Influence of chronic exercise on carotid atherosclerosis in marathon runners.
Ontology highlight
ABSTRACT: Objectives
The effect of habitual, high-intensity exercise training on the progression of atherosclerosis is unclear. We assessed indices of vascular health (central systolic blood pressure (SBP) and arterial stiffness as well as carotid intima-medial thickness (cIMT)) in addition to cardiovascular risk factors of trained runners versus their untrained spouses or partners to evaluate the impact of exercise on the development of carotid atherosclerosis.Setting
field study at Boston Marathon.Participants
42 qualifiers (mean age±SD: 46±13 years, 21 women) for the 2012 Boston Marathon and their sedentary domestic controls (46±12 years, n=21 women).Outcomes
We measured medical and running history, vital signs, anthropometrics, blood lipids, C reactive protein (CRP), 10 years Framingham risk, central arterial stiffness and SBP and cIMT.Results
Multiple cardiovascular risk factors, including CRP, non-high-density lipoprotein cholesterol, triglycerides, heart rate, body weight and body mass index (all p<0.05), were reduced in the runners. The left and right cIMT, as well as central SBP, were not different between the two groups (all p>0.31) and were associated with age (all r≥0.41; p<0.01) and Framingham risk score (all r≥0.44; p<0.01) independent of exercise group (all p>0.08 for interactions). The amplification of the central pressure waveform (augmentation pressure at heart rate 75 bpm) was also not different between the two groups (p=0.07) but was related to age (p<0.01) and group (p=0.02) in a multiple linear regression model.Conclusions
Habitual endurance exercise improves the cardiovascular risk profile, but does not reduce the magnitude of carotid atherosclerosis associated with age and cardiovascular risk factors.
SUBMITTER: Taylor BA
PROVIDER: S-EPMC3927935 | biostudies-literature |
REPOSITORIES: biostudies-literature
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| S-EPMC7488354 | biostudies-literature
Project description:A common single nucleotide polymorphism in the ACTN3 gene might result in the complete deficiency of α-actinin-3 (i.e., XX genotype). It has been found that ACTN3 XX individuals have several traits related to lessened muscle performance. This study aimed to determine the influence, if any, of ACTN3 genotypes on injury incidence of marathoners during the year preceding to participating in a competitive marathon race. Using a cross-sectional experimental design, the type and conditions of sports injuries were documented for one year in a group of 139 marathoners. Injuries were recorded following a consensus statement on injuries in Athletics. Afterward, ACTN3 genotyping was performed, and injury epidemiology was compared among RR, RX, and XX genotypes. The distribution of the RR/RX/XX genotypes was 28.8/42.8/23.5%, respectively. A total of 67 injuries were recorded. The frequency of marathoners that reported any injury during the previous year was not different across the genotypes (55.0/38.8/40.6%, P = 0.241). Although the overall injury incidence was not different among genotypes (2.78/1.65/1.94 injuries/1000 h of running, P = 0.084), the likelihood of suffering an injury was higher in RR than in RX (OR = 1.93: 95%CI = 0.87-4.30), and higher than in XX (OR = 1.79: 0.70-4.58). There was no difference in the conditions, severity, body location, time of year, or leading cause of injury among genotypes. However, XX presented a higher frequency of sudden-onset injuries (P = 0.024), and the OR for muscle-type injuries was 2.0 (0.51-7.79) times higher compared to RR runners. Although XX marathoners did not have a higher overall incidence of injury, the OR in these runners for muscle-type injuries was superior to RR and RX runners. The likelihood of suffering a muscle injury, especially with a sudden-onset, was twice in XX than in RR endurance runners.
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Project description:PurposeHeat stress exacerbates post-exercise hypotension (PEH) and cardiovascular disturbances from elevated body temperature may contribute to exertion-related incapacity. Mast cell degranulation and muscle mass are possible modifiers, though these hypotheses lack practical evidence. This study had three aims: (1) to characterise pre-post-responses in histamine and mast cell tryptase (MCT), (2) to investigate relationships between whole body muscle mass (WBMM) and changes in blood pressure post-marathon, (3) to identify any differences in incapacitated runners.Methods24 recreational runners were recruited and successfully completed the 2019 Brighton Marathon (COMPLETION). WBMM was measured at baseline. A further eight participants were recruited from incapacitated runners (COLLAPSE). Histamine, MCT, blood pressure, heart rate, body temperature and echocardiographic measures were taken before and after exercise (COMPLETION) and upon incapacitation (COLLAPSE).ResultsIn completion, MCT increased by nearly 50% from baseline (p = 0.0049), whereas histamine and body temperature did not vary (p > 0.946). Systolic (SBP), diastolic (DBP) and mean (MAP) arterial blood pressures and systemic vascular resistance (SVR) declined (p < 0.019). WBMM negatively correlated with Δ SBP (r = - 0.43, p = 0.046). For collapse versus completion, there were significant elevations in MCT (1.77 ± 0.25 μg/L vs 1.18 ± 0.43 μg/L, p = 0.001) and body temperature (39.8 ± 1.3 °C vs 36.2 ± 0.8 °C, p < 0.0001) with a non-significant rise in histamine (9.6 ± 17.9 μg/L vs 13.7 ± 33.9 μg/L, p = 0.107) and significantly lower MAP, DBP and SVR (p < 0.033).ConclusionThese data support the hypothesis that mast cell degranulation is a vasodilatory mechanism underlying PEH and exercise associated collapse. The magnitude of PEH is inversely proportional to the muscle mass and enhanced by concomitant body heating.
