Increased Risk of Upper Respiratory Infection in Military Recruits Who Report Sleeping Less Than 6 h per night.

Introduction: Professional sleep associations recommend 7-9 h of sleep per night for young adults. Habitually sleeping less than 6 h per night has been shown to increase susceptibility to common cold in otherwise healthy, adult civilians. However, no investigations have examined the importance of sleep duration on upper respiratory tract infection (URTI) and loss of training days in military recruits. The purpose of this study was to describe self-reported sleep duration in a large cohort of military recruits and to assess the relationship between reported sleep duration and incidence of URTI's. We hypothesized that recruits who reported sleeping less than the recommended 7-9 h per night during training suffered a greater incidence of URTI and, as a consequence, lost more training days compared with recruits who met sleep recommendations. Materials and Methods: Participants included 651 British Army recruits aged 22 ± 3 yr who completed 13 wk of basic military training (67% males, 33% females). Participants were members of 21 platoons (11 male, 10 female) who commenced training across four seasons (19% winter, 20% spring, 29% summer, and 32% autumn). At the start and completion of training, participants completed a questionnaire asking the typical time they went to sleep and awoke. Incidence of physician-diagnosed URTI and lost training days due to URTI were retrieved from medical records. Results: Self-reported sleep duration decreased from before to during training (8.5 ± 1.6 vs. 7.0 ± 0.8 h; p < 0.01). Prior to training, 13% of participants reported sleeping less than the recommended 7 h sleep per night; however, this increased to 38% during training (X2 = 3.8; p = 0.05). Overall, 49 participants (8%) were diagnosed by a physician with at least one URTI and 3 participants (<1%) were diagnosed with two URTI's. After controlling for sex, body mass index, season of recruitment, smoking, and alcohol, participants who reported sleeping less than 6 h per night during training were four times more likely to be diagnosed with URTI compared with participants who slept 7-9 h per night in a logistic regression model (OR 4.4; 95% CI, 1.5-12.9, p < 0.01). On average, each URTI resulted in 2.9 ± 1.5 lost training days. Participants who were diagnosed with URTI had more overall lost training days for any illness compared with participants who did not report a URTI during basic military training (3.3 ± 1.9 vs. 0.4 ± 1.3; p < 0.01). Conclusion: In a large population of British Army recruits, these findings show that more than one third of participants failed to meet sleep duration recommendations during training. Furthermore, those who reported sleeping less than 6 h per night were four times more likely to be diagnosed with an URTI and lost more training days due to URTI. Since sleep restriction is considered a necessary element of military training, future studies should examine interventions to reduce any negative effects on immunity and host defense.

Tear Fluid SIgA as a Noninvasive Biomarker of Mucosal Immunity and Common Cold Risk.

PURPOSE: Research has not convincingly demonstrated the utility of saliva secretory immunoglobulin-A (SIgA) as a biomarker of upper respiratory tract infection (URTI) risk, and disagreement exists about the influence of heavy exercise ("open-window theory") and dehydration on saliva SIgA. Prompted by the search for viable alternatives, we compared the utility of tear and saliva SIgA to predict URTI prospectively (study 1) and assessed the influence of exercise (study 2) and dehydration (study 3) using a repeated-measures crossover design. METHODS: In study 1, 40 subjects were recruited during the common-cold season. Subjects provided tear and saliva samples weekly and recorded upper respiratory symptoms (URS) daily for 3 wk. Real-time PCR confirmed common-cold pathogens in 9 of 11 subjects reporting URS (82%). Predictive utility of tear and saliva SIgA was explored by comparing healthy samples with those collected during the week before URS. In study 2, 13 subjects performed a 2-h run at 65% V˙O2peak. In study 3, 13 subjects performed exercise heat stress to 3% body mass loss followed by overnight fluid restriction. RESULTS: Tear SIgA concentration and secretion rate were 48% and 51% lower, respectively, during URTI and 34% and 46% lower the week before URS (P < 0.05), but saliva SIgA remained unchanged. The risk of URS the following week increased ninefold (95% confidence interval, 1.7-48) when the tear SIgA secretion rate was <5.5 µg·min(-1) and sixfold (95% confidence interval, 1.2-29) when the tear SIgA secretion rate decreased >30%. Tear SIgA secretion rate >5.5 µg·min(-1) or no decrease of >30% predicted subjects free of URS in >80% of cases. Tear SIgA concentration decreased after exercise (-57%, P < 0.05) in line with the "open-window theory" but was unaffected by dehydration. Saliva flow rate decreased and saliva SIgA concentration increased after exercise and during dehydration (P < 0.05). CONCLUSIONS: Tear SIgA has utility as a noninvasive biomarker of mucosal immunity and common-cold risk.

