Biomedical subjects

R J Shephard

Publications and source records attributed to R J Shephard.

At least 55 records · Page 3Linked to original sources

PubMed1999

Immune changes in humans during cold exposure: effects of prior heating and exercise.

This study examined the immunological responses to cold exposure together with the effects of pretreatment with either passive heating or exercise (with and without a thermal clamp). On four separate occasions, seven healthy men [mean age 24.0 +/- 1.9 (SE) yr, peak oxygen consumption = 45.7 +/- 2.0 ml. kg(-1). min(-1)] sat for 2 h in a climatic chamber maintained at 5 degrees C. Before exposure, subjects participated in one of four pretreatment conditions. For the thermoneutral control condition, subjects remained seated for 1 h in a water bath at 35 degrees C. In another pretreatment, subjects were passively heated in a warm (38 degrees C) water bath for 1 h. In two other pretreatments, subjects exercised for 1 h at 55% peak oxygen consumption (once immersed in 18 degrees C water and once in 35 degrees C water). Core temperature rose by 1 degrees C during passive heating and during exercise in 35 degrees C water and remained stable during exercise in 18 degrees C water (thermal clamping). Subsequent cold exposure induced a leukocytosis and granulocytosis, an increase in natural killer cell count and activity, and a rise in circulating levels of interleukin-6. Pretreatment with exercise in 18 degrees C water augmented the leukocyte, granulocyte, and monocyte response. These results indicate that acute cold exposure has immunostimulating effects and that, with thermal clamping, pretreatment with physical exercise can enhance this response. Increases in levels of circulating norepinephrine may account for the changes observed during cold exposure and their modification by changes in initial status.

Adult↗

PubMed1999

Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution.

The contribution of hyperthermia to the differential leukocytosis of exercise remains obscure. This study examined changes in circulating sympathoadrenal hormone concentrations and patterns of leukocyte and lymphocyte subset (CD3(+), CD4(+), CD8(+), CD19(+), CD3(-)16(+)/56(+)) redistribution during exercise, with and without a significant rise of rectal temperature (T(re)). Ten healthy men [age 26.9 +/- 5.7 (SD) yr, body mass 76.0 +/- 10.9 kg, body fat 13.9 +/- 4.6%, peak O(2) consumption: 48.0 +/- 12.4 ml x kg(-1) x min(-1)] exercised for 40 min (65% peak O(2) consumption) during water immersion at 39 or 18 degrees C. T(re) increased from 37.2 to 39.3 degrees C (P < 0.0001) after 40 min of exercise in 39 degrees C water but was held constant to an increment of 0.5 degrees C during exercise in 18 degrees C water. Application of this thermal clamp reduced exercise-associated increments of plasma epinephrine (Epi) and norepinephrine (NE) by >50% (P < 0.05) and abolished the postexercise increase in cortisol. Thermal clamping also reduced the exercise-induced leukocytosis and lymphocytosis. Multiple regression demonstrated that T(re) had no direct association with lymphocyte subset mobilization but was significantly (P < 0.0001) correlated with hormone levels. Epi was an important determinant of total leukocytes, lymphocytes, and CD3(+), CD4(+), CD8(+), and CD3(-)CD16(+)/56(+) subset redistribution. The relationship between NE and lymphocyte subsets was weaker than that with Epi, with the exception of CD3(-)CD16(+)/56(+) counts, which were positively (P < 0.0001) related to NE. Cortisol was negatively associated with leukocytes, CD14(+) monocytes, and CD19(+) B- and CD4(+) T-cell subsets but was positively related to granulocytes. We conclude that hyperthermia mediates exercise-induced immune cell redistribution to the extent that it causes sympathoadrenal activation, with alterations in circulating Epi, NE, and cortisol.

Adrenal Glands↗

PubMed1999

Effects of exercise and training on natural killer cell counts and cytolytic activity: a meta-analysis.

