Research on exercise and Heart rate etc...

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    • Research on exercise and Heart rate etc...

      Okay going to post some more information on this (if you get a naysayer show them this thread), will add to it as often as I can today as my internet keeps dropping out.

      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • Exercise and Diabetes Control

      This article is more for the management of diabetes but it has a good explanation on the types of exercise, heart rate etc... that show where this 60-70% recommendation comes from, the explanation will be in bold:

      A Winning Combination

      Sheri R. Colberg, PhD; David P. Swain, PhD

      THE PHYSICIAN AND SPORTSMEDICINE - VOL 28 - NO. 4 - APRIL 2000

      physsportsmed.com/issues/2000/04_00/colberg.htm



      In Brief: It is becoming evident that in many individuals, diabetes of all types can be precipitated or exacerbated by inactivity. Exercise is a cornerstone in diabetes management and conveys many health benefits. Different forms of exercise can have varying effects on the blood sugar response, especially in individuals using insulin. Appropriate exercise for effective management of blood sugar levels and published clinical exercise recommendations for individuals with type 1 and type 2 diabetes include additional blood glucose monitoring, modified insulin doses, and supplemental carbohydrate intake. Physicians who treat exercising patients with diabetes should tailor programs to meet individual requirements.

      The prevalence of diabetes mellitus is increasing worldwide. In the United States alone, an estimated 16 million individuals have diabetes mellitus, and in close to a third of them the disease is undiagnosed. A vast majority (90% to 95%) have type 2 diabetes (formerly called non-insulin-dependent, or NIDDM), but many of these individuals also use exogenous insulin (1). More than 1 million individuals have type 1 diabetes (formerly called insulin-dependent, or IDDM). Although all types of diabetes mellitus result in hyperglycemia, the etiology depends on the type. In most individuals with type 1 diabetes, an environmentally triggered autoimmune process destroys pancreatic beta-cells, rendering the body unable to manufacture insulin. Type 2 diabetes results more often from an insulin resistance syndrome that is usually exacerbated by excess body fat (2). A third form, gestational diabetes, occurs in women mainly during their third trimester of pregnancy. Although the condition usually resolves in the postpartum period, it is associated with a higher risk of type 2 diabetes later in life (3).


      Benefits of Exercise

      Exercise plays a role in the prevention of type 2 diabetes as well as other serious health problems, including cardiovascular disease and certain cancers. It is becoming evident that many cases of type 2 diabetes may be precipitated by inactivity. Manson et al (4) examined the potential role of physical activity in the primary prevention of type 2 diabetes by studying a cohort of 87,253 middle-aged US women (ages 34 to 59) for 8 years. The investigators found that women who engaged in vigorous exercise at least once a week had a lower risk of developing diabetes (age-adjusted relative risk of 0.67; P < 0.0001) compared with women who did not exercise, irrespective of obesity (4). In another study (5), participation in leisure-time physical activity was inversely related to the development of type 2 diabetes, especially for men at highest risk. Each 500-kcal increment in weekly energy expenditure reduced the age-adjusted risk of diabetes by 6%. More recently, Hu et al (6) published the results from a longitudinal study of 70,102 female nurses who were studied from 1986 to 1992. The researchers showed that exercise need not be vigorous to have the same preventive effect. In these women, a greater physical activity level, even in those who did only moderately paced activities such as walking, was associated with a substantial risk reduction for the development of type 2 diabetes.

      Being physically active not only can reduce the risk for developing type 2 diabetes, but exercising regularly can also bring many health benefits to all, especially for those with diabetes. Recent research has shown that exercise lowers the risk of macrovascular disease (7), obesity, hypertension (8), certain cancers such as breast (9) and colorectal (10), and all-cause mortality in the general population. Kampert et al (11) studied 7,080 women and 25,341 men (mean age, 43 years; age range, 20 to 88) for about 8 years and assessed baseline physical fitness with a maximal treadmill test and physical activity via questionnaire. They found a strong inverse relationship between all-cause mortality and level of physical fitness in both men and women (P for trend < 0.01). Physically active men, but not women, were also at lower risk of death from cancer and all causes.


      Exercise and Diabetes Therapy

      Exercise is a cornerstone in the treatment of diabetes, along with proper diet and medication, but it may present greater obstacles for the type 1 patient (see below). Physical exercise confers the well-established benefit of improved insulin sensitivity for all patients (12). Increased sensitivity may improve glucose homeostasis and necessitate lower doses of medications. Physically conditioned individuals with diabetes also have a heightened insulin sensitivity, which allows glucose to enter muscle cells more efficiently, both acutely and chronically with exercise (13). Acute changes probably stem from an increased rate of muscle glycogen repletion, while chronic changes likely indicate increases in the total amount of metabolically active muscle. These adaptations may result in lower basal and postprandial insulin needs for diabetic patients (12). Increased insulin sensitivity begins to decline, however, in as little as 1 to 2 days without exercise (14).

      While exercise is considered a cornerstone in type 2 management, glycemic control in individuals with type 1 diabetes can be challenging for medical care-givers because of the complexities of regulating blood sugar with the added, and often unpredictable, variable of exercise. Furthermore, unlike most exercisers with type 2 diabetes, some patients with type 1 diabetes may not have improved glycemic control with regular exercise training if changes in their diet and insulin dosage do not appropriately match exercise requirements (15).


      Choosing Appropriate Exercise

      Different forms of exercise have varying effects on the blood sugar response, especially in patients using insulin. Variables that must be considered include exercise type, duration, and intensity and the patient's fitness level.

      Exercise type. For individuals with diabetes, the type of exercise done (aerobic vs anaerobic) exerts a significant effect on blood sugar responses during the activity.

      Anaerobic. Activities lasting less than 2 minutes (such as sprinting or power lifting) are primarily anaerobic in nature and are fueled by phosphagens (adenosine triphosphate [ATP] and creatine phosphate) and carbohydrates (glycogen) stored in skeletal muscle. The contributions of phosphagenic and glycolytic metabolism depend on the duration and intensity of the activity (figure 1).

      [Figure 1]

      Feed-forward glycemic control (that due to immediate activation of the sympathetic nervous system at the onset of exercise) causes an immediate rise in blood glucose levels, and only a minimal amount of blood glucose is used to fuel anaerobic activities. Blood glucose levels are easier to maintain during such exercise but can also rise as a result. Kjaer et al (16) demonstrated that individuals with type 2 diabetes experienced an exaggerated rise in blood glucose levels during, and for 60 minutes after, maximal exercise on a dynamic cycle ergometer. But patients then experienced increased insulin sensitivity that lasted for at least 24 hours postexercise.

      Repeated bouts of an intense activity (eg, interval or circuit-type weight training) can result in significant muscle glycogen depletion that greatly increases postactivity insulin sensitivity. Eriksson et al (17), who studied individuals who had impaired glucose tolerance, found that several months of resistance training led to a much greater increase in insulin sensitivity than seen in patients who engaged in aerobic or no training. This was attributed primarily to an increase in glycogen storage.

      Aerobic. For any exercise lasting 2 minutes or longer, the body uses all three of the different energy systems (see figure 1): phosphagens, anaerobic glycolysis (use of glycogen stores), and ATP derived from aerobic metabolism of fats and carbohydrates. In addition, many hormonal changes occur in normal individuals to maintain blood sugar levels around 100 mg/dL (5.5 mM). Sustained aerobic activities such as running, cycling, swimming, and aerobic dance rely on a mix of aerobically processed fuels, but the major sources are fats and carbohydrates (both muscle glycogen and blood glucose).

      For exercise done at higher intensities (70% to 75% of maximal aerobic capacity or higher), carbohydrates are the body's fuel of choice regardless of training status. Blood glucose use can become quite significant during these activities, especially as muscle glycogen stores become more depleted during prolonged exercise. As more glycogen is depleted, the risk of hypoglycemia occurring during muscle glycogen replenishment increases, especially in those who do not adjust their insulin doses. For shorter duration and more intense activities, carbohydrate supplementation alone is effective in maintaining euglycemia. For prolonged exercise such as in marathons, triathlons, and long practices, most diabetic athletes must reduce their insulin dose because an increased carbohydrate intake by itself is not adequate to compensate for the accelerated glucose uptake during the activity (18).

      An individual's training status will additionally affect the fuels used during an activity. As exercise intensity increases, the body switches from using a mix of fats and carbohydrates to primarily carbohydrates for fueling prolonged activity. Chronic training increases the proportion of fat used during low- or moderate-intensity activity, delaying the "crossover" point to greater carbohydrate use with increasing exercise intensity (19). Metabolism of more fats (both intramuscular triglycerides and circulating plasma free fatty acids) spares muscle glycogen and blood glucose and allows trained individuals with diabetes to maintain blood sugar levels more effectively during endurance activities.



      Exercise Prescription for Individuals With Diabetes

      Before beginning an exercise program, individuals with diabetes should have a medical evaluation to screen for macrovascular and microvascular complications that may be exacerbated by exercise. The exam should screen for cardiovascular health, peripheral arterial disease, retinopathy, nephropathy, and peripheral and autonomic neuropathy. A graded exercise test is recommended to screen for cardiovascular disease in individuals who meet any of the criteria in table 1 and who wish to participate in moderate- to high-intensity exercise programs (20).

      TABLE 1. Criteria* for Assessing the Need for Graded Exercise Testing Among Patients Who Have Type 1 or Type 2 Diabetes

      Age > 35 years

      Type 2 diabetes > 10 years' duration

      Type 1 diabetes > 15 years' duration

      Presence of any additional risk factor for coronary artery disease

      Presence of microvascular disease (proliferative retinopathy or nephropathy, including microalbuminuria)

      Peripheral vascular disease

      Autonomic neuropathy

      *If an individual meets any one of these criteria, exercise testing is recommended prior to participation in moderate- to high-intensity exercise programs.

