Alan R. Morton

Overtraining in athletes. An update.

SummaryOvertraining 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.

Exercise and the Immune Response

SummaryA growing number of reports have become available which implicate infectious disease with reduced performance in athletes.The immune system consists of both nonspecific and specific components geared to control infections. Adaptive immunity functions through both antibody-mediated and cell-mediated compartments to establish and maintain long term immunity to infectious agents. Evidence is accumulating to support the view that physical exercise can lead to modification of the cells of the immune system. However, studies have often not been well designed to control exercise protocols when examining the effects of exercise on the immune system.Large numbers of peripheral blood lymphocytes are mobilised with exercise and in vitro tests indicate that temporarily these cells may not be capable of responding normally to mitogens. These reactions appear to be influenced by hormones to some degree and there are reports that the cells of the immune system are extremely active biochemically and may depend on products from muscles to maintain their activity.Specific populations within the circulating leucocyte pool vary significantly with exercise and there is some evidence that the T4/T8 lymphocyte ratio may become significantly reduced. This reduction in ratio may be related to the variable responses to T and B cell mitogens recorded in vitro which overall suggests that a temporary immune suppression may exist following certain training or performance schedules. It is argued that this may lead to a temporary susceptibility to infection and could result from overtraining.

Resistance Training over 2 Years Increases Bone Mass in Calcium-Replete Postmenopausal Women†

Understanding the stress/strain relationship between exercise and bone is critical to understanding the potential benefit of exercise in preventing postmenopausal bone loss. This study examined the effect of a 2‐year exercise intervention and calcium supplementation (600 mg) on bone mineral density (BMD) in 126 postmenopausal women (mean age, 60 ± 5 years). Assignment was by block randomization to one of three groups: strength (S), fitness (F), or nonexercise control (C). The two exercise groups completed three sets of the same nine exercises, three times a week. The S group increased the loading, while the F group had additional stationary bicycle riding with minimal increase in loading. Retention at 2 years was 71% (59% in the S group, 69% in the F group, and 83% in the C group), while the exercise compliance did not differ between the exercise groups (S group, 74 ± 13%; F group, 77 ± 14%). BMD was measured at the hip, lumbar spine, and forearm sites every 6 months using a Hologic 4500. Whole body BMD also was measured every 6 months on a Hologic 2000. There was no difference between the groups at the forearm, lumbar spine, or whole body sites. There was a significant effect of the strength program at the total (0.9 ± 2.6%; p < 0.05) and intertrochanter hip site (1.1 ± 3.0%; p < 0.01). There was a significant time and group interaction (p < 0.05) at the intertrochanter site by repeated measures. This study shows the effectiveness of a progressive strength program in increasing bone density at the clinically important hip site. We concluded that a strength program could be recommended as an adjunct lifestyle approach to osteoporosis treatment or used in combination with other therapies.

Effects of a short-term circuit weight training program on glycaemic control in NIDDM

This study assessed the effects of short-term circuit weight training (CWT) on glycaemic control in NIDDM. Twenty-seven untrained, sedentary subjects (mean age, 51) with NIDDM participated in an 8-week randomised, controlled study, involving either CWT 3 days/week (n = 15) or no formal exercise (control) (n = 12). All subjects performed regular self-blood glucose monitoring throughout. Fasting serum glucose and insulin were measured following a 12-h fast and during an oral glucose tolerance test (75 g) before and after 8 weeks. Twenty-one subjects completed the study (CWT, n = 11) (Control, n = 10). Strength for all exercises improved significantly after CWT. Pooled time-series analysis, using a random effects model, revealed an overall decrease in self-monitored glucose levels with CWT compared to controls. Significant reductions from baseline values were observed in both the glucose (-213 mmol l-1 per 120 min, P < 0.05) and insulin (-6130 pmol l-1 per 120 min, P < 0.05) area under the curve following CWT relative to controls. After adjustment for body mass changes, the change in self-monitored glucose levels and insulin area under the curve, but not glucose area under the curve, remained significant. Short-term CWT therefore may provide a practical exercise alternative in the lifestyle management of this condition.

The emerging role of glutamine as an indicator of exercise stress and overtraining

SummaryGlutamine is an amino acid essential for many important homeostatic functions and for the optimal functioning of a number of tissues in the body, particularly the immune system and the gut. However, during various catabolic states, such as infection, surgery, trauma and acidosis, glutamine homeostasis is placed under stress, and glutamine reserves, particularly in the skeletal muscle, are depleted.With regard to glutamine metabolism, exercise stress may be viewed in a similar light to other catabolic stresses. Plasma glutamine responses to both prolonged and high intensity exercise are characterised by increased levels during exercise followed by significant decreases during the post-exercise recovery period, with several hours of recovery required for restoration of pre-exercise levels, depending on the intensity and duration of exercise. If recovery between exercise bouts is inadequate, the acute effects of exercise on plasma glutamine level may be cumulative, since overload training has been shown to result in low plasma glutamine levels requiring prolonged recovery. Athletes suffering from the overtraining syndrome (OTS) appear to maintain low plasma glutamine levels for months or years. All these observations have important implications for organ functions in these athletes, particularly with regard to the gut and the cells of the immune system, which may be adversely affected. In conclusion, if methodological issues are carefully considered, plasma glutamine level may be useful as an indicator of an overtrained state.

