Was thinking of cardio, and HR levels, and then stimulants...

  1. Was thinking of cardio, and HR levels, and then stimulants...

    So I know the basic philosophy of 60% or lower HR for low intensity (burning fat as the primary source) versus going higher HR and switching to glycogen metabolism for fuel.

    My question involves the use of stimulants now. For instance, if normal cardio for me brings my HR to 50%, but now I add in stimulants and it goes up to 70%, will I be burning glycogen? Even though normally I wouldnt be?

    And vice versa, for instance DCP actually helps maintain my HR during cardio that otherwise would send it skyrocketing. Can I do more intense with DCP if I wished to stay below 60% (lets say, for argument's sake, that sprinting kept my HR below 60% with DCP).

    Basically, is HR really tied in with the substrate usage by the body for fuel? Or is it more complicated than that?

  2. excellent Q!

  3. Im pretty excited to hear the responses to this question. Does DCP reall change Hrt that much?

    Also I was doing a cardio program mainly on an elliptical called Sprint 8 by Phil Cambell, the idea is a 3min warm up at low intensity then 30 second sprint high rpms and max hrt followed by 1 min 30 sec cool down then Sprint 30 sec. followed by same cool down etc. and you do this for a total of 8 sprints which is about 20 min work out with only 4 total min. of exertion. The idea behind it is to release HGH naturally in the body. Try it some time you really have to push yourself I do it until I almost throw up.

  4. I dont know if anyone has the answers to this, as it seems no one wants to respond...

    Now, remember my argument put forth regarding DCP is somewhat hypothetical. In addition, I have noticed that after a couple weeks of DCP my heart rate has basically returned to normal during cardio (the buffer effect has diminished).

    However, I can state that I immediately noticed HR effects from DCP; at home, when I started DCP, I woudl routinely do a bicycle routine for 45 min-1 hour, and my HR would hit mid 130s. Once starting DCP, I was able to keep it in the mid teens-20s with the exact same program.

    I guess I am more interested in the action of stimulants; what I keep thinking of is the rise in metabolism initiated by stimulants. I guess I'll do some digging and see how closely HR is correlated with substrate use.

  5. Maximal fat oxidation during exercise in trained men.

    * Achten J,
    * Jeukendrup AE.

    School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom.

    Fat oxidation increases from low to moderate exercise intensities and decreases from moderate to high exercise intensities. Recently, a protocol has been developed to determine the exercise intensity, which elicits maximal fat oxidation rates (Fat(max)). The main aim of the present study was to establish the reliability of the estimation of Fat(max) using this protocol (n = 10). An additional aim was to determine Fat(max) in a large group of endurance-trained individuals (n = 55). For the assessment of reliability, subjects performed three graded exercise tests to exhaustion on a cycle ergometer. Tests were performed after an overnight fast and diet and exercise regime on the day before all tests were similar. Fifty-five male subjects performed the graded exercise test on one occasion. The typical error (root mean square error and CV) for Fat(max) and Fat(min) was 0.23 and 0.33 l O(2) x min(-1) and 9.6 and 9.4 % respectively. Maximal fat oxidation rates of 0.52 +/- 0.15 g x min(-1) were reached at 62.5 +/- 9.8 % VO(2)max, while Fat(min) was located at 86.1 +/- 6.8 % VO(2)max. When the subjects were divided in two groups according to their VO(2)max, the large spread in Fat(max) and maximal fat oxidation rates remained present. The CV of the estimation of Fat(max) and Fa(min) is 9.0 - 9.5 %. In the present study the average intensity of maximal fat oxidation was located at 63 % VO(2)max. Even within a homogeneous group of subjects, there was a relatively large inter-individual variation in Fat(max) and the rate of maximal fat oxidation.

    PMID: 14598198 [PubMed - indexed for MEDLINE]

    Caffeine ingestion and muscle metabolism during prolonged exercise in humans.

    * Spriet LL,
    * MacLean DA,
    * Dyck DJ,
    * Hultman E,
    * Cederblad G,
    * Graham TE.

    School of Human Biology, University of Guelph, Ontario, Canada.

    We examined the effects of a high-caffeine dose on endurance performance and muscle acetyl group metabolism during prolonged exercise. Eight subjects cycled to exhaustion at approximately 80% maximal oxygen uptake (VO2max) 1 h after ingestion of 9 mg/kg body wt dextrose (Pl) or caffeine (Caf). In the Pl trial, muscle biopsies were taken at rest (1 h postingestion) and at 15 min and exhaustion during exercise. The Caf trial followed the same protocol 1 wk later, with an additional biopsy at the time corresponding to Pl exhaustion. The subjects cycled significantly longer during the Caf trial (96.2 +/- 8.8 min) than in the Pl trial (75.8 +/- 4.8 min). Net glycogenolysis during the initial 15 min of cycling was reduced in the Caf vs. Pl trial (4.7 +/- 1.5 vs. 10.6 +/- 1.3 mmol.kg dry muscle-1.min-1; P less than 0.05). Muscle citrate concentration was increased at rest with Caf (0.59 +/- 0.07 vs. 0.37 +/- 0.05 mmol/kg dry muscle; P less than 0.05) but increased to similar values in both trials during cycling. Caf elevated the acetyl-CoA/CoA-SH ratio at rest (0.316 +/- 0.046 vs. 0.201 +/- 0.023; P less than 0.05) but had no effect on the increases in muscle acetyl-CoA and acetylcarnitine during exercise. The results indicate that Caf before exercise decreased muscle glycogenolysis by approximately 55% over the first 15 min of exercise at approximately 80% VO2max. This "spared glycogen" was available late in exercise and coincided with a prolonged time to exhaustion. Increased utilization of intramuscular triacylglycerol and/or extramuscular free fatty acids after caffeine ingestion may inhibit carbohydrate use at rest and early during exercise via elevations in muscle citrate and the acetyl-CoA/CoA-SH ratio. Muscle acetyl-CoA and acetylcarnitine were maintained above resting contents even at exhaustion when muscle glycogen was depleted.

    PMID: 1616022 [PubMed - indexed for MEDLINE]

    It might be more complicated than just VO2 % and HR % when adding in stimulants. Most studies, however, use VO2 max as the indicator of substrate metabolism, not HR; they convert VO2 % into HR %. Also, note in the top study that each individual had varying VO2 percentages for substrate usage - therefore, the old 60% rule probably isnt as solid as people make it seem.



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