Effects of posture and ergometer-specific exercise modality on plasma viscosity and plasma fibrinogen: the role of plasma volume changes.

The aim of the present study was ascertain the effects posture and exercise modality on the main determinants of blood rheology. Thirteen subjects performed two exercise trials, in random order, at approximately 70% VO(2) max for 45-min. One trial was performed on a motorized treadmill at an intensity corresponding to 70% VO(2) max, while the other was performed on a stationary pike at an intensity corresponding to 70% VO(2) max. In the cycling trial subjects stood for 30-min, followed by sitting for 30-min then cycled for 30-min at 70% VO(2) max. In the treadmill trial, subjects sat for 30-min followed by standing for 30-min then ran on the treadmill for 30-min at 70% VO(2) max. Variations of body postures prior to exercise were associated with opposite changes in plasma volume, plasma viscosity and plasma fibrinogen. When post exercise raw data were not adjusted for plasma volume changes, a significant increase (p < 0.05) in plasma viscosity and plasma fibrinogen was found with no difference between the cycling and running trials. However, the increase in plasma viscosity and fibrinogen were no longer apparent when the raw data post exercises were adjusted for plasma volume changes. Changing body posture from standing to sitting and vice versa were associated with opposite changes in plasma volume and mirrored the changes in plasma viscosity and fibrinogen. In addition, ergometer-specific vigorous exercises at the same relative intensity, irrespective of its modality, transiently increased plasma viscosity and plasma fibrinogen mainly due to exercise-associated haemoconcentration.

Does ambient temperature affect exercise-induced changes in the main determinants of blood rheology?

To ascertain the effects of environmental temperature on blood rheology, ten subjects performed two exercise trials, in random order, at approximately 60% VO(2) max for 45-min. One trial was conducted in thermoneutral environment (20 ± 1°C), while the other was performed in hot dry condition (36 ± 1°C). Venous blood was removed at rest; following exercise and recovery. Blood was measured for lactate, haematocrit, and hemoglobin, while plasma was measured for viscosity, and fibrinogen. Plasma volume changes were estimated from Hct and Hb readings. Exercise was followed by a significant (P < 0.05) reduction in plasma volume in both test trials. Lactate increased significantly (P < 0.05) following exercise with no difference being observed between trials. When post exercise raw data were not adjusted for plasma volume changes, a significant increase (P < 0.05) in plasma viscosity (PV) and plasma fibrinogen (Fb) was found with no difference between thermoneutral and hot trials. When the raw data post exercise for PV and Fb were adjusted for plasma volume changes, no significant difference between rest and post exercise was demonstrated. Rheological variables returned to the pre-exercise level at the end of recovery. In conclusion, vigorous exercise transiently increased PV and Fb, and the added heat stress did not affect these responses more than exercise alone. The mechanism responsible for the increase in PV and Fb in response to vigorous exercise appears to be related to plasma shifts from intravascular to the extravascular spaces rather than plasma volume loss.

Effects of time of day and acute resistance exercise on platelet activation and function.

The present study was designed to ascertain the interaction between time of day and resistance exercise on platelet activation and function. Ten healthy male subjects (age, 29.3 +/- 4.5 yr) undertook identical bouts of resistance exercise on two separate occasions. Tests were randomised and performed at two different time of day (08:00 and 20:00 h). Subjects performed 3 sets of 7 repetitions of six exercises at 80% of 1RM, which was followed by 30 min recovery. Beta-thromboglobulin (B-TG) and platelet indices were measured at rest, post-exercise and at the completion of recovery. Platelet aggregation was determined in platelet rich plasma using collagen and three different concentrations of adenosine-5'-diphosphate. Platelet aggregations induced by different aggregating agents at rest were significantly higher in the morning (p < 0.05). Although platelet aggregations induced by collagen and ADP did not change in response to resistance exercise, significant differences between the results in the morning and evening trials were observed (p < 0.01). These differences emulated the differences observed at rest. A significant (P < 0.05) increase in B-TG was found following exercise with no difference between morning and evening trials. It was concluded that resistance exercise induces significant changes in platelet activation, irrespective of time of day, as assessed by beta-thromboglobulin.

Aerobic power and the main determinants of blood rheology: is there a relationship?

