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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.

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 ( V?O 2max)=43.0?(3.1)?ml?·?kg -1?·?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% V?O 2max (AO), a standard circuit-training routine (CT), 2?h cycle ergometer exercise at 60% V?O 2max (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 a (TNF-a). 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-a. 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.

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°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°C. In another pretreatment, subjects were passively heated in a warm (38°C) water bath for 1 h. In two other pretreatments, subjects exercised for 1 h at 55% peak oxygen consumption (once immersed in 18°C water and once in 35°C water). Core temperature rose by 1°C during passive heating and during exercise in 35°C water and remained stable during exercise in 18°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°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.

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, VO2maxO2 peak = 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°C) or heated (40°C, 30% relative humidity, r.h.), subjects performed either two 30-min bouts of cycle-ergometer exercise at ˜50% VO2maxO2 peak (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.

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, V?O 2max?=?47.6 (6.2) ml?·?kg?· min -1; mean (SD)] were assigned to four different experimental conditions according to a randomized-block design. While in a thermoneutral (23°C) or heated (40°C, 30% relative humidity) climatic chamber, subjects performed either cycle ergometer exercise (two 30-min bouts at ˜50% V?O 2max, 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°C during bout 1: E?=?393 (199) pmol?·?l -1 (CEx) vs 174 (85) pmol?·?l -1 (CS), NE?=?4593 (2640) pmol?·?l -1 (CEx) vs 1548 (505) pmol?·?l -1 (CS), and hGH?=?274 (340) pmol?·?l -1 (CEx)vs 64 (112) pmol?·?l -1 (CS). At 40°C, bout 1: E?=?596 (346) pmol?·?l -1 (HEx) vs 323 (181) pmol?·?l -1 (HS), NE?=?7789 (5129) pmol?·?l -1 (HEx) vs 1527 (605) pmol?·?l -1 (HS), and hGH?=?453 (494) pmol?·?l -1 (HEx) vs 172 (355) pmol?·?l -1 (HS). However, concentrations of plasma cortisol were increased only in response to exercise in the heat [HEx?=?364 (168) nmol?·?l -1vs HS?=?295 (114) nmol?·?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 ( V?O 2 max)= 48.1 (7.6) ml?·?kg -1?·?min -1, 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 2 max, 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 (P HF?:?P T) [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.