Exercise physiology Flashcards
Resting oxygen consumption (VO2)
250ml/min for 70kg man and 220ml/min for 70kg woman
Power generated calculation
250ml per min/60 sec per min x 20 joule/sec = 83 Watts
Max oxygen consumption during exervise
About 1700ml/min
Change in muscle blood flow
15% of blood flow to muscle at rest, can be about 80% maximum during exercise
Net oxygen transport (VO2) change is dependent on
Cardiac output
Difference in oxygen concentrations in arterial and venous blood - so fall in venous saturation must occur during exercise.
Static exercise effect on muscle flow
Muscle at >75% of it’s maximum tension, blood flow is halted and so is overall intermittent. Increases effect of metabotropic reflex.
Increased blood flow to muscles cause
Dilation of local resistance (arteriolar) vessels in exercising muscle, such that capillaries are recruited. Eithre due to metabolic dilation or some sympathetic Beta2 input. Also environment leads to the Bohr shift of the oxygen dissociation curve and so more O2 unloading.
Metabolic dilation
K+, adenosine, H+, pCO2, pO2 and increased warmth all have an unknown contribution on local vasodilation
Redistribution of blood flow in exercise
Increased in muscle, coronary blood flow and respiratory muscle perfusion. Decreased in splanchnic, renal and and non-exercising muscle vasculature due to sympathetic output. Skin is mixed as rising core temperature stimulates dilation for thermoregulation. Contribution of vasoconstriction is overall trivial in redistribution, and more is in homeostatic control of arterial blood pressure by adjusting the total peripheral resistance.
Muscle mechanoreceptors
Small myelinated axons within the muscle, which are stimulated by local pressure and muscle contraction to signal to inccrease sympathetic vasomotor activity
Metaboreceptors
Chemosensitive endings of unmyelinated acons which also reflexly increase sympathetic vasomotor activity, so contributing to exercise pressor response. Activated by ATP, K+, prostaglandings, bradykinin, metabolites of arachidonic acid, lacic acid and adenosine. Chemicals particularly accumulate in static exercise, so causing BP to rise more.
Experiment showing metaboreflex response
Alam and Smirk, 1937. Made subject perform forearm exercises and then inflated a pneumatic cuff around the upper arm to trap local chemical stimulants in the forearm. Exercise pressor response partly maintained after the active exercise had finished and only stopped entirely when the cuff was released.
Experiment showing contribution of circulating catecholamines to CV response
Denervated racing greyhounds remain tachycardic with only slightly lower and slower onset. Due to rising circulating adrenaline and noradrenlaine. In total run only 5% slower. Noradrenaline increase by about 1-10nM due to spill from peripheral terminals, and adrenaline released from adrenal glands.
Central command experiment
Krogh and Lindhard 1913, noted that subjects showed increased ventilation in expectation of work even when the heavy load was not administered. Followed by many experiments, including using hypnosis, eg subjects told to imagine cycling uphill even on same level. Suggests ‘central command’ system by which exercise response (also heart rate and ABP) are controlled.
Increased filling pressure in exercise
Skeletal muscle pump action, alpha venoconstriction and respiratory pump (decreased intrathoracic pressure on deep breath in) all increase venous return, and so right ventricle filling pressure. Hence Frank-Starling mechanism leads to greater strength of contraction.
