Exercise and training during graded leg ischaemia in healthy man with special reference to effects on skeletal muscle.
The influence of graded leg muscle ischaemia on the adaptation to training and on the acute response to exercise was studied in healthy subjects. Graded ischaemia during supine exercise was induced by application of 50 mmHg external pressure on the legs. This procedure reduced leg blood flow by 16%, venous oxygen saturation by 12 percentage units, and markedly increased lactate release (p < 0.05 for all). One-legged training was performed during four weeks, 4 sessions per week. Each session started with one leg training for 45 min with reduced blood flow (ischaemic training). The contralateral leg, serving as a control, was then trained with an identical power-output profile for 45 min but without flow restriction (non-ischaemic training). Ischaemic training enhanced the adaptation to training. Peak oxygen uptake and time to fatigue increased more (p < 0.05) with ischaemic than with non-ischaemic training. Citrate synthase activity, capillaries per fibre, and glycogen content were greater (p < 0.05) in the trained than in the detrained state. In the ischaemically trained leg, the type IIb fibre proportion was lower (p < 0.05) and the I fibre proportion tended to be higher (p = 0.06) in the trained than in the detrained state. Maximum voluntary dynamic strength was decreased by 8% (p < 0.01) in the ischaemically trained leg, but was unaffected in the non-ischaemically trained leg. During acute ischaemic exercise, as compared to non-ischaemic exercise, there was a higher degree of glycogen depletion, a greater depletion of type II, but not of type I fibres, a greater electromyographic activity, higher catecholamine concentrations, lower intramuscular ATP and creatine phosphate content, and an increased nitric oxide formation as estimated by increased plasma nitrate content. In conclusion, the mechanisms underlying the potentiation of the adaptation to training by ischaemia are assumed to depend on the operation of stimuli which were amplified during acute ischaemic exercise.
Sundberg
C J
CJ
Karolinska Institutet, Department of Physiology and Pharmacology, Stockholm, Sweden.
D000208:Acute Disease; D000222:Adaptation, Physiological / Q000502:physiology*; D000255:Adenosine Triphosphate / Q000032:analysis; D000293:Adolescent; D000328:Adult; D001706:Biopsy; D001783:Blood Flow Velocity; D001784:Blood Gas Analysis; D002196:Capillaries / Q000473:pathology; D002395:Catecholamines / Q000032:analysis; D002950:Citrate (si)-Synthase / Q000032:analysis; D004576:Electromyography; D005081:Exercise Therapy; D006003:Glycogen / Q000032:analysis; D006801:Humans; D007511:Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D007866:Leg / Q000098:blood supply*; D008297:Male; D008955:Models, Cardiovascular; D009132:Muscles / Q000098:blood supply / Q000737:chemistry / Q000473:pathology; D009569:Nitric Oxide / Q000096:biosynthesis / Q000097:blood; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000032:analysis
D002395:Catecholamines; D007773:Lactates; D010725:Phosphocreatine; D009569:Nitric Oxide; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D006003:Glycogen; D002950:Citrate (si)-Synthase; D010100:Oxygen