To determine the potential for mechanical stimulation of skeletal muscle to contribute to the reflex cardiovascular response to static contraction (exercise reflex), we examined the cardiovascular effects caused by either passive stretch or external pressure applied to the triceps surae muscles. First, the triceps surae were stretched to an average developed tension of 4.8 ± 0.3 kg. This resulted in increases in mean arterial pressure (MAP) of 28 ± 7 mmHg, dP/dt of 1,060 ± 676 mmHg/s, and heart rate (HR) of 6 ± 2 beats/min (P <0.05). Additionally, increments of 0.3, 0.5, 1.0, 2.0, 4.0, and 8.0 kg of tension produced by passive stretch elicited pressor responses of -6 ± 1, 7 ± 1, 16 ± 3, 21 ± 8, 28 ± 6, and 54 ± 9 mmHg, respectively. External pressure, applied with a cuff to the triceps surae to produce intramuscular pressures (125-300 mmHg) that were similar to those seen during static contraction, also elicited small increases in MAP (4 ± 1 to 10 ± 1 mmHg) but did not alter HR. Transection of dorsal roots L5-L7 and S1 abolished the responses to passive stretch and external pressure. Moreover, when the triceps surae were stretched passively to produce a pattern and amount of tension similar to that seen during static hindlimb contraction, a significant reflex cardiovascular response occurred. During this maneuver, the pressor response averaged 51% of that seen during contraction. In six other cats, we observed no changes in triceps surae venous O2 content, PCO2, K+, pH, and lactate during passive stretch or application of external pressure. These data suggest that stimulation of mechanosensitive or polymodal muscle afferents during static contraction contributes to a substantial portion of the exercise reflex.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Applied Physiology|
|State||Published - 1988|
ASJC Scopus subject areas
- Orthopedics and Sports Medicine
- Physical Therapy, Sports Therapy and Rehabilitation