Fuel selection, muscle fibre

Hultman, E.

doi:10.1079/pns19950041

Cited by 52 publications

(43 citation statements)

References 40 publications

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“…50,51 Another important factor in this context is the recruitment of muscle fibres at different exercise intensities. Generally, type II fibres are recruited at higher intensities 52 and this could also influence substrate utilization.…”

Section: Distribution Of Muscle Fibresmentioning

confidence: 99%

Optimal exercise intensities for fat metabolism in handbike cycling and cycling

2004

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Study design: Energy expenditure (EE) and fat oxidation in handbike cycling compared to cycling in order to determine the intensity that elicits maximal fat oxidation in handbike cycling. Objective: To establish the exercise intensity with the highest fat oxidation rate in handbike cycling compared with cycling (control group) in order to give training recommendations for spinal cord-injured (SCI) athletes performing handbike cycling. Setting: Institute of Sports Medicine, Swiss Paraplegic Centre, Nottwil, Switzerland. Methods: Eight endurance-trained handbike cyclists (VO 2 peak handbike cycling 37.577.8 ml/kg/ min) and eight endurance trained cyclists (VO 2 peak cycling 62.574.5 ml/kg/min) performed three 20-min exercise blocks at 55, 65 and 75% VO 2 peak in handbike cycling on a treadmill or in cycling on a cycling ergometer, respectively, in order to find the intensity with the absolutely highest fat oxidation. Results: The contribution of fat to total EE was highest (39.1716.3% EE) at 55% VO 2 peak in handbike cycling compared to cycling, where highest contribution of fat to EE (50.8713.8%) was found at 75% VO 2 peak. In handbike cycling, the highest absolute fat oxidation (0.2870.10 g/min) was found at 55% VO 2 peak compared to cycling, where highest fat oxidation (0.6770.20 g/min) was found at 75% VO 2 peak. Conclusion: Well-trained handbike cyclists have their highest fat oxidation at 55% VO 2 peak handbike cycling compared to well-trained cyclists at 75% VO 2 peak cycling . Handbike cyclists should perform endurance exercise training at 55% VO 2 peak handbike cycling , whereas well-trained cyclists should be able to exercise at 75% VO 2 peak cycling . For training recommendations, the heart rate at 55% VO 2 peak handbike cycling lies at 13576 bpm in handbike cycling in SCI compared to 147714 bpm at 75% VO 2 peak cycling in well-trained cyclists. We presume that the reduced muscle mass involved in exercise during handbike cycling is the most important factor for impaired fat oxidation compared to cycling. But also other factors as fitness level and haemodynamic differences should be considered. Our results are only applicable to well-trained handbike cyclists with SCI and not for the general SCI population.

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Section: Distribution Of Muscle Fibresmentioning

confidence: 99%

Optimal exercise intensities for fat metabolism in handbike cycling and cycling

2004

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“…In addition, type I fibres show low activity of ATPase, creatine kinase and glycolytic enzymes. Their activating motor neurons are small (35) . In this context, it is important to acknowledge that mitochondria produce about 90 % of ATP required for cellular functioning during oxidative phosphorylation (29) .…”

Section: Mechanisms Of Wasting: Skeletal Musclementioning

confidence: 99%

“…The first description of different muscle fibre types dates back to 1873, when Louis Ranvier described red and white muscles in rabbits and rays as either tonicslow or tetanic-fast, respectively (34) . Red muscles, now known to be primarily composed of type I fibres, possess high oxidative capacity due to high mitochondrial density, high myoglobin content and a high number of capillaries (35) . Their metabolic profile is adjusted to their long twitch contraction time and their low force production, which also makes them resistant to fatigue.…”

Section: Mechanisms Of Wasting: Skeletal Musclementioning

confidence: 99%

“…Not only are they activated by larger motoneurons, which means that the level of excitation will determine the pool of neurons and thus the fibre type that will contract, but they also possess high ATPase, creatine kinase and anaerobic glycolysis activity. Further, type II fibres are differentiated into type IIA and IIB fibres, which have different oxidative capacities (35) . The fibre composition of any muscle can be subject to change in response to appropriate stimuli; for example, reduced muscular activity will yield slow-to-fast fibre transformation (36) .…”

Section: Mechanisms Of Wasting: Skeletal Musclementioning

confidence: 99%

See 1 more Smart Citation

The wasting continuum in heart failure: from sarcopenia to cachexia

Haehling

2015

Proc. Nutr. Soc.

104

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Conference on 'Nutrition and age-related muscle loss, sarcopenia and cachexia' Symposium 2: Mechanisms for loss of muscle mass, strength and clinical measurement of malnutrition and cachexiaThe wasting continuum in heart failure: from sarcopenia to cachexiaStephan von Haehling Sarcopenia (muscle wasting) and cachexia share some pathophysiological aspects.Sarcopenia affects approximately 20 %, cachexia <10 % of ambulatory patients with heart failure (HF). Whilst sarcopenia means loss of skeletal muscle mass and strength that predominantly affects postural rather than non-postural muscles, cachexia means loss of muscle and fat tissue that leads to weight loss. The wasting continuum in HF implies that skeletal muscle is lost earlier than fat tissue and may lead from sarcopenia to cachexia. Both tissues require conservation, and therapies that stop the wasting process have tremendous therapeutic appeal. The present paper reviews the pathophysiology of muscle and fat wasting in HF and discusses potential treatments, including exercise training, appetite stimulants, essential amino acids, growth hormone, testosterone, electrical muscle stimulation, ghrelin and its analogues, ghrelin receptor agonists and myostatin antibodies.

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“…Nonetheless, prolonged endurance exercise primarily involves recruitment of type I motor units, leaving a large fraction of the type II motor units inactive (Hultman 1995;Vollestad and Blom 1985). Therefore, such approach conceivably underestimates the true amplitude of contraction-induced regulation of intramyocellular signalling pathways.…”

Section: Pln (mentioning

confidence: 99%