Meta-analysis techniques have been used to accumulate data from 94 studies describing the natural killer (NK) cell response of some 900 volunteers to acute and chronic exercise. NK cell numbers have been indicated in terms of CD3-CD16+CD56+, CD16+ or CD56+ phenotypes, and cytolytic activity has been expressed per 10,000 peripheral blood mononuclear cells or in terms of lytic units. Acute exercise has been categorised as sustained moderate (50 to 65% of aerobic power), sustained vigorous (>75% of aerobic power), brief maximal or 'supramaximal', prolonged, eccentric or resistance, and repeated exercise. In general, there was a marked increase in NK cell count at the end of exercise, probably attributable to a catecholamine-mediated demargination of cells. Following exercise, cell counts dropped to less than half of normal levels for a couple of hours but, except in unusual circumstances (e.g. prolonged, intense and stressful exercise), normal resting values are restored within 24 hours. If activity is both prolonged and vigorous, the decrease in NK cell counts and cytolytic activity may begin during the exercise session. Although the usual depression of NK cell count seems too brief to have major practical importance for health, there could be a cumulative adverse effect on immunosurveillance and health experience in athletes who induce such changes several times per week. There is a weak suggestion of an offsetting increase in resting NK cell counts and cytolytic action in trained individuals, and this merits further exploration in studies where effects of recent training sessions are carefully controlled.

Adult↗

PubMed1999

Immune responses to training: how critical is training volume?

BACKGROUND: If the volume of training undertaken is sufficient to induce a negative energy balance, the anticipated benefit of an enhanced immune response may be reduced or lost. METHODS: 33 sedentary but healthy male volunteers aged 19-29 years, recruited from the university community. A peak oxygen intake measurement (cycle ergometer) and a 60-min exercise challenge at 60% of aerobic power were performed before and after 12 wk of treatment. Total leukocytes, subsets, CD3+, CD4+, CD8+, CD16+, CD19+, and CD25+ counts (FACScan), cytolytic activity (51Cr release) and cell proliferation (PHA and PWM) were measured, with subjects assigned arbitrarily to one of three groups: light training (18 subjects, aerobic exercise at 70-85% HRmax 3 times/wk), moderate training (9 subjects, similar programme 4-5 times/wk) and control (6 subjects). RESULTS: Groups were initially well-matched in physical and physiological terms. Training increased aerobic power (8%, light, 21% moderate training), with a loss of body mass and fat in the moderate training group. Controls showed no changes. Resting CD16+ counts increased by 27% (light training) and CD16+ CD56+ counts by 21% (moderate training), with less post-exercise suppression of counts than at recruitment. Light training also decreased CD3+ and CD4+ counts without changing the CD4+/CD8+ ratio. Moderate training decreased resting CD19+ count. CONCLUSIONS: From the viewpoint of immune function, the optimal training regimen is of low volume. Moderate training sufficient to induce a negative energy balance yields a smaller increase in numbers of non-MHC-restricted cytotoxic cells, and carries the negative consequence of diminished B cell counts.

Adult↗

PubMed1999

Immune function in hyperbaric environments, diving, and decompression.

The purpose of this review is to examine the influence of exposure to hyperbaric oxygen (HBO2) deep diving, and decompression on various facets of the immune response. Potential changes during exposure include a decrease in the CD4+:CD8+ ratio, a decreased proliferation of lymphocytes, and an activation of neutrophils with migration to regions of high oxygen pressure. There may also be an activation of the complement cascade during decompression. Clinical indicators of overall immune suppression include a decreased response to antigens, a weakening of autoimmune responses, and a slower rejection of allografts. In professional divers, immune changes are at least partially offset by acclimatization, and seem to have little clinical significance. However, patients receiving HBO2 are a more vulnerable group; in their case, exposure may impair immune surveillance, and a careful monitoring of immune function may be important to the success of treatment.

Animals↗

PubMed1999

Immune dysfunction as a factor in heat illness.

The influence of stress on immune function is well recognized. Indeed for some authors, the changes induced by combinations of vigorous exercise and heat exposure are merely examples of a more generalized stress response. However, there has been surprisingly little consideration of how far disturbances of immune function contribute to heat illness and heat fatalities. The physiology of exercise in hot environments has recently been reviewed. This article provides a brief outline of the main features of heat illness. It then summarizes current knowledge of general immune responses to stress and specific reactions to heat exposure and heavy exercise, and discusses the potential impact of such changes on the outcome of heat illness.