This cross-sectional study aimed to explore the relationship between aerobic power and the main determinants of blood rheology namely plasma viscosity, plasma fibrinogen concentration and haematocrit. Ninety-three normal healthy individuals (VO2max 48.3 ml/kg per min), who were familiarized with the laboratory environment and testing procedures, participated in the study. Aerobic power as assessed by maximal oxygen consumption (VO2max) was determined by using an incremental exercise protocol on either a treadmill or a stationary bike. Oxygen consumption was measured online using a computer-based metabolic system. In a standardized resting condition, venous blood samples were removed from a prominent vein of the nondominant arm. Aliquots of whole blood were measured for haematocrit (in triplicate), whereas plasma was assayed for fibrinogen concentration and viscosity (in duplicate) using semiautomatic coagulometer and capillary viscometer; respectively. The mean values for haematocrit (41.9 +/- 2.5%), plasma viscosity (1.56 +/- 0.27 mPa s) and plasma fibrinogen (272.1 +/- 86.9 mg/dl) were within the normal range for normal participants. Pearson correlation coefficients and regression analysis were used for statistical evaluations. In this population, VO2max negatively correlated with plasma viscosity (P < 0.01) and plasma fibrinogen concentration (P < 0.01). Although VO2max positively correlated with haematocrit, this correlation was not as strong. Thus, high aerobic power as assessed by maximal oxygen consumption appears to be associated with lower plasma viscosity and lower plasma fibrinogen. The significant negative relationships between VO2max and plasma viscosity and plasma fibrinogen might suggest that blood is more dilute in individuals with high aerobic power. This could probably be due to an expansion of plasma volume, which is commonly seen in those who are physically active and exhibit a higher level of cardiorespiratory fitness.

Bone health in men: influencing factors.

OBJECTIVE: To describe osteoporosis health beliefs, osteoporosis risk factors, and lifestyle habits that affect bone health in men. METHODS: Data were collected from 272 men using the Bone Health in Men questionnaire. RESULTS: The majority of participants reported that they were unlikely to develop osteoporosis, that osteoporosis in men is less serious than in women, and that osteoporosis is preventable. Few osteoporosis risk factors were reported. The lifestyle habits reported were below the suggested recommendations. CONCLUSIONS: Increasing men's awareness of osteoporosis risk factors, changing their beliefs, and encouraging them to adopt healthy lifestyle habits are necessary strategies to promote bone health.

Physical fitness indices and anthropometrics profiles in schoolchildren with sickle cell trait/disease.

The current studies aimed at determining physical fitness indices and anthropometrics profiles of school children with sickle cell trait (SCT) and sickle cell disease (SCD). Male school children (150) comprising 3 Groups participated in the studies. Group 1 has 50 normal healthy controls, while Groups 2 and 3 each has 50 children who were suffering from SCT and SCD, respectively. Anthropometrics measurement and parameters of physical fitness were assessed in all subjects. All children were also subjected to a 5-min running exercise test on a flat motorized treadmill at speed corresponding to 5 km/hr. Throughout the test, heart rate was monitored and recorded during exercise and for 10-min during recovery. Blood lactate was measured before and 5 min following the completion of test. The mean values of lean body mass and height were lower in the SCD children (P < 0.05) compared with the healthy subjects and SCT individuals. Children with SCD exhibited a higher mean value (P < 0.05) for percent body fat and fat mass than the normal healthy subjects and SCT individuals. Although all groups tolerated well the treadmill exercise protocol, the SCD group exhibited higher (P < 0.05) mean values of heart rate during exercise than those observed in the SCT and normal control children. In addition, SCD children showed higher serum lactate values before and after treadmill exercise compared to the other groups. Children with SCD exhibit high level of adiposity; low level of fitness and their exercise performance appears to be physiologically more stressful as indicated by heart rate and blood lactate concentration responses.

Responses of platelet activation and function to a single bout of resistance exercise and recovery.

