The oxi-inflammatory response is part of the natural process mobilizing leukocytes and satellite cells that contribute to clearance and regeneration of damaged muscle tissue. In sports medicine, a number of post-injury recovery strategies, such as whole-body cryotherapy (WBC), are used to improve skeletal muscle regeneration often without scientific evidence of their benefits. The study was designed to assess the impact of WBC on circulating mediators of skeletal muscle regeneration. Twenty elite athletes were randomized to WBC group (3-min exposure to −120 °C, twice a day for 7 days) and control group. Blood samples were collected before the first WBC session and 1 day after the last cryotherapy exposure. WBC did not affect the indirect markers of muscle damage but significantly reduced the generation of reactive oxygen and nitrogen species (H2O2 and NO) as well as the concentrations of serum interleukin 1β (IL-1β) and C-reactive protein (CRP). The changes in circulating growth factors, hepatocyte growth factor (HGF), insulin-like growth factor (IGF-1), platelet-derived growth factor (PDGFBB), vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor (BDNF), were also reduced by WBC exposure. The study demonstrated that WBC attenuates the cascade of injury–repair–regeneration of skeletal muscles whereby it may delay skeletal muscle regeneration.

Intermittent exposure to hypoxia (IHE) increases the production of reactive oxygen and nitrogen species as well as erythropoietin (EPO), which stimulates the adaptation to intense physical activity. However, several studies suggest a protective effect of moderate hypoxia in cardiovascular disease (CVD) events. The effects of intense physical activity with IHE on oxi-inflammatory mediators and their interaction with conventional CVD risk factors were investigated. Blood samples were collected from elite athletes (control n=6, IHE n=6) during a 6-day IHE cycle using hypoxicator GO2 altitude. IHE was held once a day, at least 2 hours after training. In serum, hydrogen peroxide (H2O2), nitric oxide (NO), 3-nitrotyrosine (3-Nitro), proinflammatory cytokines (IL-1β and TNFα), high sensitivity C-reactive protein (hsCRP), and heat shock protein 27 (HSP27) were determined by the commercial immunoenzyme (ELISA kits) or colorimetric methods. Serum erythropoietin (EPO) level was measured by ELISA kit every day of hypoxia. IHE was found to significantly increase H2O2, NO, and HSP27 but to decrease 3NT concentrations. The changes in 3NT and HSP27 following hypoxia proved to enhance NO bioavailability and endothelial function. In the present study, the oxi-inflammatory mediators IL-1β and hsCRP increased in IHE group but they did not exceed the reference values. The serum EPO level increased on the 3rd day of IHE, then decreased on 5th day of IHE, and correlated with NO/H2O2 ratio (rs=0.640, P<0.05). There were no changes in haematological markers contrary to lipoproteins such as low-density lipoprotein (LDL) and non-high-density lipoprotein (non-HDL) which showed a decreasing trend in response to hypoxic exposure. The study demonstrated that IHE combined with sports activity reduced a risk of endothelial dysfunction and atherogenesis in athletes even though the oxi-inflammatory processes were enhanced. Therefore, 6-day IHE seems to be a potential therapeutic and nonpharmacological method to reduce CVD risk, especially in elite athletes participating in strenuous training.

One of the latest theories on ageing focuses on immune response, and considers the activation of subclinical and chronic inflammation. The study was designed to explain whether anti-inflammatory diet and lifestyle exercise affect an inflammatory profile in the Polish elderly population. Sixty individuals (80.2 ± 7.9 years) were allocated to a low-grade inflammation (LGI n = 33) or high-grade inflammation (HGI n = 27) group, based on C-reactive protein concentration (<3 or ≥3 mg/L) as a conventional marker of systemic inflammation. Diet analysis focused on vitamins D, C, E, A, β-carotene, n-3 and n-6 PUFA using single 24-h dietary recall. LGI demonstrated a lower n-6/n-3 PUFA but higher vitamin D intake than HGI. Physical performance based on 6-min walk test (6MWT) classified the elderly as physically inactive, whereby LGI demonstrated a significantly higher gait speed (1.09 ± 0.26 m/s) than HGI (0.72 ± 0.28 m/s). Circulating interleukins IL-1β, IL-6, IL-13, TNFα and cfDNA demonstrated high concentrations in the elderly with low 6MWT, confirming an impairment of physical performance by persistent systemic inflammation. These findings reveal that increased intake of anti-inflammatory diet ingredients and physical activity sustained throughout life attenuate progression of inflammaging in the elderly and indicate potential therapeutic strategies to counteract pathophysiological effects of ageing.