Animals↗

PubMed1998

Worksite physical activity interventions.

BACKGROUND: National objectives for public health have targeted worksite as important settings for interventions to increase physical activity. However, expert reviews reveal no scientific consensus about the effectiveness of worksite interventions for increasing physical activity or fitness. METHODS: We judged the quantity and quality of existing evidence against scientific standards for the internal and external validity of the research design and the validity of measurements. Meta-analytic methods were used to quantify the size of effects expressed as Pearson correlation coefficients (r). Variation in effect was examined in relation to several features of the studies deemed important for implementing successful worksite interventions. Pre-experimental cohort studies were excluded because they are sensitive to secular trends in physical activity. RESULTS: Twenty-six studies involving nearly 9,000 subjects yielded 45 effects. The mean effect was heterogeneous and small, r = 0.11 (95% CI, -0.20 to 0.40), approximating 1/4 S.D., or an increase in binomial success rate from 50% to 56%. Although effects varied slightly according to some of the study features we examined, effects were heterogeneous within levels of these features. Hence, the moderating variables examined did not explain variation in the effects (P > 0.05). The exception was that effects were smaller in randomized studies compared with studies using quasi-experimental designs (P < 0.05). CONCLUSIONS: Our results indicate that the typical worksite intervention has yet to demonstrate a statistically significant increase in physical activity or fitness. The few studies that have used an exemplary sample, research design, and outcome measure have also yielded small or no effects. The generally poor scientific quality of the literature on this topic precludes the judgment that interventions at worksites cannot increase physical activity or fitness, but such an increase remains to be demonstrated by studies using valid research designs and measures.

Adolescent↗

PubMed1998

Stress hormones and the immunological responses to heat and exercise.

This review focuses on the response of "stress" hormones to heat, exercise (single or repeated bouts), and combinations of these stimuli, with particular reference to their impact upon immune function. Very hot conditions induce a typical stress response, with secretion of catecholamines and cortisol. The catecholamines induce a demargination of leukocytes, and cortisol subsequently causes cells to migrate to lymphoid tissue. Sustained exercise, even in a thermally comfortable environment, induces a larger hormonal response than moderate thermal stress. With moderate exercise, increases in leukocyte numbers are related mainly to plasma norepinephrine concentrations, but with more intense exercise epinephrine concentrations assume a major importance. As exercise continues, plasma cortisol levels also rise, inducing an influx of neutrophils from bone marrow and an efflux of other leukocyte subsets. A combination of exercise and heat stress augments both hormonal and leukocyte responses. But these changes seem to be reversed if temperatures are clamped by exercising in cold water. If a second bout of exercise is performed with an inter-test interval of 30-45 min, neither hormone concentrations nor immune responses show any great cumulative effect under temperate conditions. However, in a hot environment the second exercise bout induces a larger and more persistent neutrophilia. Training influences these various responses mainly by decreasing the stress imposed when exercising at a given absolute work-rate.

Body Temperature Regulation↗

PubMed1998

Acute and chronic over-exertion: do depressed immune responses provide useful markers?

There are ethical objections to inducing cumulative muscle damage and associated decrements of performance deliberately in a healthy athlete. Available data on acute and chronic over-exertion thus include the changes of immune response observed following a single bout of exhausting exercise, sequential observations made on top-level competitors as they approach peak training periods, and longitudinal laboratory studies of heavy (but not necessarily damaging) bouts of training. In all three of these situations, subclinical muscle damage initiates an acute inflammatory response, with a resulting deterioration in physical performance. Although much smaller in degree and shorter in duration, the associated changes in immune function are similar to those seen in sepsis. There have been major advances in immunological technique over the past decade, and significant changes in a number of elements of the immune response can be identified in athletes during periods of heavy training. The most promising immunological marker of excessive training seems a decrease in salivary IgA concentration. However, no single change occurs with sufficient consistency to identify the individual competitor who is at risk of overtraining. Mechanisms can be conceived that convert a sequence of excessive training bouts into an acute and then a chronic inflammatory process, but the syndrome of overtraining has a complex overlay of biological and psychological influences. It remains more easily detected by decreases in physical performance and alterations in mood state than by changes in immune function.