The present study was designed to investigate the effects of resistance exercise and recovery on platelet activation and function. Twenty one healthy male subjects (27.9 +/- 4.8 years) completed three sets of five to seven repetitions of six exercises at an intensity corresponding to 80% of one repetition maximum (1RM), which was followed by 30 minutes recovery. Venous blood samples (20 ml) were obtained before, immediately after exercise and at the end of recovery and were analysed for platelet indices, platelet aggregation using collagen and various final concentrations of adenosine-5'-diphosphate (ADP), and beta thromboglobulin (B-TG). Resistance exercise was followed by a significant increase in corrected platelet count, corrected plateletcrit, and B-TG. These increases were transient and decreased to pre-exercise level at the end of recovery. When plasma samples were not corrected for changes in platelet count, exercise was followed by a significant increase (P < 0.05) in platelet aggregation using high concentration of ADP. With corrected samples, platelet aggregation and B-TG were not altered after exercise and recovery. It was concluded that heavy resistance exercise induces in vivo activation of platelets as manifested by an increase in platelet aggregation and a rise in B-TG and that these changes could be explained partially by changes in plasma volume and platelet count induced by exercise.

Effects of water intake on the responses of haemorheological variables to resistance exercise.

To examine the effects of drinking an amount of water equal to weight loss on the responses of blood rheological variables, eleven healthy male subjects performed three resistance exercise trials. The aim of the first session was to determine the amount of weight loss following a resistance exercise trial at 80% of one repletion maximum (1RM). In the second and third sessions subjects performed the same resistance exercise protocol without and with drinking an amount of water equal to that recorded for body weight loss. Three venous blood samples were taken before exercise, immediately after exercise, and at the end of 30-min recovery and were analysed for haematocrit (Hct), haemoglobin (Hb), blood cells count and the main determinant of blood rheology. Haematocrit, plasma viscosity, fibrinogen, albumin, and total protein were significantly increased in response to resistance exercise and returned to pre-exercise level following 30-min of recovery. The changes in blood rheological variables in response to resistance exercise occurred similarly in both control and water trials with no significant difference being observed between trials. Plasma volume loss through sweating and respiratory tract during resistance exercise could have contributed to the decrease in plasma volume, though, this contribution was negligible. Therefore, it is concluded that the increases in blood rheological variables in response to resistance exercise are mainly due to plasma shifts from intravascular space to extravascular spaces rather than plasma volume loss through sweating and respiratory tract.

Haemorheology in exercise and training.

Disruption of the normal rheological properties of blood is considered an independent risk factor for cardiovascular disease and plays a significant role in the aetiology of atherothrombogenesis. The acute increase in whole blood viscosity may unfavourably affect the microcirculatory blood flow and oxygen delivery to the tissues. It is universally accepted that exercise and physical activity performed on a regular basis has health benefits. However, the effects of exercise on the rheological properties of blood have not received much research attention. Recent, limited evidence indicates that the viscosities of whole blood and plasma increase in response to a variety of exercise protocols. The increase in whole blood viscosity is mainly attributed to an increase in haematocrit and plasma viscosity, whereas the deformability and aggregability of red blood cells remain unaltered. The increases in plasma viscosity and haematocrit have been ascribed to exercise-induced haemoconcentration as a result of fluid transfer from the blood to the interstitial spaces. The haemorheological changes associated with strenuous exercise appear to be linked with enhanced oxidative stress and depletion of antioxidant capacity, and that may affect oxygen delivery and availability to the tissues. Although significant advances have been made in many areas of exercise haematology, the long-term effects of endurance training on blood rheology have been very briefly examined and the exact effect of training has not as yet been determined. Available cross-sectional and longitudinal studies indicate that the blood of endurance athletes is more dilute and this has been attributed to an expansion of blood volume, particularly plasma volume as a result of training. The low haematocrit values in trained athletes represent a hydration condition rather than iron stores deficiency. It has been suggested that this hypervolaemia and blood dilutional effect of endurance training may be advantageous for heat dissipation and greater cardiac stroke volume and lower heart rates during exercise. Enhanced blood fluidity also facilitates oxygen delivery to the exercising muscles because of a reduced resistance to blood flow within the microcirculation. Furthermore, the increase in plasma volume may contribute to the body water pool and help offset dehydration. The influence of strength and power training on blood rheology is not known. The physiological mechanisms responsible for and the functional consequences of the haemorheological changes associated with exercise to a large extent remain speculative. The paradox of haematocrit and blood rheology in exercise and training warrants additional studies. Likewise, further investigations are necessary to determine the possible link between overtraining and blood rheological profiles.

