Benefits of Aspirin
Exercise Induced Stress
Exercise and Effect on Thyroid Hormone
Ray Peat, PhD and Concentric Exercise
Ray Peat, PhD: Quotes Relating to Exercise
Lactate Paradox: High Altitude and Exercise
Carbohydrate Lowers Exercise Induced Stress
Exercise Induced Menstrual Disorders
Synergistic Effect of Creatine and Baking Soda on Performance
Protective Carbon Dioxide, Exercise, and Performance
Eur J Appl Physiol. 2003 Apr;89(2):177-83. Epub 2003 Feb 1.
The influence of aspirin on exercise-induced changes in adrenocorticotrophic hormone (ACTH), cortisol and aldosterone (ALD) concentrations.
Przybyłowski J, Obodyński K, Lewicki C, Kuźniar J, Zaborniak S, Drozd S, Czarny W, Garmulewicz M.
The influence of aspirin (ASA) on the endocrinology system and prostaglandin (PGs) synthesis is not completely clear. The aim of the study was to estimate the influence of ASA on the changes in the concentration of ACTH, cortisol and aldosterone (ALD) induced by physical exercise. This study was conducted on 19 healthy students (age 21-23 years). They were subjected to intensive physical exercise on a cycle ergometer. On the day prior to the experiment, 12 subjects took two 0.5-g doses of ASA in a wafer, and another 0.5 g 3-4 h before the test on the day of the investigation (ASA group). The remaining seven subjects (control group) received placebo. Hematocrit, lactate concentration and concentrations of ACTH, cortisol and ALD were determined before exercise, after exercise, and after 30 min of recovery, in a blood sample taken from a cubital vein. Before exercise, the degree of platelet aggregation in response to arachidonic acid was estimated, in order to confirm the correct allocation to the two groups. Aggregation should only occur in the ASA group. ASA and control groups exercised for 30.3 (3.1) min and 30.2 (1.6) min, respectively. Maximal heart rate and lactate concentration were similar in both groups, as were the basal concentrations of ACTH and cortisol; the ALD concentration seemed lower in the ASA group, but the difference was not significant (p<0.1). In both groups after exercise ACTH, cortisol and ALD concentrations were significantly increased, however when compared to the control group, the increase of ACTH in the ASA group was significantly higher, and ALD increase significantly lower. After recovery there was a significant decrease in ACTH concentration, whereas the concentrations of ALD and cortisol did not change. The concentrations of cortisol in both groups after exercise and recovery were similar. That is most likely because the ACTH concentrations in the ASA and control groups were sufficient for almost maximal cortisol secretion. It is proposed that ASA administration caused prostaglandin synthesis to decrease, and that this led to a lower basal concentration of ALD and a significantly lower level of ALD after exercise.
Int J Sports Med. 2007 Oct;28(10):809-14. Epub 2007 May 11.
Do non-steroidal anti-inflammatory drugs influence the steroid hormone milieu in male athletes?
Di Luigi L, Rossi C, Sgrò P, Fierro V, Romanelli F, Baldari C, Guidetti L.
Prostaglandins modulate the hypothalamus-pituitary-adrenal and -gonadal axis pathways. We explored the effects of a single course of treatment with acetylsalicylic acid (ASA), an inhibitor of prostaglandin synthesis, on the steroid milieu in athletes. Morning plasma cortisol (F), dehydroepiandrosterone sulphate, free-testosterone, testosterone (T) and their ratios were evaluated before and after the administration of either ASA or placebo in twelve male athletes, when affected by minor musculoskeletal trauma and, as control, after a five/six week wash-out in healthy conditions respectively. One tablet of ASA (800 mg), or placebo, was administered two times daily for 10 days during treatment. All the volunteers suspended exercise training during treatment. The results revealed that compared to placebo, plasma F was significantly lower after ASA treatment (p = 0.023). Furthermore, the comparison of hormone’s absolute and percentage of variations (Delta and Delta%) between ASA and placebo treatment showed significant differences respectively for DeltaF (p = 0.045), for DeltaT (p = 0.047), for DeltaT/F (p = 0.042), for DeltaF% (p = 0.04) and for DeltaT% (p = 0.049). Our data suggest that in comparison to placebo, a short-term ASA treatment is able to influence the plasma steroid milieu in athletes. Due to the observed variability of the individual hormonal patterns, further research is required to substantiate these findings.
Med Sci Sports Exerc. 2001 Dec;33(12):2029-35.
Acetylsalicylic acid inhibits the pituitary response to exercise-related stress in humans.
