Why the study?
Does ischemia during dynamic exercise alter interstitial K+ concentration and muscle pain in young healthy subjects?
Does ischemia during dynamic exercise alter interstitial K+ concentration and muscle pain in young healthy subjects?
Ischemia reduces interstitial potassium concentration during exercise, demonstrating that factors other than potassium accumulation are responsible for ischemic muscle pain.
Questions K+ mediation of ischemic pain in healthy subjects; leaves open alternative mechanisms for targeted investigation.
Changes in the concentration of interstitial K+ surrounding skeletal muscle fibres ([K+]I) probably play some role in the regulation of cardiovascular adjustments to muscular activity, as well as in the aetiology of muscle pain and fatigue during high-intensity exercise. However, there is very little information on the response of [K+]I to exercise in human skeletal muscle. Five young healthy subjects performed plantar flexion exercise for four 5 min periods at increasing power outputs ( approximately 1-6 W) with 10 min intervening recovery periods, as well as for two 5 min periods with ischaemia at approximately 1 and approximately 3 W. Microdialysis probes were inserted into the gastrocnemius medialis muscle of the right leg to measure [K+]I, and K+ release from the plantar flexors during and after incremental exercise was calculated from plasma flow and arterial-venous differences for K+. Calf muscle pain was assessed using a visual analogue scale. On average, [K+]I was 4.4 mmol l(-1) at rest and increased during minutes 3-5 of incremental exercise by approximately 1-7 mmol l(-1) as a positive function of power output. K+ release also increased as a function of exercise intensity, although there was a progressive increase by approximately 1-6 mmol l-1 in the [K+] gradient between the interstitium and arterial-venous plasma. [K+]I was lower during ischaemic exercise than control exercise. In contrast to this effect of ischaemia on [K+]I, muscle pain was relatively higher during ischaemic exercise, which demonstrates that factors other than changes in [K+]I are responsible for ischaemic muscle pain. In conclusion, this study has demonstrated that during 5 min of dynamic exercise, [K+]I increases during the later period of exercise as a positive function of exercise intensity, ischaemia reduces [K+]I during rest and exercise, and the increase in [K+]I is not responsible for muscle pain during ischaemic exercise.
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Green et al. (2000) studied this question.
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