Hey - sorry for the delay, been super busy at work which, sadly, doesn’t involve fun things like bikes. As mentioned to Helv, apologies for mixing up your name with someone else, certainly not intentional.
Below please find three studies/articles on strength training and glycolysis.
The first, which I’ve posted previously, shows trained endurance athletes obtaining a significant increase in OBLA as a result of 12-15 rep strength training (while maintaining their endurance training) for two months. I personally believe the weights used should have been much heavier, but they followed NSCA guidelines (which suck IMO) so it is what it is.
https://journals.lww.com/nsca-jscr/fulltext/2018/05000/aerobic_exercise_supplemented_with_muscular.25.aspx
The second examines a 5x10 rep leg press routine vs. 10x5 rep leg press routine and, using muscle biopsies and blood samples, shows that glycolysis is clearly taking place. An interesting part of this study is the comparison of muscle lactate (not blood lactate) in the leg press compared to high intensity cycling/running (13.5 mmol-kg vs. 8 mmol-kg). In my opinion this provides a fantastic training benefit, as your leg muscles develop physiologically in response to work done under highly glycolytic conditions that are not experienced even when doing intervals. My criticism with the protocol used here is that the weight was too light - I would love to see the findings with heavier weights for 12-15 reps.
https://journals.lww.com/nsca-jscr/fulltext/2014/10000/blood_ammonia_and_lactate_as_markers_of_muscle.11.aspx
The third is an article in Nature, which analyzes resistance exercise and glycolysis. It is rather technical so you might enjoy that aspect of it. To use their own words, “Here, we show that an RET-induced increase in PGC-1α4 (an isoform of the transcriptional co-activator PGC-1α) expression not only promotes muscle hypertrophy but also enhances glycolysis, providing a rapid supply of ATP for muscle contractions. In human skeletal muscle, PGC-1α4 binds to the nuclear receptor PPARβ following RET, resulting in downstream effects on the expressions of key glycolytic genes. In myotubes, we show that PGC-1α4 overexpression increases anaerobic glycolysis in a PPARβ-dependent manner and promotes muscle glucose uptake and fat oxidation.”
https://www.nature.com/articles/s41467-022-30056-6
In strength training circles people often use the term “metabolic strength training” when referring to higher rep sets. I don’t care for that term since, as long as you’re not dead, metabolism is occurring. I use the term glycolytic strength training to refer to how the body is fueling the work, and when you’re performing maximal strength training for 30+ seconds you are fueling it glycolytically, as the ATP-CP system is pretty much spent by 12-15 seconds. Cyclists like to structure training by energy system and this is a simple way of incorporating strength training into a cycling program. In any case, strength training can be neurologic if you structure it that way with the goal of increasing your 1 RM, but it can also be highly glycolytic, producing enormous quantities of muscle lactate, if you set it up properly. That’s the kind of strength training I advocate and I see no reason why, given the studies I provided that show either increased OBLA on the bike or glycolytic response under the microscope, your muscles won’t respond in a way that increases your FTP - you’re training to increase the amount of force (torque) you can produce while using lactate as fuel. Perhaps too many people are too busy pushing too much neuro weight lifting nonsense and should adapt a protocol that begins at the edge of neuromuscular training before moving into higher reps using that same weight (i.e. glycolytic strength training).