The effects of voluntary isocapnic hyperpnea (VIH) training (10 h over 4 weeks, 30 min/day) on ventilatory system and running performance were studied in 15 male competitive runners, 8 of whom trained twice weekly for 3 more months. Control subjects (n = 7) performed sham-VIH. Vital capacity (VC), FEV1, maximum voluntary ventilation (MVV), maximal inspiratory and expiratory mouth pressures, VO2max, 4-mile run time, treadmill run time to exhaustion at 80% VO2max, serum lactate, total ventilation (V(E)), oxygen consumption (VO2) oxygen saturation and cardiac output were measured before and after 4 weeks of VIH. Respiratory parameters and 4-mile run time were measured monthly during the 3-month maintenance period. There were no significant changes in post-VIH VC and FEV1 but MVV improved significantly (+10%). Maximal inspiratory and expiratory mouth pressures, arterial oxygen saturation and cardiac output did not change post-VIH. Respiratory and running performances were better 7- versus 1 day after VIH. Seven days post-VIH, respiratory endurance (+208%) and treadmill run time (+50%) increased significantly accompanied by significant reductions in respiratory frequency (-6%), V(E) (-7%), VO2 (-6%) and lactate (-18%) during the treadmill run. Post-VIH 4-mile run time did not improve in the control group whereas it improved in the experimental group (-4%) and remained improved over a 3 month period of reduced VIH frequency. The improvements cannot be ascribed to improved blood oxygen delivery to muscle or to psychological factors.
There is no consensus on the best diet for exercise, as many variables influence it. We propose an approach that is based on the total energy expenditure of exercise and the specific macro- and micronutrients used. di Prampero quantified the impact of intensity and duration on the energy cost of exercise. This can be used to determine the total energy needs and the balance of fats and carbohydrates (CHO). There are metabolic differences between sedentary and trained persons, thus the total energy intake to prevent overfeeding of sedentary persons and underfeeding athletes is important. During submaximal sustained exercise, fat oxidation (FO) plays an important role. This role is diminished and CHO's role increases as exercise intensity increases. At super-maximal exercise intensities, anaerobic glycolysis dominates. In the case of protein and micronutrients, specific recommendations are required. We propose that for submaximal exercise, the balance of CHO and fat favors fat for longer exercise and CHO for shorter exercise, while always maintaining the minimal requirements of each (CHO: 40% and fat: 30%). A case for higher protein (above 15%) as well as creatine supplementation for resistance exercise has been proposed. One may also consider increasing bicarbonate intake for exercise that relies on anaerobic glycolysis, whereas there appears to be little support for antioxidant supplementation. Insuring minimal levels of substrate will prevent exercise intolerance, while increasing some components may increase exercise tolerance.
Although statin therapy normalizes blood lipoproteins, it reduced fat metabolism in older individuals, which cannot be a result of lower availability from blood.
Cholesterol lowering drugs are associated with myopathic side effects in 7% of those on therapy, which is reversible in most, but not all patients. This study tested the hypothesis that total body fat oxidation (TBFO) is reduced by statins in patients with genetic deficiencies in FO, determined by white blood cells (FOwbc) and by molecular analysis of common deficiencies, and would cause intolerance in some patients. Six patients on statin therapy without myopathic side effects (tolerant) and 7 patients who had previously developed statin-induced myopathic symptoms (intolerant) (age = 58 +/- 8.25 yrs, ht. = 169 +/- 11 cm, and wt. = 75.4 +/- 14.2 kg) were tested for TBFO (Respiratory Exchange Ratio, RER) pre- and during exercise. FOwbc was not significantly different between tolerant and intolerant (0.261 +/- 0.078 vs. 0.296 +/- 0.042 nmol/h per 10(9) wbc), or normals (0.27 +/- 0.09 nmol/h per 10(9) wbc) and no common molecular abnormalities were found. Pre-exercise RER (0.73 +/- 0.05 vs. 0.84 +/- 0.05) was significantly lower in the intolerant group and the VO2 at RER = 1.0 (1.27 +/- 0.32 vs. 1.87 +/- 0.60 L/min) greater than the tolerant. Post-exercise lactates were not different between groups. Although dietary fat intake was not different, blood lipoprotein levels, particularly triglycerides were 35% lower in tolerant than previously intolerant. TBFO and blood lipoproteins were reduced in tolerant patients in spite of the absence of genetic limitations, but not in the intolerant group as hypothesized. Although not conclusive, these data suggest the need for a prospective study of the effects of statins on fat oxidation.
Background: Previous studies have suggested reduced fat metabolism in older subjects. However, corrections for their reduced maximal oxygen consumption and the effects of training and substrate availability have not been fully examined. Objectives: Fat metabolism (FM) in older subjects (n = 14, 75 ± 7 yrs), and the effects of exercise training were compared with FM in younger subjects (n = 16, 22 ± 3 yrs). Materials and Methods: All subjects completed a maximal exercise test and a sustained submaximal run at 70% of their maximal capacity. The respiratory exchange ratio (RER) and blood substrate levels were determined. Older subjects were re-tested after training. Results: Young subjects had higher oxygen consumption (VO 2 ) peak (36.3 ± 6.7 vs. 23.7 ± 6.2 ml/kg/min) and lower slope of RER vs. VO 2 than older subjects. However, the slope of the RER vs. VO 2 relationship was not different between younger and older subjects, after correction for their VO 2 peaks. Younger subjects had longer sustained exercise times (45.5 ± 17.6 min) than the elderly (30.2 ± 14.0 min), pre-training. Posttraining, there was a significant increase in VO 2 peak (25%) in older subjects (P = 0.001) and submaximal exercise time (30.2 ± 14.0 vs. 58.3 ± 27.3min, P = 0.020). Respiratory exchange ratio was reduced during both exercises after training (0.90 ± 0.03 vs. 1.00 ± 0.03, P = 0.04). Conclusions: The RER of older subjects was not different from that of younger subjects, after correction for the VO 2 peak. The VO 2 peak, sustained exercise time, and RER decreased after training in older subjects, indicating increased fat metabolism.
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