Antibody Formation↗

PubMed1998

Effects of endurance training and heat acclimation on psychological strain in exercising men wearing protective clothing.

Two experiments examined the influences of endurance training and heat acclimation on ratings of perceived exertion (RPE) and thermal discomfort (RTD) during exercise in the heat while wearing two types of clothing. In experiment 1, young men underwent 8 weeks of physical training [60-80% of maximal aerobic power (VO2max) for 30-45 min day-1, 3-4 days week-1 at 20-22 degrees C dry bulb (db) temperature] followed by 6 days of heat acclimation [45-55% VO2max for 60 min day-1 at 40 degrees C db, 30% relative humidity (rh)] (n = 7) or corresponding periods of control observation followed by heat acclimation (n = 9). In experiment 2, young men were heat-acclimated for 6 or 12 days (n = 8 each). Before and after each treatment, subjects completed bouts of treadmill exercise (1.34 m s-1, 2% grade in experiment 1 and 0% grade in experiment 2) in a climatic chamber (40 degrees C db, 30% rh), wearing in turn normal light clothing (continuous exercise at 37-45% VO2max for a tolerated exposure of 116-120 min in experiment 1 and at 31-34% VO2max for 146-150 min in experiment 2) or clothing protective against nuclear, biological, and chemical agents (continuous exercise at 42-51% VO2max for a tolerated exposure of 47-52 min in experiment 1 and intermittent exercise at 23% VO2max for 97-120 min in experiment 2). In experiment 1, when wearing normal clothing, endurance training and/or heat acclimation significantly decreased RPE and/or RTD at a fixed power output. There were concomitant reductions in relative work intensity (% VO2max) [an unchanged oxygen consumption (VO2) but an increased VO2max, or a reduced VO2 with no change of VO2max], rectal temperature (Tre), mean skin temperature (Tsk), and/or heart rate (HR). When wearing protective clothing, in contrast, there were no significant changes in RPE or RTD. Although training and/or acclimation reduced %VO2max or Tre, any added sweat that was secreted did not evaporate through the protective clothing, thus increasing discomfort after training or acclimation. Tolerance times were unchanged in either normal or protective clothing. In experiment 2, when wearing normal clothing, heat acclimation significantly decreased RPE and RTD at a fixed power output, with concomitant reductions in Tre, Tsk, and HR; the response was greater after 12 than after 6 days of acclimation, significantly so for RPE and HR. When wearing protective clothing, the subjects exercised at a lower intensity for a longer duration than in the moderate exercise trial. Given this tactic, either 6 or 12 days of heat acclimation induces significant reductions RPE and/or RTD, accompanied by reductions in Tre, Tsk, and/or HR. Tolerance times in protective clothing were also increased by 11-15% after acclimation, despite some increase of sweat accumulation in the protective clothing. The results suggest that (1) neither endurance training nor heat acclimation reduce psychological strain when protective clothing is worn during vigorous exercise, because increased sweat accumulation adds to discomfort, and (2) in contrast to the experience during more vigorous exercise, heat acclimation is beneficial to the subject wearing protective clothing if the intensity of effort is kept to a level that allows permeation of sweat through the clothing. This condition is likely to be met in most modern industrial applications.

Acclimatization↗

PubMed1998

Immune responses to inflammation and trauma: a physical training model.

Physical activity and training have some potential as tools for examining immune responses to inflammation and trauma. Contributors to the present symposium review various aspects of the inflammatory process, including issues of lymphocyte recirculation and endotoxemia. They examine also the extent and nature of the immune disturbances induced by acute and chronic exercise and consider parallels between such responses and cellular manifestations of clinical sepsis. Factors modulating immune responses during physical activity include changes in the circulating levels of various cytokines, alterations in nutritional status, an altered expression of adhesion molecules, and the possible intervention of reactive species. Factors that can exacerbate exercise-induced changes include exposure to adverse environments, particularly hot conditions, and disturbances of the normal sleep-wakefulness cycle. Current research in exercise immunology finds clinical application in attempts to regulate aging, acute viral infections, and neoplasia.

Animals↗

PubMed1998

Immune changes induced by exercise in an adverse environment.

Both physical activity and exposure to environmental stressors such as cold, heat, and high altitudes modify various components of immune function: T cell counts, natural killer (NK) cell counts, and cytolytic activity, cytokine secretion, lymphocyte proliferation and immunoglobulin levels. Light physical activity or a moderate level of environmental stress stimulate the immune response, but exhausting physical activity or more severe environmental stress have a suppressant effect, manifested by a temporary increase in susceptibility to viral infections. Combinations of physical activity and environmental stress generally have at least an additive effect. Thus, an intensity of physical activity or of environmental stress that is beneficial in itself can readily cause immunosuppression if the body is challenged by the two stimuli simultaneously.

Altitude↗

PubMed1998

Aging and immune response to exercise.

Human immune function undergoes adverse changes with aging. The T cells, which have a central role in cellular immunity, show the largest age-related differences in distribution and function, with thymus involution as the apparent underlying cause. The immune responses to acute exercise and training have not been studied extensively in the elderly. The natural killer (NK) cell response to a single exercise challenge is normal in older individuals, but immediately after exercise the elderly subjects manifest less suppression of phytohemagglutinin (PHA)-induced lymphocyte proliferation than younger individuals. In contrast, a strenuous exercise seems to induce a more sustained postexercise suppression of cellular immunity in older individuals than in their young peers. A few cross-sectional comparisons of immune status between physically fit elderly individuals and young sedentary controls suggest that habitual physical activity may enhance NK cell activity, checking certain aspects of the age-related decline in T cell function, such as reduced mitogenesis in response to plant lectins and decreases in the production of certain types of cytokine. The clinical implications, however, remain to be clarified by future study.

Adult↗

PubMed1998

Physical exercise as a human model of limited inflammatory response.

An inflammatory response represents a fundamental series of humoral and cellular reaction cascades in response to infection, tissue injury, and related insults. An excessive response is commonly seen under the pathological conditions of trauma, sepsis, and burns. It is becoming increasingly evident that most, if not all, of the distinguishing features of a classical inflammatory response are detectable in an exercising individual, namely mobilization and activation of granulocytes, lymphocytes, and monocytes; release of inflammatory factors and soluble mediators; involvement of active phase reactants; and activation of the complement and other reactive humoral cascade systems. While the manifestation of many exercise-induced immune and related changes has been reported and confirmed repeatedly, the underlying mechanisms triggering and modulating the elicited immune responses are, at best, poorly understood. Unlike the exaggerated and sometimes uncontrollable inflammatory response in septic and trauma patients resulting in morbidity and mortality, strenuous and severe exercise normally elicits an inflammatory response of a subclinical nature to facilitate the repairing process for site-specific tissue damage. Regardless of the inciting event, for example trauma, infection, or exercise, and given an appropriate triggering signal, a remarkably similar sequence of inflammatory reactions can be reproduced in the affected host. Therefore, physical exercise and training represent an acceptable and good model for the study of limited inflammatory responses in humans.

Cytokines↗

PubMed1998

Cold exposure and immune function.

The influence of cold exposure on immune function is reviewed. Data obtained mainly on small mammals suggest that the acute effect of severe chilling is a suppression of several cellular and humoral components of the immune response, including a decrease of lymphocyte proliferation, a down-regulation of the immune cascade, a reduction of natural killer (NK) cell count, cytolytic activity, activation of complement, and the induction of heat shock proteins. However, adaptation to a given cold stimulus appears to develop over the course of 2-3 weeks. Further work is needed to examine interactions between cold exposure and exercise, and to determine whether the disturbances of immune response are sufficient to impair immunosurveillance in human subjects.

Animals↗

PubMed1998

beta-Endorphin and natural killer cell cytolytic activity during prolonged exercise. is there a connection?

This study was designed to test whether a single 50-mg dose of the opioid antagonist naltrexone hydrochloride, ingested 60 min before 2 h of moderate-intensity exercise (i.e., 65% peak O2 consumption), influenced the exercise-induced augmentation of peripheral blood natural killer cell cytolytic activity (NKCA). Ten healthy male subjects were tested on four occasions separated by intervals of at least 14 days. A rested-state control trial was followed by three double-blind exercise trials [placebo (P), naltrexone (N), and indomethacin] arranged according to a random block design. The indomethacin exercise trial is discussed elsewhere (S. G. Rhind, G. A. Gannon, P. N. Shek, and R. J. Shepherd. Med. Sci. Sports Exerc. 30: S20, 1998). For both the P and N trials, plasma levels of beta-endorphin were increased (P < 0.05) at 90 and 120 min of exercise but returned to resting (preexercise) levels 2 h postexercise. CD3(-)CD16(+)CD56(+) NK cell counts and NKCA were significantly (P < 0.05) elevated at each 30-min interval of exercise compared with correspondingly timed resting control values. However, there were no differences in NK cell counts or NKCA between P and N trials at any time point during the two trials. Changes in NKCA reflected mainly changes in NK cell count (r = 0.72; P < 0.001). The results do not support the hypothesis that the enhancement of NKCA during prolonged submaximal aerobic exercise is mediated by beta-endorphin.

Adult↗

PubMed1998

Immune deficits induced by strenuous exertion under adverse environmental conditions: manifestations and countermeasures.

A brief description is given of the various laboratory and clinical manifestations of immune suppression that arise when strenuous exertion must be carried out in the face of a negative energy balance, shifts of circadian rhythm, sleep deprivation, psychological stressors, and exposure to hostile environments (extremes of heat or cold, high or low ambient pressures, and hyper- or hypo-gravity conditions). From the operational viewpoint, immune suppression could impair both physical and mental performance by increasing susceptibility to opportunistic microorganisms. It is also likely to increase susceptibility to sepsis following trauma or extensive burns, and has occasionally predisposed to fatal myocarditis. The effects of such challenges are complex, in part because of interactions between the various stressors. It is thus important to investigate the impact and to devise appropriate countermeasures with the full physical and intellectual resources of a defense environmental research laboratory. Existing knowledge of the topic is reviewed, and suggestions are made for research that may lead to new and more effective countermeasures.

Energy Metabolism↗

PubMed1998

Autonomic regulation of the circulation during exercise and heat exposure. Inferences from heart rate variability.

Minimal information is available on the autonomic response to exercise under adverse environmental conditions. Traditionally, pharmacological blockade has been used to study autonomic responsiveness but, owing to its invasive nature, such studies have been limited in their scope. Recent advances in electrocardiographic tape recording, telemetry and associated computing systems have provided investigators with noninvasive methods for assessing the autonomic response to various physiological stressors. This article describes methods for the analysis of heart rate variability (HRV) and discusses the reports of those who have used HRV analysis to evaluate autonomic regulation during exercise, heat exposure and the combination of these 2 stressors. Spectral analysis of HRV reduces variations in the R-R interval into component sine waves of differing amplitude and frequency. Amplitude (variance) is displayed as a function of frequency, and power (cumulative variance) is calculated for specified frequency ranges (< 0.03 Hz, 0.03 to 0.15 Hz and 0.15 to 0.5 Hz). Parasympathetic nervous system activity can be inferred from the several indices of high frequency power; however, the estimation of sympathetic nervous system activity from low frequency power is more problematic. Data on HRV have shown that sympathovagal regulation during exercise is dependent on the intensity of the activity and the environmental conditions. At the onset of exercise, heart rate is increased by a reduction in vagal tone and a temporary increase in sympathetic tone. A continuation of physical activity is associated with a continued withdrawal of vagal activity and an attenuation of sympathetic nervous system tone. However, with the additional stimulus of a heated environment, sympathetic activity remains increased throughout exercise.

Adult↗