Influence of exercise-induced plasma volume changes on the interpretation of biochemical data following high-intensity exercise.

OBJECTIVE: To assess the effects that exercise-induced plasma volume changes (PVCs) have on the interpretation of biochemical and hormonal parameters in the blood of athletes after high-intensity exercise. It was hypothesized that two unrelated high-intensity exercise protocols, performed by two separate subject groups each using different exercise modes, would result in similar percentage changes in plasma volume (% delta PV). It was further hypothesized that the % delta PV, measured in both protocols, would comparably influence the interpretation of biochemical variables measured following exercise. DESIGN: An experimental before-after trial on volunteers was performed. Two different exercise modes employing two different high-intensity acute exercise protocols were investigated. Eight male swimmers performed an interval training session (ITS) consisting of 15 x 100-m freestyle efforts at 95% of their maximal exercise intensity, and eight male runners performed a multistage discontinuous treadmill test (MSD) to volitional exhaustion. SETTING: The Human Performance Laboratory at the Department of Human Movement at the University of Western Australia. MAIN OUTCOME MEASURES: Blood samples obtained before, immediately after, and 30, 60, and 120 min during recovery were analyzed for plasma volume changes, urea, uric acid, creatinine, albumin, calcium, iron, transferrin, testosterone, cortisol, and sex hormone-binding globulin (SHBG). MAIN RESULTS: The ITS and MSD protocols produced similar and significant alterations (p < 0.01) in plasma volume. Both protocols also elicited significant fluctuations (p < 0.01) in the concentration of most of the parameters measured (excluding iron). When albumin, transferrin, testosterone, and SHBG values were adjusted for the significant % delta PV, their concentrations did not change over the experimental period, suggesting that the changes in measured concentration of these parameters may be, in part, due to changes in plasma volume. However, urea, uric acid, creatinine, calcium, and cortisol, when corrected for % delta PVC, still demonstrated significant changes (p < 0.01). CONCLUSIONS: It is recommended, when sampling biochemical and hormonal parameters in blood following an acute bout of exercise, that corrections for PVCs should be conducted. Apparent changes in blood solutes may reflect PVCs. PVCs should be taken into consideration when interpreting results regardless of exercise protocol and exercise mode performed.

Depression of plasma glutamine concentration after exercise stress and its possible influence on the immune system.

OBJECTIVE: To determine whether plasma glutamine levels can be used as an indicator of exercise-induced stress, and to consider the possible effects of low plasma glutamine concentrations on the immune system. METHODS: We used two exercise regimens: in Trial 1 seven male subjects were randomly stressed on a treadmill at 0, 30%, 60%, 90% and 120% of their maximal oxygen uptake (VO2max); in Trial 2 five highly trained male subjects underwent intensive interval training sessions twice daily for ten days, followed by a six-day recovery period. RESULTS: Plasma glutamine concentrations decreased significantly from an average of 1244 +/- 121 mumol/L to 702 +/- 101 mumol/L after acute exercise at 90% VO2max (P < 0.05) and to 560 +/- 79 mumol/L at 120% VO2max (P < 0.001). Four of the five subjects showed reduced plasma glutamine concentrations by Day 6 of the overload training trial, with all subjects displaying significantly lower glutamine levels by Day 11. However, glutamine levels showed a variable rate of recovery over the six-day recovery period, with two subjects' levels remaining low by Day 16. CONCLUSIONS: Reduced plasma glutamine concentrations may provide a good indication of severe exercise stress.

Psychological and immunological correlates of acute overtraining.

Five men undertook two intensive interval training sessions per day for 10 days, followed by 5 days of active recovery. Subjects supplied a venous blood sample and completed a mood-state questionnaire on days 1, 6, 11 and 16 of the study. Performance capabilities were assessed on days 1, 11 and 16 using a timed treadmill test to exhaustion at 18 kmh-1 and 1% grade. These individuals became acutely overtrained as indicated by significant reductions in running performance from day 1 to day 11. The overtrained state was accompanied by severe fatigue, immune system deficits, mood disturbance, physical complaints, sleep difficulties, and reduced appetite. Mood states moved toward baseline during recovery, but feelings of fatigue and immune system deficits persisted throughout the study.