Intermittent exposure to hypoxia (IHE) increases production of reactive oxygen and nitrogen species which, as signalling molecules, participate in tissue injury–repair–regeneration cascade. The process is also stimulated by arginine whose bioavailability is a limiting factor for NO synthesis. The effects of IHE in combination with arginine (Arg) intake on myogenesis and angiogenesis mediators were examined in a randomized and placebo-controlled trial. Blood samples were collected from 38 elite athletes on the 1st, 7th and 14th days during the training camp. The oral doses of arginine (2 × 6 g/day) and/or IHE using hypoxicator GO2Altitude (IHE and Arg/IHE) were applied. Serum NO and H2O2 concentrations increased significantly and were related to muscle damage (CK activity >900 IU/mL) in IHE and Arg/IHE compared to placebo. The changes in NO and H2O2 elevated the levels of circulating growth factors such as HGF, IHG-1, PDGFBB, BDNF, VEGF and EPO. Modification of the lipid profile, especially reduced non-HDL, was an additional beneficial effect of hypoxic exposure with arginine intake. Intermittent hypoxic exposure combined with high-dose arginine intake was demonstrated to affect circulating mediators of injury–repair–regeneration. Therefore, a combination of IHE and arginine seems to be a potential therapeutic and non-pharmacological method to modulate the myogenesis and angiogenesis in elite athletes.

Exposure to intense physical exercise increases reactive oxygen and nitrogen species production. The process can be modulated by dipeptide bioavailability with antioxidant scavenger properties. The effects of dipeptide intake in combination with physical exercise on the oxi-antioxidant response were examined in a randomized and placebo-controlled trial. Blood samples were collected from 20 males aged 21.2 ± 1.8 years before and after 14-day intake of chicken breast extract (4 g/day), which is a good source of bioactive dipeptides. A significant increase in the NO/H2O2 ratio was observed in the 1st and 30th minute after intense incremental exercise in dipeptides compared to the placebo group. Total antioxidant and thiol redox status were significantly higher in the dipeptide group both before and after exercise; η2 ≥ 0.64 showed a large effect of dipeptides on antioxidant and glutathione status. The level of 8-isoprostanes, markers of oxidative damage, did not change under the influence of dipeptides. By contrast, reduced C-reactive protein levels were found during the post-exercise period in the dipeptide group, which indicates the anti-inflammatory properties of dipeptides. High pre-exercise dipeptide intake enhances antioxidant status and thus reduces the oxi-inflammatory response to intense exercise. Therefore, the application of dipeptides seems to have favourable potential for modulating oxidative stress and inflammation in physically active individuals following a strenuous exercise schedule.

The immunosenescence-related disproportion in T lymphocytes may have important consequences for endothelial dysfunction, which is a key event in vascular aging. The study was designed to assess the prognostic values of the inflammatory-immune profile to better predict and prevent vascular diseases associated with old age. Eighty individuals aged 70.9 ± 5.3 years were allocated to a low- (LGI) or high-grade inflammation (HGI) group based on CRP (< 3 or ≥ 3 mg/L) as a conventional risk marker of cardiovascular diseases. Significant changes in inflammatory and endothelium-specific variables IL-1β, IL-6, TNFα, oxLDL, H2O2, NO, 3-nitrotyrosine, and endothelial progenitor cells (OR 7.61, 95% CI 2.56–29.05, p < 0.0001), confirmed their interplay in vascular inflammation. The flow-cytometry analysis demonstrated a high disproportion in T lymphocytes CD4+ and CD8+ between LGI and HGI groups. CRP was < 3 mg/mL for the CD4/CD8 ratio within the reference values ≥ 1 or ≤ 2.5, unlike for the CD4/CD8 ratio < 1 and > 2.5. The odds ratios for the distribution of CD4+ (OR 5.98, 95% CI 0.001–0.008, p < 0.001), CD8+ (OR 0.23, 95% CI 0.08–0.59, p < 0.01), and CD8CD45RO+ T naïve cells (OR 0.27, 95% CI 0.097–0.695, p < 0.01) and CD4/CD8 (OR 5.69, 95% CI 2.07–17.32, p < 0.001) indicated a potential diagnostic value of T lymphocytes for clinical prognosis in aging-related vascular dysfunction.

Aging-related anemia contributes to frailty syndrome, cognitive decline and early mortality. The study aim was to evaluate inflammaging in relation to anemia as a prognostic indicator in affected older patients. The participants (73.0 ± 7.2 years) were allocated into anemic (n = 47) and non-anemic (n = 66) groups. The hematological variables RBC, MCV, MCH, RDW, iron and ferritin were significantly lower, whereas erythropoietin EPO and transferrin Tf tended toward higher values in the anemic group. Approx. 26% of individuals demonstrated transferrin saturation TfS < 20%, which clearly indicates age-related iron deficiency. The cut-off values for pro-inflammatory cytokine IL-1β, TNFα and hepcidin were 5.3 ng/mL, 97.7 ng/mL and 9.4 ng/mL, respectively. High IL-1β negatively affected Hb concentration (rs = −0.581, p < 0.0001). Relatively high odds ratios were observed for IL-1β (OR = 72.374, 95%Cl 19.688–354.366) and peripheral blood mononuclear cells CD34 (OR = 3.264, 95%Cl 1.263–8.747) and CD38 (OR = 4.398, 95%Cl 1.701–11.906), which together indicates a higher probability of developing anemia. The results endorse the interplay between inflammatory status and iron metabolism and demonstrated a high usefulness of IL-1β in identification of the underlying causes of anemia, while CD34 and CD38 appeared useful in compensatory response assessment and, in the longer term, as part of a comprehensive approach to anemia monitoring in older adults.