Exercise Intensity and Duration Effects on In Vivo Immunity.

PURPOSE: To examine the effects of intensity and duration of exercise stress on induction of in vivo immunity in humans using experimental contact hypersensitivity (CHS) with the novel antigen diphenylcyclopropenone (DPCP). METHODS: Sixty-four healthy males completed either 30 min running at 60% V˙O2peak (30MI), 30 min running at 80% V˙O2peak (30HI), 120 min running at 60% V˙O2peak (120MI), or seated rest (CON). Twenty min later, the subjects received a sensitizing dose of DPCP; and 4 wk later, the strength of immune reactivity was quantified by measuring the cutaneous responses to a low dose-series challenge with DPCP on the upper inner arm. Circulating epinephrine, norepinephrine and cortisol were measured before, after, and 1 h after exercise or CON. Next, to understand better whether the decrease in CHS response on 120MI was due to local inflammatory or T-cell-mediated processes, in a crossover design, 11 healthy males performed 120MI and CON, and cutaneous responses to a dose series of the irritant, croton oil (CO), were assessed on the upper inner arm. RESULTS: Immune induction by DPCP was impaired by 120MI (skinfold thickness -67% vs CON; P < 0.05). However, immune induction was unaffected by 30MI and 30HI despite elevated circulating catecholamines (30HI vs pre: P < 0.01) and greater circulating cortisol post 30HI (vs CON; P < 0.01). There was no effect of 120MI on skin irritant responses to CO. CONCLUSIONS: Prolonged moderate-intensity exercise, but not short-lasting high- or short-lasting moderate-intensity exercise, decreases the induction of in vivo immunity. No effect of prolonged moderate-intensity exercise on the skin's response to irritant challenge points toward a suppression of cell-mediated immunity in the observed decrease in CHS. Diphenylcyclopropenone provides an attractive tool to assess the effect of exercise on in vivo immunity.

Exercise-induced stress inhibits both the induction and elicitation phases of in vivo T-cell-mediated immune responses in humans.

Little is known about the influence of exercise on induction and elicitation phases of in vivo immunity in humans. We used experimental contact-hypersensitivity, a clinically relevant in vivo measure of T cell-mediated immunity, to investigate the effects of exercise on induction and elicitation phases of immune responses to a novel antigen. The effects of 2 h-moderate-intensity-exercise upon the induction (Study One) and elicitation of in vivo immune memory (Study Two) to diphenylcyclopropenone (DPCP) were examined. Study One: matched, healthy males were randomly-assigned to exercise (N=16) or control (N=16) and received a primary DPCP exposure (sensitization), 20 min after either 2 h running at 60% V O(2peak) (EX) or 2 h seated rest (CON). Four weeks later, participants received a low, dose-series DPCP challenge (elicitation) on their upper inner arm, which was read at 24 and 48 h as clinical score, oedema (skinfold thickness) and redness (erythema). Study Two: pilot; 13 healthy males were sensitized to DPCP. Elicitation challenges were repeated every 4 weeks until responses reached a reproducible plateau. Then, N=9 from the pilot study completed both EX and CON trials in a randomized order. Elicitation challenges were applied and evaluated as in Study One. Results demonstrate that exercise-induced stress significantly impairs both the induction (oedema -53% at 48 h; P<0.001) and elicitation (oedema -19% at 48 h; P<0.05) phases of the in vivo T-cell-mediated immune response. These findings demonstrate that prolonged moderate-intensity exercise impairs the induction and elicitation phases of in vivo T-cell-mediated immunity. Moreover, the induction component of new immune responses appears more sensitive to systemic-stress-induced modulation than the elicitation component.