This study evaluated blood flow in the peritendinous space of the human Achilles tendon during rest and 40-min dynamical contraction of m. triceps surae. In 10 healthy volunteers 133Xe was injected in to the peritendinous space just ventrally to the Achilles tendon 2 and 5 cm proximal to the calcaneal insertion of the tendon, respectively. Blood flow 5 cm proximal to the Achilles tendon insertion was found to increase 4-fold from rest to exercise whereas the exercise induced increase in blood flow was less pronounced, only 2.5-fold, when measured 2 cm proximal to the Achilles tendon insertion. Lymph drainage from the area was found to be negligible both during rest and exercise. We conclude that dynamical calf muscle contractions result in increased peritendinous blood flow at the Achilles tendon in humans.

This survey provides insight into the guidelines used at various polyposis registries for the surveillance and management of FAP patients, and this insight may contribute to the appropriate management of these patients.

To elucidate the underlying mechanism behind the thermogenic effect of adrenaline in human skeletal muscle, nine healthy subjects were studied during intravenous infusion of adrenaline. Restriction of blood flow to one forearm was obtained by external compression of the brachial artery, to separate a direct metabolic effect of adrenaline from an effect dependent on increased blood flow. The other arm served as the control arm. In the control arm, the forearm blood flow increased 4.7-fold (from 2.0 +/- 0.3 to 9.3 +/- 1.5 mL 100 g(-1) min(-1), P < 0.001) during the adrenaline infusion. Adrenaline significantly increased forearm oxygen consumption (from 4.7 +/- 2.1 to 7.0 +/- 3.6 micromol 100 g(-1) min(-1), P < 0.025). In the arm with restricted blood flow, the forearm blood flow increased 2.9-fold (from 1.6 +/- 0.3 to 4.6 +/- 0.8 mL 100 g(-1) min(-1), P < 0.002) but the forearm oxygen consumption did not increase (baseline period: 5.6 +/- 2.3 micromol 100 g(-1) min(-1), adrenaline period: 6.1 +/- 2.1 micromol 100 g(-1) min(-1), P = 0.54). The experimental design and the difficulties in interpretation of the result are discussed. The results give evidence for the hypothesis that the vascular system plays a key role in the thermogenic effect of adrenaline in skeletal muscle in vivo.

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