      ACSM recommendations. The American College of Sports Medicine (ACSM) recommendations (table 2) for all individuals (including those with diabetes) is that aerobic physical activity be done a minimum of 3 to 5 days a week, for 20 to 60 minutes at 40% to 85% of maximum oxygen uptake reserve (VO2R or heart rate reserve [HRR]), or at 55% to 90% of maximal heart rate (21). For less conditioned individuals, exercise can be done at the lower intensity level for a longer duration, at least until a higher level of fitness can be achieved. Individuals with type 2 diabetes should especially be encouraged to progress to a higher total duration of exercise (eg, 1 hour daily) to facilitate fat loss.

      TABLE 2. American College of Sports Medicine Guidelines for Aerobic Exercise Programs
      Exercise Characteristic Recommendation*
      Mode Continuous, rhythmic, prolonged activities using the large muscle groups of the arms and/or legs
      Intensity Range of 55%-90% of maximal heart rate, 40%-85% of VO2R or HRR, or RPE of 12-16 (somewhat hard to hard)
      Duration Minimum of 20-60 min of continuous aerobic activity to improve fitness and endurance capacity
      Frequency Minimum of 3-5 dy/wk, with frequency determined by exercise duration and intensity
      Rate of progression Initial conditioning of 4-6 wk, improvement phase lasting 4-5 mo, and maintenance thereafter

      *Resistance-type and flexibility training are recommended 2-3 days per week. VO2R = VO2 reserve; HRR = heart rate reserve; RPE = rating of perceived exertion

      Monitoring intensity. Exercise intensity can be prescribed and monitored in several ways. Oxygen uptake reserve is a percentage of the difference between maximal and resting oxygen uptake (VO2) (22). If metabolic data from an exercise stress test are available, a target VO2 can be determined at a desired percentage of VO2R and then translated into a workload for a given exercise. More typically, exercise intensity is established using heart rate. Calculation of a training heart rate or range using the HRR method is done with the following formula:

      Training HR = intensity fraction 3 (HRmax - HRrest) + HRrest, where the intensity fraction is chosen between 0.40 and 0.85 (the lower end of the range is used for patients with low initial fitness). A known value of HRmax, obtained from a maximal stress test, should be used if available; otherwise, HRmax may be estimated by subtracting the patient's age from 220. For example, calculation of a training HR at 50% of HRR for a patient with a maximal HR of 170 beats per minute (bpm) and a resting HR of 80 bpm would result in a training HR of 125 bpm:

      Training HR = 0.50 3 (170 - 80) + 80 = 45 + 80 = 125 bpm.

      Resistance training. Resistance or weight training that includes at least one set of each of 8 to 10 different exercises using the major muscle groups is also recommended 2 to 3 days a week. Each set should consist of 8 to 12 repetitions, with the amount of weight increased when the individual can complete 12 or more repetitions. For those age 50 or older who have diabetes or preexisting health concerns such as hypertension, more repetitions (12 to 15) done at a lower weight may be more suitable. Flexibility training should be incorporated into the overall fitness routine a minimum of 2 to 3 days per week to develop and maintain joint range of motion and to minimize the potential loss of flexibility resulting from glycosylation of various joint structures. Stretching for 5 to 10 minutes should be done either after an aerobic warm-up or following the completion of an exercise session.

      Warm-up and cooldown. No matter what type of activity is done, the standard recommendation for all individuals (with or without diabetes) is to include proper warm-up and cooldown periods. A warm-up consists of 5 to 10 minutes of a lower-intensity aerobic activity that uses the same muscles that will be exercised at a higher intensity (eg, walking before starting to jog). The cooldown consists of 5 to 10 minutes of less intense activity. Such activities may ease the cardiovascular transition between rest and exercise and help prevent muscle and joint injuries.

      Exercise Recommendations for Blood Glucose Management

      Exercise recommendations published collaboratively by the American Diabetes Association and the ACSM give general guidelines for maintaining metabolic control and avoiding hypoglycemia (20). The recommendations address management of blood sugar levels in type 1 diabetes during exercise and explain metabolic control before exercise, blood glucose monitoring before and after exercise, and food intake (table 3). The following sections serve to assist the physician in fully understanding all aspects of the recommendations.

      TABLE 3. American College of Sports Medicine and American Diabetes Association General Guidelines for Exercise and Type 1 Diabetes

      Metabolic Control Before Exercise
      Avoid exercising if fasting glucose levels are > 250 mg/dL and ketosis is present; use caution if glucose levels are > 300 mg/dL and no ketosis is present

      Ingest added carbohydrates if glucose levels are < 100 mg/dL

      Blood Glucose Monitoring Before and After Exercise
      Identify when changes in insulin or food intake are necessary

      Learn the glycemic response to different exercise conditions

      Food Intake
      Consume added carbohydrate as needed to avoid hypoglycemia

      Carbohydrate-based foods should be readily available during and after exercise

      Maintaining glycemic control. Individuals should identify when changes in insulin or food intake are necessary and learn their own glycemic response to different exercise conditions. Glycemic balance is essential to optimal exercise performance. The key to sustaining normal blood glucose levels during physical activity is frequent blood sugar monitoring coupled with appropriate preventive and corrective changes to insulin dosage and/or food intake.

      In a recent study (23), one of us (SRC) reported on the extent of usage of current recommendations by 238 exercisers with type 1 diabetes. Participants stated that the general nature of available guidelines requires a trial-and-error period when they participate in new or unusual physical activities. To establish their usual glycemic patterns, exercisers had to engage in more blood sugar monitoring before, during, and after exercise. Once a pattern was found, then each one's subsequent response was easier to predict.

      A recommendation addressing metabolic control states that type 1 diabetic individuals should avoid exercise if blood glucose levels are greater than 250 mg/dL (13.9 mM) and ketosis is present, and use caution if glucose levels are greater than 300 mg/dL (16.8 mM) and no ketosis is present (table 4) (23). While this recommendation is well advised in most cases, the physician should allow for individual variations if an exerciser has an established pattern such as short excursions in blood glucose levels postprandially without ketosis. Trained athletes with type 1 diabetes report optimal performance when starting exercise at lower levels of blood glucose (70 to 200 mg/dL) (23).

      TABLE 4. Exercise Recommendations for Type 1 Diabetes Based on Preexercise Blood Glucose Levels
      Glucose
      Level Ketones Exercise
      Advised?
      < 100 mg/dL - Yes, but carbohydrate snack may be needed first (allows for individual variation in response)
      100-250 mg/dL - Yes
      > 250 mg/dL No Yes*
      > 250 mg/dL Yes No
      > 300 mg/dL No Use caution*
      > 300 mg/dL Yes No

      *At these levels, some athletes may choose to inject a small dose of short-acting insulin prior to exercise.

      Reprinted with permission from Colberg S: Use of clinical practice recommendations for exercise by individuals with type 1 diabetes. Diabetes Educator 2000;26(2);265-271.

      Modifying insulin dosage. The current ubiquity of blood glucose monitors affords many individualized modifications of insulin and diet to avoid hypoglycemia during exercise. Although the actual reduction will be affected by the individual's insulin regimen, fitness level, exercise choice, and other factors, a general guideline for insulin users is to reduce by 30% to 50% their dose of short-acting insulin (usually regular or lispro, a modified insulin) within 2 to 3 hours of beginning exercise. Alternately, some insulin pump users simply choose to reduce or eliminate their basal infusion of insulin during exercise. These recommendations are, however, merely starting points, as individual responses will vary greatly. The onset and peak of lispro insulin action are much more rapid than those of regular insulin, and greater reductions may be needed if lispro is given before exercise.

      Because "tighter" (closer to recommended) metabolic control is achievable with various insulin regimens and frequent blood glucose monitoring, most diabetic exercisers can experience a decrease in their blood sugar levels while doing aerobic exercise, regardless of their starting blood sugar levels, as long as they have some circulating insulin "on board." Many exercisers report injecting 1 to 3 units of regular or lispro insulin before exercising when they have preexercise blood sugars of 250 to 300 mg/dL or greater (23). They find that the combination of exercise-induced and insulin-mediated glucose uptake lowers blood sugar levels more rapidly than exercise or insulin alone.

      Carbohydrates for exercise.

      Other exercise recommendations for individuals with type 1 diabetes advise having extra carbohydrates handy and consuming them as needed to avoid hypoglycemia during and after exercise. When insulin doses can be reduced before exercise, additional carbohydrates may not be needed. For more spontaneous exercise, or if an individual prefers not to modify insulin dosages, glucose monitoring should be used to determine the actual amount of carbohydrate needed; a typical intake for endurance activities is 15 to 30 g of simple carbohydrates (such as sports drinks, juice, regular soda, glucose tablets, hard candy, bagels, fruit, or dried fruit) every 30 to 60 minutes during prolonged exercise. Access to simple carbohydrates is essential for the rapid treatment of hypoglycemia, should it occur. In addition, a glucagon emergency kit should be available, especially during longer endurance sporting activities.

      Another recommendation is that exercisers ingest additional carbohydrates if glucose levels are below 100 mg/dL (5.5 mM) before exercise. At this level, an exerciser may need to ingest 10 to 15 g of simple carbohydrates and wait 5 to 10 minutes before beginning to exercise. As noted for other recommendations, this serves as a starting point until an individual's glycemic response can be determined. Additional carbohydrates may not be needed for exercise of short duration (< 30 minutes) if the exerciser has sufficiently reduced the preexercise insulin dosage. Intense, shorter exercise usually requires a lower carbohydrate intake as well.

      Although a snack may not be needed immediately to maintain blood glucose levels after exercise, research has shown that consuming carbohydrates within 30 minutes after exhaustive, glycogen-depleting exercise allows for more efficient restoration of muscle glycogen (24). This step may also help prevent postexercise, late-onset hypoglycemia, which can occur up to 24 hours following such exercise (25). During the time of heightened insulin sensitivity, muscle uptake of glucose to restore glycogen can be accomplished with minimal circulating insulin. However, some individuals will require supplemental insulin--albeit less than usual--along with these carbohydrates to prevent hyperglycemia.

