Showing papers on "Interval training published in 1992"

Biological responses to overload training in endurance sports.

Abstract: 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.

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Abstract: Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.

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

Abstract: 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.

The effect of interval and continuous training on the aerobic parameters.

Abstract: The purpose of this study was to investigate changes in the parameters of aerobic function resulting from continuous training (CT) and interval training of both low power (LPO-IT) and high power output (HPO-IT). Untrained males (n = 17, 25.1 yrs) trained 10 weeks on cycle ergometers (four 40-min sessions a week) at 80% VO2max. Cycle ramp function tests at 0 and 10 weeks were used to determine the four aerobic parameters:VO2max, ventilation threshold (VeT), effective time constant for O2 uptake kinetics (MRT), and work efficiency (eta): VO2max increased significantly (3.30 to 3.66 l.min-1). Absolute VeT increased significantly (2.17 to 2.45 l.min-1) but there was no change in the relative threshold (VeT/VO2max). MRT decreased significantly from 38.8 to 33.1 seconds and there was no change in eta. There were no between-group differences; thus neither low power output nor high power output interval training offers an advantage over continuous training of the same average power output in altering the aerobic parameters.

Acute intensive interval training and T-lymphocyte function.

Abstract: : FRY, R. W., A. R. MORTON, and D. KEAST. Acute intensive interval training and T-lymphocyte function. Med. Sci. Sports Exerc., Vol. 24, No. 3, pp. 339–345, 1992. 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. The addition of interleukin-2 (IL-2) or indomethacin to the mitogen-stimulated cultures of preexercise and postexercise cells demonstrated that the postexercise suppression in 3H-DNA synthesis of the leukocytes could not be accounted for by either an inability of the T-cells to produce IL-2 or the inhibitory action of prostaglandin production.

Training Practices of Athletes Who Participated in the National Wheelchair Athletic Association Training Camps

Abstract: A survey designed to record training practices of athletes with disabilities was administered to participants in the 1990 and 1991 National Wheelchair Athletic Association Elite and Developmental Athlete Training Camp. Information on age, weight, nature and level of disability, the sport and experience in it, sources of training information, dietary practices, and alcohol and cigarette consumption was requested. The athletes were also asked to report their weekly training practices by quarters for the previous year concerning average number of workouts per week, number of hours per workout, number of miles per week, percent of time spent on speed work and/or interval training per week, number of weight training sessions per week, and the number of competitions entered per quarter. Results indicate that most of the athletes derived much of their training information from personal contact with coaches, other athletes, and sport scientists. Many do not set goals in developing training routines, training diet...

Adenosine in exercise adaptation.

Abstract: By influencing the regulation of the mechanisms of angiogenesis, erythropoietin production, blood flow, myocardial glucose uptake, glycogenolysis, systolic blood pressure, respiration, plasma norepinephrine and epinephrine levels, adenosine may exert a significant effect on the body's adaptation response to exercise. However, adenosine's possible influence over the vasodilatory response to exercise in skeletal muscle is controversial and more research is required to resolve this issue. Various popular exercise training methods, such as cyclic training, interval training, and the 'warm down' from training may increase adenosine levels and thereby might enhance the response of adenosine-influenced adaptive mechanisms. Among the several classes of drugs which may enhance extracellular adenosine levels and thereby might augment adenosine-influenced adaptive mechanisms, are the anabolic steroidal and some readily available non-steroidal anti-inflammatory drugs (NSAIDs).

[An epidemiologic study of the value and limits of physical therapy/exercise therapy in Fontaine stage II arterial occlusive disease].

Abstract: Using a questionaire the members of the German Society for Angiology (DGA) were interrogated on the use of physical training for the treatment of peripheral arterial occlusive disease; from a total of n = 431 as much as n = 156 responded, i.e. making up a response of 36%. 104 of them conduct physical training either on their own or assign patients to it (67%). In most of the institutions exclusively walking/interval training (83%) or medical exercise (74%) are performed. In most cases the training is conducted by physiotherapeutists (71%). 13% of the patients are admitted exclusively to physical training, 34% undergo combined therapy, i.e. physical training and vaso-active medication. 22% receive mere medical, 31% surgical treatment. A general evaluation on the success of the different therapies applied turned out following frequency: 1. combined therapy (medical treatment/physical training); 2. surgical procedures as a therapeutic measure; 3. physical training; 4. medical treatment. A further study performed at three ambulatory centres offering physical training were to show what kind and to which extent such training is useful. In 34% of the cases (from a total of n = 201 patients with peripheral arterial occlusive disease in state II according to Fontaine) contraindications argue against the application of physical training. From a rest of 66% as much as 36% of the patients refuse to undergo physical training the reasons of which were stated with large transport distances and time problems. The remaining rest accepts the offer, although 24% attend such training only sporadically. The results show that mainly contraindications and insufficient patient compliance account for the fact that only one third of the patients attend physical training. The results are discussed and proposals are made to improve patient compliance.

Cautions with the use of data from incremental work‐rate tests for the prescription of work rates for interval training

Abstract: Ventilation per minute (VE) and percent fractional expired oxygen [FEO2(%)] data were used to determine the work rate at which the ventilatory threshold occurred during an incremental kayak test. Although an exponential curve fitted the ventilation data significantly, a quartic curve was more useful for subjective determination of the ventilatory threshold. A cubic polynomial curve fitted the blood lactate, pH, carbon dioxide pressure, bicarbonate, and base‐excess data from an incremental test on a treadmill, indicating the more complex curvilinear nature of these parameters as exercise intensity increased. This creates difficulties for the objective determination of a training intensity, which is likely to induce optimal training adaptation. In addition, the prescription of training based on a set blood lactate concentration may result in different physiologic stress for different individuals. Heart rate was found to vary little within a range of work rates that induced maximum variation in lactate conce...

Enhancement of functional power in patients with coronary artery disease by circuit interval training

Abstract: The purpose of this study was to investigate the effect of a 12‐week circuit interval training (CIT) program on several indices of functional power in coronary artery disease (CAD) patients following from the exercise regimen. Twenty‐two patients with documented CAD served as subjects. After training, peak oxygen consumption (ml kg−1 min−1) and maximal MET level achieved in these patients increased significantly (p ≤ 0.05). Several hemodynamic variables and electrocardiographic data were studied to try to assess whether functional power was enhanced predominantly by central or peripheral hemodynamic and metabolic events. Maximal ST‐segment depression did not decrease significantly, and peak heart rate (HR), systolic blood pressure, rate‐pressure product, and the HR at the time of ST‐segment depression did not increase significantly. These data imply that the change in functional power observed was primarily the result of adaptation in the periphery.