The acute effects of resistance exercise on the main determinants of blood rheology.

The aim of this study was to examine short-term changes in blood rheological variables after a single bout of resistance exercise. Twenty-one healthy males completed three sets of 5 - 7 repetitions of six exercises at an intensity corresponding to 80% of one-repetition maximum (1-RM). The average duration of the exercise bout was 35 min. Venous blood samples were obtained before exercise, immediately after exercise and after 30 min of recovery and analysed for lactate, red blood cell count, haematocrit, haemoglobin, plasma viscosity, fibrinogen, total protein and albumin concentration. Plasma volume decreased 10.1% following resistance exercise. This occurred in parallel with an increase of 5.6%, 5.4% and 6.2% in red blood cell count, haemoglobin and haematocrit; respectively. Plasma viscosity increased from 1.55 +/- 0.01 to 1.64 +/- 0.01 mPa s immediately after resistance exercise before decreasing to 1.57 +/- 0.01 mPa s at the end of the recovery period. Similarly, fibrinogen, albumin and total protein increased significantly following resistance exercise. However, the rises in all these rheological parameters were transient and returned to pre-exercise values by the end of recovery. We conclude that a single session of heavy resistance exercise performed by normal healthy individuals alters blood rheological variables and that these changes are transient and could be attributed to exercise-induced haemoconcentration.

Interaction between alcohol and exercise: physiological and haematological implications.

Alcohol use, particularly excessive alcohol consumption is one of the most serious health risks in the world. A relationship between sport, exercise and alcohol consumption is clear and long-standing. Alcohol continues to be the most frequently consumed drug among athletes and habitual exercisers and alcohol-related problems appear to be more common in these individuals. Alcohol use is directly linked to the rate of injury sustained in sport events and appears to evoke detrimental effects on exercise performance capacity. The model of alcohol consumption in human experimental studies has either been acute (single dose) or chronic (repeated doses over a period). These studies suggested that alcohol consumption decreases the use of glucose and amino acids by skeletal muscles, adversely affects energy supply and impairs the metabolic process during exercise. In addition, chronic alcohol use is associated with increased citrate synthase activity and decreased cross-sectional area of type I, IIa and IIb fibres. There is evidence to suggest that exercise may attenuate the ethanol-induced decline in hepatic mitochondria and accelerates ethanol metabolism by the liver. Exercise training seems to reduce the extent of the oxidative damage caused by ethanol. Evidence generated from in vitro experiments and animal studies have also suggested that ethanol administration decreased skeletal muscle capillarity and increased pyruvate kinase and lactate dehydrogenase activities. Substantial epidemiological evidence has been accrued showing that moderate ingestion of alcohol may reduce the incidence of cardiovascular diseases. Although the existing evidence is often confusing and disparate, one of the mechanisms by which alcohol may reduce the incidence of mortality of cardiovascular diseases is through raising levels of high-density lipoprotein cholesterol. Available evidence suggests that exercise and moderate alcohol consumption may have favourable effects on blood coagulation and fibrinolysis; however, compelling experimental evidence is lacking to endorse this notion. Occasional and chronic alcohol consumption is usually linked with unfavourable alterations in platelet aggregation and function and may be associated with platelet-related thrombus formation. Although the effects of alcohol consumption on the rheological properties of the blood are not known, recent experimental evidence suggests that alcohol use following exercise is associated with unfavourable changes in the main determinants of blood viscosity. It is well documented that alcohol use modulates the immune system and impairs host defence. Compelling evidence is also mounting to suggest that chronic alcohol use is linked with adverse effects on the body systems and organs including the brain, the cardiovascular system and the liver.

Aggregation and activation of blood platelets in exercise and training.