      Type 2 diabetes. For individuals with type 2 diabetes who are not using supplemental insulin, such stringent recommendations are not necessary to maintain proper blood glucose levels during exercise. Blood glucose monitoring should be done before and after an activity to assess its effect on glycemia. Supplemental carbohydrates are generally not needed in these patients; however, blood glucose monitoring will reveal which individuals may need additional carbohydrates to prevent hypoglycemia during and following exercise. Use of certain oral hypoglycemic agents such as sulfonylureas carries a higher risk of exercise-induced hypoglycemia due to their longer half-lives. Other recommendations concern safe participation for type 2 exercisers with existing or developing diabetes-related complications such as cardiovascular disease, hypertension, neuropathy, or microvascular changes.
      Exercise Risks and Precautions

      Exercise under some hyperglycemic conditions--especially if insulin deficiency and ketosis are present--can actually worsen metabolic control. This disruption stems from excessive secretion of counterregulatory hormones that may increase already high levels of glucose and ketones. Hyperglycemia alone can stimulate urine production and increase fluid losses; this phenomenon combined with sweat and other fluid losses from exercise can cause dehydration in diabetic individuals.

      Avoiding hypoglycemia. The most immediate and serious potential risk is that exercise can result in hypoglycemia (blood glucose level of 65 mg/dL [3.6 mM] or lower). Supranormal levels of circulating insulin resulting from the mobilization of injected insulin during exercise can attenuate or prevent the normal mobilization of glucose and other substrates and increase muscle uptake of glucose (26). In fact, the risk of hypoglycemia during or following exercise is substantial, especially in insulin users who take a preset insulin dosage, unless appropriate modifications in food or insulin are made.

      A preventive strategy is to exercise when circulating insulin levels are lower (at least 3 to 4 hours after the last injection of short-acting insulin, and not during a dose peak). This makes insulin levels during exercise more similar to those in a nondiabetic individual. Morning exercise, especially if done before any insulin injection, usually exerts less hypoglycemic effect than the same exercise done later in the day. This results from the effects of higher circulating cortisol and other glucose-raising hormone levels early in the day (ie, insulin resistance is generally greater in the morning), along with lower circulating levels of insulin (27). Conversely, evening exercise conveys the greatest risk for nocturnal hypoglycemia unless the patient makes preventive changes in food intake or insulin doses.

      Mitigating diabetic complications. People with diabetes may experience a variety of macrovascular and microvascular complications that can complicate exercise. Any individual with a high risk for underlying cardiovascular disease should be considered for a graded exercise test before beginning a moderate- to high-intensity exercise program (22). For exercise involving the feet, precautionary measures are recommended, especially if peripheral neuropathy is present. Use of silica gel or cushioned midsoles, polyester or synthetic-blend socks, and proper footwear is essential to prevent blisters, keep the feet dry, and minimize or prevent trauma. Non-weight-bearing exercise such as aqua aerobics can be substituted for weight-bearing activities.

      Hypotension and hypertension following vigorous exercise are more likely to develop in individuals with autonomic neuropathy. Their thermoregulatory capacity may be inadequate, and special care is needed to maintain adequate hydration. Active, strenuous exercise is contraindicated for individuals with active vitreous hemorrhages due to unstable proliferative retinopathy. Intense exercise involving straining, jarring, or Valsalva-like maneuvers should be avoided as well. When nephropathy is present, individuals may have a reduced exercise capacity, but low- to moderate-intensity activities can be done.


      Parting Advice

      Individuals with diabetes can learn how to improve their blood glucose management during exercise. Making the appropriate regimen adjustments before, during, and after exercise is a trial-and-error process for each new activity. Physicians should encourage diabetic exercisers to test their blood glucose levels before, during (for new activities), and after exercise. They should also assist these individuals in predicting their exercise responses to new or unusual activities based on the type, duration, and intensity of exercise, insulin regimens, starting blood sugar levels, carbohydrate intake, and timing of exercise; all can affect blood sugar responses. All exercisers should be advised to consume extra rapidly absorbed carbohydrates as necessary to prevent or treat hypoglycemia during and following exercise.

      Although the general exercise recommendations can be helpful, physicians may have to aid patients in modifying diet and insulin regimens because the recommendations require tailoring to meet individual needs (23). Furthermore, if a patient's preexercise metabolic control is poor or diabetes-related complications are present, clinical recommendations should be followed to prevent worsening or onset of complications. Exercise can be done safely by individuals with diabetes, and the health benefits are undeniable. Diabetes control and regular exercise truly form a winning combination.
      References

      1. Harris M, Flegal K, Cowie C, et al: Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in US adults: the Third National Health and Nutrition Survey, 1988-1994. Diab Care 1998;21(4):518-524
      2. Weyer C, Bogardus C, Mott DM, et al: The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest 1999;104(6):787-794
      3. Buchanan TA, Kjos SL: Gestational diabetes: risk or myth? J Clin Endocrinol Metab 1999;84(6):1854-1857
      4. Manson JE, Rimm EB, Stampfer MJ, et al: Physical activity and incidence of non-insulin-dependent diabetes mellitus in women. Lancet 1991;338(8770):774-778
      5. Helmrich SP, Ragland, DR, Leung RW, et al: Physical activity and reduced occurrence of non-insulin-dependent diabetes mellitus. N Engl J Med 1991;325(3):147-152
      6. Hu FB, Sigal RJ, Rich-Edwards JW, et al: Walking compared with vigorous physical activity and risk of type 2 diabetes in women: a prospective study. JAMA 1999;282(15):1433-1439
      7. Haapanen N, Miilunpalo S, Vuori I, et al: Association of leisure time physical activity with the risk of coronary heart disease, hypertension and diabetes in middle-aged men and women. Int J Epidemiol 1997;26(4):739-747
      8. Engstrom G, Helblad B, Janzon L: Hypertensive men who exercise regularly have lower rate of cardiovascular mortality. J Hypertens 1999;17(6):737-742
      9. Thune I, Brenn T, Lund E, et al: Physical activity and the risk of breast cancer. N Engl J Med 1997;336(18):1269-1275
      10. 10. Thune I, Lund E: Physical activity and risk of colorectal cancer in men and women. Br J Cancer 1996;73(9):1134-1140
      11. Kampert JB, Blair SN, Barlow CE, et al: Physical activity, physical fitness, and all-cause and cancer mortality: a prospective study of men and women. Ann Epidemiol 1996;6(5):452-457
      12. Devlin J: Effects of exercise on insulin sensitivity in humans. Diab Care 1992;15(11):1690-1693
      13. Dela F, Mikines K, Von Linstow M, et al: Effect of training on insulin-mediated glucose uptake in human muscle. Am J Physiol 1992;263(6):E1134-E1143
      14. King D, Dalsky G, Clutter W, et al: Effects of lack of exercise on insulin secretion and action in trained subjects. Am J Physiol 1988;254(5):E537-E542
      15. Ebeling P, Tuominen J, Bourey R, et al: Athletes with IDDM exhibit impaired metabolic control and increased lipid utilization with no increase in insulin sensitivity. Diabetes 1995;44(4):471-477
      16. Kjaer M, Hollenbeck CB, Frey-Hewitt B, et al: Glucoregulation and hormonal responses to maximal exercise in non-insulin-dependent diabetes. J Appl Physiol 1990;68(5):2067-2074
      17. Eriksson J, Tuominen J, Valle T, et al: Aerobic endurance exercise or circuit-type resistance training for individuals with impaired glucose tolerance? Horm Metab Res 1998;30(1):37-41
      18. Sane T, Helve E, Pelkonen R, et al: The adjustment of diet and insulin dose during long-term endurance exercise in type 1 (insulin-dependent) diabetic man. Diabetologia 1988;31(1):35-40
      19. Brooks G, Mercier J: The balance of carbohydrate and lipid utilization during exercise: the 'crossover' concept. J Appl Physiol 1994;76(6):2253-2261
      20. American Diabetes Association: Clinical Practice Recommendations 2000: diabetes mellitus and exercise. Diab Care 2000;23(suppl 1):S50-S54
      21. Pollack ML, Gaesser GA, Butcher JD, et al: The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness and flexibility in healthy adults. Med Sci Sports Exerc 1998;30(6):975-991
      22. Swain DP, Leutholtz BC: Heart rate reserve is equivalent to % VO2reserve, not to % VO2max. Med Sci Sports Exerc 1997;29(3):410-414
      23. Colberg S: Use of clinical practice recommendations for exercise by individuals with type 1 diabetes. Diabetes Educator 2000;26(2):265-271
      24. Ivy J, Katz A, Cutler C, et al: Muscle glycogen synthesis after exercise: effect of time of carbohydrate ingestion. J Appl Physiol 1988;64(4):1480-1485
      25. MacDonald M: Post-exercise late-onset hypoglycemia in insulin-dependent diabetic patients. Diab Care 1987;10(5):584-588
      26. Kemmer F: Prevention of hypoglycemia during exercise in type 1 diabetes. Diab Care 1992;15(suppl 4):1732-1735
      27. Ruegemer J, Squires R, Marsh H, et al: Differences between prebreakfast and late afternoon glycemic responses to exercise in IDDM patients. Diab Care 1990;13(2):104-110

      Dr Colberg is an assistant professor and Dr Swain is an associate professor in the department of exercise science, physical education, and recreation at Old Dominion University in Norfolk, Virginia. Address correspondence to Sheri R. Colberg, PhD, Dept of Exercise Science, Physical Education and Recreation, Old Dominion University, HPE Bldg, Rm 140, Norfolk, VA 23529-0196; e-mail to scolberg@odu.edu.
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


      Let me know if you think of anything else handy from the site to put here.
    • Training on the Cyclical Ketogenic Diet: Effects of Cyclical Ketogenic Diets on Exerc

      One from Lyle, keep in mind that CKD is 5-6 days of LC and 1-2 days of HC. So when he talks about doing very high intensity of exercise to get into ketosis this is for the purpose of depleting Glycogen (carbohydrates) from the body after a day or two of very high sugar intake.