Di Luigi L, Guidetti L, Romanelli F, Baldari C, Conte D.
PURPOSE: Prostaglandins (PGs) modulate the activity of the hypothalamus-pituitary axis, and pituitary hormones are largely involved in the physiological responses to exercise. The purpose of this study was to analyze the effects of acetylsalicylic acid (ASA), an inhibitor of PGs synthesis, in the pituitary responses to physical stress in humans.
METHODS: Adrenocorticotropin (ACTH), beta-endorphin, cortisol, growth hormone (GH), and prolactin (PRL) responses to exercise were evaluated after administration of either placebo or ASA. Blood samples for hormone evaluations before (-30, -15, and 0 pre) and after (0 post, +15, +30, +45, +60, and +90 min) a 30-min treadmill exercise (75% of .VO(2max)) were taken from 12 male athletes during two exercise trials. One tablet of ASA (800 mg), or placebo, was administered two times daily for 3 d before and on the morning of each exercise-test.
RESULTS: The results clearly show that, compared with placebo, ASA ingestion significantly blunted the increased serum ACTH, beta-endorphin, cortisol, and GH levels before exercise (anticipatory response) and was associated with reduced cortisol concentrations after exercise. Furthermore, although no differences in the GH response to exercise were shown, a significantly reduced total PRL response to stress condition was observed after ASA.
CONCLUSION: ASA influences ACTH, beta-endorphin, cortisol, GH, and PRL responses to exercise-related stress in humans (preexercise activation/exercise-linked response). Even though it is not possible to exclude direct action for ASA, our data indirectly confirm a role of PGs in these responses. We have to further evaluate the nature of the preexercise endocrine activation and, because of the large use of anti-inflammatory drugs in athletes, whether the interaction between ASA and hormones might positively or negatively influence health status, performance, and/or recovery.
Respir Physiol Neurobiol. 2002 Apr;130(2):189-99.
The post-exercise oxidative stress is depressed by acetylsalicylic acid.
Steinberg J, Gainnier M, Michel F, Faucher M, Arnaud C, Jammes Y.
In order to assess whether oxidative stress occurs after fatiguing dynamic contractions of a small forearm muscle group, we estimated the kinetics of changes in some of its biomarkers (thiobarbituric acid reactive substances or TBARS; plasma reduced ascorbic acid or RAA; erythrocyte reduced glutathione or GSH). We also tested the hypothesis that acetylsalicylic acid (ASA) may compete with endogenous radical targets, attenuating the post-exercise oxidative stress. Seven male subjects successively performed a 3-min dynamic handgrip exercise with the dominant and then the contralateral forearm. Blood samples were taken from an antecubital vein in each exercising forearm. Biochemical analyses, including the concentration measurements of lactic acid, potassium, and oxidative stress markers were performed at rest and then during the 30-min period of recovery following each exercise. The same day, exercises were repeated after ingestion of a single dose (10 mg/kg) of ASA, and the same exercises were performed after a 3-day ASA treatment (30 mg/kg/day). In control condition, the changes in TBARS, RAA and GSH were already significant immediately after the end of the forearm exercise. They culminated after 5 min, and control values were recovered by a 30-min rest period. We verified that repeated bouts failed to alter the post-exercise variations. ASA did not modify the lactic acid production significantly, though the 3-day ASA treatment significantly reduced the efflux of potassium (-74%, P < 0.05), and the post-exercise variations of TBARS (-45%, P < 0.01), RAA (-44%, P < 0.01) and GSH (-48%, P < 0.01). These results suggest that the dynamic handgrip exercise is a good model for studying the post-exercise oxidative stress and also that ASA seems to offer an efficient protection against oxidative stress and the changes in membrane permeability to potassium.
Brazilian Journal of Biomotricity, v. 4, n. 3, p. 206-213, Aug 2010
Aspirin may be an effective treatment for exercise-induced muscle soreness.
Sahar Riasati, Mehrzad Moghadasi, Ahmad Torkfar, Rahim Shirazinejad ,Hamid Arvin
Delayed onset muscle soreness (DOMS) refers to the skeletal muscle pain that is experienced following eccentric exercise. The aim of the present study was to examine the effect of aspirin supplementation on DOMS after an eccentric exercise. Sixteen healthy female [age, 21.05 ± 3.7 years; body mass index (BMI), 24.03 ± 0.8 kg/m2; (mean ± SD)] participated as subjects in this study. The subjects were assigned to either an experimental (200 mg of aspirin; n=8) or a placebo group (Same dosage of lactose; n=8) using a double-blind research design. Knee range of motion (ROM), perceived pain, thigh circumference and serum activity of the enzyme creatine kinase (CK) were taken before, immediately, 24 and 48 hours after the eccentric exercise. No differences among groups were observed for thigh circumference and ROM before, immediately, 24 and 48 hours after the eccentric exercise. Serum CK levels and pain increased (P<0.05) in the both groups immediately after the eccentric exercise and increased to maximum at 48 hours after the eccentric exercise. The aspirin supplementation decreased (P<0.05) the serum CK levels and pain compare to the placebo group at 24 and 48 hours after the eccentric exercise. In conclusion, aspirin supplementation can be effective to minimize DOMS induced by eccentric exercise.