The effects of an acute bout of sleep on running economy and VO2 max.

Synchronized human sleep has been shown to decrease activation of the sympathetic nervous system, resulting in reduced levels of oxygen consumption. This is in direct conflict with sympathetic arousal, which coincides with the initiation of exercise. Although a considerable body of research has investigated the effects of sleep deprivation on exercise performance, the effects of an acute bout of sleep on exercise response have not been previously reported. This question appears relevant considering the occurrence of acute sleep bouts among athletes competing in prolonged multi-event competition (e.g. swimming, track and field). To investigate the effects of an acute bout of sleep on submaximal (running economy) and maximal oxygen consumption, seven male volunteers participated in a continuous, progressive treadmill test to volitional exhaustion immediately following a 1-h bout of sleep (SB) or no sleep (Control). The subjects served as their own controls and the order of trials was randomized. A MANOVA with repeated measures indicated no difference between groups for running economy or VO2 (P < 0.05). However, a significant interaction effect was observed in which SB resulted in greater running economy (lower VO2) through the first two stages of the protocol, while the control treatment yielded a greater economy throughout the remaining stages. While the implications of the findings are uncertain, they may indicate differences in psychological arousal or anxiety as a result of treatments or the possibility of a delayed sympathetic arousal in the early stages of exercise following sleep.

Periodisation of training stress--a review.

Athletic performance improves as the athlete adapts to progressively increasing training loads. Empirical observations and studies investigating fluctuations in performance indicate that this adaptation occurs during periods of reduced training, termed regeneration periods. Thus it is essential that adequate regeneration time be included in training programmes so that adaptation can be achieved. In order to induce adaptation, heavy periods of training are used to provide a stimulus for adaptive processes to become functional. The literature and anecdotal accounts suggest that the cycling of light, medium, and heavy periods of training is an optimal method for combining the heavy periods of training with the periods of light training needed to allow adaptation and supercompensation.

Periodisation and the prevention of overtraining.

It may be essential for the athlete to train in cycles in order to induce optimal improvements and prevent overtraining. Without sufficient recovery time, adaptation may not occur and the athlete may develop the symptoms of overtraining due to continuous and/or excessive exposure to training stress. Training in cycles provides guidelines for the times in the training programme when regeneration should be complete, and therefore the times when the athlete can be screened for overtraining without confusing the fatigue of overload training with that of overtraining. A periodised training structure provides guidelines for conducting research into the mechanisms of training adaptation and overtraining.

Acute intensive interval training and T-lymphocyte function.

Immune suppression has been suggested to occur as a result of acute exercise although results of previous studies are variable, possibly due to the failure of some researchers to control exercise intensity and duration. Most of the studies so far have investigated immediate effects after bouts of exercise mainly in subjects undertaking lower body exercise (running or cycling), and the time course of recovery has rarely been determined. We chose two groups of athletes for our studies. One group represented subjects of a range of fitness levels from recreational runners to high-performance runners. The second group represented kayakists with a similar range of fitness levels. Following interval training designed to stress either the lower or upper body anaerobically, we have now shown that upper body exercise (kayaking) induces similar in vitro responses to those described for lower body exercise. There were no differences between the responses of low-fitness versus high-fitness subjects. In addition we have studied the in vitro responses of leukocytes following acute anaerobic exercise over a 24-h recovery period. The results showed that the reduced lymphocyte proliferative response, in vitro, to the T-cell mitogen CONA experienced immediately after exercise returned to normal levels within 2 h of recovery time. This suggests that the reduction in lymphocyte proliferative response is a short transient one.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell numbers and in vitro responses of leucocytes and lymphocyte subpopulations following maximal exercise and interval training sessions of different intensities.