      Training on the Cyclical Ketogenic Diet: Effects of Cyclical Ketogenic Diets on Exercise Performance

      by Lyle McDonald, CSCS
      Author of The Ketogenic Diet

      thinkmuscle.com/articles/mcdon…ing-on-ketogenic-diet.htm

      Please send us your feedback on this article.

      Introduction

      As the Cyclical Ketogenic Diet (CKD) becomes more popular among natural bodybuilders, a great many questions have arisen regarding any and all manners of topics. One of the primary has to do with exercise on a CKD. First and foremost, individuals want to know what types of exercise can and can not be sustained on a CKD. Secondly questions arise as to what is the optimal training structure to maximize either fat loss or muscle gains on a CKD.

      To answer these two questions, a lot of topics have to be covered ranging from exercise biochemistry to the hormonal response to different types of exercise to the implications of a diet which does not contain

      carbohydrates during the week. The goal of this article will be to discuss the CKD primarily for fat loss. For reasons beyond the scope of this article, the CKD is most likely not the optimal diet for mass gains.

      What is the CKD?

      The Cyclical Ketogenic Diet, CKD, is a general term to describe diets such as The Anabolic Diet (by Dr. Mauro DiPasquale) and BODYOPUS (by Dan Duchaine). While there are many variants, the most common structure for a CKD is 5-6 days of strict low carbohydrate eating (less than 30 grams per day) with a 1-2 day carb-loading period (where carbohydrate intakes is roughly 60-70% of the total calories consumed). The idea behind the CKD (which will be discussed in a later article) is to force the body to burn fat during the lowcarb days, while sustaining exercise intensity by refilling muscle glycogen stores during the weekend carb-load.

      Some Basic Exercise Metabolism

      To better understand the effects of a CKD on exercise performance, we have to look briefly at how different forms of exercise affect fuel utilization in the body. There are four potential fuels which the body can use during exercise: glycogen, fat, protein and ketones. Except under certain conditions (which will be mentioned when necessary), protein and ketones do not provide a significant amount of energy during exercise. Therefore this discussion will focus primarily on glycogen and fat use during exercise. To simplify this article, exercise will be delineated as either aerobic or anaerobic (which will include interval training and weight training).

      Aerobic Exercise

      Aerobic exercise is generally defined as any activity which can be sustained continuously for periods of at least three minutes or longer. Examples would be walking, jogging, cycling, swimming, aerobics classes, etc.

      The primary fuels during aerobic exercise are carbohydrate (muscle glycogen and blood glucose) and fat (from adipose tissue as well as intramuscular triglyceride) (1,2). At low intensities, fat is the primary fuel source during exercise.

      As exercise intensity increases, less fat and more glycogen is used as fuel. At some intensity, sometimes called the "Crossover point", glycogen becomes the primary fuel during exercise. (3) This point corresponds roughly with something called the lactate threshold. The increase in glycogen utilization at higher intensities is related to a number of factors including greater adrenaline release (3,4) decreased availability of free fatty acids (5), and greater recruitment of Type II muscle fibers (3,6,8). The ketogenic diet shifts the crossover (i.e. lactate threshold) point to higher training intensities (3) as does regular endurance training (4).

      Under normal (non-ketotic) conditions, ketones may provide 1% of the total energy yield during exercise (8). During the initial stage of a ketogenic diet, ketones may provide up to 20% of the total energy yield during exercise (9). After adaptation, even under conditions of heavy ketosis, ketones rarely provide more than 7-8% of the total energy yield which is a relatively insignificant amount (10,11,12).

      Generally, protein use during aerobic exercise is minimal, accounting for perhaps 5% of the total energy yield. With glycogen depletion, this may increase to 10% of the total energy yield, amounting to the oxidation of about 10-13 grams of protein per hour of continuous exercise (14). This is at least part of the reason that excessive aerobic exercise, especially under low glycogen conditions, can cause muscle loss while dieting.


      Studies on ketogenic diets (2 to 6 weeks) find a maintenance (15, 16) or increase (17,18) in aerobic endurance during low intensity exercise (75% of maximum heart rate and below). At higher exercise intensities (around 85% of maximum heart rate which is likely above the lactate threshold), as glycogen use increases, performance decreases on a ketogenic diet (19).

      Anaerobic Exercise

      While anaerobic exercise refers generally to any activity which lasts less than three minutes or so, most individuals are interested in the effects of a CKD on weight training. However athletes involved in sports such as sprinting, or any activity lasting less than three minutes, will have the same considerations discussed in this section.

      Weight training refers to any activity involving the use of heavy resistance which lasts less than three minutes (i.e. it is anaerobic). Weight training is slightly more complicated to discuss in terms of fuel use than aerobic exercise. For very short activities (less than 20 seconds), muscles use ATP (adenosine triphosphate) which is stored directly in the muscle. Activities lasting greater than 30 seconds will rely on the breakdown of glycogen (carbohydrate stored in the muscle). During anaerobic exercise, fat can not be used directly as a fuel (1).

      Relatively few studies have examined the effects of carbohydrate depletion on resistance training. In fact no studies have studies the effects of a ketogenic diet on weight training performance. However since weight training can only use glycogen for fuel, we can logically conclude that carbohydrates are critical for weight training performance. In fact, this is the primary reason to insert the carb-loading phase of the CKD on the weekend: to sustain high intensity exercise performance while still deriving the benefits of ketosis. Other issues pertaining to glycogen levels and depletion appear below.
      The Hormonal Response to Exercise

      The hormonal response to exercise is important from two standpoints. First and foremost, manipulation of the type of exercise done on a CKD can affect how efficiently fat loss or muscle gain occur. Second, to most rapidly enter ketosis (which requires a depletion of liver glycogen), certain types of exercise will be more effective than others. The primary hormonal response to both aerobic and anaerobic exercise are discussed below.

      There are several hormones which are affected by aerobic exercise depending on exercise intensity and duration. They primarily impact on fuel utilization.

      Catecholamines:

      Adrenaline and noradrenaline are both involved in energy production. The catecholamines raise heart rate and blood pressure, stimulate fat breakdown (lipolysis), increase liver and muscle glycogen breakdown, and inhibit insulin release from the pancreas (20). Both adrenaline and noradrenaline increase during aerobic exercise although in differing amounts depending on intensity of exercise. Noradrenaline levels rise at relatively low exercise intensities stimulating FFA utilization in the muscles but relatively low levels of liver and muscle glycogen breakdown.

      Insulin:

      During aerobic exercise, insulin levels drop quickly due to an inhibitory effect on it's release from the pancreas by adrenaline (20, 21). The drop in insulin allows free fatty acid release to occur from the fat cells during exercise. Lowering insulin is also important for establishing ketosis. Despite a decrease in insulin levels during exercise, there is an increased uptake of blood glucose by the muscle. An increase in glucose uptake with a decrease in insulin indicates improved insulin sensitivity at the muscle cells during exercise.

      Glucagon:

      As the mirror hormone of insulin, glucagon levels increase during aerobic exercise (20). Thus the overall response to aerobic exercise is pro-ketogenic in that it causes the necessary shift in the Insulin/Glucagon ratio to occur.

      Thus the overall response to aerobic exercise is to decrease the use of glucose and increase the use of free fatty acids for fuel. This is beneficial from the standpoint of establishing ketosis, as will be discussed in greater detail below.

      Weight training affects levels of many hormones in the human body depending on factors such as order of exercise, loads, number of sets, number of repetitions, etc. The primary hormones we are interested in which are affected by weight training are the androgens (primarily testosterone, growth hormone and IGF-1. With the exception of testosterone, the hormonal response to weight training primarily affects fuel availability and utilization (22).

      Growth hormone (GH):

      GH is a peptide hormone released from the hypothalamus in response to many different stimuli including sleep and breath holding (23). Although growth hormone is thought to be muscle building, at the levels seen in humans, it's main role is to mobilize fat and decrease carbohydrate and protein utilization (24).

      The main role of GH on muscle growth is most likely indirect by increasing release of Insulin-like Growth Factor 1 (IGF-1) from the liver (24). The primary stimulus for GH release with weight training appears to be related to lactic acid levels and the highest GH response to training is seen with moderate weights (~75% of maximum), multiple long sets (3-4 sets of 10-12 repetitions, about 40-60 seconds per set) with short rest periods (60-90 seconds). Studies using this type of protocol (generally 3X10 Rep maximum with a 1' rest period) have repeatedly shown increases in GH levels in men (25, 26) and women (27,28) and may be useful for fat loss due to the lipolytic (fat mobilizing) actions of GH. Multiple sets of the same exercise are required for GH release (28).

      Testosterone

      Testosterone is frequently described as the 'male' hormone although women possess testosterone as well (at about 1/10th the level of men or less) (4).

      Testosterone's main role in muscle growth is by directly stimulating protein synthesis (23,29). Increases in testosterone occur in response to the use of basic exercises (squats, deadlifts, bench presses), heavy weights (85% of maximum and higher), multiple short sets (3 sets of 5 repetitions, about 20-30 seconds per set) and long rest periods (3-5 minutes). Studies have found a regimen of 3X5 rep max. with 3' rest to increases testosterone significantly in men (25,26,30) but not in women (27). It is unknown whether the transient increase in testosterone following training has any impact on muscle growth.

      Insulin like growth factor 1 (IGF-1)

      IGF-1 is a hormone released from the liver, most likely in response to increases in GH levels (31). However the small increases in GH seen with training do not appear to affect IGF-1 levels (32). More likely, IGF-1 is released from damaged muscle cells (due to eccentric muscle actions) and acts locally only to stimulate growth (33,34).
      Exercise and Ketosis

      In that ketosis indicates that the body has shifted to using fat as it's primary fuel, and since only five to six days exist per week to be in ketosis, a question which arises is how to most quickly establish ketosis.

      Aerobic and anaerobic exercise have somewhat differential effects on ketosis and are discussed here.

      It has been known for almost a century that ketones appear in higher concentrations in the blood following aerobic exercise (35). The overall effect of aerobic exercise below the lactate threshold is to induce or enhance ketosis. Liver glycogen decreases, insulin decreases, glucagon increases and there is an increase in free fatty acid levels in the bloodstream.

      Aerobic exercise can quickly induce ketosis following an overnight fast. One hour at 65% of maximum heart rate causes a large increase in ketone body levels but the ketones do not contribute to energy production to any significant degree (36). 2 hours of exercise at 65% of maximum heart rate will raise ketone levels to 3mM after 3 hours. High levels of ketonemia (similar to those seen in prolonged fasting) can be achieved five hours post-exercise (36).

      During high intensity exercise, the same overall hormonal picture described above occurs, just to a greater degree. Adrenaline and noradrenaline both increase during high intensity activities (both interval and weight training). The large increase in adrenaline causes the liver to over-release liver glycogen raising blood glucose (4,20). While this may impair ketogenesis in the short term, it is ultimately helpful in establishing ketosis initially. Insulin goes down during exercise but may increase after training due to increases in blood glucose. Glucagon goes up also helping to establish ketosis. Probably the biggest difference between high and low intensity exercise is that free fatty acid release is inhibited during high intensity activity, due to the increases in lactic acid (5).
      Glycogen Levels and Depletion

      To understand how to optimize training for a CKD, a discussion of glycogen levels under a variety of conditions are necessary. As well, some estimations must be made in terms of the amount of training which can and should be done as well as how much carbohydrate should be consumed at a given time.

      Muscle glycogen is measured in millimoles per kilogram of muscle (mmol/kg). An individual following a normal mixed diet will maintain glycogen levels around 80-100 mmol/kg. Athletes following a mixed diet have higher levels, around 110-130 mmol/kg (37). On a standard ketogenic diet, with aerobic exercise only, muscle glycogen levels maintain around 70 mmol/kg with about 50 mmol/kg of that in the Type II muscle fibers (38,39).

      Fat oxidation increases, both at rest and during aerobic exercise around 70 mmol/kg. Below 40 mmol/kg, exercise performance is generally impaired. Total exhaustion during exercise occurs at 15-25 mmol/kg. Additionally when glycogen levels fall too low (about 40 mmol/kg), protein can be used as a fuel source during exercise to a greater degree (14).

      Following total depletion, if an individual consumes enough carbohydrates over a sufficient amount of time (generally 24-48 hours), muscle glycogen can reach 175 mmol/kg or higher (38). The level of supercompensation which can be achieved depends on the amount of glycogen depleted (40,41). That is, the lower that muscle glycogen levels are taken, the greater compensation will be seen. If glycogen levels are depleted too far (below 25 mmol/kg), glycogen supercompensation is impaired as the enzymes involved in glycogen synthesis are impaired (42). A summary of glycogen levels under different conditions appears in figure 1.

      Figure 1: Summary of glycogen levels under different conditions



      Condition Diet Glycogen

      level (mmol/kg)

      48 hour carb-up High carb 175

      36 hour carb-up ~150

      24 hour carb-up ~120-130

      Athlete Mixed diet 110-130

      Normal individual Mixed diet 80-100

      Normal individual, Ketogenic diet 70

      Aerobic exercise only

      Fat burning increases 70

      Exercise performance decreased 40

      Exhaustion 15-25
      Glycogen Depletion During Weight Training

      Having looked at glycogen levels under various conditions, we can now examine the rates of glycogen depletion during weight training and use those values to make estimations of how much training can and should be done for the CKD.

      Very few studies have examined glycogen depletion rates during weight training. One early study found a very low rate of glycogen depletion of about 2 mmol/kg/set during 20 sets of leg exercise (43). In contrast, two later studies both found glycogen depletion levels of approximately 7-7.5 mmol/kg/set (44,45). As the difference between these studies cannot be adequately explained, we will assume a glycogen depletion rate of 7 mmol/kg/set.

      Examining the data of these two studies further, we can estimate glycogen utilization relative to how long each set lasts. At 70% of maximum weight, both researchers found a glycogen depletion rate of roughly 1.3 mmol/kg/repetition or 0.35 mmol/kg/second of work performed (44,45).

      Rates of glycogen depletion during weight training at an intensity at 70% max

      Depletion per set 7.5 mmol/kg/set

      Depletion per repetition 1.3 mmol/kg/rep

      Depletion per second of work 0.35 mmol/kg/second
      Designing the Workout

      With all of the above information presented, we can go through the steps to develop a CKD workout for fat loss. The goals of the workout are:

      1. Deplete muscle glycogen in all bodyparts to approximately 70 mmol/kg by Tuesday as this will maximize fat utilization by the muscles but will not increase protein utilization.

      2. Maximize Growth Hormone output (which is a lipolytic hormone) on Mon/Tue with a combination of long sets, multiple sets, and short rest periods.

      3. Maintain muscle mass with tension work outs on Monday and Tuesday.

      4. Deplete muscle glycogen to between 25 and 40 mmol/kg on Friday to stimulate optimal glycogen supercompensation.

      5. Stimulate mass gains during the weekend of overfeeding with a full body tension workout (a high rep depletion workout is also an option)

      6. Use cardio to quickly establish ketosis and enhance fat loss

      The primary goal that still needs to be discussed is how much training is necessary to achieve goals #1 and #4.

      We will assume a lifter has completed a 36 hour carb-up, ending Saturday evening, with a muscle glycogen level of 150 mmol/kg in all major muscle groups. To deplete to 70 mmol/kg in the first two workouts, this person needs to deplete:

      150 mmol/kg - 70 mmol/kg = 80 mmol/kg of total glycogen.

      Using the rate of glycogen depletion listed above we see that

      80 mmol/kg divided by 1.3 mmol/kg/rep = 61 total reps.

      or

      80 mmol/kg divided by 0.35 mmol/kg/sec = 228 seconds of total set time.

      Assuming an average set time of 45 seconds (10-12 reps at 4 seconds per repetition) this level of glycogen depletion would require approximately 5-6 sets per bodypart.

      For the Friday workout, our lifter now wants to deplete muscle glycogen to between 25-40 mmol/kg before starting the carb-up. This would require a further glycogen depletion of

      70 mmol/kg - 25 mmol/kg = 45 mmol/kg

      70 mmol/kg - 40 mmol/kg = 30 mmol/kg

      30-45 mmol/kg.

      This would be

      30-45 mmol/kg divided by 1.3 mmol/kg/rep = 20-30 reps

      30-45 mmol/kg divided by 0.35 mmol/kg/second = 85-128 seconds.
      The CKD Workout Routine

      With the above estimations for sets and reps having been made, we can develop a sample workout routine. The format for the CKD week is:

      Day Workout type Diet

      Sunday: 30'+ of low intensity cardio in Ketogenic

      morning to establish ketosis

      Monday: Tension weight training workout Ketogenic

      Tuesday: Tension weight training workout Ketogenic

      Wed/Thu: cardio optional for fat loss Ketogenic

      Fri: Full body workout Ketogenic prior to workout

      Begin carb-load after

      workout

      Saturday: No workout Carb load

      Sample workouts appear below.

      Mon: Legs and abs

      Exercise Sets Reps Rest

      Squats 4 8-10 90"

      Leg curl 4 8-10 90"

      Leg extension OR 2 10-12 60"

      feet high leg press

      Seated leg curl 2 10-12 60"

      Standing calf raise 4 8-10 90"

      Seated calf raise 2 10-12 60"

      Reverse crunch 2 15-20 60"

      Crunch 2 15-20 60"

      Total sets 24

      Tue: Upper body

      Exercise Sets Reps Rest

      Incline bench press 4 8-10 60"

      Cable row 4 8-10 60"

      Flat bench press 2 10-12 60"

      Pulldown to front 2 10-12 60"

      Shoulder press 3 10-12 60"

      Barbell curl 2 12-15 45"

      Triceps pushdown 2 12-15 45"

      Total sets 20

      There are two options for the Friday workout. One is to perform a tension workout to stimulate growth during the carb-load. The second is to do a high-rep depletion workout, which should be done in circuit fashion solely to deplete muscle glycogen.

      Sample Friday tension workout:

      Exercise Sets Reps Rest

      Leg press 3 8-10 90"

      Leg curl 1 10-12 60"

      Calf raise 2 10-12 60"

      Bench press 3 8-10 90"

      Wide grip row 3 8-10 90"

      Shoulder press 1-2 10-12 60"

      Undergrip pulldown 1-2 10-12 60"

      Total sets 14-16

      Sample circuits for Friday depletion workout:

      leg press, dumbbell bench press, cable row, leg curl, shoulder press, overgrip pulldown, calf raise, triceps pushdown, barbell curl, reverse crunch.

      leg extension, incline DB bench press, narrow grip row, seated leg curl, lateral raise, undergrip pulldown, seated calf raise, close grip bench press, alternate DB curl, twisting crunch.

      squat, flat flye, cable row, standing leg curl, upright row, overgrip pulldown, donkey calf raise, overhead triceps extension, hammer curl, crunch.

      Since the intensity is lower (roughly 50-60% of maximum) glycogen depletion per set will also be lower. Additionally, 20 reps will only require about 20-40 seconds to complete. Assuming glycogen had started at 70 mmol/kg, it will likely take 4-5 circuits to fully deplete glycogen.

      Perform 10-20 quick reps per set (1 second up/1 second down). Take 1' between exercises, and 5' between circuits. The sets should not be taken to failure; the goal is simply to deplete muscle glycogen. Many trainees complain of nausea during this workout, which is caused by not resting long enough between sets.
      References
      1. Eric Hultman "Fuel selection, muscle fibre" Proceedings of the Nutrition Society (1995) 54: 107-121.

      2. Edward F. Coyle "Substrate Utilization during exercise in active people" Am J Clin Nutr (1995) 61 (suppl): 968S-979S.

      3. George Brooks and Jacques Mercier "Balance of carbohydrate and lipid utilization during exercise: the "crossover" concept" J Appl Physiol (1994) 76: 2253-2261.

      4. "Physiology of Sport and Exercise" Jack H. Wilmore and David L. Costill. Human Kinetics Publishers 1994.

      5. Romijn J.A. et. al. "Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration" Am J Physiol (1993) 265: E380-391.

      6. Vollestad, NK et al. "Muscle glycogen depletion patterns in type I and subgroups of Type II fibers during prolonged severe exercise in man" Acta Physiol Scand (1984) 122: 433-441.

      7. Gollnick, P.D. et. al. "Selective glycogen depletion in skeletal muscle fibres of man following sustained contractions" J Physiol (1974) 241: 59-67.

      8. "Exercise Metabolism" Ed. Mark Hargreaves. Human Kinetics Publishers 1995.

      9. Elia, M. et. al. "Ketone body metabolism in lean male adults during short-term starvation, with particular reference to forearm muscle metabolism" Clinical Science (1990) 78: 579-584.

      10. Bergstrom, J. et. al. "Diet, muscle glycogen and physical performance" Acta Physiol Scand (1967) 71: 140-150.

      11. Edmond O. Balasse and F. Fery "Ketone body production and disposal: Effects of fasting, diabetes and exercise" Diabetes/Metabolism Reviews (1989) 5: 247-270.

      12. Wahren J. et. al. "Turnover and splanchnic metabolism of free fatty acids and ketones in insulin-dependent diabetics at rest and in response to exercise" J Clin Invest (1984) 73: 1367-1376.

      14. Lemon, P.R. and J.P. Mullin "Effect of initial muscle glycogen level on protein catabolism during exercise" J Appl Physiol (1980) 48: 624-629.

      15. Phinney, S.D. et. al. "The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capacity with reduced carbohydrate oxidation" Metabolism (1983) 32: 769-776.

      16. Phinney, S.D. et. al. "Effects of aerobic exercise on energy expenditure and nitrogen balance durin very low calorie dieting." Metabolism (1988) 37: 758-765.

      17. Phinney, SD et. al. "Capacity for moderate exercise in obese subjects after adaptation to a hypocaloric, ketogenic diet" J Clin Invest (1980) 66: 1152-1161.

      18. Lambert E.V. et. al. "Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet" Eur J Apply Physiol (1994) 69: 387-293.

      19. Hargreaves M. et. al. "Influence of muscle glycogen on glycogenolysis and glucose uptake during exercise in humans" J Appl Physiol (1995) 78: 288-292.

      20. "Exercise Physiology: Human Bioenergetics and it's applications" George A Brooks, Thomas D. Fahey, and Timothy P. White. Mayfield Publishing Company 1996.

      21. Wade H. Martin III "Effects of acute and chronic exercise on fat metabolism" Exercise and Sports Science Reviews (1994) Vol 22: 203-231.

      22. Katarina Borer "Neurohumoral mediation of exercise-induced growth" Med Sci Sports Exerc (1994) 26:741-754.

      23. William Kraemer "Endocrine responses to resistance exercise" Med Sci Sports Exerc (1989) 20 (suppl): S152-S157.

      24. Rogol, A.D. "Growth hormone: physiology, therapeutic use, and potential for abuse" ESSR (1989) 17: 353-377.

      25. K. Hakkinen and A. Pakarinen "Acute hormonal responses to two different fatiguing heavy-resistance protocols in male athletes" J Appl Physiol (1993) 74: 882-887.

      26. Kraemer, W.J. et. al. "Hormonal and growth factor responses to heavy resistance exercise protocols" J Appl Physiol (1990) 69: 1442-1450.

      27. Kraemer, W.J. et. al. "Changes in hormonal concentrations following different heavy resistance exercise protocols in women." J Appl Physiol (1993) 75: 594-604.

      28. Mulligan, S.E. et. al. "Influence of resistance exercise volume on serum growth hormone and cortisol concentrations in women" J Strength Cond Res (1996) 10: 256-262.

      29. Griggs, R.C. et . al. "Effect of testosterone on muscle mass and protein synthesis" J Appl Physiol (1989) 66: 498-503.

      30. Schwab, R. et. al. "Acute effects of different intensities of weight lifting on serum testosterone." Med Sci Sports Exerc (1993) 25(12): 1381-1385.

      31. Kraemer, W.J. et. al. "Responses of IGF-1 to endogenous increases in growth hormone after heavy-resistance exercise" J Appl Physiol (1995) 79:1310-1315.

      32. Katarina Borer "Neurohumoral mediation of exercise-induced growth" Med Sci Sports Exerc (1994) 26:741-754.

      33. R. Smith and O.M. Rutherford "The role of metabolites in strength training I. A comparison of eccentric and concentric contractions" Eur J apply Physiol (1995) 71: 332-336.

      34. DeVol, DL et. al. "Activation of insulin-like work-induced skeletal muscle growth" Am J Physiol (1990) 259: E89-E95.

      35. J. H. Koeslag "Post-exercise ketosis and the hormone response to exercise: a review" Med Sci Sports Exerc (1982) 14: 327-334.

      36. Edmond O. Balasse and F. Fery "Ketone body production and disposal: Effects of fasting, diabetes and exercise" Diabetes/Metabolism Reviews (1989) 5: 247-270.

      37. John Ivy "Muscle glycogen syntehsis before and after exercise" Sports Medicine (1991) 11: 6-19.

      38. Phinney S.D. et. al. "The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptations" Metabolism (1983) 32: 757-768.

      39. Phinney, S.D. et. al. "The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capacity with reduced carbohydrate oxidation" Metabolism (1983) 32: 769-776.

      40. Zachweija, J.J. et. al. "Influence of muscle glycogen depletion on the rate of resynthesis" Med Sci Sports Exerc (1991) 23: 44-48.

      41. Price, TB et. al. "Human muscle glycogen resynthesis after exercise: insulin-dependent and -independent phases" J Appl Physiol (1994) 76: 104-111.

      42. Yan Z. et. al. "Effect of low glycogen on glycogen synthase during and after exercise" Acta Physiol Scand (1992) 145: 345-352.

      43. D.D. Pascoe and L.B. Gladden "Muscle glycogen resynthesis after short term, high intensity exercise and resistance exercise" Sports Med (1996) 21: 98-118.

      44. Robergs, RA et. al. "Muscle glycogenolysis during different intensities of weight-resistance exercise" J Appl Physiol (1991) 70: 1700-1706.

      45. Tesch, PA et. al. "Muscle metabolism during intense, heavy resistance exercise" Eur J Appl Physiol (1986) 55: 362-366.


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    • What is the best exercise to burn fat?

      What is the best exercise to burn fat?

      medicdirectsport.com/exerciset…default.asp?step=4&pid=52

      So You Want To Lose Some Body Fat?

      Carrying excess fat is unhealthy. The only effective way to lose body fat is to increase energy expenditure by exercising more and/or decrease energy intake by eating less. A combination of the two in moderation is probably most effective, since dieting alone is often accompanied by an adaptive reduction in metabolic rate (resting energy expenditure). Many people exercise in order to lose fat, enhance muscle tone and improve their body shape. But what exercise intensity should be performed in order to optimise the burning of fat?
      Exercise Expends Energy And So Requires Fuel

      During dynamic aerobic exercise your muscles use oxygen to burn fuel in the form of both fat and carbohydrate, which releases energy that can be used to perform muscular work. The precise fuel mixture that the muscles use for exercise depends mostly on the exercise intensity and duration. During short-term high intensity exercise, the muscles predominantly use carbohydrate in the form of muscle glycogen (a storage form of sugar) and glucose that is absorbed from the blood. For exercise of low-moderate intensity the muscles oxidise mostly fat. Even for moderate intensity exercise, in the first few minutes we tend to use mostly carbohydrate, but as exercise duration increases, the contribution of fat becomes greater.

      At rest we expend about 1 kilocalorie (or 4 kilojoules) of energy per minute. Moderate intensity exercise will typically raise the rate of energy expenditure to around 6 kilocalories (25 kilojoules) per minute. So if you exercised for one hour at this intensity you would expend about 360 kilocalories (1500 kilojoules), burning up to 40 grams (2 ounces) of fat in the process. Although this doesn't sound a lot, when exercise is performed on a regular basis (e.g. one hour every day) this mounts up to over 1 kilogram (2.2 pounds) of fat loss per month.

      How Is Exercise Intensity Quantified?

      Exercise requires energy to fuel the contracting muscles. For sustained activity, oxygen is also required and is pumped from the lungs to the muscles via the red blood cells in the circulation. The heart is the pump and the heart rate can increase from around 70 beats per minute at rest up to around 200 beats per minute during exercise, depending on age. You can estimate your own maximal heart rate (HRmax) by subtracting your age in years from 220 (e.g. a typical 40 year-old person will have a predicted maximum heart rate of 220 - 40 = 180 beats per minute). With increasing exercise intensity, oxygen uptake increases proportionally until a plateau is reached. At this point further increases in work rate do not elicit further increases in oxygen uptake and the plateau value is called the maximal oxygen uptake or VO2max. This can also be referred to as the aerobic capacity and is strongly associated with a person's capacity to perform prolonged exercise.

      At rest, the rate of oxygen uptake of an adult is about 0.25 litres per minute. During exercise this can increase up to about 10-20 times, though this is dependent on fitness and genetic factors. An elite endurance runner or cyclist can have a VO2max of over 5 litres per minute, whereas a typical middle-aged couch potato might only have a VO2max of less than 2 litres per minute. Because different people have different maximal oxygen uptakes, one way of quantifying relative exercise intensity is to express the work rate as a percentage of a particular person's maximal oxygen uptake (%VO2max).

      Measuring oxygen uptake requires rather sophisticated and expensive scientific equipment, but the heart rate can be measured by counting the pulse at the wrist or with the use of relatively inexpensive heart rate monitors. Another way of easily quantifying relative exercise intensity is to measure the heart rate during exercise and express it as a percentage of the maximal heart rate (%HRmax). The HRmax can either be determined in an incremental exercise test to fatigue or predicted (with ±10% accuracy) from the person's age as described above.


      What Is The Optimal Exercise Intensity To Burn Fat?

