In order to assess the influence of physical stress, such as exercise and nutritional restriction, on immunity, there is a need for well-controlled field studies and use of clinically relevant and practical in vivo measures of immune competence. The broad aim of this thesis was to examine the reductive effects of physical stress on immune responses in humans. Firstly, a daily mixed nutritional supplement prevented the decrease in circulating total leukocytes, lymphocytes and monocytes and increased saliva secretory immunoglobulin-A during 8 weeks of arduous military training, compared with a comparative control group (Chapter 4). A stronger approach to investigate the effects of physical stress includes utilising a measure of in vivo immunity, such as experimental contact hypersensitivity (CHS) with the novel antigen Diphenylcyclopropenone (DPCP). Prolonged, moderate intensity exercise, but not short, high or short, moderate intensity exercise, impaired induction to DPCP, despite elevated circulating catecholamines and greater circulating cortisol following short, high intensity exercise (Chapter 5). Experimental CHS was then coupled with a suction blister technique at the site of DPCP sensitisation to measure cutaneous cytokines thought to orchestrate dendritic cell migration and successful induction of new immune memory. After demonstrating this technique to be repeatable (Chapter 6) and identifying 6 h of patch exposure as a suitable time to initiate suction blisters (Chapter 7), results showed prolonged, moderate intensity exercise had no effect on local cutaneous interleukin (IL)-1β, tumour necrosis factor (TNF)-α and IL-10 (Chapter 8), thought to be implicated in the initial events of immune induction. Therefore it is possible that prolonged, moderate intensity exercise suppresses further downstream events of immune induction, rather than local inflammatory processes at the skin. Topical application of DPCP provides an attractive tool for the assessment of in vivo immunity in future exercise stress and nutritional intervention studies. Further research is required to identify the mechanisms involved in the suppression of CHS responses to DPCP after prolonged, moderate intensity exercise.