Athanasios Z. Jamurtas

Acute impact of active and passive electronic cigarette smoking on serum cotinine and lung function

Abstract Context: Electronic cigarettes (e-cigarettes) are becoming increasingly popular yet their effects on health remain unknown. Objective: To conduct the first comprehensive and standardized assessment of the acute impact of active and passive e-cigarette smoking on serum cotinine and lung function, as compared to active and passive tobacco cigarette smoking. Materials and methods: Fifteen smokers (≥15 cigarettes/day; seven females; eight males) and 15 never-smokers (seven females; eight males) completed this repeated-measures controlled study. Smokers underwent a control session, an active tobacco cigarette (their favorite brand) smoking session and an active e-cigarette smoking session. Never-smokers underwent a control session, a passive tobacco cigarette smoking session and a passive e-cigarette smoking session. Serum cotinine, lung function, exhaled carbon monoxide and nitric oxide were assessed. The level of significance was set at p ≤ 0.001 to adjust for multiple comparisons. Results: e-Cigarettes and tobacco cigarettes generated similar (p > 0.001) effects on serum cotinine levels after active (60.6 ± 34.3 versus 61.3 ± 36.6 ng/ml) and passive (2.4 ± 0.9 versus 2.6 ± 0.6 ng/ml) smoking. Neither a brief session of active e-cigarette smoking (indicative: 3% reduction in FEV1/FVC) nor a 1 h passive e-cigarette smoking (indicative: 2.3% reduction in FEV1/FVC) significantly affected the lung function (p > 0.001). In contrast, active (indicative: 7.2% reduction in FEV1/FVC; p < 0.001) but not passive (indicative: 3.4% reduction in FEV1/FVC; p = 0.005) tobacco cigarette smoking undermined lung function. Conclusion: Regarding short-term usage, the studied e-cigarettes generate smaller changes in lung function but similar nicotinergic impact to tobacco cigarettes. Future research should target the health effects of long-term e-cigarette usage, including the effects of nicotine dosage.

The dancer as a performing athlete: physiological considerations.

The physical demands placed on dancers from current choreography and performance schedules make their physiology and fitness just as important as skill development. However, even at the height of their professional careers, dancers’ aerobic power, muscular strength, muscular balance, bone and joint integrity are the ‘Achilles heels’ of the dance-only selection and training system. This partly reflects the unfounded view, shared by sections of the dance world, that any exercise training that is not directly related to dance would diminish dancers’ aesthetic appearances.Given that performing dance itself elicits only limited stimuli for positive fitness adaptations, it is not surprising that professional dancers often demonstrate values similar to those obtained from healthy sedentary individuals of comparable age in key fitness-related parameters. In contrast, recent data on male and female dancers revealed that supplementary exercise training can lead to improvements of such fitness parameters and reduce incidents of dance injuries, without interfering with key artistic and aesthetic requirements. It seems, however, that strict selection and training regimens have succeeded in transforming dance to an activity practised by individuals who have selectively developed different flexibility characteristics compared with athletes. Bodyweight targets are normally met by low energy intakes, with female dance students and professional ballerinas reported to consume below 70% and 80% of the recommended daily allowance of energy intake, respectively, while the female athlete ‘triad’ of disordered eating, amenorrhoea and osteoporosis is now well recognised and is seen just as commonly in dancers.An awareness of these factors will assist dancers and their teachers to improve training techniques, to employ effective injury prevention strategies and to determine better physical conditioning. However, any change in the traditional training regimes must be approached cautiously to ensure that the aesthetic content of the dance is not affected by new training techniques. Since physiological aspects of performing dance have been viewed primarily in the context of ballet, further scientific research on all forms of dance is required.

Time-course of changes in inflammatory and performance responses following a soccer game.

Objective:To study the effects of a single soccer game on indices of performance, muscle damage, and inflammation during a 6-day recovery period. Design:Participants were assigned to either an experimental group (E, played in the game; n = 14) or a control group (C, did not participate in the game; n = 10). Setting:Data were collected on a soccer field and at the Physical Education and Sports Science laboratory of the Democritus University of Thrace before and after the soccer game. Participants:Twenty-four elite male soccer players (age, 20.1 ± 0.8 years; height, 1.78 ± 0.08 m; weight, 75.2 ± 6.8 kg). Main Outcome Measurements:Muscle strength, vertical jumping, speed, DOMS, muscle swelling, leukocyte count, creatine kinase (CK), lactate dehydrogenase (LDH), C-reactive protein (CRP), cortisol, testosterone, cytokines IL-6 and IL-1b, thioburbituric acid-reactive substances (TBARS), protein carbnyls (PC), and uric acid (UA). Results:Performance deteriorated 1 to 4 days post-game. An acute-phase inflammatory response consisted of a post-game peak of leukocyte count, cytokines, and cortisol, a 24-hour peak of CRP, TBARS, and DOMS, a 48-hour peak of CK, LDH, and PC, and a 72-hour peak of uric acid. Conclusion:A single soccer game induces short-term muscle damage and marked but transient inflammatory responses. Anaerobic performance seems to deteriorate for as long as 72-hour post-game. The acute phase inflammatory response in soccer appears to follow the same pattern as in other forms of exercise. These results clearly indicate the need of sufficient recovery for elite soccer players after a game.