The Independent and Combined Effects of Aerobic Exercise and Dietary Fish Intake on Serum Lipids and Glycemic Control in NIDDM: A randomized controlled study

OBJECTIVE The triglyceride-lowering effects of ω-3 fats and HDL cholesterol-raising effects of exercise may be appropriate management for dyslipidemia in NIDDM. However, fish oil may impair glycemic control in NIDDM. The present study examined the effects of moderate aerobic exercise and the incorporation of fish into a low-fat (30% total energy) diet on serum lipids and glycemic control in dyslipidemic NIDDM patients. RESEARCH DESIGN AND METHODS In a controlled, 8-week intervention, 55 sedentary NIDDM subjects with serum triglycerides > 1.8 mmol/l and/or HDL cholesterol < 1.0 mmol/l were randomly assigned to a low-fat diet (30% daily energy intake) with or without one fish meal daily (3.6 g ω-3/day) and further randomized to a moderate (55–65% VO2max) or light (heart rate < 100 bpm) exercise program. An oral glucose tolerance test (75 g), fasting serum glucose, insulin, lipids, and GHb were measured before and after intervention. Self-monitoring of blood glucose was performed throughout. RESULTS In the 49 subjects who completed the study, moderate exercise improved aerobic fitness (VO2max) by 12% (from 1.87 to 2.07 l/min, P = 0.0001). Fish consumption reduced triglycerides (0.80 mmol/l, P = 0.03) and HDL3 cholesterol (0.05 mmol/l, P = 0.02) and increased HDL2 cholesterol (0.06 mmol/l, P = 0.01). After adjustment for age, sex, and changes in body weight, fish diets were associated with increases in GHb (0.50%, P = 0.05) and self-monitored glucose (0.57 mmol/l, P = 0.0002), which were prevented by moderate exercise. CONCLUSIONS A reduced fat diet incorporating one daily fish meal reduces serum triglycerides and increases HDL2 cholesterol in dyslipidemic NIDDM patients. Associated deterioration in glycemic control can be prevented by a concomitant program of moderate exercise.

The Influence of Exercise-Induced Plasma Volume Changes on the Interpretation of Biochemical Parameters Used for Monitoring Exercise, Training and Sport

A number of studies have demonstrated considerable plasma volume changes during and after exposure to different environmental and physiological conditions. These changes are thought to result from transient fluid shifts into (haemodilution) and out of (haemoconcentration) the intravascular space. If the levels of plasma constituents are to be routinely measured for research purposes or used as indicators of training adaptation or the health of an athlete, then it is important to consider the dynamic nature of plasma volume.Controversy still exists over the relevance of plasma volume interactions with plasma constituent levels, and while some investigators have taken plasma volume shifts into account, others have chosen to ignore these changes. Bouts of acute exercise have been shown to produce a transient haemoconcentration immediately after long distance running, bicycle ergometry and both maximal and submaximal swimming exercise. While these changes are transient, lasting only a few hours, other studies have reported a longer term haemodilution following acute exercise. In addition, endurance training has been shown to cause long term expansion of the plasma volume.It would, therefore, seem important to consider the influence of plasma volume changes on plasma solutes routinely measured for research, and as markers of training adaptation, prior to arriving at conclusions and recommendations based purely on their measured plasma level. To further confound this issue, plasma volume changes are known to be associated with heat acclimatisation, hydration state, physical training and postural changes, all of which may differ from one experiment or exercise bout to the next, and should thus be taken into account.

Biological responses to overload training in endurance sports

SummaryFive 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 overtraining. 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.

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

SummaryIn 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.

The haematological, biochemical and immunological profile of athletes suffering from the overtraining syndrome.

To help clarify the overtraining syndrome (OTS), a combination of parameters were measured in ten athletes who were suffering from OTS. Blood samples were obtained at rest and a range of haematological, biochemical and immunological tests were carried out on the samples. For each parameter, the mean value for the group was compared to an established normal range amongst age-matched controls. The subjects were also asked to complete a questionnaire to establish the severity of their condition. The data indicated that the debilitating fatigue experienced by the OTS sufferers was not related to any of the blood parameters traditionally associated with chronic exercise stress, since levels were normal in OTS. The only parameter measured which deviated significantly from the normal range for both the sedentary controls and the athletes was the plasma concentration of glutamine. Although the data in this study would suggest that plasma glutamine concentrations represented an objective, measurable difference between OTS subjects and normal controls, it remains to be shown that there is any correlation between glutamine concentrations and other clinical symptoms of OTS such as physical capability.