Eur J Heart Fail (2004) 6 (6)
The effect of aspirin on the ventilatory response to exercise in chronic heart failure
Klaus K.A. Witte and Andrew L. Clark
Introduction: Patients with chronic heart failure (CHF) experience breathlessness and fatigue on exercise. One of the abnormalities seen on maximal exercise testing is an increased ventilatory response to exercise (VE/VCO2 slope). The cause of this is unknown, but is likely to be due to a combination of interacting peripheral and central factors. Recent data have demonstrated a relation between VE/VCO2 slope and prostaglandin levels in contracting muscles. The present study examined the influence of the presence of a potent non-selective prostaglandin inhibitor, aspirin, on the ventilatory response to exercise in a group of patients with CHF.
Methods: We investigated the ventilatory response to exercise of 120 consecutive patients in sinus rhythm attending a specialist heart failure clinic. We excluded those taking clopidogrel (six patients) and those on both warfarin and aspirin or taking other non-steroidal anti-inflammatory agents (five patients). The other 109 patients were grouped according to whether they were taking aspirin (n=52 (48%)) or not (n=57 (52%)). Each patient underwent echocardiography to assess left ventricular function, and exercise testing with metabolic gas exchange to derive peak oxygen consumption (pVO2) and the VE/VCO2 slope.
Results: The groups were similar in terms of age, (67 (13) vs. 66 (12) years; P=0.34) drug use, heart failure aetiology, left ventricular function (ejection fraction; 33.3 (9.4) vs. 31.8 (9.9)%; P=0.05)) and exercise tolerance (pVO2; 20.4 (5.3) vs. 19.9 (6.0); P=0.68, and VE/VCO2 slope; 35.4 (6.2) vs. 35.7 (9.3); P=0.73). There was no difference in the ventilatory response to exercise or the symptoms of breathlessness between the two groups.
Conclusions: Aspirin does not appear to affect exercise performance in CHF.
Circulation 1980, 61:62-65
Production of Circulating Platelet Aggregates by Exercise in Coronary Patients
ANDREW G. KUMPURIS, M.D., ROBERT J. LUCHI, M.D., CAROLINE C. WADDELL, M.D.,
AND RICHARD R. MILLER, M.D.
SUMMARY To determine the effect of exercise on the in vivo formation of circulating platelet aggregates in patients with severe coronary artery disease (CAD), platelet aggregate ratios (PAR) (normal 0.8-1.1) were measured immediately before and after treadmill exercise and 30 minutes after exercise in 17 CAD patients (group 1, mean age 55 years), 12 age-matched normal subjects (group 2), and 13 young normals (mean age 27 years, group 3). Coronary patients had lower resting PAR than group 3 (0.79 ± 0.05 vs 0.98 ± 0.03; p <0.01), while group 2 had an intermediate value 0.86 4- 0.04 (p > 0.05 vs CAD and group 3). Immediately after exercise, group I PAR declined from 0.79 i 0.05 to 0.53 ± 0.04 (p < 0.001), while groups 2 and 3 were unchanged (p > 0.05; both p < 0.001 vs group 1); 30 minutes after exercise, PAR in group 1 rose to 0.66 ± 0.05 (p < 0.05 vs pre- and immediately postexercise); groups 2 and 3 remained unchanged vs pre- and immediately postexercise (p > 0.05; both p < 0.001 vs group 1). Six group 1 patients received 1300 mg aspirin daily for 10 days and repeated the protocol. Resting PARs were unchanged (p > 0.05) from resting values without aspirin. The exercise-induced decline in PAR was attenuated by aspirin: without aspirin, 0.73 ± 0.02 preexercise to 0.54 ± 0.04 postexercise; with aspirin, 0.73 ± 0.03 to 0.82 ± 0.03 (p < 0.05 vs no aspirin). These data indicate that platelet aggregation occurs with exercise in CAD. In addition, these data suggest that as