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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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The diagnosis of familial Mediterranean fever (FMF) is primarily based on clinical standards. The purpose of this study was to investigate the relevance of Mediterranean fever (MEFV) genetic testing in the diagnosis of FMF as well as to identify the most frequent variant alleles and their relationship to clinical symptoms in Egyptian patients. Egyptian patients with a clinical suspicion of having FMF were studied in order to determine MEFV genotypes. Each patient was meticulously evaluated through an extensive collection of their medical history, a thorough clinical examination, and a series of laboratory tests, encompassing CBC, ESR, and CRP measurements. The MEFV variant screening procedure included the use of reverse dot blot hybridization. The average age of our patients when they were given a diagnosis was 22.8 ± 1.404 years old. The predominant clinical manifestations identified were abdominal pain, fever, and arthralgia.  Molecular interrogation of the MEFV gene unveiled that a significant proportion of the cohort, constituting 72 individuals (60%), displayed heterozygosity, whereas a smaller fraction, comprising 12 subjects (10%), demonstrated homozygosity and an equivalent number (10%) exhibited compound heterozygosity. Pertaining to the distribution of allele variants, E148Q emerged as the most prevalent, succeeded by M694I, accounting for 12.5% of the cases, and M680I (G/A), representing 10.41%. This notable prevalence of heterozygous genotypes among the Egyptian demographic, preliminarily identified as potential FMF cases, underscores the imperative for molecular diagnostics to enhance the precision of FMF identification.

Infections with Mycoplasma gallisepticum (MG) in poultry are associated with a wide range of disease conditions, including those affecting the respiratory and reproductive systems. The purpose of this study was to endorse the more sensitive diagnostic scheme for MG infection and identify the best molecular marker for MG phylogenetic analysis using six housekeeping genes: mgc2 , mraW , atpG , ugpA , DUF31196, and lgT . For these purposes, 55 poultry flocks of different species were screened using either qRT-PCR or PCR techniques analogous to conventional culturing from non-cultured and cultured swabs on PPLO broth. The rate of MG positivity was the highest when using qRT-PCR from cultured broth (89.0%) and the lowest when using conventional culturing (34.5%). Compared to qRT-PCR from broth, statistical analysis using the Roc curve in MedCalc statistical software showed that the PCR schemes (qRT-PCR from swabs and PCR from swabs and broth) performed better than conventional culturing in terms of sensitivity, accuracy, and area under the curve (AUC), suggesting that they may be more reliable schemes. Further support was added by Cohen's kappa test, showing moderate agreement between the molecular approaches. Among the six screened genes, mgc2 and mraW had the highest detection rates (69% and 65.4%, respectively). The comparative phylogenetic analysis revealed that mgc2 or atpG gene sequences distinguished MG isolates into different clades with high discriminatory power.

Objective: The aim was to investigate the effect of dapagliflozin on non-alcoholic fatty liver disease and dyslipidemia in type 2 diabetic rats by studying the histopathological structure of the liver and detecting possible underlying mechanisms for this impact by evaluating the potential anti-inflammatory action of dapagliflozin., Materials and Methods: 100 albino rats were used in this work and divided into five equal groups: group I (Control group), group II (Control diabetic group), group III (was administered dapagliflozin, 0.75 mg/kg, p.o.), group IV (was administered dapagliflozin, 1.5 mg/kg, p.o.), and group V (was administered dapagliflozin, 3 mg/kg, p.o.)., Results: In our study, the total body weight, liver weight, liver index, blood glucose level, insulin level, insulin resistance, total cholesterol, triglycerides, liver enzymes, IL-1 β, and MDA were significantly higher in the control diabetic group than the normal group. The dapagliflozin reduced all the above variables significantly in a dose-dependent manner compared to the control diabetic group (p-value = 0.001 for all)., Conclusions: Dapagliflozin may be a promising novel treatment strategy for treating T2DM-related non-alcoholic fatty liver disease (NAFLD), and dyslipidemia where it possesses anti-oxidative, anti-inflammatory and anti-dyslipidemic effects.

