The CSF and arterial to internal jugular venous hormonal differences during exercise in humans

Abstract

Strenuous exercise increases the cerebral uptake of carbohydrate out of proportion to that of oxygen, but it is unknown whether such enhanced carbohydrate uptake is influenced by the marked endocrine response to exercise. During exhaustive exercise this study evaluated the a-v differences across the brain (a-v diff) of hormones that could influence its carbohydrate uptake (n = 9). In addition, neuroendocrine activity and a potential uptake of hormones via the cerebrospinal fluid (CSF) were assessed by lumbar puncture postexercise and at rest (n = 6). Exercise increased the arterial concentration of noradrenaline and adrenaline, but there was no cerebral uptake. However, following exercise CSF noradrenaline was 1.4 (0.73-5.5) nmol l −1 , and higher than at rest, 0.3 (0.19-1.84) nmol l −1 (P < 0.05), whereas adrenaline could not be detected. Exercise increased both the arterial concentration of NH 4 + and its a-v diff, which increased from 1 (-12 to 5) to 17 (5-41) µmol l −1 (P < 0.05), while the CSF NH 4 + was reduced to 7 (0-10) versus 11 (7-16) µmol l −1 (P < 0.05). There was no release from, or accumulation in the brain of interleukin (IL)-6, tumour necrosis factor (TNF-α), heatshock protein (HSP72), insulin, or insulin-like growth factor (IGF)-I. The findings indicate that for maximal exercise, the concentration of noradrenaline is increased within the brain, whereas blood borne hormones and cytokines are seemingly unimportant. The results support the notion that the exercise-induced changes in brain metabolism are controlled by factors intrinsic to the brain.

Fuelling Cerebral Activity in Exercising Man

“…Thus, noradrenaline in the CSF increases by 50% with intense exercise in the dog (Radosevich et al, 1989). Likewise, exhaustive exercise elicits a B300% increase in CSF noradrenaline after both brief (Dalsgaard et al, 2004b) and 2 h of maximal exercise (unpublished), which seems to be related to factors within the brain rather than the blood glucose homeostasis. Although noradrenaline in CSF may increase with the blood level, exercise per se seems not to be the cause (Dalsgaard et al, 2004b).…”

“…Conversely, the blood concentration of insulin-like growth factor (IGF)-I increases during exercise (Schwarz et al, 1996) and IGF-I is superior to insulin in regard to both glucose transport into the brain (Reinhardt and Bondy, 1994) and its stimulatory effect on brain glucose metabolism (Cheng et al, 2000;Dringen and Hamprecht, 1992). However, increased levels of IGF-I in blood with exercise do not affect A-JV IGF and IGF-I remains low in the CSF ( < 21 ng) as a potential site of entry (Dalsgaard et al, 2004b). ; 'Submax, 10 mins', mean value from four bouts of light exercise (Dalsgaard et al, 2002(Dalsgaard et al, , 2003; 'Max arm, 35 mins' (Dalsgaard et al, 2004d); 'Leg + curare, 10 mins' (Dalsgaard et al, 2002); 'Leg, 10 mins + PEMI (post-exercise muscle ischemia), 5 mins' and 'Leg + thigh cuffs, 10 mins' (Dalsgaard et al, 2003); 'Max leg + heat, 60 mins' (Nybo et al, 2003b); 'Max leg, 12 mins' (Dalsgaard et al, 2002;Ide et al, 2000b); Max leg, 25 mins (Dalsgaard et al, 2004a); 'Max leg + arm, 12 mins' (Dalsgaard et al, 2004c); 'Max leg + heat, 6 mins' (Gonzalez-Alonso et al, 2004); Visual cortex (Fox et al, 1988).…”

“…Furthermore, during exercise blood glucose homeostasis is maintained with low systemic levels of insulin (Guezennec et al, 1982). Thus, during maximal exercise the reduction in MR takes place without any change in A-JV insulin or in CSF insulin concentration (Dalsgaard et al, 2004b). Moreover, the effects of insulin would be exerted only after the fast reduction and normalisation of MR that commonly takes place within few minutes after cessation of exercise.…”

“…Furthermore, at different exercise intensities, cortical lactate metabolism seems elevated in well-trained compared with untrained subjects (Kemppainen et al, 2005) and that could be of importance for exercise capacity. During exercise, the lactate taken up by the brain is not released to blood within a 1-h recovery period (Dalsgaard et al, 2002;Ide et al, 2000b) and it does not accumulate in CSF or within the brain as determined by MRS (Figure 4) (Dalsgaard et al, 2004b). Of note, the extracellular lactate pool would be expected also to receive lactate from glycolysis and glycogenolysis.…”

“…For example, moderate exercise at an arterial lactate concentration greater than 3 mmol/L is associated with slight lactate uptake by the brain (Ahlborg and Wahren, 1972;Dalsgaard et al, 2002). Indeed, when maximal exercise raises the arterial lactate concentrations to B15 mmol/L or higher, the cerebral lactate uptake (in molar amounts) may exceed that of glucose ( Figure 3) (Dalsgaard et al, 2002(Dalsgaard et al, , 2004bGonzalez-Alonso et al, 2004;Ide et al, 2000b). With such marked concentration gradient from blood to brain, lactate would be expected to reach high concentrations locally in the extracellular fluid of importance for the cellular uptake.…”