      From low to moderate intensities of exercise the absolute rate of fat oxidation increases and then declines as exercise becomes even more intense. Generally the highest rates of fat oxidation are found at low to moderate exercise intensities (range 33-65% VO2max). Most published scientific studies, however, have measured fat oxidation at only two or three different exercise intensities. This has made it difficult to accurately determine the exercise intensity that elicits maximal fat oxidation. Hence, very recently in our human performance laboratory at the University of Birmingham we have systematically studied fat oxidation over a large range of exercise intensities in order to identify the exercise intensity at which fat oxidation is maximal, which we have called "Fatmax".

      In our study we used an incremental cycling exercise protocol with 5-minute stages and 35-watt work rate increments to determine Fatmax. We found that Fatmax was located at 64±4%VO2max, corresponding to 74±3%HRmax. In addition to Fatmax, a Fatmax-zone was also determined. This zone was defined as a range of exercise intensities with fat oxidation rates within 10% of fat oxidation rates at Fatmax. The results of this study are shown in Figure 1 and indicate that fat oxidation rates are within 10% of the peak rate over a relatively large range of intensities (between 55±3% and 72±4%VO2max; corresponding to between 68±3% and 79±3%HRmax).

      So this is the intensity of exercise that people should aim to do in order to maximise their fat burning. It would be advisable for those unaccustomed to exercise to do dynamic exercise (e.g. cycling, running, aerobics or swimming) at the low end of this range, as of course the other important factor is how long you exercise for. No point in trying to exercise at the upper end of this range if you are going to have to stop due to fatigue after only a few minutes!

      Figure 1: Data from the University of Birmingham Fatmax study. Fat oxidation rates (in grams per minute) are plotted against exercise intensity expressed as percentage of VO2max (%VO2max). Data are based on 11 male subjects of moderate fitness. Need to put in fatmax zone bit


      It must be noted that the absolute rates of fat oxidation are dependent on carbohydrate intake. It has been shown in numerous studies that ingestion of carbohydrate (e.g. starchy foods such as potatoes, cereals, rice, bread and pasta, sweets and sports drinks) in the hours before exercise, reduces the rate of fat oxidation in a subsequent exercise bout. To prevent a carbohydrate-induced decrease in fat oxidation rates, all exercise tests in our study were performed after an overnight fast. However, although it is known that carbohydrate intake can influence the absolute rate of fat oxidation during exercise, it is not known whether the intensity at which this occurs is also influenced.



      Exercise training

      Endurance training increases the capability for fat oxidation. In the trained muscles there are more mitochondria (the powerhouses of the cell where oxidation of fuel takes place) and increased concentrations of enzymes involved in fat oxidation. There is a greater reliance on fat as a source of energy during submaximal exercise at the same absolute work rate in trained individuals compared with the untrained. Adipose fat tissue becomes more sensitive to the effects of hormones such as adrenaline which mobilise fat from its storage sites when needed for exercise. Training also increases the activities of both muscle and adipose tissue lipoprotein lipase, an enzyme that facilitates the use of circulating triglyceride fat as a fuel source for the trained muscles and promotes the clearance of circulating triglycerides even at rest. Hence, one advantage of becoming fitter is that you can burn even more fat when you exercise.
      References and further reading
      Achen J, Gleeson M and Jeukendrup AE. (2001). Determination of the optimal exercise
      intensity that elicits maximal fat oxidation. Medicine and Science in Sports and Exercise, 33 Supplement: S52.
      Arnos PM, Sowash J and Andres FF. (1997). Fat oxidation at varied work intensities using
      different exercise modes. Medicine and Science in Sports and Exercise, 29
      Supplement: S199.
      Horowitz J, Mora-Rodriguez R, Byerley L and Coyle E. (1997). Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. American
      Journal of Physiology, 273: E768-E775.
      Maughan RJ, Gleeson M and Greenhaff PL (1997). Biochemistry of exercise and training.
      Oxford: Oxford University Press.
      Thompson DL, Townsend KM, Boughey R, Patterson K and Basset DR. (1998). Substrate
      use during and following moderate- and low-intensity exercise: Implications for weight control. European Journal of Applied Physiology, 78: 43-49.

      By Professor Mike Gleeson
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • I'd appreciate it if you state where you got these from.
      Nothing personal but I've been at this since 9 this morning and just had my pc crash on me and have to start all over again :rolleyes:

      BTW I am still researching this, one thing that is not easy is finding research on high intenity exercise during ketosis. All research I'm finding that is recommending ketosis and exercise (for example cyclist on 85% fat diets) are all based on moderate </= 70% max heart rate which is what we recommend anyway :rolleyes:

      But heres a little snippet on the atkins site on what heart rate they recommend which if my reading is correct is 60-70% of max heart rate:

      Find Your Target Heart-Rate Zone
      Here's how to calculate your Target Heart-Rate zone: Subtract your age from 220, and then take 60 per cent and 70 per cent of that number. Mathematically, the formula works out as follows: (220 – age) x .60, and (220 – age) x .70 = THR zone.

      So the sample calculation for a 58-year-old woman would be: 220 – 58 = 162 x .60 = 97, and 162 x .70 = 113

      This woman should keep her pulse between 97 and 113 beats per minute while exercising. Very overweight people should be especially careful because they may reach the high end of their zone quite quickly.


      atkins-uk.com/Archive/2001/11/30-428919.html
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • Optimizing fat oxidation through exercise and diet.

      Optimizing fat oxidation through exercise and diet.

      Achten J, Jeukendrup AE.

      ncbi.nlm.nih.gov/entrez/query.…stract&list_uids=15212756

      School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom. jachten@bham.ac.uk

      Interventions aimed at increasing fat metabolism could potentially reduce the symptoms of metabolic diseases such as obesity and type 2 diabetes and may have tremendous clinical relevance. Hence, an understanding of the factors that increase or decrease fat oxidation is important. Exercise intensity and duration are important determinants of fat oxidation. Fat oxidation rates increase from low to moderate intensities and then decrease when the intensity becomes high. Maximal rates of fat oxidation have been shown to be reached at intensities between 59% and 64% of maximum oxygen consumption in trained individuals and between 47% and 52% of maximum oxygen consumption in a large sample of the general population. The mode of exercise can also affect fat oxidation, with fat oxidation being higher during running than cycling. Endurance training induces a multitude of adaptations that result in increased fat oxidation. The duration and intensity of exercise training required to induce changes in fat oxidation is currently unknown. Ingestion of carbohydrate in the hours before or on commencement of exercise reduces the rate of fat oxidation significantly compared with fasted conditions, whereas fasting longer than 6 h optimizes fat oxidation. Fat oxidation rates have been shown to decrease after ingestion of high-fat diets, partly as a result of decreased glycogen stores and partly because of adaptations at the muscle level.
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • Maximal fat oxidation during exercise in trained men.

      Maximal fat oxidation during exercise in trained men.

      Achten J, Jeukendrup AE.

      ncbi.nlm.nih.gov/entrez/query.…stract&list_uids=14598198

      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.

      Publication Types:

      * Clinical Trial
      * Validation Studies


      PMID: 14598198 [PubMed - indexed for MEDLINE]
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • Effect of exercise intensity on skeletal muscle AMPK signaling in humans.

      Effect of exercise intensity on skeletal muscle AMPK signaling in humans.

      Chen ZP, Stephens TJ, Murthy S, Canny BJ, Hargreaves M, Witters LA, Kemp BE, McConell GK.

      St. Vincent's Institute of Medical Research, University of Melbourne, Fitzroy, Victoria, Australia.

      ncbi.nlm.nih.gov/entrez/query.…stract&list_uids=12941758

      The effect of exercise intensity on skeletal muscle AMP-activated protein kinase (AMPK) signaling and substrate metabolism was examined in eight men cycling for 20 min at each of three sequential intensities: low (40 +/- 2% VO(2) peak), medium (59 +/- 1% VO(2) peak), and high (79 +/- 1% VO(2) peak). Muscle free AMP/ATP ratio only increased at the two higher exercise intensities (P < 0.05). AMPK alpha 1 (1.5-fold) and AMPK alpha 2 (5-fold) activities increased from low to medium intensity, with AMPK alpha 2 activity increasing further from medium to high intensity. The upstream AMPK kinase activity was substantial at rest and only increased 50% with exercise, indicating that, initially, signaling through AMPK did not require AMPK kinase posttranslational modification. Acetyl-CoA carboxylase (ACC)-beta phosphorylation was sensitive to exercise, increasing threefold from rest to low intensity, whereas neuronal NO synthase (nNOS) micro phosphorylation was only observed at the higher exercise intensities. Glucose disappearance (tracer) did not increase from rest to low intensity, but increased sequentially from low to medium to high intensity. Calculated fat oxidation increased from rest to low intensity in parallel with ACC beta phosphorylation, then declined during high intensity. These results indicate that ACC beta phosphorylation is especially sensitive to exercise and tightly coupled to AMPK signaling and that AMPK activation does not depend on AMPK kinase activation during exercise.

      PMID: 12941758 [PubMed - indexed for MEDLINE]
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    • Thanks Sam :)

      I will find some more today. I tell you this has been very interesting and I have found out lots of interesting tidbits whilst sifting though all of these articles.
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • Yeah I just had a quick look and I don't see what point hes trying to make :confused:

      I know there seems to be contradictions, but the biggest ones I see are all the studies proving exercise in ketosis (ones atkins uses) are all using moderate intensity and not high...

      For example those cyclists who were on an 85% high fat diet for 4 weeks were tested at moderate intensity (70% or lower).

      Did you know also the trend for higher fat diets on exercise are also meaning lower protien.

      The one fact that all these studies here are showing is that as you get to a higher intensity your body switches over to using carbohydrates as fuel, making it even more reason to use lower intensities for fat loss no matter what diet you are on

      On top of that your lactic threshhold can be lower then elite athletes as it is individual which gives even more reason to play it safe...

      The theme that I seem to be getting from all this is higher intensities are much better in short durations for fitness not fat loss.

      Oh and one other theme I am finding is that lower intensities are even more important for males as they tend to have a lower threshhold...
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • i haven't even made it through half of this fascinating stuff you've been posting yet!! let alone understanding it.
      I don't see what point hes trying to make
      i think that he doesn't believe this:
      The one fact that all these studies here are showing is that as you get to a higher intensity your body switches over to using carbohydrates as fuel, making it even more reason to use lower intensities for fat loss no matter what diet you are on
      .
      cheers, sam

      go hard...or go home
    • i think that he doesn't believe this:

      quote:The one fact that all these studies here are showing is that as you get to a higher intensity your body switches over to using carbohydrates as fuel, making it even more reason to use lower intensities for fat loss no matter what diet you are on

      .


      If anything is going to answer that this will: bioscience.org/1998/v3/d/holloszy/holloszy.pdf

      It is a great article on the crossover point and the carbohydrate and fat metabolism during exercise. It looks at both high carb and low carb. It explains about carbohydrates needing to be utilised the high the level of intensity.

      It also explains why people say that low carbohydrate diets spare muscle and a good thing to note is it does mention that we utilize fat better during exercise after a prolonged high fat diet.

      This actually helps us use less carbohydrates during exercise but we still utilise more fat during moderate to low exercise.
      Low Carb in a Nutshell ~ Carb Counts ~ Research ~ Measurements/Conversions ~ Glossary


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    • "He" speaks!:)

      Hi Sherrie,

      1. Thanks for doing all Sam’s homework!
      2. I have read all that plus a whole lot more.
      3. You may have come in a bit late into this discussion, but what “he” is “on about” stems from Sam’s advice to a newcomer to restrict her exercise to 70% of her heart rate – and, as I understood her comment, this was because she was on a low carb diet (not that she needed to start a new exercise program cautiously – which I think is what Atkins means).
      4. I don’t believe this to be a specific limitation of low carb diets, but as you rightly point out there are issues that affect the proportion of fat being oxidised which occur at around this point, which may have an impact on the efficiency of various types of exercise as they relate to fat loss.

      OK, lets start with the basic energy pathways (something we can agree on!).

      During the initial 2-3 seconds of (anaerobic) exercise, energy is derived from the splitting of adenosine triphosphate (ATP) producing adenosine diphosphate (ADP) that is stored in the muscle. This low reserve (approx. 85 g in the whole body) is only enough to perform maximum exertion for a few seconds (power lifters executing lifts of their 1 rep max, for example). ATP is quickly depleted after which the body resorts to the next energy pathway - splitting creatine phosphate (CP) into creatine and phosphate (a reaction catalylzed by the enzyme creatine kinase that produces more energy) - this liberated phosphate combines with ADP to regenerate ATP. As CP becomes depleted (circa. 4-20 seconds of maximum effort), the body engages the anaerobic lactate (glycolytic) system in which the energy source is the muscle's storage form of glucose (glycogen). Glycogen is broken down in order to produce more CP (which in turn is used to produce more ATP). A by-product of this process is lactic acid (i.e., when you feel the 'burn' you are burning sugar). The fourth energetic pathway is the aerobic pathway, which utilizes oxygen to eliminate the lactic acid (and indirectly produce more ATP) resulting in carbon dioxide and water as by-products (eliminated via respiration). This pathway takes place at times beyond which maximum physical exertion is possible (or desirable). Note: this is why some moderate aerobic activity is useful following a heavy anaerobic training session as it helps clear out residual lactic acid. The aerobic or oxidative pathway uses mobilized fatty acids as a predominant fuel source, however when intensity increases (at higher heart rate levels) for example when performing exercises such as sprints and HIIT (where you literally become out of breath) you are no longer performing in this pathway and the training becomes anaerobic in nature - the dominant fuel is once again muscle glycogen. NB you will actually still be burning more fat than you were at lower intensity but a greater proportion of total energy will be coming from glycogen.

      In terms of elite athletic performance the primary energy source for sprinting distances up to 400 m is stored ATP/CP. From 400 m to 1,500 m, anaerobic glycolysis is the primary energy source. For distances longer than 1,500 m, athletes rely primarily on aerobic metabolism.

      It appears, from the limited research done in the context of restricted carbohydrate diets, that when this “cross over point” occurs (when anaerobic glycolysis again provides more than 50% of energy requirements) can be changed by both dietary adaptation and muscle building/training. In “Ketogenic diets and physical performance” - Stephen D. Phinney in the August issue of Nutrition & Metabolism cites the studies that have demonstrated that ketogenic diets (and also those understood as "very low" in carbohydrates) do not necessarily impair physical performance' in fact they may actually improve it provided that adaptation is allowed so the body adjusts. For how long? Those studies show that takes about 4-6 weeks. It would be very interesting to see longer term studies to examine whether this adaptation improved further with time. One thing that does appear clear from this research is that for any such adaptation to have effect consistent adherence to the low carb diet is essential or the adaptive benefits are lost. This calls into question the wisdom of CKD type strategies at least in terms of endurance fitness.

      This brings into focus the reason that the average low carb dieter exercises in the first place, because optimal performance is not our primary goal – stimulating fat metabolism and obtaining ongoing health benefits are.

      As Gabriel Guzman points out, “ (this) tells you that whatever exercise you do must be accord to your nutritional approach. To say that "on a low carb diet you shouldn’t exercise at over 70% of your age related maximum heart rate" is arguable and it depends on the type of exercise is being referred to. For example, most people think that weight lifting cannot be done on a carbohydrate restricted diet. In fact, it can. Moreover, it can be done so it becomes an "aerobic" exercise instead of the common "anaerobic" strength training. How is that possible? In short, by adjusting the load to give enough resistance to the muscle and by working the muscle at a pace that will take the energy production system beyond the utilization of glycogen. The word "aerobic" has little to do with how fast one breathes, but with how efficient is the extraction of oxygen from the blood. How fast we breathe is just a signal that the body is trying to get rid of excess carbon dioxide …

      ... Health benefits come as a result of adaptation to exercise and include lower heartbeat at rest (the heart doesn't need to pump too fast), higher "pump" (the heart pumps strongly enough so it doesn't need to pump too fast), which of course results in an improvement in blood pressure. Weight loss, cardiovascular tone, improved aerobic capacity, all those are health benefits. Fitness benefits, on the other hand, come after health benefits have been achieved, normally as a result in an increase in the intensity and the frequency of exercise. An overweight person doesn't achieve a great time sprinting or swimming or bicycling before his/her health has improved a great deal - after exercise is incorporated.”

      Now I am sure we would agree that the most suitable exercise for fat burning would be one that uses mainly fat as fuel and for longer time. In that regard, we must remember that only trained muscles become efficient fat burners and strength training is not the only way of training muscles. Resistance exercise, which can be done focused either on strength or power, provides the necessary stimulus to the muscles to develop. Such development is translated in either increase in muscle mass (if the exercise is tailored so it is sustained mainly by glycogen utilization) or increase in density (if the exercise encourages the muscles to rely on fat utilization to supply the energy demand imposed by resistance training). In both instances, enough resistance encourages muscle repair, which in turn encourages more protein synthesis, which in turn requires a great deal of energy. That doesn't happen during the actual training session but afterwards and it lasts even hours after the training session. At rest, it is not likely that already depleted muscle glycogen will be called to supply for the energy that supports protein synthesis, thus it is the energy that is in store that is called upon to supply this demand, resulting in the utilization of fatty acids for that purpose.

      Even if training at a higher heart rate may appear to offer diminishing returns for fat oxidation, it can still act as a trigger to stimulate lipolysis in the hours following exercise. Intense exercise stimulates the production of more mitochondria (“fat burning furnaces”) within the cells. Intense exercise, such as taking a muscle group to ‘failure’ point, stimulates the production and activity of an enzyme called “AMP kinase” which ‘switches on’ fat burning and keeps it going for some hours after you stop exercising. The danger often cited of this approach for low carb dieters - that of muscle catabolism as an alternative energy supply if glycogen is sufficiently depleted and fatty acid oxidation cannot keep up with energy demand in reality should only apply to elite athletes. For ordinary mortals like me, you, or the average overweight low carber, the reality is that the build up of lactic acid in the muscles will of itself prevent a long enough period of maximal exercise intensity to cause such problems. In the mean time, occasional bursts of high intensity exercise (such as interval training) combined with resistance training of the muscles involved plus the long term adaptation of the body to diet are all highly conducive to a low carb way of life.

      Cheers,

      Malcolm
      Started LC (PP) Dec 2003
      114/86.5/85
      BF 30+/17/15
    • In the mean time, occasional bursts of high intensity exercise (such as interval training) combined with resistance training of the muscles involved plus the long term adaptation of the body to diet are all highly conducive to a low carb way of life.


      Yes I don't disagree with you (ofcourse HIIT is something people have to work up to), my reason for looking into this which I must say was alot of fun (I learnt alot) was because we have a few members here wanting to go full on and run etc... So I wanted to do this not only in hope that they may read it and be careful ;) but for my own knowledge aswell.

      I've seen lots of good feedback on HIIT (when doing this I saw a few good studies on this too), you just have to look at the bodies of sprinters for example.
      I tried it last year but I had been at the dieting for way too long by then which could be why for me it didn't work.
      One way you could incorporate this into your walk is by adding in some hills.

      But at the same token there seems to be an equal amount of encouraging feedback about longer duration low to moderate exercise and alot of people swear by that from their experiences too (For example body builders trying to reach or helping others to reach those ultra low bodyfat levels). Which I wouldn't ignore either as first hand experience is always a good thing and being easier on the body is the best place to start.
      Maybe which one is the best of the two is individual?

      Those studies you speak of if they were the ones that I am thinking of (for example the ones atkins speaks of) they were still only doing moderate exercise. I didn't actually find much where people on ketogenic diets did high intensity exercise for longer then the shorter bursts involved in HIIT. Mind you for most of these I could only find abstracts.

      But regardless of any strength or resistance training this was more for the argument of longer periods of low to moderate excerise compared to say doing a long run, aerobics for an hour etc...

      BTW I'm glad you posted, its always good to have more people to learn from.
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