Objective: Urinary incontinence is defined as involuntary loss of urine, a common health condition that is more frequent in women. It disturbs the affected individuals and interferes with their daily activities. This study aimed to estimate the prevalence of urinary incontinence among Saudi women in the western area of the Kingdom of Saudi Arabia., Subjects and Methods: A descriptive cross-sectional design was used for this study. A survey was administered to Saudi women in the western area of the Kingdom of Saudi Arabia ranging in age from 18 to 70 years. The data were collected using the Arabic version of the Questionnaire for Urinary Incontinence Diagnosis. Descriptive statistics were generated by calculating numbers and percentages of information on the prevalence of incontinence in women. p-values < 0.05 were considered statistically significant., Results: The prevalence of urinary incontinence was 44.2%, with the urge type being the most reported. Stress urinary incontinence was reported by 155 women (15.4%), urgency urinary incontinence by 257 women (25.6%), and mixed urinary incontinence by 102 women (10.15%)., Conclusions: Urinary incontinence is prevalent in women in Western Saudi Arabia. Age, multiparty obesity, and vaginal surgery are significant risk factors influencing its occurrence.

Objective: The purpose of this systematic review was to study the incidence, risk factors and patients subjected to Guillain-Barré syndrome (GBS) after COVID-19., Materials and Methods: For qualitative assessment and assessing the methodological quality, the Cochrane Handbook for Systematic Reviews of Interventions and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) checklist were utilized. Data from PubMed, Cochrane, Embase, CINAHIL, Medline, ResearchGate, and Scopus were searched. The relevant studies involved patients with confirmed COVID-19 diagnosis by RT-PCR, and GBS diagnosis based on typical clinical symptoms and/or confirmatory diagnostic results. A total of 12 English relevant articles (6 papers were case reports and 8 were case series with a total of 32 patients) published in a peer-reviewed journal from 2019 to 2021 were included. Following the review methodology, two independent raters were responsible for retrieving, extracting and checking for data eligibility. Demographic characteristics are presented as frequencies and percentages. Based on distribution of values, continuous data were expressed as median and interquartile range (IQR)., Results: Out of 32 patients, 26 patients reported neurological symptoms, 6 cases went unnoticed, 7 cases showed involvement of the cranial nerves, 12 cases did not, and 13 cases went unreported., Conclusions: It is too early to draw any conclusions concerning a potential relationship between SARS-CoV-2 infection and GBS. More large-scale observational studies are required to understand the pathogenesis of SARS-CoV-2-associated GBS and to demonstrate a definite causal relationship between GBS and SARS-CoV-2 infection.

The human brain can effortlessly perform vision processes using the visual system, which helps solve multi-object tracking (MOT) problems. However, few algorithms simulate human strategies for solving MOT. Therefore, devising a method that simulates human activity in vision has become a good choice for improving MOT results, especially occlusion. Eight brain strategies have been studied from a cognitive perspective and imitated to build a novel algorithm. Two of these strategies gave our algorithm novel and outstanding results, rescuing saccades and stimulus attributes. First, rescue saccades were imitated by detecting the occlusion state in each frame, representing the critical situation that the human brain saccades toward. Then, stimulus attributes were mimicked by using semantic attributes to reidentify the person in these occlusion states. Our algorithm favourably performs on the MOT17 dataset compared to state-of-the-art trackers. In addition, we created a new dataset of 40,000 images, 190,000 annotations and 4 classes to train the detection model to detect occlusion and semantic attributes. The experimental results demonstrate that our new dataset achieves an outstanding performance on the scaled YOLOv4 detection model by achieving a 0.89 mAP 0.5.

Objectives: Reactive axillary lymph nodes (ALN) may occur post-COVID-19 vaccination. This may be confused with malignant nodal metastases on oncological imaging. We aimed to determine the reactive ALN incidence and duration on 18 F-fluorodeoxyglucose positron emission tomography - computed tomography ( 18 F-FDG PET-CT), and its relationship with gender, age and vaccine type., Methods: A retrospective study was performed. Two-hundred and four eligible patients had 18 F-FDG PET-CT between 01 January 2021 and 31 March 2021, post-vaccination with Pfizer-BioNTech or Oxford-AstraZeneca vaccine. Image analysis was performed on dedicated workstations. SPSS was used for statistical analysis., Results: Thirty-six per cent of patients had reactive ALN until 10 weeks post-vaccination; reducing in frequency and intensity with time. Women were more likely to have reactive ALN compared with men. The frequency and intensity were higher in patients aged <65 years compared with those aged ≥65 years. However, no difference was found between both vaccine types in our study cohort., Conclusions: Physicians' awareness of COVID-19 vaccine-related reactive ALN on 18 F-FDG PET-CT is important to avoid inappropriate upstaging of cancers., (© Royal College of Physicians 2021. All rights reserved.)

Aim: To compare the incidence of pulmonary embolism (PE) in COVID-19 pneumonia and non-COVID-19-related community-acquired pneumonia (CAP) in hospitalised patients., Materials and Methods: A retrospective case-control study was conducted. This included patients hospitalised with pneumonia and investigated for suspected PE with computed tomography pulmonary angiogram (CTPA). Cases were defined as patients with COVID-19 pneumonia from 1 March 2020 to 17 May 2020; controls were patients with CAP from 5 July 2019 to 31 January 2020. The primary outcome was to determine the risk of developing PE in both groups. Multivariable logistic regression was used to calculate the adjusted odds ratio for PE., Results: One hundred and forty-four patients were included; 72 cases (47% male; mean age 59 (±15) years), and 72 controls (56% male; mean age 58 (±20) years). PE was diagnosed in 23.6% of the cases versus 6.9% of the controls. The adjusted odds ratio for PE in hospitalised patients with COVID-19 pneumonia compared with those with CAP was 3.23 (95% confidence interval [CI] 1.04-10.04, p=0.04)., Conclusion: The odds of developing PE in hospitalised patients with COVID-19 pneumonia are three-times higher than in those with CAP. The results provide a quantitative assessment of the risk of PE in COVID-19 pneumonia, a condition new to healthcare, compared to other forms of pneumonia with a well-established scientific basis., (Crown Copyright © 2021. Published by Elsevier Ltd. All rights reserved.)

The present study was performed on 180-day-old commercial Cobb chicks to assess the effects of the probiotic candidate Enterococcus faecalis-1, the Poulvac Escherichia coli vaccine, and their combination on growth parameters, intestinal microbial composition, immune response, and protection against challenge with the avian pathogen E. coli O78. The experimental groups were as follows: G1, basal diet; G2, basal diet and challenge with O78 at 28 days of growth; G3, basal diet, vaccination with Poulvac (1 and 15 days), and challenge with O78 at 28 days of growth; G4, basal diet, E. faecalis-1 supplementation for the first 3 days of growth, and challenge with O78 at 28 days of growth; G5, basal diet, E. faecalis-1 supplementation for the first 3 days of growth, vaccination with Poulvac (1 and 15 days), and challenge with O78 at 28 days of growth; G6, basal diet and E. faecalis-1 supplementation for the first 3 days of growth. The results showed that E. faecalis-1 in drinking water significantly improved the growth performance and immune response, increased the total Enterococcus counts, reduced the mortality, and decreased the visceral invasion by O78 in challenged broilers. While the effect of the Poulvac vaccine alone or with E. faecalis-1 was not significant compared with that of the E. faecalis-1 supplement, the vaccine improved the growth rate and decreased the mortality and visceral invasion by APEC O78 in challenged broilers. These results showed that E. faecalis-1 supplementation and routine vaccination with the Poulvac vaccine could improve the growth performance and immune response of broiler chickens and protect against challenge with APEC O78.

The current study conducted to investigate the effects of a multi-strain commercial probiotic mix and prebiotic (isomaltooligosaccharide, IMO) on broiler performance parameters, cecal microbiota composition, and protection against challenge with avian pathogenic Escherichia coli (APEC) O78. For this purpose, 101-day-old Cobb chicks were randomly allocated into four experimental groups (G)-G01: basal diet, G02: basal diet and challenged with E. coli O78 at 28 days old, G03: basal diet with probiotic mix and challenged with E. coli O78 at 28 days old, and G04: basal diet with IMO and challenged with E. coli O78 at 28 days old. Results showed that weekly body weights in G03 were heavier (P < 0.05) than those of G01 and G02 at the fourth and fifth week. The body gain at the fourth and fifth week was higher (P < 0.05) in G03 than those of the other groups. The hot carcass weight (g) was significantly higher in broiler chickens kept in G03 and G04 compared with those in the control groups (G01 and G02). The probiotic mix and IMO significantly increased the total lactobacilli and total lactobacilli-enterococci populations in the ceca of treated broilers, respectively compared with those in the control groups. The treated broilers (G03 and G04) also showed lower mortality percentage and E. coli recovery rates the liver and spleen than those in G02. It was concluded that probiotic mix or IMO significantly improved the growth performance and modulated the intestinal microbiota of broiler chickens challenged with APEC O78.