In vitro lymphocyte function and the mobilisation of peripheral blood leucocytes was examined in eight trained subjects who undertook an incremental exercise test to exhaustion and a series of interval training sessions. Venous blood samples were obtained before the incremental test, immediately after, and 30, 60, and 120 min after the test. Interval training sessions were undertaken on separate days and the exercise intensities for each of the different sessions were 30%, 60%, 90% and 120% of their maximal work capacity respectively, as determined from the incremental exercise test. There were 15 exercise periods of 1-min duration separated by recovery intervals of 2 min in each session. Venous blood samples were obtained immediately after each training session. Significant increases in lymphocyte subpopulations (CD3+, CD4+, CD8+, CD20+, and CD56+) occurred following both maximal and supramaximal exercise. This was accompanied by a significant decrease in the response of cultures of peripheral blood lymphocytes to Concanavalin A (ConA), a T-cell mitogen. The state of lymphocyte activation in vivo as measured by CD25+ surface antigen was not, however, affected by acute exercise. The total number of lymphocytes, distribution of lymphocyte subpopulations and in vitro lymphocyte response to ConA had returned to pre-exercise levels within half an hour of termination of exercise but serum cortisol concentrations had not begun to fall at this time. There was a significant decrease in the CD4+:CD8+ cell ratio following exercise; this was more the result of increases in CD3-CD8+ cells (CD8+ natural killer cells) than to CD3+CD8+ cells (CD8+ T-lymphocytes). Decreased responsiveness of T-cells to T-cell mitogens, postexercise, may have been the result of decreases in the percentage of T-cells in postexercise mixed lymphocyte cultures rather than depressed cell function. The cause of this was an increase in the percentage of natural killer cells which did not respond to the T-cell mitogen. The results indicated that while a substantial immediate in vitro "immunomodulation" occurred with acute exercise, this did not reflect an immunosuppression but was rather the result of changes in the proportions of reactive cells in mononuclear cell cultures. We have also demonstrated that the degree of the change in distribution of lymphocyte subpopulation numbers and responsiveness of peripheral blood mononuclear cells in in vitro mitogen reactions increased with increasing exercise intensity. Plasma volume changes may have contributed to some of the changes seen in leucocyte population and subpopulation numbers during and following exercise.

Biological responses to overload training in endurance sports.

Five subjects undertook 10 days of twice daily interval training sessions on a treadmill followed by 5 days of active recovery. On days 1, 6, 11, and 16 the subjects were required to undertake a test of submaximal and maximal work capacity on a treadmill combined with a performance test consisting of a run to exhaustion with the treadmill set at 18 km.h-1 and 1% gradient. Also on these days a pre-exercise blood sample was collected and analysed for a range of haematological, biochemical and immunological parameters. The subjects experienced a significant fall in performance on day 11 which had returned to pretraining levels on day 16. Serum ferritin concentrations were depressed significantly from pretraining concentrations at the conclusion of the recovery period while the expression of lymphocyte activation antigens (CD25+ and HLA-DR+) was increased both after the training phase and the recovery phase. The number of CD56+ cells in the peripheral circulation was depressed at the conclusion of the recovery period. Several parameters previously reported to change in association with overload training failing to reflect the decrease in performance experienced by subjects in this study, suggesting that overtraining may best be diagnosed through a multifactorial approach to the recognition of symptoms. The most important factor to consider may be a decrease in the level of performance following a regeneration period. The magnitude of this decreased performance necessary for the diagnosis of overtraining and the nature of an "appropriate" regeneration period are, however, difficult to define and may vary depending upon the training background of the subjects and the nature of the preceding training. It may or may not be associated with biochemical, haematological, physiological and immunological indicators. Individual cases may present a different range of symptoms and diagnosis of overtraining should not be excluded based on the failure of blood parameters to demonstrate variation. However, blood parameters may be useful to identify possible aetiology in each separate case report of over-training. An outstanding factor to emerge from this study was the difficulty associated with an objective diagnosis of overtraining and this is a possible reason why there have been new accounts of overtraining research in the literature.