Association analysis of the ACTN3 R577X polymorphism and complex quantitative body composition and performance phenotypes in adolescent Greeks.

The functional allele (577R) of ACTN3, which encodes human α-actinin-3, has been reported to be associated with elite athletic status and with response to resistance training, while the nonfunctional allele (577X) has been proposed as a candidate metabolically thrifty allele. In a study of 992 adolescent Greeks, we show that there is a significant association (P=0.003) between the ACTN3 R577X polymorphism and 40 m sprint time in males that accounts for 2.3% of phenotypic variance, with the 577R allele contributing to faster times in an additive manner. The R577X polymorphism is not associated with other power phenotypes related to 40 m sprint, nor with an endurance phenotype. Furthermore, the polymorphism is not associated with obesity-related phenotypes in our population, suggesting that the 577X allele is not a thrifty allele, and thus the persistence of this null allele must be explained in other terms.

The Effect of Muscle-Damaging Exercise on Blood and Skeletal Muscle Oxidative Stress : Magnitude and Time-Course Considerations

The aim of this article is to present the effects of acute muscle-damaging exercise on oxidative stress/damage of animal and human tissues using a quantitative approach and focusing on the time-course of exercise effects. The reviewed studies employed eccentric contractions on a dynamometer or downhill running. The statistical power of each study to detect a 20% or 40% post-exercise change compared with pre-exercise value in each oxidative stress/damage biomarker was calculated. Muscle-damaging exercise can increase free radical levels and augment oxidation of lipids, proteins, glutathione and possibly DNA in the blood. In contrast, the effect of muscle-damaging exercise on concentration of antioxidants in the blood, except for glutathione, was little. Muscle-damaging exercise induces oxidative stress/damage in skeletal muscle, even though this is not fully supported by the original statistical analysis of some studies. In contrast, muscle-damaging exercise does not appear to affect — at least to similar extent as the oxidative stress/ damage markers — the levels of antioxidants in skeletal muscle. Based on the rather limited data available, the oxidative stress response of skeletal muscle to exercise was generally independent of muscle fibre type. Most of the changes in oxidative stress/damage appeared and were sustained for days after muscledamaging exercise. The major part of the delayed oxidative stress/damage production that follows muscle-damaging exercise probably comes from phagocytic cells that are activated and recruited to the site of the initial damage. A point that emerged and potentially explains much of the lack of consensus among studies is the low statistical power of many of them. In summary, muscle-damaging exercise can increase oxidative stress/damage in blood and skeletal muscle of rats and humans that may persist for and/or appear several days after exercise.

Blood as a reactive species generator and redox status regulator during exercise.

The exact origin of reactive species and oxidative damage detected in blood is largely unknown. Blood interacts with all organs and tissues and, consequently, with many possible sources of reactive species. In addition, a multitude of oxidizable substrates are already in blood. A muscle-centric approach is frequently adopted to explain reactive species generation, which obscures the possibility that sources of reactive species and oxidative damage other than skeletal muscle may be also at work during exercise. Plasma and blood cells can autonomously produce significant amounts of reactive species at rest and during exercise. The major reactive species generators located in blood during exercise may be erythrocytes (mainly due to their quantity) and leukocytes (mainly due to their drastic activation during exercise). Therefore, it is plausible to assume that oxidative stress/damage measured frequently in blood after exercise or any other experimental intervention derives, at least in part, from the blood.

Equal volumes of high and low intensity of eccentric exercise in relation to muscle damage and performance.

We examined differences in muscle damage and muscle performance perturbations in relation to the same volumes of high (HI) and low intensity (LI) of eccentric exercise. Untrained young healthy men (n = 12) underwent 2 isokinetic quadriceps eccentric exercise sessions, 1 on each randomly selected leg, separated by a 2-week interval. In the first session subjects performed HI exercise (i.e., 12 sets of 10 maximal voluntary efforts). In the second session, volunteers were subjected to continuous exercise of LI (50% of peak torque) until the total work done was approximately equal to that generated during HI. Muscle damage (serum creatine kinase concentration [CK], delayed onset of muscle soreness, and range of motion) and muscle performance (eccentric [EPT] and isometric peak torque [IPT]) indicators were assessed pre-exercise and 24, 48, 72, and 96 hours postexercise. Compared to baseline data, changes in muscle damage indicators were significantly different (p < 0.05) at almost all post-exercise time points in both conditions. However, apart from the significant elevation of CK at 24 hours after HI (p < 0.05), no other significant differences were observed between the 2 exercise conditions (p > 0.05). The main finding in relation to muscle performance was that decrements following HI exercise were significantly greater (p < 0.05) compared to LI. Compared with baseline data, the EPT values following HI and LI exercise were as follows: 24 hours, 72.1% vs. 92%; 48 hours, 81.9% vs. 94.8%; 72 hours, 77.7% vs. 100.6%; 96 hours, 86.8% vs. 107.9%. The corresponding data for IPT were as follows: 24 hours, 86.4% vs. 102.8%; 48 hours, 84.2% vs. 107%; 72 hours, 84.8% vs. 109.2%; 96 hours, 86.8% vs. 114.4%. These results indicate that matching volumes of HI and LI eccentric exercise have similar effects on muscle damage, but HI has a more prominent effect on muscle performance.