Diabetic polyneuropathy (DPN) is a complex and multifactorial entity in which various factors besides hyperglycemia play an important role. Symptoms of DPN are sensory, motor or autonomic. Intensive research proved that oxidative stress is the common denominator for the four major destructive pathways of hyperglycemia including increased hexosamine pathway flux, activation of Protein kinase-C (PKC) pathway, increased Advanced Glycated End-products (AGEs) formation, and increased Polyol Pathway flux. National data in Egypt confirms that more than 60% of Egyptian diabetic patients suffer from neuropathy. The most common complications of DPN are Cardiac Autonomic Neuropathy (CAN), diabetic foot and ulcers, neuromuscular disability, and anxiety. In addition, DPN affects the Quality of Life (QoL). According to common clinical practice, the common diagnostic tools are bed-side diagnosis and electrophysiological tests. Early diagnosis is critical to improve the prognosis of DPN and therapeutic intervention in the early phase. In this review, we provide a clear understanding of the pathogenesis, early diagnosis and the good management of DPN. Since the pathogenesis of DPN is multifactorial, its management is based on combination therapy of symptomatic; either pharmacological or non-pharmacological treatments, and pathogenic treatment. Alpha Lipoic Acid (ALA) is a potent anti-oxidant that has several advantages as a pathogenic treatment of DPN. So, in clinical practice, ALA may be prescribed for patients with early neuropathic deficits and symptoms. Patient education has an important role in the managemement of DPN., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

[Purpose] This study aimed to investigate the effect of auditory rhythmic cueing on gross motor skills in children with autism. [Participants and Methods] A total of 30 autistic children aged 8-10 years with mild to moderate autistic features participated in this study. They were randomly allocated to either the control group (n=15), which underwent a specially designed physical therapy program, or the study group (n=15), which underwent the same program in addition to gait training with rhythmic auditory stimulation. To provide rhythmic auditory stimulation, combination of a metronome beat set to the child's cadence and rhythmic cueing from the MIDI Cuebase musical program was used. Both groups received 3 sessions per week for 3 months. The Bruininks-Oseretsky Test of Motor Proficiency 2nd Edition was used to assess gross motor skills at baseline and after 3 months of intervention. [Results] The study found statistically significant improvements in bilateral coordination, balance, running speed and agility, and strength in both groups after treatment. Moreover, there were statistically significant differences between the 2 groups, with the study group showing better improvement in all outcome measures. [Conclusion] Gait training with auditory rhythmic cueing elicited a positive effect on the gross motor skills of children with autism.

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.

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.

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.

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.

Objective: The repair of a persistently leaking migrating tracheoesophageal fistula (TEF) represents a particular challenge owing to the low site of the fistula down to the tracheoesophageal septum (TES). A simple microscopic approach to repair a migrating TEF is described., Design: A description of five cases of migrating TEF. The repair technique and surgical outcome are described in detail., Setting: Tertiary care referral hospital., Methods: Excision of the fistula tract was done under local anesthesia and microscopic vision using microlaryngoscopic instruments followed by one-layer repair without soft tissue interposition. This technique was used in one patient with a leaking migrating TEF when planned dissection through the TES was abandoned. Subsequently, the technique was employed in four other patients with a similar TEF., Main Outcome Measures: Evidence of complete closure of the fistula was assessed clinically 1 week postoperatively. This was followed by methylene blue and Gastrografin swallowing tests. The methylene blue test was repeated after 6 months to exclude recurrence of the fistula and confirm persistent closure., Result: Complete closure of the fistulae was achieved when assessed clinically and by methylene blue and Gastrografin tests. All patients were discharged on a normal diet. Stable closure was confirmed by the methylene blue test after 6 months. The microlaryngoscopic instruments and surgical microscope have greatly facilitated access and dissection of the migrating fistula with minimum soft tissue loss., Conclusion: The described technique is simple, relatively safe, and reproducible for closure of a small migrating TEF. It can also be used to repair small, nonmigrating TEF.

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., ((c) 2006 Wiley-Liss, Inc.)

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.

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.

Study Design: A prospective, two-group comparative intervention study., Objective: To determine the acute and training effects of arm cranking exercise on blood lipid profiles in wheel chair bound individuals with spinal cord injury (SCI) and normal able-bodied subjects., Setting: Faculty of Science, School of Sport and Exercise Science, Liverpool John Moores University, England., Methods: Total cholesterol, triglyceride and high-density lipoprotein cholesterol (HDL-C) at rest and in response to arm cranking exercise before and after 12 weeks of training were compared between individuals with SCI (N = 5) and able-bodied subjects (N = 7). Following the determination of peak oxygen consumption (VO2peak), all subjects performed a submaximal arm cranking exercise at an intensity corresponding to 60-65% VO2peak for 30 min. Venous blood samples were obtained before and after submaximal exercise and measured for total cholesterol, triglycerides and HDL-C concentrations. These lipid parameters were remeasured in all subjects at rest and in response to the same submaximal arm cranking exercise after 12 weeks of individually supervised arm cranking training programme., Results: Before training, the resting mean value of triglyceride in individuals with SCI was significantly (P < 0.05) higher than that found in able-bodied persons. Acute arm cranking exercise did not change total cholesterol or triglyceride concentrations in either the SCI or the able-bodied groups. However, HDL-C increased significantly following exercise in the able-bodied subjects. Following training, the resting mean value of total cholesterol in the group with SCI was significantly (P < 0.05) higher compared with able-bodied individuals. Furthermore, the resting and post submaximal arm cranking exercise mean values of total cholesterol in the able-bodied group, but not in the group with SCI, were significantly lower than those observed before training. While the resting mean value of HDL-C before training in the group with SCI was lower than that found in the able-bodied, this difference did not reach the designated level of significance (P > 0.05). Submaximal arm cranking exercise was followed by a significant increase in HDL-C only in the able-bodied individuals. Compared to pretraining, the resting and post arm cranking exercise levels of HDL-C in the group with SCI increased significantly (P < 0.05) after training., Conclusion: It is concluded that acute arm cranking exercise and training in individuals with SCI is associated with favourable effects on HDL-C, whereas total cholesterols and triglycerides were not altered. The mechanism responsible for the increase in HDL-C with training in individuals with SCI is not known, but it is likely to be related to increased activity of cholesterol transport enzymes lipoprotein lipase and acyltransferase.

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.

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.

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.

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.

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.

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.

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.

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.

The present study examined the influence of ingesting a moderate dose of alcohol on the main determinants of blood rheology namely: plasma viscosity, plasma fibrinogen concentration, plasma total protein concentration, and haematocrit. Eleven moderately active young men were studied immediately after a standardised cycle ergometer test and during the 24 h period of recovery. 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. A significant reduction in plasma volume was observed immediately after exercise, but this decrease was restored 1-h post drink 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. Exercise induced significant changes (P<0.05) in blood rheology as manifested by a significant increase (P<0.05) in plasma viscosity and plasma fibrinogen. Parallel increase (P<0.05) in haematocrit and total protein was also observed after exercise. The increase in these rheological variables immediately after exercise was mainly due to exercise-induced plasma volume loss. During recovery, while the increase in haematocrit post-exercise returned to the baseline level in both control and alcohol trials, plasma viscosity and plasma fibrinogen remained significantly high during recovery in the alcohol trial compared with control condition. It is concluded that exercise induces significant changes in the main determinants of blood rheology and the consumption of alcohol after physical exercise delays the normal return of plasma viscosity, plasma fibrinogen to the resting baseline levels during recovery. Although the mechanism responsible for these findings is not, as yet known, it might be linked with alcohol induce dehydration.

The study determined the effect of alcohol ingestion postexercise on postprandial lipemia during recovery. The mean values were compared with those obtained in a control experiment during which no alcohol was given. Nineteen normolipidemic subjects (11 males and 8 females) performed two exercise trials at an intensity corresponding to 70% VO2max for 35 min. In a random order, alcoholic (0.7 g/kg) or alcohol-free drinks were given 1 h after the completion of exercise. Venous blood samples were obtained pre- (before breakfast) and postexercise and pre- and postprandially during recovery. Total cholesterol and high-density lipoprotein cholesterol showed no change with exercise or alcohol ingestion. In the control trial, when subjects consumed a standardized lunch, triglycerides showed no significant change, but when alcohol was consumed postexercise triglyceride concentration increased substantially 5 h during recovery in both males and females. The mechanism responsible for the rise in triglyceride concentration during recovery when alcohol was ingested following exercise is not known, but this appears to be a late phenomenon.

