Little is known about the strain and consequences of very prolonged and sustained exercise lasting multiple days. This thesis comprises two multi-day exercise field studies and a 24-h, controlled-trial field/laboratory study. The field studies were undertaken using international adventure races (2003 and 2004 Southern Traverses: 86-120 h) to profile exercise intensity and associated physiological and psychophysical strain, and physical and cognitive performance. The 2003 study showed that exercise intensity (from heart rate range) averaged 64% during the first 12 h, dropped to 41% by 24 h, and remained so thereafter. Body core temperature (gastrointestinal pills), throughout racing (n=8) was relatively stable (min 36.0�C and only briefly >39�C), despite widely varying endogenous and exogenous thermal stress. Blood samples obtained before (n=34), during (n=11) and after (n=34) racing revealed a large plasma volume expansion (24%), with stable [sodium]plasma (n=6). Acute (15-30 h) and chronic (96-120 h) elevation of neutrophil, monocyte and lymphocyte numbers were observed across the race. Standardised exercise tests (rest, 25 and 50% peak power output (PPO)) before and after racing (n=9) revealed an extreme shift toward fat utilisation, consistent with lowered fat mass (11%; n=44) and high [free fatty acids]plasma (up 370%; n=9) at race-finish, although [HAD]muscle was unchanged. Muscle glycogen was only 50% lower post-race (290 nmol�kg⁻�d.w.). Complex cognitive performance (Stroop test) impairment was attenuated during 50% PPO post-race. Perceived exertion uncoupled from HR at standardised workloads. Explosive power (jump test; n=24) and anaerobic power (30-s Wingate; n=27) were modestly (<10%) impacted. Strength reduction of arms (11%) and legs (17%) was equivalent (p=0.17). The 2004 study (n=4) involved dissimilar terrain, vegetation, and sequence of exercise modes, yet the profile of exercise intensity was similar: first 12 h 65%, then 45% by 24 h and thereafter. Thus, athletes reliably attain sustainable, low-to-moderate exercise intensity by 24 h. Plasma volume, neutrophil and monocyte responses were reliable across races, whereas lymphocytes were not. Plasma [IL-6] and [S100β] were elevated, substantially in some individuals (IL-6: 223 pg�mL⁻�; S100β: 113 pg�mL⁻�), during racing. A 24-h adventure race simulation (n=9) was then undertaken to investigate physiological and psychophysical factors influencing exercise intensity, autonomic function and orthostatic tolerance. Tests were at 0, ~7, ~15 and 24 h. The 24-h HR profile matched that observed during racing: first 12 h 58% (including 3-h testing), remainder 41%. The shift toward fat utilisation was almost complete within 7 h, and similar to that following 2003 race. The perceived exertion-to-HR uncoupling was also similar; being complete within 15 h. Plasma [noradrenaline] for rest and 12-km�h⁻� run was elevated post-simulation. Plasma [IL-6] peaked by 7 h, although not as high as field observations. The timeframe of metabolic change and perceived exertion uncoupling coincided with that of pace reduction, and may be important regulatory components of very prolonged exercise intensity. Orthostatic intolerance was evident during the simulation (n=6/9), as was cerebral hypo-perfusion (15 h & 24 h). Autonomic function (baroreflex sensitivity, sympathetic activation, parasympathetic withdrawal) was altered only at 7 h, whereas postural-induced hypotension (via impaired venous response) and hypocapnia were always present.

Little is known about the strain and consequences of very prolonged and sustained exercise lasting multiple days. This thesis comprises two multi-day exercise field studies and a 24-h, controlled-trial field/laboratory study. The field studies were undertaken using international adventure races (2003 and 2004 Southern Traverses: 86-120 h) to profile exercise intensity and associated physiological and psychophysical strain, and physical and cognitive performance. The 2003 study showed that exercise intensity (from heart rate range) averaged 64% during the first 12 h, dropped to 41% by 24 h, and remained so thereafter. Body core temperature (gastrointestinal pills), throughout racing (n=8) was relatively stable (min 36.0�C and only briefly >39�C), despite widely varying endogenous and exogenous thermal stress. Blood samples obtained before (n=34), during (n=11) and after (n=34) racing revealed a large plasma volume expansion (24%), with stable [sodium]plasma (n=6). Acute (15-30 h) and chronic (96-120 h) elevation of neutrophil, monocyte and lymphocyte numbers were observed across the race. Standardised exercise tests (rest, 25 and 50% peak power output (PPO)) before and after racing (n=9) revealed an extreme shift toward fat utilisation, consistent with lowered fat mass (11%; n=44) and high [free fatty acids]plasma (up 370%; n=9) at race-finish, although [HAD]muscle was unchanged. Muscle glycogen was only 50% lower post-race (290 nmol�kg⁻�d.w.). Complex cognitive performance (Stroop test) impairment was attenuated during 50% PPO post-race. Perceived exertion uncoupled from HR at standardised workloads. Explosive power (jump test; n=24) and anaerobic power (30-s Wingate; n=27) were modestly (<10%) impacted. Strength reduction of arms (11%) and legs (17%) was equivalent (p=0.17). The 2004 study (n=4) involved dissimilar terrain, vegetation, and sequence of exercise modes, yet the profile of exercise intensity was similar: first 12 h 65%, then 45% by 24 h and thereafter. Thus, athletes reliably attain sustainable, low-to-moderate exercise intensity by 24 h. Plasma volume, neutrophil and monocyte responses were reliable across races, whereas lymphocytes were not. Plasma [IL-6] and [S100β] were elevated, substantially in some individuals (IL-6: 223 pg�mL⁻�; S100β: 113 pg�mL⁻�), during racing. A 24-h adventure race simulation (n=9) was then undertaken to investigate physiological and psychophysical factors influencing exercise intensity, autonomic function and orthostatic tolerance. Tests were at 0, ~7, ~15 and 24 h. The 24-h HR profile matched that observed during racing: first 12 h 58% (including 3-h testing), remainder 41%. The shift toward fat utilisation was almost complete within 7 h, and similar to that following 2003 race. The perceived exertion-to-HR uncoupling was also similar; being complete within 15 h. Plasma [noradrenaline] for rest and 12-km�h⁻� run was elevated post-simulation. Plasma [IL-6] peaked by 7 h, although not as high as field observations. The timeframe of metabolic change and perceived exertion uncoupling coincided with that of pace reduction, and may be important regulatory components of very prolonged exercise intensity. Orthostatic intolerance was evident during the simulation (n=6/9), as was cerebral hypo-perfusion (15 h & 24 h). Autonomic function (baroreflex sensitivity, sympathetic activation, parasympathetic withdrawal) was altered only at 7 h, whereas postural-induced hypotension (via impaired venous response) and hypocapnia were always present.