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Project description:An ultra-marathon trail (UMT) represents a significant physical and psychological effort. However, little is known about the gene expression response to an UMT although this approach has been explored in shorter races. The objective is to identify the affected pathways in response to an 82km UMT considering a genome-wide analysis. Such response is interpreted as a global effect and as a sum of independent sources identified through an Independent Component Analysis.
2017-06-19 | GSE93945 | GEO
Project description:BackgroundRecreational marathon runners face strong physiological challenges. Assessment of potential biomarkers for the biological responses of runners will help to discriminate individual race responsiveness and their physiological consequences. This study sought to analyze the changes in the plasma levels of GDF15 and FGF21, novel endocrine factors related to metabolic stress, in runners following the strenuous exercise of a marathon race.MethodsBlood samples were obtained from eighteen male runners (mean ±SD, age: 41.7 ±5.0 years, BMI: 23.6 ± 1.8) 48 h before, immediately after, and 48 h after a marathon race, and from age-matched sedentary individuals. The level of GDF15, FGF21, and 38 additional biochemical and hematological parameters were determined.ResultsThe basal levels of GDF15 and FGF21 did not differ between runners before the race and sedentary individuals. Significant increases in the mean levels of GDF15 (4.2-fold) and FGF21 (20-fold) were found in runners immediately after the race. The magnitudes of these increases differed markedly among individuals and did not correlate with each other. The GDF15 and FGF21 levels had returned to the basal level 48 h post-race. The post-race value of GDF15 (but not FGF21) correlated positively with increased total white cell count (r = 0.50, P = 0.01) and neutrophilia (r = 0.10, P = 0.01).ConclusionGDF15 and FGF21 are transiently increased in runners following a marathon race. The induction of GDF15 levels is associated with alterations in circulating immune cells levels.
| S-EPMC7711067 | biostudies-literature
Project description:Among several serious medical conditions, arrhythmia and heat stroke are two important causes of death during endurance races. Clinically, collapsing might be the first sign of these serious conditions and may mimic the more common and benign exercise-associated collapse. Several risk factors have been reported in the literature. We aimed to conduct a qualitative study to find a perceived risk profile among runners who collapsed and who were transported by ambulances to the nearest hospital during Gothenburg's half marathon (2010-2017). Collapsing runners seem to lack the ability to make a decision to withdraw from the contest despite being exhausted. They feel the pain, but are unable to put meaning to their feeling, to adjust their pacing, and to handle other influences. Consequently, they do not overcome the problem or assess the situation. These individual mental characteristics may indicate a unique profile for collapsing runners. Pre-race health control and educational initiatives aiming at mental preparedness and information before endurance races might be a necessary step to avoid life-threatening complications.
| S-EPMC7022577 | biostudies-literature
Project description:BACKGROUND:Investigation into strenuous activity and kidney function has gained interest given increasing marathon participation. STUDY DESIGN:Prospective observational study. SETTING & PARTICIPANTS:Runners participating in the 2015 Hartford Marathon. PREDICTOR:Completing a marathon. OUTCOMES:Acute kidney injury (AKI) as defined by AKI Network (AKIN) criteria. Stage 1 AKI was defined as 1.5- to 2-fold or 0.3-mg/dL increase in serum creatinine level within 48 hours of day 0 and stage 2 was defined as a more than 2- to 3-fold increase in creatinine level. Microscopy score was defined by the number of granular casts and renal tubular epithelial cells. MEASUREMENTS:Samples were collected 24 hours premarathon (day 0), immediately postmarathon (day 1), and 24 hours postmarathon (day 2). Measurements of serum creatinine, creatine kinase, and urine albumin were completed, as well as urine microscopy analysis. 6 injury urine biomarkers (IL-6, IL-8, IL-18, kidney injury molecule 1, neutrophil gelatinase-associated lipocalin, and tumor necrosis factor ?) and 2 repair urine biomarkers (YKL-40 and monocyte chemoattractant protein 1) were measured. RESULTS:22 marathon runners were included. Mean age was 44 years and 41% were men. 82% of runners developed an increase in creatinine level equivalent to AKIN-defined AKI stages 1 and 2. 73% had microscopy diagnoses of tubular injury. Serum creatinine, urine albumin, and injury and repair biomarker levels peaked on day 1 and were significantly elevated compared to day 0 and day 2. Serum creatine kinase levels continued to significantly increase from day 0 to day 2. LIMITATIONS:Small sample size and limited clinical data available at all time points. CONCLUSIONS:Marathon runners developed AKI and urine sediment diagnostic of tubular injury. An increase in injury and repair biomarker levels suggests structural damage to renal tubules occurring after marathon. The results of our study should be validated in larger cohorts with longer follow-up of kidney function.
| S-EPMC5526736 | biostudies-literature