The present study examined the influence of ingesting a moderate dose of alcohol on plasminogen activator activity (t-PA), plasma fibrinogen (Fb), total degradation products (TDP) and the degradation products of fibrin (FbDP) and fibrinogen (FgDP) at rest and in response to exercise. Eleven male subjects performed two separate experimental trials at an exercise intensity corresponding to 70% maximal oxygen consumption for 35 min. Prior to trials, subjects were either given 0.5 g/kg alcohol in orange-flavoured drink or an equal volume of non-caloric non-alcoholic drink 45 min before exercise. Comparison of the levels of t-PA, Fb, TDP, FbDP, and FgDP at rest, before and 45 min after the ingestion of alcohol revealed no significant differences between alcohol and control experiments. Exercise resulted in a marked increase in t-PA, TDP, and FgDP, with no appreciable change in FbDP. Although plasma fibrinogen level showed significant decrease post-exercise when subjects ingested alcohol, this difference was small and its biological significance is questionable. While t-PA level increased similarly in response to exercise during alcohol and control trials, a significantly higher response of TDP was found during the control trial compared with alcohol trial. It was concluded that exercise with and without alcohol ingestion is followed by a substantial increase in t-PA, which coincided with an increase in TDP. The increase in TDP was mainly due to an increase in FgDP, but not to FbDP. These findings support the hypothesis that a significant fibrinogenolysis occurs in response to exercise, and moderate intoxication with alcohol prior to exercise reduced this response.

This study examined the effect of exercise on plasma fibrinogen concentrations with simultaneous measurements of plasma volume changes. Eight moderately active males aged 26.6+/-3.6 years (mean +/- SD) completed maximal (VO2max) and submaximal (75% VO2max for 30 minutes) exercise trials separated by 7 days. Venous blood samples were obtained at rest, immediately postexercise, and following 30 minutes of recovery. Whole blood was analysed for haematocrit and haemoglobin, while citrated plasma was assayed for fibrinogen levels. Values of haematocrit and haemoglobin before and after exercise were utilised for the estimation of plasma volume changes. Plasma volume decreased (p<0.05) immediately following both maximal (-17.7+/-5.1%) and submaximal (-14.3+/-4.1%) exercise. Exercise resulted in decreased plasma fibrinogen levels (maximal exercise: from 266.3+/-14.5 to 222.2+/-23.9 mg x dL(-1); submaximal exercise: from 239.5+/-45.4 to 209.7+/-42.4 mg x dL(-1)) only when postexercise raw data were corrected for the contraction of plasma volume. It is concluded therefore that changes in plasma volume in response to exercise should be taken into account when interpreting exercise effects on plasma fibrinogen concentration.

The effect of alcohol ingestion before exercise on blood haemostasis is not known. The present study examined the effects of moderate alcohol ingestion on blood haemostatic variables at rest and in response to exercise. Eleven normal healthy individuals randomly performed two tests separated by 7 days. A moderate dose of ethanol (0.5 g.kg-1) was administered before one test, whereas an equal volume of an alcohol-free drink was administered before the other. Forty-five minutes after the ingestion of either drink, the participants cycled at 65% VO2max for 30 min followed by a 5-min all-out performance. Venous blood samples were obtained before and 45 min after the ingestion of both drinks, and also immediately after exercise. Exercise induced a significant increase in tissue-type plasminogen activator activity and antigen, and factor VIII procoagulant activity. The post-exercise data also showed a significant decrease in plasminogen activator inhibitor activity and soluble fibrin, with a significant shortening in prothrombin time and activated partial thromboplastin time, but not thrombin time. No significant changes were observed in antithrombin III. Although no significant differences were found between trials in the haemostatic and fibrinolytic variables at rest, a significant decrease in fibrinogen concentration was observed after exercise in the alcohol trial. This suggests that ingesting a moderate dose of alcohol does not alter blood coagulation and fibrinolysis at rest. Apart from fibrinogen concentration, which was significantly decreased after exercise in the alcohol trial, most of the haemostatic and fibrinolytic variables were not affected by alcohol. The mechanism responsible for the decrease in fibrinogen following exercise in the alcohol trial remains unknown, but might be related to inhibition of fibrinogen synthesis by the liver or an enhanced rate of its catabolism.

