the brain, such as the cardiovascular system, gut microbiome, liver, testes, and kidney. These observations make AD a complex systemic disorder. Still, no effective medications have been found, but regular physical activity has been considered to have a positive impact on this challenging disease. While several articles have been published on the benefits of physical activity on AD development in the CNS, its peripheral effects have not been discussed in detail. The provocative question arising is the following: is it possible that the beneficial effects of regular exercise on AD are due to the systemic impact of training, rather than just the effects of exercise on the brain? If so, does this mean that the level of fitness of these peripheral organs can directly or indirectly influence the incidence or progress of AD? Therefore, the present paper aims to summarize the systemic effects of both regular exercise and AD and point out how common exercise-induced adaptation via peripheral organs can decrease the incidence of AD or attenuate the progress of AD.

Despite the intensive investigation of the molecular mechanism of skeletal muscle hypertrophy, the underlying signaling processes are not completely understood. Therefore, we used an overload model, in which the main synergist muscles (gastrocnemius, soleus) of the plantaris muscle were surgically removed, to cause a significant overload in the remaining plantaris muscle of 8-month-old Wistar male rats. SIRT1-associated pro-anabolic, pro-catabolic molecular signaling pathways, NAD and H₂S levels of this overload-induced hypertrophy were studied. Fourteen days of overload resulted in a significant 43% (p < 0.01) increase in the mass of plantaris muscle compared to sham operated animals. Cystathionine-β-synthase (CBS) activities and bioavailable H₂S levels were not modified by overload. On the other hand, overload-induced hypertrophy of skeletal muscle was associated with increased SIRT1 (p < 0.01), Akt (p < 0.01), mTOR, S6 (p < 0.01) and suppressed sestrin 2 levels (p < 0.01), which are mostly responsible for anabolic signaling. Decreased FOXO1 and SIRT3 signaling (p < 0.01) suggest downregulation of protein breakdown and mitophagy. Decreased levels of NAD⁺, sestrin2, OGG1 (p < 0.01) indicate that the redox milieu of skeletal muscle after 14 days of overloading is reduced. The present investigation revealed novel cellular interactions that regulate anabolic and catabolic processes in the hypertrophy of skeletal muscle.

Regular exercise can upgrade the efficiency of the immune system and beneficially alter the composition of the gastro-intestinal microbiome. We tested the hypothesis that active athletes have a more diverse microbiome than sedentary subjects, which could provide better protection against COVID-19 during infection. Twenty active competing athletes (CA) (16 male and 4 females of the national first and second leagues), aged 24.15 ± 4.7 years, and 20 sedentary subjects (SED) (15 male and 5 females), aged 27.75 ± 7.5 years, who had been diagnosed as positive for COVID-19 by a PCR test, served as subjects for the study. Fecal samples collected five to eight days after diagnosis and three weeks after a negative COVID-19 PCR test were used for microbiome analysis. Except for two individuals, all subjects reported very mild and/or mild symptoms of COVID-19 and stayed at home under quarantine. Significant differences were not found in the bacterial flora of trained and untrained subjects. On the other hand, during COVID-19 infection, at the phylum level, the relative abundance of Bacteroidetes was elevated during COVID-19 compared to the level measured three weeks after a negative PCR test (p < 0.05) when all subjects were included in the statistical analysis. Since it is known that Bacteroidetes can suppress toll-like receptor 4 and ACE2-dependent signaling, thus enhancing resistance against pro-inflammatory cytokines, it is suggested that Bacteroidetes provide protection against severe COVID-19 infection. There is no difference in the microbiome bacterial flora of trained and untrained subjects during and after a mild level of COVID-19 infection.

Laboratory-based assessment of cardiorespiratory function is a widely applied method in sports science. Most performance evaluations focus on oxygen uptake parameters. Despite the well-established concept of oxygen deficit introduced by Hill in the 1920s, relatively few studies have examined its behavior during submaximal exercise, with limited exploration of deficit dynamics. The present study aimed to analyze the behavior of oxygen deficit in young female handball players (N = 42, age: 15.4 ± 1.3 years) during graded exercise. Oxygen deficit was estimated using the American College of Sports Medicine (ACSM) algorithm, restricted to subanaerobic threshold segments of a quasi-ramp exercise protocol. Cardiorespiratory parameters were measured with the spiroergometry test on treadmills, and body composition was assessed via Dual Energy X-ray Absorptiometry (DEXA). Cluster and principal component analyzes revealed two distinct athlete profiles with statistically significant differences in both morphological and physiological traits. Cluster 2 showed significantly higher relative VO₂ peak (51.43 ± 3.70 vs. 45.70 ± 2.87 mL·kg⁻¹·min⁻¹; p < 0.001; Cohen’s d = 1.76), yet also exhibited a greater oxygen deficit per kilogram (39.03 ± 16.71 vs. 32.56 ± 14.33 mL·kg⁻¹; p = 0.018; d = 0.80). Cluster 1 had higher absolute body mass (69.67 ± 8.13 vs. 59.66 ± 6.81 kg; p < 0.001), skeletal muscle mass (p < 0.001), and fat mass (p < 0.001), indicating that body composition strongly influenced oxygen deficit values. The observed differences in oxygen deficit profiles suggest a strong influence of genetic predispositions, particularly in cardiovascular and muscular oxygen utilization capacity. Age also emerged as a critical factor in determining the potential for adaptation. Oxygen deficit during submaximal exercise appears to be a multifactorial phenomenon shaped by structural and physiological traits. While certain influencing factors can be modified through training, others especially those of genetic origin pose inherent limitations. Early development of cardiorespiratory capacity may offer the most effective strategy for long-term optimization.