RESUMO
The aim of the present study was to analyze the effects of traffic-related air pollution (TRAP) on markers of inflammatory, neuroplasticity, and endurance performance-related parameters in recreationally trained cyclists who were adapted to TRAP during a 50-km cycling time trial (50-km cycling TT). Ten male cyclists performed a 50-km cycling TT inside an environmental chamber located in downtown Sao Paulo (Brazil), under TRAP or filtered air conditions. Blood samples were obtained before and after the 50-km cycling TT to measure markers of inflammatory [interleukin-6 (IL-6), C-reactive protein (CRP), interleukin-10 (IL-10), intercellular adhesion molecule-1 (ICAM-1)] and neuroplasticity [brain-derived neurotrophic factor (BDNF)]. Rating of perceived exertion (RPE), heart rate (HR), and power output (PO) were measured throughout the 50-km cycling TT. There were no significant differences between experimental conditions for responses of IL-6, CRP, and IL-10 (P > 0.05). When compared with exercise-induced changes in filtered air condition, TRAP provoked greater exercise-induced increase in BDNF levels (TRAP = 3.3 ± 2.4-fold change; Filtered = 1.3 ± 0.5-fold change; P = 0.04) and lower exercise-induced increase in ICAM-1 (Filtered = 1.1 ± 0.1-fold change; TRAP = 1.0 ± 0.1-fold change; P = 0.01). The endurance performance-related parameters (RPE, HR, PO, and time to complete the 50-km cycling TT) were not different between TRAP and filtered air conditions (P > 0.05). These findings suggest that the potential negative impacts of exposure to pollution on inflammatory, neuroplasticity, and performance-related parameters do not occur in recreationally trained cyclists who are adapted to TRAP.
Assuntos
Poluição do Ar , Desempenho Atlético , Ciclismo , Resistência Física , Poluição do Ar/efeitos adversos , Desempenho Atlético/fisiologia , Ciclismo/fisiologia , Fator Neurotrófico Derivado do Encéfalo , Brasil , Humanos , Inflamação , Molécula 1 de Adesão Intercelular , Interleucina-10 , Interleucina-6 , MasculinoRESUMO
High-intensity interval exercise (HIIE) is an effective non-pharmacological tool for improving physiological responses related to health. When HIIE is performed in urban centers, however, the exerciser is exposed to traffic-related air pollution (TRAP), which is associated with metabolic, anti-inflammatory imbalance and cardiovascular diseases. This paradoxical combination has the potential for conflicting health effects. Thus, the aim of this study was to determine the effects of HIIE performed in TRAP exposure on serum cytokines, non-target metabolomics and cardiovascular parameters. Fifteen participants performed HIIE in a chamber capable to deliver filtered air (FA condition) or non-filtered air (TRAP condition) from a polluted site adjacent to the exposure chamber. Non-target blood serum metabolomics, blood serum cytokines and blood pressure analyses were collected in both FA and TRAP conditions at baseline, 10 min after exercise, and 1 h after exercise. The TRAP increased IL-6 concentration by 1.7 times 1 h after exercise (p < 0.01) and did not change the anti-inflammatory balance (IL-10/TNF-α ratio). In contrast, FA led to an increase in IL-10 and IL-10/TNF-α ratio (p < 0.01), by 2.1 and 2.3 times, respectively. The enrichment analysis showed incomplete fatty acid metabolism under the TRAP condition (p < 0.05) 10 min after exercise. There was also an overactivity of ketone body metabolism (p < 0.05) at 10 min and at 1 h after exercise with TRAP. Exercise-induced acute decrease in systolic blood pressure (SBP) was not observed at 10 min and impaired at 1 h after exercise (p < 0.05). These findings reveal that TRAP potentially attenuates health benefits often related to HIIE. For instance, the anti-inflammatory balance was impaired, accompanied by accumulation of metabolites related to energy supply and reduction to exercise-induced decrease in SBP.
Assuntos
Poluição do Ar , Poluição Relacionada com o Tráfego , Poluição do Ar/análise , Anti-Inflamatórios , Exercício Físico , Humanos , MetabolomaRESUMO
The aim of this study was to develop predictive equations for minute ventilation based on heart rate, and to test the precision of the equations in two forms of endurance exercise. Eighteen men (age 27.8 ± 5.4 years old, maximal oxygen uptake 45.4 ± 8.3 ml·kg-1·min-1) performed a maximal progressive cycle test in which minute ventilation and heart rate were continually measured and further used to establish the proposed equations with quadratic and exponential adjustments. In the second and third laboratory visits, sixteen participants completed two cycling bouts, one high-intensity interval exercise and one low-intensity continuous exercise. The minute ventilation and heart rate were measured in both exercises and the validity of the equations tested. The Bland-Altman analysis showed agreement between the minute ventilation and estimated equations for interval and continuous exercise. There was no difference between the minute ventilation obtained from both equations and the minute ventilation directly measured during the interval exercise. However, the quadratic equation underestimated the minute ventilation during continuous exercise (p < 0.05). While both equations seem to be suitable to estimate minute ventilation during high-intensity interval exercise, the exponential equation is recommended for low-intensity continuous exercise.
Assuntos
Exercício Físico/fisiologia , Frequência Cardíaca/fisiologia , Testes de Função Respiratória/métodos , Adulto , Humanos , Masculino , Modelos Teóricos , Respiração , Medicina Esportiva , Adulto JovemRESUMO
Endothelial nitric oxide synthase (eNOS) is a vascular enzyme that produces nitric oxide, a transient signaling molecule that by vasodilatation regulates blood flow and pressure. Nitric oxide is believed to play roles in both short-term acclimatization and long-term evolutionary adaptation to environmental hypoxia. Several laboratories, including ours, have shown that variants in NOS3 (the gene encoding eNOS) are overrepresented in individuals with altitude-related illnesses such as high altitude pulmonary edema (HAPE) and acute mountain sickness (AMS), suggesting that NOS3 genotypes contribute to altitude tolerance. To further test our hypothesis that the G allele at the G894T polymorphism in NOS3 (dbSNP number: rs1799983; protein polymorphism Glu298Asp) is beneficial in hypoxic environments, we compared frequencies of this allele in an altitude-adapted Amerindian population, Quechua of the Andean altiplano, with those in a lowland Amerindian population, Maya of the Yucatan Peninsula. While common in both populations, the G allele was significantly more frequent in the highlanders. Taken together, our data suggest that this variant in NOS3, which has been previously associated with higher levels of nitric oxide, contributes to both acclimatization and adaptation to altitude.