Physiological and kinanthropometric attributes of elite flatwater kayakists.

Physical and physiological factors accounting for the variability of performance in 500, 1000, 10,000, and 42,000 m flatwater kayaking were investigated using linear regression. Times achieved for each distance were used as the dependent variable for analysis while the independent variables were the parameters derived from the test battery. The 38 kayakists who participated were categorized as either state team members or nonselected paddlers, based on an objective selection policy. Several of the participant subjects were Australian international representatives. All selected paddlers were grouped together and Student's t-tests performed to determine which variables could distinguish between selected and nonselected paddlers. Simple regression was used to determine the strength of association of each parameter with performance time over each race distance, and multiple regression was used to generate equations for the prediction of performance times. Aerobic power and variables related to the aerobic-anaerobic transition were examined using gas analysis during an incremental workload test on a kayak ergometer. A 1-min all-out test also on a kayak ergometer was used to obtain an indication of anaerobic capacity and power. Muscular strength and fatigue were assessed using a simulated kayak stroke on a Cybex isokinetic dynamometer. Physical characteristics were determined using kinanthropometric tests. Aerobic power, anaerobic power and capacity, muscular strength, resistance to muscular fatigue, and measures of body size were significantly greater in more successful kayakists. All of the parameters measured correlated significantly with performance time over at least one of the four race distances.(ABSTRACT TRUNCATED AT 250 WORDS)

Overtraining in athletes. An update.

Overtraining appears to be caused by too much high intensity training and/or too little regeneration (recovery) time often combined with other training and nontraining stressors. There are a multitude of symptoms of overtraining, the expression of which vary depending upon the athlete's physical and physiological makeup, type of exercise undertaken and other factors. The aetiology of overtraining may therefore be different in different people suggesting the need to be aware of a wide variety of parameters as markers of overtraining. At present there is no one single diagnostic test that can define overtraining. The recognition of overtraining requires the identification of stress indicators which do not return to baseline following a period of regeneration. Possible indicators include an imbalance of the neuroendocrine system, suppression of the immune system, indicators of muscle damage, depressed muscle glycogen reserves, deteriorating aerobic, ventilatory and cardiac efficiency, a depressed psychological profile, and poor performance in sport specific tests, e.g. time trials. Screening for changes in parameters indicative of overtraining needs to be a routine component of the training programme and must be incorporated into the programme in such a way that the short term fatigue associated with overload training is not confused with the chronic fatigue characteristic of overtraining. An in-depth knowledge of periodisation of training theory may be necessary to promote optimal performance improvements, prevent overtraining, and develop a system for incorporating a screening system into the training programme. Screening for overtraining and performance improvements must occur at the culmination of regeneration periods.

Monitoring exercise stress by changes in metabolic and hormonal responses over a 24-h period.

Metabolic and endocrine responses of 14 subjects of varying levels of fitness to an intensive anaerobic interval training session were assessed before exercise and at 2 h, 4 h, 8 h and 24 h postexercise. The endocrine response of the same subjects to a control day, where they were required not to exercise, was also assessed and compared with the values obtained on the interval training day. Uric acid, urea, and creatine phosphokinase concentrations still remained elevated above pre-exercise values 24 h postexercise. Lactate, creatinine, testosterone and cortisol concentrations were significantly elevated above pre-exercise values immediately postexercise but these had reversed by 2 h postexercise. Over the remainder of the recovery period testosterone concentrations remained significantly lower than values measured at similar times on the control day. This was shown to be due directly to a change in testosterone as sex hormone binding globulin concentration remained constant throughout the recovery period. The data indicate that when comparisons of data were made to control (rest) days, imbalances in homeostasis, due to intensive training, are not totally reversed within the next 24-h. The data also demonstrate that the parameters measured undergo the same variations in subjects with a wide range of physical fitness, indicating that these parameters could be used to monitor exercise stress and recovery in athletes of a wide range of abilities.(ABSTRACT TRUNCATED AT 250 WORDS)