Physical exercise activates blood coagulation and enhances fibrinolytic activity. To investigate whether these activations of blood coagulation and fibrinolysis are balanced post-exercise and during the period of recovery, 11 moderately active young men were examined immediately after a standardised cycle ergometer test and during the 24 h period of recovery. Blood samples were obtained at rest, immediately after exercise, and 2, 6 and 24 h after exercise. All post-exercise values were corrected for any change in plasma volume. Exercise induced a significant increase in factor VIII activity and this occurred with a significant shortening of activated partial thromboplastin time. A concomitant enhancement of tissue plasminogen activity resulted in significant increases in tissue plasminogen activity antigen and total fibrin/fibrinogen degradation products, and a significant decrease in tissue plasminogen activator inhibitor-1 activity. Increases in coagulation and fibrinolytic activity changed in parallel during exercise. However, during recovery, while the increase in factor VIII activity post-exercise persisted 2 and 6 h into recovery, fibrinolytic activity demonstrated a sharp fall. It is concluded that whereas the enhanced fibrinolytic activity during exercise appears to counterbalance the increase in blood coagulability, this haemostatic balance is not maintained during recovery. This perturbed blood haemostasis could constitute an enhanced risk for coronary artery thrombosis and may contribute to exercise-related cardiovascular events.

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. Although the long term effects of endurance training on blood rheology have been very briefly examined, the exact effect of training has not as yet been determined. However, 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 plasma volume as a result of training. It has been suggested that this blood dilutional effect of endurance training may be advantageous in delivering oxygen to the exercising muscles because of a reduced resistance to blood flow. The increase in plasma volume may also contribute to the body water pool and help offset dehydration. The influence of strength and power training on blood rheology is not known.

It is generally recognized that a decrease in carbohydrate availability can lead to the development of fatigue during prolonged exercise in humans. Administration of glucose or other carbohydrates before or during exercise has been shown to postpone fatigue, conserve muscle glycogen and improve performance. Carbohydrates can be categorised according to their ability to increase blood glucose concentration (known as glycaemic index) and by the extent they stimulate the release of insulin. The glycaemic index is reflected in the rate at which consumed carbohydrate is made available in the blood. Glucose is the only type of carbohydrate that can readily be oxidised by skeletal muscle for energy production. Gastric emptying is the primary factor limiting the rate of carbohydrate delivery to the blood and therefore influences the utilisation of exogenous carbohydrate ingested before or during exercise. Various methods have been used to assess the oxidation of exogenous carbohydrates during exercise. Peak rates of CHO oxidation during exercise have been reported between 0.4 and 1.0 g/min, and the rates of oxidation do not appear to be influenced to a major extent by the use of multiple drinking schedule in comparison with a single bolus schedule. Previous studies also suggest that the ingestion of fructose during exercise does not offer any additional benefits over ingestion of glucose or glucose polymer solutions of similar concentration. The hormones insulin, glucagon and adrenaline together with cortisol and growth hormone play key roles in the regulation of carbohydrate metabolism during exercise. Ingestion of moderately concentrated carbohydrate solutions (4-8%) enhances prolonged exercise performance and is appropriate for optimising energy and fluid delivery without causing adverse effects. The ergogenic effects of carbohydrate ingestion on performance during intermittent exercise such as competitive sports are less well established, although the evidence to date suggests diminished performance when carbohydrate are limiting.

This study examined the effect of carbohydrate ingestion on metabolic and performance-related responses during and after a simulated 1 h cycling time trial. Eight trained male cyclists (VO2 peak = 66.5 ml kg-1 min-1) rode their own bicycles mounted on a windload simulator to imitate real riding conditions. At a self-selected maximal pace, the cyclists performed two 1 h rides (separated by 7 days) and were fed either an 8% carbohydrate or placebo solution. The beverages were administered 25 min before (4.5 ml kg-1) and at the end (4.5 ml kg-1) of the ride. With carbohydrate feeding, plasma glucose tended (P = 0.21) to rise before the time trial. Compared with rest, the plasma glucose concentration decreased significantly (P < 0.05) at the end of both rides, with no statistically significant difference being observed between treatments. Thereafter, plasma glucose increased significantly (P < 0.05) at 15 and 30 min into recovery and was significantly higher at 30 min during the carbohydrate trial compared with the placebo trial. No significant changes in plasma free fatty acids were observed during the ride. However, a significant increase (P < 0.05) in free fatty acids was found at 15 and 30 min into recovery, with no difference between trials. Mean power output was significantly (P < 0.05) greater during the carbohydrate compared with the placebo trial (mean +/- S.E.: 277 +/- 3 and 269 +/- 3 W, respectively). The greater distance covered in the carbohydrate compared with the placebo trial (41.5 +/- 1.06 and 41.0 +/- 1.06 km, respectively; P < 0.05) was equivalent to a 44 s improvement. We conclude that pre-exercise carbohydrate ingestion significantly increases endurance performance in trained cyclists during a 1 h simulated time trial. Although the mechanism for this enhancement in performance with carbohydrate ingestion cannot be surmised from the present results, it could be related to a higher rate of carbohydrate oxidation, or to favourable effects of carbohydrate ingestion on the central component of fatigue.

We examined the effects of active warm-down (AWD) and carbohydrate ingestion on plasma levels of free fatty acids (FFAs) and glucose changes into recovery following prolonged submaximal exercise. Subjects in Group 1 cycled at 70% of maximal oxygen uptake (VO2max); carbohydrate (CHO) or placebo (PLA) was ingested 15 min before and 45 min during exercise. In the AWD experiment, exercise was followed immediately by an AWD and subjects were given a placebo solution. Group 2 subjects consumed CHO or PLA at 75 min during and after exercise at 70% VO2max. ANOVA revealed a significant decrease in blood glucose levels only in Group 1, with a concomitant increase in FFA concentrations during exercise in both groups. Carbohydrate ingestion in Groups 1 and 2 significantly decreased the normal response of FFAs during exercise and markedly reduced the normal elevation of FFAs in recovery. AWD following submaximal exercise had no effect on plasma FFA elevations in recovery. These results suggest that carbohydrate ingestion, but not active warm-down, attenuates FFA elevations in recovery.

Disturbances of the haemostatic balance may result in thrombosis or bleeding tendency. There have been abundant reports on the effects of exercise on blood haemostasis, but the results reported have been conflicting and difficult to interpret. This review outlines and critically evaluates the relevant literature on the effects of short term exercise and physical training on the 3 systems of blood haemostasis i.e. blood coagulation, fibrinolysis and platelet aggregation. Short term exercise is usually associated with a significant shortening of activated partial thromboplastin time (APTT) and a marked increase in factor VIII (FVIII). The rise in FVIII is directly related to exercise intensity and the individuals' training status. Exercise also induces a significant increase in blood fibrinolysis which is dependent on exercise intensity, duration and training condition. The rise in blood fibrinolysis is mainly due to an increase in tissue-type plasminogen activator (t-PA) and a decrease in its main inhibitor plasminogen activator inhibitor (PAI-1) which are released from the endothelial cells of the vessel wall. Platelet count increases in exercise and this is probably due to a fresh release of platelets from the spleen, bone marrow and lungs. Studies on the effects of exercise on platelet aggregation and markers of platelet activation have produced conflicting results, and the exact effects of exercise remain as yet undetermined. It is suggested that short term exercise activates blood coagulation and enhances blood fibrinolysis and the delicate balance between clot formation and clot dissolution is maintained in normal populations. No valid conclusion could be reached regarding the actual effects of physical training on blood coagulation, fibrinolysis and platelet aggregation. This is undoubtedly due to variations in training programmes employed, populations studied, and the analytical methods used.

The purpose of this study was to determine the effect of high and low intensity exercise conditioning programs on components pertinent to blood fibrinolysis and selected lipid profile variables in sedentary, but healthy individuals. Eighteen normal subjects were divided into two equal groups: high intensity, and low intensity exercise groups. Each subject in the high and low intensity groups exercised on a bicycle ergometer for 20 min, three times a week for 12 weeks at an intensity corresponding to 80% and 30% VO2 max, respectively. One week before and 1 week after the conditioning programs data were collected for body weight, percentage body fat, VO2 max and 12 h fasting blood levels of total tissue-type plasminogen activator (t-PA), tissue-type plasminogen activator activity (t-PAa), total plasminogen activator inhibitor (PAI-1), plasminogen activator inhibitor activity (PAI-1a), cholesterol (CHOL), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C). Post-conditioning, maximum oxygen consumption increased significantly (P < 0.05) only in the high intensity exercise group while body weight and percentage body fat did not change (P > 0.05) in either of the groups. Physical conditioning induced no statistically significant (P > 0.05) changes in the resting baseline of CHOL, TG or HDL-C. The resting baseline values of t-PA, t-PAa, PAI-1 and PAI-1a before conditioning did not vary significantly (P > 0.05) between two groups. Similarly, after training no significant change in t-PA, t-PAa or PAI-1. However, PAI-1a decreased significantly (P < 0.05) in the high intensity group, but not in the low intensity (P > 0.05). It is concluded that high, but not low, intensity physical conditioning significantly enhances the cardiorespiratory fitness and reduces the resting level of plasminogen activator inhibitor activity which may be linked with the favourable effects of exercise conditioning.