No effect of antioxidant supplementation on muscle performance and blood redox status adaptations to eccentric training

BACKGROUND It was recently reported that antioxidant supplementation decreases training efficiency and prevents cellular adaptations to chronic exercise. OBJECTIVE This study aimed to investigate the effects of vitamin C and vitamin E supplementation on muscle performance, blood and muscle redox status biomarkers, and hemolysis in trained and untrained men after acute and chronic exercise. A specific type of exercise was applied (eccentric) to produce long-lasting and extensive changes in redox status biomarkers and to examine more easily the potential effects of antioxidant supplementation. DESIGN In a double-blinded fashion, men received either a daily oral supplement of vitamin C and vitamin E (n = 14) or placebo (n = 14) for 11 wk (started 4 wk before the pretraining exercise testing and continued until the posttraining exercise testing). After baseline testing, the subjects performed an eccentric exercise session 2 times/wk for 4 wk. Before and after the chronic eccentric exercise, the subjects underwent one session of acute eccentric exercise, physiologic measurements were performed, and blood samples and muscle biopsy samples (from 4 men) were collected. RESULTS The results failed to support any effect of antioxidant supplementation. Eccentric exercise similarly modified muscle damage and performance, blood redox status biomarkers, and hemolysis in both the supplemented and nonsupplemented groups. This occurred despite the fact that eccentric exercise induced marked changes in muscle damage and performance and in redox status after exercise. CONCLUSION The complete lack of any effect on the physiologic and biochemical outcome measures used raises questions about the validity of using oral antioxidant supplementation as a redox modulator of muscle and redox status in healthy humans.

Acute effects of electronic and tobacco cigarette smoking on complete blood count

The World Health Organisation called for research assessing the safety of electronic cigarette (e-cigarette). We evaluated the acute effect of active and passive e-cigarette and tobacco cigarette smoking on complete blood count (CBC) markers in 15 smokers and 15 never-smokers, respectively. Smokers underwent a control session, an active tobacco cigarette smoking session, and an active e-cigarette smoking session. Never-smokers underwent a control session, a passive tobacco cigarette smoking session, and a passive e-cigarette smoking session. The results demonstrated that CBC indices remained unchanged during the control session and the active and passive e-cigarette smoking sessions (P>0.05). Active and passive tobacco cigarette smoking increased white blood cell, lymphocyte, and granulocyte counts for at least one hour in smokers and never smokers (P<0.05). It is concluded that acute active and passive smoking using the e-cigarettes tested in the current study does not influence CBC indices in smokers and never smokers, respectively. In contrast, acute active and passive tobacco cigarette smoking increase the secondary proteins of acute inflammatory load for at least one hour. More research is needed to evaluate chemical safety issues and other areas of consumer product safety of e-cigarettes, because the nicotine content in the liquids used may vary considerably.

Acute and Short-term Effects of Secondhand Smoke on Lung Function and Cytokine Production

RATIONALE The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. OBJECTIVES To assess the SHS effects and their duration on lung function and inflammatory markers. METHODS In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/restaurant SHS levels. MEASUREMENTS AND MAIN RESULTS Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-alpha, and IFN-gamma. At 0 hours most lung function parameters were significantly reduced (indicative: FEV(1), 4.3 +/- 0.4 vs. 3.8 +/- 0.3 L; FEV(1)/FVC, 0.9 +/- 0.1 vs. 0.8 +/- 0.1; P < 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 +/- 3.2 vs. 35.5 +/- 10.2 ng x ml(-1)), IL-4 (41.3 +/- 5.8 vs. 44.2 +/- 4.5 pg x ml(-1)), IL-5 (36.1 +/- 3.2 vs. 60.1 +/- 7.0 pg x ml(-1)), IL-6 (2.5 +/- 0.3 vs. 7.6 +/- 1.4 pg x ml(-1)) and IFN-gamma (0.3 +/- 0.2 vs. 0.6 +/- 0.2 IU x ml(-1)) at 3 hours were higher than at baseline (P < 0.05). IL-4 and TNF-alpha increased only in men, whereas IL-5, IL-6, and IFN-gamma were different between sexes after exposure (P < 0.05). Regression analyses revealed inverse associations of FEV(1) and FEV(1)/FVC ratio with IL-5 (P < 0.05) in men and with IL-5 (P = 0.01), IL-6 (P < 0.001), IFN-gamma (P = 0.034) and serum cotinine (P < 0.001) in women. CONCLUSIONS We conclude that 1 hour of SHS exposure at bar/restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS.