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Context: High-intensity exercise causes tissue damage, production of stress hormones, and alterations in the function and quantity of various immune cells. Many clinical-physical stressors such as surgery, trauma, burns and sepsis induce a pattern of hormonal and immunological response similar to that of exercise. It has thus been suggested that heavy exercise might be used to cause graded and well-defined amounts of muscle trauma, thereby serving as an experimental model for inflammation and sepsis., Objective: In order to explore whether some form of strenuous exercise might provide an useful model for the inflammatory process, we studied the effects of three different exercise protocols on blood leukocyte count during and following exercise., Design: Four different experimental conditions, using a randomized-block design., Setting: Defence and Civil Institute of Environmental Medicine, North York, Ontario, Canada., Participants: Eight healthy and moderately fit males., Procedures: Participants were each assigned to four experimental conditions. Subjects performed 5 minutes of cycle-ergometry exercise at 90%, 2 hours of cycle-ergometry exercise at 60%, a standard circuit of resistance exercises with 3 sets of 10 repetitions at 60 to 70% of one-repetition maximum (1-RM) force at each of 5 different stations; or they remained seated for 5 hours. DIAGNOSTIC TEST USED: Flow cytometric analysis., Main Measurements: Blood samples were analyzed for total leukocyte counts, total T cells, T helper/inducer cells, T suppressor/cytotoxic cells, B cells, cytolytic T cells, and natural killer cells., Results: The peak aerobic and prolonged submaximal exercise induced similar alterations in cell counts. These changes were generally larger than those produced by the resistance exercise, although both resistance and peak aerobic exercise resulted in a significantly longer-lasting decrease in the CD4+/CD8+ ratio than the submaximal exercise bout did., Conclusion: The data suggest that, of the three exercise patterns tested, prolonged aerobic exercise induced the largest and most readily measured patterns of immune response. Nevertheless, the changes provided only a partial model for the clinical inflammatory process.

It is commonly believed that exposure to cold environmental temperatures depresses immune function and increases the risk for infection. This review paper will 1) present an overview of human physiological responses to cold exposure, 2) present the human studies examining the effects of cold exposure on immune responses, and 3) summarize recent experiments from our laboratories examining the effects of exercise and fatigue on immune responses during subsequent cold exposure. Based on the review of the literature, there is no support for the concept that cold exposure depresses immune function.

The present review examines the impact of basic recruit training on health and lifestyle. Many of those recruited begin training with a less than optimal lifestyle with respect to fitness, smoking habits, alcohol consumption, drug abuse, and exposure to sexually transmitted diseases. Thus, there is scope to enhance training programs that address fitness and lifestyle, minimizing potential losses in health and efficiency from upper respiratory infections, musculoskeletal injuries, cardiac catastrophes, mental disturbances, and adverse responses to extreme environments.

This study tested the hypothesis that exercise elicits monocytic cytokine expression and that prolonged cold exposure modulates such responses. Nine men (age, 24.6 +/- 3.8 y; VO(2 peak), 56.8 +/- 5.6 ml. kg(-1). min(-1)) completed 7 days of exhausting exercise (aerobic, anaerobic, resistive) and underwent three cold, wet exposures (CW). CW trials comprised

The effect of an 18.5-week infantry training program on health status was studied in 23 male military personnel (aged 22.0 +/- 0.5 years, mean +/- SE). Aerobic power, body composition, and immune function (including natural killer cell activity, mitogen-stimulated lymphocyte proliferation, in vivo cell-mediated immunity, and secretory immunoglobulin A levels) were measured in subjects at the beginning and end of the course. Subjects self-reported their symptoms of sickness in health logs using a precoded checklist. Data from this study indicate that subjects became leaner and maintained, but did not increase, their aerobic fitness by the end of the course. Cell function was enhanced significantly; however, in vivo cell-mediated immunity remained the same, and levels of secretory immunoglobulin A were lower by the end of the course. The incidence of infection remained stable throughout the course. These results indicate that the current pattern of infantry training does not have an adverse effect on the health status of recruits.

It was hypothesized that muscle injury would be greater with eccentric than with all-out or prolonged exercise, and that immune changes might provide an indication that supplements the information provided by traditional markers such as creatine kinase (CK) or delayed-onset muscle soreness. Eight healthy males [mean (SE): age = 24.9 (2.3) years, maximum oxygen consumption (VO2(max)) = 43.0 (3.1) ml x kg(-1) x min(-1)] were each assigned to four experimental conditions, one at a time, using a randomized-block design: 5 min of cycle ergometer exercise at 90% VO2(max) (AO), a standard circuit-training routine (CT), 2 h cycle ergometer exercise at 60% VO2(max) (Long), or remained seated for 5 h. Blood samples were analyzed for CK, natural killer (NK) cell counts (CD3(-)/CD16(+)56(+)), cytolytic activity and plasma levels of the cytokines interleukin (IL)-6, IL-10, and tissue necrosis factor alpha (TNF-alpha). CK levels were only elevated significantly 72 h following CT. NK cell counts increased significantly during all three types of exercise, but returned to pre-exercise baseline values within 3 h of recovery. Cytolytic activity per NK cell was not significantly modified by any type of exercise. Prolonged exercise induced significant increases in plasma IL-6 and TNF-alpha. We conclude that the lack of correlation between traditional markers of muscle injury (plasma CK concentrations and muscle soreness rankings) and immune markers of the inflammatory response suggests that, for the types and intensities of exercise examined in this study, the exercise-induced inflammatory response is modified by humoral and cardiovascular correlates of exercise.

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.

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.

Purpose: This study examined the effects of advancing gestational age and maternal aerobic conditioning (stationary cycling) on fetal heart rate (FHR) responses to strenuous non-steady-state maternal exercise., Methods: Subjects chose to participate in either an exercise group (EG) or control group (CG). Fourteen healthy, previously sedentary pregnant women participated in the exercise group, and six pregnant controls remained sedentary. Stationary cycling (heart rate target: 145 beats x min(-1)) was performed 3 d x wk(-1) by the exercised group. Exercise duration was increased from 14 to 25 min x session(-1) during the second trimester and was maintained at 25 min x session(-1) throughout the third trimester. FHR was monitored before, during, and after a progressive submaximal cycle ergometer test (peak heart rate = 170 beats x min(-1)) performed at approximately 27 and 37 wk gestation., Results: Mean FHR increased significantly (P < 0.05) during exercise, followed by a modest suppression and then a delayed rise during the recovery period at both observation times. Fetal bradycardia was not observed in any of the exercise tests. Effects of advancing gestational age included a lower FHR baseline both at rest and in response to maternal exercise and a lower incidence of exercise-induced tachycardia. Maternal physical conditioning did not significantly alter FHR response to maternal exercise., Conclusion: Our results support the hypothesis that FHR responses to strenuous exercise are altered by advancing gestational age and a brief progressive exercise test terminated at a maternal heart rate of 170 beats x min(-1) does not induce fetal distress during a healthy pregnancy.

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.

To determine if heat exposure alters the hormonal responses to moderate, repeated exercise, 11 healthy male subjects [age = 27.1 (3.0) years; maximal oxygen consumption, VO2max = 47.6 (6.2) ml x kg x min(-1); mean (SD)] were assigned to four different experimental conditions according to a randomized-block design. While in a thermoneutral (23 degrees C) or heated (40 degrees C, 30% relative humidity) climatic chamber, subjects performed either cycle ergometer exercise (two 30-min bouts at approximately 50% VO2max, separated by a 45-min recovery interval, CEx and HEx conditions), or remained seated for 3 h (CS and HS conditions). Blood samples were analyzed for various exercise stress hormones [epinephrine (E), norepinephrine (NE), dopamine, cortisol and human growth hormone (hGH)]. Passive heating did not alter the concentrations of any of these hormones significantly. During both environmental conditions, exercise induced significant (P < 0.001) elevations in plasma E, NE and hGH levels. At 23 degrees C during bout 1: E = 393 (199) pmol x l(-1) (CEx) vs 174 (85) pmol x l(-1) (CS), NE = 4593 (2640) pmol x l(-1) (CEx) vs 1548 (505) pmol x l(-1) (CS), and hGH = 274 (340) pmol x l(-1) (CEx)vs 64 (112) pmol x l(-1) (CS). At 40 degrees C, bout 1: E = 596 (346) pmol x l(-1) (HEx) vs 323 (181) pmol x l(-1) (HS), NE = 7789 (5129) pmol x l(-1) (HEx) vs 1527 (605) pmol x l(-1) (HS), and hGH = 453 (494) pmol x l(-1) (HEx) vs 172 (355) pmol x l(-1) (HS). However, concentrations of plasma cortisol were increased only in response to exercise in the heat [HEx = 364 (168) nmol x l(-1) vs HS = 295 (114) nmol x l(-1)]. Compared to exercise at room temperature, plasma levels of E, NE and cortisol were all higher during exercise in the heat (P < 0.001 in all cases). The repetition of exercise did not significantly alter the pattern of change in cortisol or hGH levels in either environmental condition. However, repetition of exercise in the heat increased circulatory and psychological stress, with significantly (P < 0.001) higher plasma concentrations of E and NE. These results indicate a differential response of the various stress hormones to heat exposure and repeated moderate exercise.

This study examined indices of parasympathetic (PNS) and sympathetic (SNS) nerve activity during exposure to heat and/or two successive bouts of exercise. Seven healthy males [age = 27.1 (3.6) years; mean (SD), maximum oxygen consumption (VO2max) = 48.1 (7.6) ml x kg(-1) x min(-1)] were assigned to each of four experimental conditions according to a randomized-block design. While in a thermoneutral (23 degrees C) or heated (40 degrees C, 30% relative humidity) climatic chamber subjects performed exercise on a cycle ergometer (two 30-min bouts at approximately 50% VO2max, separated by a 45-min recovery period, (CEx and HEx, respectively) or remained seated (CS and HS, respectively) for 2 h. The R-R intervals of the subjects' ECGs were analyzed for selected near-steady-state time periods [termed Phase I (25-40 min) and Phase II (100-115 min)] according to the method of Yamamoto and Hughson (J Appl Physiol 71:1143-1150, 1991). Total (P(T)), low-frequency (P(LF) = 0-0.15 Hz) and high-frequency (P(HF) = 0.15-0.5 Hz) power spectra were calculated using coarse-graining spectral analysis. Heat exposure alone did not alter autonomic balance or levels of circulating catecholamines significantly. Exercise in both environmental conditions induced a significant decrease in an index of PNS tone (PHF:PT) [PNS indicator for CS = 0.084 (0.04) vs CEx = 0.023 (0.015) and HS = 0.065 (0.027) vs HEx = 0.015 (0.009)], with an increase in catecholamine concentrations. Although the index of SNS activity (P(LF):P(HF)) tended to rise with exercise in both environmental conditions, increments reached levels of significance only during exercise in the heat [SNS indicator for CS = 8.22 (5.58) vs CEx = 34.06 (21.73) and HS = 8.94 (5.49) vs HEx = 54.29 (49.80)]. The relative magnitudes of SNS and PNS indicators did not differ significantly between the first and second bouts of exercise. These results indicate the substantial contribution of vagal withdrawal and catecholamine secretion to the increase in heart rate that occurs during repeated moderate exercise at room temperature and the additional contribution from SNS activity during such exercise in the heat.

This study examined the impact of heat exposure and moderate, intermittent exercise on the CD16+ and CD56+ cell counts and cytolytic activity. Eleven healthy male subjects [mean (SD): age = 27.1 (3.0) years, peak oxygen intake, VO2peak = 47.6 (6.2) ml. kg-1. min-1] were assigned to each of four different experimental conditions according to a randomized-block design. While in a climatic chamber maintained at a comfortable temperature (23 degrees C) or heated (40 degrees C, 30% relative humidity, r.h.), subjects performed either two 30-min bouts of cycle-ergometer exercise at approximately 50% VO2peak (separated by a 45-min recovery interval), or remained seated for 3 h. Blood samples were analyzed for CD16+ and CD56+ cell counts, cytolytic activity and the concentrations of various exercise stress hormones (norepinephrine, epinephrine and cortisol). Heat exposure alone had no significant effect on cytolytic cells. The (CD16+ and CD56+) cell count increased significantly (P < 0.0001) during each exercise bout under both environmental conditions, but returned to baseline levels 15-45 min following each exercise bout. Total cytolytic activity (determined by a standard 51Cr release assay using K562 cells) followed a similar pattern, but cytolytic activity per CD16+ or CD56+ cell was not significantly modified by exercise. Our findings show a strong association between hemodynamic factors and recruitment of cytolytic cells into the peripheral circulation. Alterations in cytolytic activity of the whole blood during and following moderate exercise seem to be the result of changes in CD16+ and CD56+ cell counts.

Coaches and athletic team physicians have provided anecdotal information and case studies to support their beliefs that athletes may be unusually prone to illness during strenuous training or competition. Many athletes, in contrast, believe that physical activity improves their resistance to infectious disease. However, it is generally agreed that the stress of competition may make athletes temporarily more susceptible to infectious illness. A review of the literature shows that upper respiratory tract infections and skin infections are more prevalent in top level athletes than in the general population, particularly during periods of intensive training. Exercise induced changes occur in both the innate and adaptive components of the immune system; however, the relative importance of each component is unknown. Strenuous exertion and contact sports may compromise host defence both by reducing physical protection and by impairing immunosurveillance. Skin lacerations, vigorous sweating and maceration of the dermis impair the defence normally provided by the skin surface. In addition, adverse changes in soluble and cellular components of the immune system can increase susceptibility to infection. Persistence with strenuous training during an infectious illness can have deleterious effects; not only is athletic performance impaired, but the severity of the disease process can be augmented.