This article presents an overview of the progress that has been made in recent years in our understanding of the interaction between exercise and platelets in health and disease. Although platelets are important in normal haemostasis, recent evidence emphasises the pivotal role of abnormal platelet function in acute coronary artery diseases, myocardial infarction, unstable angina and stroke. In light of the positive health benefits of exercise, interest has been heightened on the association between exercise and platelet aggregation and function, not only in normal healthy subjects but also in patients. However, the study of exercise effects on blood platelets are highly contentious because of the fact that the analytical methods employed to study platelets are bedevilled by numerous methodological problems. While exercise effects on platelet aggregation and function in healthy individuals have been extensively examined, the evidence reported has been conflicting. Somewhat less contradictory are the results generated from studies in patients with coronary heart disease, as the preponderance of evidence available would strongly suggest that platelet aggregation and function are increased with exercise. Several drugs are known to influence platelet aggregation and function, the most examined among these medications is aspirin (acetylsalicylic acid). However, aspirin appears to be ineffective to attenuate exercise-induced increases in platelet aggregation and activation. Few studies are available on the effect of training on blood platelets and the exact effects of exercise training on platelet activation and function is not as yet known. This lack of information makes further studies particularly important, in order to clarify whether there are favourable effects of exercise training on platelet aggregation and function in health and disease.

The effects of arm cranking exercise and training on platelet aggregation in male spinal cord individuals.

Platelet aggregation at rest and in responses to exercise and training were compared between spinal cord injured (SCI) individuals (N=5) and able-bodied subjects (N=7). All participants performed arm cranking exercise at 60-65% VO(2peak) for 30 min. Venous blood samples were obtained before and after sub-maximal exercise and measured for platelet aggregation using ADP and collagen. To assess the effects of arm cranking training, platelet aggregation was re-measured in all subjects at rest and in response to the sub-maximal arm cranking exercise after 12 weeks of individually supervised training programme. Before training, the resting mean values of platelet aggregation induced by ADP and collagen were not different (P>0.05) between SCI and able-bodied. However the SCI individuals, but not the able-bodied subjects, exhibited a significantly (P<0.05) higher maximal platelet aggregation induced by ADP and collagen following sub-maximal arm cranking exercise. Although VO(2peak) after training was significantly increased (P<0.05) in both groups, the resting mean values of platelet aggregation induced with ADP and collagen were not significantly different (P>0.05) from those observed before training and were not different (P>0.05) between SCI and able-bodied. Post-training, the SCI individuals, but not able-bodied individuals, exhibited a significant decrease (P<0.05) in platelet aggregation following sub-maximal arm cranking exercise and this occurred with both ADP and collagen. These results suggest that SCI individuals, but not normal subjects increase their platelet aggregation following sub-maximal arm cranking exercise. Furthermore, arm cranking training in SCI individuals, appears to diminish the percentage of platelet aggregation ex vivo.

Exercise and training effects on blood haemostasis in health and disease: an update.

In recent years, the dysfunction of the haemostatic system in relation to the clinical complications from arterioscleroses and cardiovascular diseases has become more recognised. Blood coagulation and fibrinolysis comprise two important physiological systems, which are regulated by a balance between activators and inhibitors. Activation of blood coagulation is associated with accelerated clot formation, whereas activation of blood fibrinolysis enhances the breakdown of the blood clot. Available evidence suggests that strenuous exercise induces activation of blood coagulation with simultaneous enhancement of blood fibrinolysis. Although the responses of blood coagulation and fibrinolysis appear to be related to the exercise intensity and its duration, recent reports suggest that moderate exercise intensity is followed by activation of blood fibrinolysis without concomitant hyper-coagulability, while very intense exercise is associated with concurrent activation of blood coagulation and fibrinolysis. Similar to blood coagulation and fibrinolysis, systemic platelet-related thrombogenic factors have been shown to be involved in the initiation and progression of atherogenesis and plaque growth. Although exercise effects on platelet aggregation and function in healthy individuals have been examined, the results reported have been conflicting. However, for patients with coronary heart disease, the balance of evidence available would strongly suggest that platelet aggregation and functions are increased with exercise. Few studies are available concerning the influence of training on blood coagulation and fibrinolysis and the exact effects of exercise training on the equilibrium between blood coagulation and fibrinolysis is not as yet known. Although the effects of physical training on platelets have been briefly investigated, available meagre evidence suggests that exercise training is associated with favourable effects on platelet aggregation and activation in both men and women.

The effects of graded resistance exercise on platelet aggregation and activation.

