The Effects of Stroke Rate on Blood Flow
Over the past few months I've been interested in trying to understand the effect that SPM (strokes per minute) have on rowing economy when rowing at a fixed pace that is at a supra-threshold (lets approximate it as a ~2-3k PR pace). This would be the difference between rowing your 2k at a 1:35/500m split at 25 SPM versus a 1:35/500m split at 35 SPM.
What I'm most interested in is understanding how changes to SPM at a fixed work rate impact blood flow to the working muscles. My hypothesis going in was that the increased SPM would enhance the skeletal muscle pump, which would result in an increased cardiac output. My thought was that by keeping the work output (pace) fixed and increasing the SPM, each stroke would be lower force (and higher velocity) which would decrease the likelihood of generating so much intra-muscular tension that venous outflow was restricted. This would effectively allow for a greater venous return, which would increase cardiac preload, stroke volume, and subsequently cardiac output.
This is something we can identify with NIRS by looking at blood flow trends in the muscle. If this were to play out how I expected then we'd see higher THb levels in the working muscle with steadier blood flow (compressions during each stroke followed by a return of flow on the catch phase, or mild venous occlusion on each stroke with complete relaxation on the catch which would allow for steadier flow). Interestingly, I saw these trends in about ~50% of the athlete's I tested when they rowed their 2k pace at 35 SPM versus 25 SPM. Those who had the steadier blood flow trends at the higher cadence reported being able to row at that pace with a lower RPE, where those that did not reported an increased RPE with that strategy.
Naturally, this made me question why this strategy was more effective some some individuals, and less so for others. The more comparable research I could find was looking at cycling cadence, and the findings showed that higher cadences lent themselves to increased oxygen utilization (15% increase), higher heart rate, higher stroke volume. hight cardiac output (35% increase), a decrease in vascular resistance, BUT increased blood pressure.
Perhaps the athletes who did not handle the increased SPM as well were those who were more prone to delivery issues, though that doesn't seem like the only plausible explanation. My hunch is that it could also be an intra-muscular coordination issue, which is something that can be trained. This would mean developing the ability to contract and relax in shorter time spans, being able to coordinate breathing with the higher SPM (while maintaining depth of inhale and exhale), and improving the ability of the skeletal muscle pump to increase muscle blood flow and venous return at these faster work rates.