PURPOSE: The purpose of this study was to examine the effects of resistance exercise with varying intensity but with similar volume on platelet aggregation and activation. METHODS: Thirteen healthy male subjects randomly completed three resistance exercise test trials at an intensity corresponding to 40%, 60%, and 80% of one repetition maximum (1-RM) in which the subjects performed six exercises including upper- and lower-body parts. Venous blood samples were obtained before and immediately after each exercise trial and analyzed for platelet count (PLT), plateletcrit (PCT), mean platelet volume (MPV), platelet aggregation, and beta-thromboglobulin (B-TG). Plasma volume changes were estimated from hemoglobin and hematocrit readings before and after each exercise trial. RESULTS: Although all exercise trials were followed by a significant (P < 0.05) increase in PLT (thrombocytosis), PCT, and MPV, this rise was not related to the exercise intensity (P > 0.05). Exercise was also followed by a significant increase (P < 0.05) in platelet aggregation, but this only occurred with the high but not with the low concentrations of adenosine diphosphate (ADP). Although ANOVA showed a significant overall increase (P < 0.05) in the concentration of B-TG after exercise, this rise only reached the assigned level of significance (P < 0.05) after 80% exercise trial. CONCLUSION: It was concluded therefore that resistance exercise is followed by an increase in PLT, PCT, and MPV, and this occurred in parallel with an in vivo activation of platelet as manifested by an increase in platelet aggregation and a rise in B-TG.

Exercise and training effects on platelets in health and disease.

In recent years the involvement of platelets dysfunction in atherogenesis and in the clinical complications from atherosclerosis has become more recognised. Systemic platelet-related thrombogenic factors have been shown to be involved in the initiation and progression of atherogenesis and plaque growth. Over the last two decades, interest has been heightened regarding the changes in platelet aggregation and functions that are associated with exercise in normal subjects and also patients, particularly those suffering from coronary artery disease. Although exercise effects on platelet aggregation and function in healthy individuals have been examined, the results reported have been conflicting, most likely due to methodological problems in the measurements of platelet aggregation and activation during and after exercise. However for patients suffering from coronary heart disease, the balance of evidence available would strongly suggest that platelet aggregation and function are increased with exercise. Several drugs are known to affect platelets, the most studied among them is aspirin. The evidence available would suggest that aspirin is ineffective in attenuating enhanced platelet aggregation and activation induced by exercise. Although the effects of physical training have been briefly investigated, available meagre evidence suggests that exercise on a regular basis is associated with favourable effects on platelets aggregation and activation in both men and women.

Effects of alcohol ingestion post-exercise on platelet aggregation.

The present study examined the influence of ingesting a moderate dose of alcohol on platelet count and platelet aggregation during recovery following exercise. Nineteen subjects (11 male and 8 female) were studied immediately after a standardised cycle ergometer test and during the 24-h period of recovery. In random order, alcohol (0.7 g/kg body mass) was given 1 h after exercise on one test occasion, while an equal volume of alcohol-free solution was administered on the other. Venous blood samples were obtained at baseline, post-exercise, and at 1, 5, and 22 h post-alcohol ingestion. Blood alcohol level increased significantly 1 h after the ingestion of alcohol, but decreased and returned to the resting baseline level at 5 h during recovery. Males and females subjects exhibited similar mean values of platelet count, platelet aggregation, and beta-thromboglobulin concentration at rest and following exercise and recovery. A significant increase in platelet count and a decrease in platelet aggregation using adenosine diphosphate (ADP) was found following exercise. Although plasma beta-thromboglobulin level (pooled data for males and females) showed an increase by 26.0% (from a mean pre-exercise value of 22.3-28.1 IU/ml), this rise was not significant (P>.05). The post-exercise increase in platelet count was mainly due to exercise-induced plasma volume loss. During recovery, while the increase in platelet count post-exercise returned to the baseline level in control and alcohol trials, the optical density of platelet aggregation remained significantly depressed at 5-h during recovery in the alcohol trial but not in the normal control condition. It is concluded that exercise induces significant reduction in platelet aggregation and the consumption of alcohol after physical exercise delays the normal return of platelet aggregation to the resting baseline levels during recovery.