Research Blog

Exercise and Heart Physiology

heart physiology

A 2011 paper uses MRI technique to challenge a hypothesis developed in 1975. The study found that endurance training increases left ventricular mass by increasing ventricular wall thickness and volume. Resistance training produced no affect on the heart.  

The body adapts to exercise by changing the physiological parameters of the heart. Changes are observed in the left ventricle, the chamber responsible for pumping blood throughout the body (as opposed to the right ventricle, which pumps blood through the pulmonary circuit). The left ventricular end-diastolic volume is the volume of the left ventricle just before contraction (systole).

In 1975 the Morganroth Hypothesis was proposed (Comparative Left Ventricular Dimensions in Trained Athletes, 1975, Joel Morganroth, et al.). Morganroth and team studied the hearts of varsity college athletes in the sports of wrestling, swimming and endurance running as well as world-class track and field athletes.  The hearts were studied echocardiographically, a revolutionary, non-invasive technique at the time, but primitive compared to today's MRI instruments. They found that the athletes involved in isotonic exercise (swimming and running) had a greater left ventricular mass due to a greater left ventricular end-diastolic volume. However, their ventricular wall thickness was no different than non-athletes. The athletes involved in isometric exercise (shot put and wrestling) were found to have a greater left-ventricular wall thickness than non-athletes. However, no difference in left ventricular end-diastole volume was observed.  The increase in ventricular volume in isotonic athletes and ventricular wall thickness in ventricular wall thickness in isometric athletes independently resulted in an increase in left ventricular mass as the figure below demonstrates.

Screen Shot 2012-06-28 at 12.39.37 PM

The Morganroth hypothesis was challenged by a paper released in 2011 (A prospective randomised longitudinal MRI study of left ventricular adaptation to endurance and resistance exercise training in humans, 2011, Spence AL, et al.).  Study participants were put through a 24-week training program. The training program came in two flavors: endurance or resistance. The longitudinal study measured heart parameters using MRI at baseline, at the end of the training program and after a detraining period. The study found no significant difference in the heart physiology in the resistance trained group. However, the endurance trained group showed an increase in both left ventricle volume and ventricular wall thickness. As the figure below shows, after the detraining period the left ventricle wall thickness decreased, but the left ventricular volume did not change in the endurance trained participants.

                 Impact of exercise training and detraining on MRI derived measures of cardiac mass, volume and wall thickness Bars represent percentage change from baseline after training (filled bars) and detraining (open bars) values in the endurance (upper panel) and resistance-trained (lower panel) groups. *P < 0.05 post-training vs. baseline, †P < 0.05 post-detraining vs. baseline. For measures of IVS, PWT, LVIDd and LVIDs, n= 7 for endurance group.  EDV, end-diastolic volume; ESV, end-systolic volume; LVM, left ventricular mass; LVMi, left ventricular mass index; LVIDd, left ventricular internal diameter during diastole; LVIDs, left ventricular internal diameter during systole; IVS, interventricular septal thickness; PWT, posterior wall thickness.

In the endurance trained group left ventricular mass increased an average of 8%. Some other interesting findings from the study include the fact that fitness was retained in the resistance group and endurance group as measured by bench press, push-ups and squats after detraining. Leanness was conserved in the resistance group, but not the endurance group, after detraining.

In summary, advances in MRI imaging of the heart allow more precise measurements of changes in the heart. Using MRI, researchers found that left ventricular mass increased via volume and thickness in endurance trained athletes. However, no physiological changes in the heart were seen in the resistance trained group.

Muscle Fiber Influence on Motor Neurons


A team of Harvard researchers found that muscle fibers have retrograde influence on motoneurons.

Athletes generally refer to muscle fibers as "fast twitch" and "slow twitch" depending on muscle contraction speed. From slowest to fastest, the muscles are designated type I, IIA, IIX, IIB. Studies have shown that each motor neuron is homogenous for the muscle fibers it operates. Thus, a slow motoneuron would operate a bundle of slow twitch motor muscle fibers.

Muscle fibers can be converted to a different muscle fiber type by attachment to a alternate motoneuron. For example, a slow twitch muscle fiber can be converted to a fast twitch muscle fiber via attachment to a fast motoneuron. The question then becomes can this mechanism operate in reverse?  In other words, can muscle fibers cause the motoneurons to change from fast to slow and vice versa?  

This is the question a team of Harvard researchers sought to address (Retrograde influence of muscle fibers on their innervation revealed by a novel marker for slow motor neurons, 2010, Joe V. Chakkalakal, et al.). 

The researchers introduced a novel marker of slow motoneurons, SV2A. Using immunofluorescence staining the researchers could mark slow motoneurons.  Fast twitch muscle fibers were converted to slow twitch muscle fibers using the transcriptional cofactor PGC-1alpha (discussed in this post on smoking). It was found that an increase in slow twitch muscle fibers led to an increase in slow motoneurons. The possible mechanisms by which an increase in slow-twitch muscle fibers (via PGC-1alpha) increases slow motoneurons synaptic connections is shown below.

Three possible mechanisms by which PGC-1alpha can increase the amount of slow motor neuron terminals.  This study confirms that the mechanism is conversion.

The increase in slow motoneurons demonstrates that the mechanism increasing slow synaptic connections is the conversion of motoneurons from fast to slow.  Motoneurons ability to undergo conversion suggests that they have some postnatal plasticity. The authors suggest that there may be a combination of prenatal and postnatal determinants of motoneuron type.  

The physiology of motoneurons and their relationship with muscle fibers may have interesting ramifications on the way we look at training. Evidently more than muscle fiber type and capillary proliferation are at play during training. 

Why Caffeine Boosts Performance

clif bar shots

Caffeine, packed into the gel packs to the right, boosts athletic performance by regulating glucose-related metabolic pathways.

If you are an endurance athlete you have probably taken caffeine before a competition. Many studies have shown that caffeine boosts both maximum speed and endurance. The question that will be addressed here is how caffeine boosts performance from a biological stand point.  

Caffeine raises blood glucose levels by influencing the regulation of cellular respiration (breakdown of glucose to energy), glycogen metabolism and fatty acid metabolism.  So to understand how caffeine works, a basic understanding of the regulation of cellular respiration, glycogen metabolism and fatty acid metabolism are necessary. These three metabolic pathways are all regulated by Protein Kinase A (PKA). PKA targets 6 different enzymes in our metabolism.  

Structure of Caffeine

PKA blocks fatty acid biosynthesis, the synthesis of fat from the glucose derivative acetyl CoA. Fatty acid oxidation, the breakdown of fatty acids to energy (in the form of free fatty acids which are exported to muscle cells) is inhibited by fatty acid biosynthesis. This prevents fatty acid biosynthesis and fatty acid oxidation from occurring in a cell simultaneously.  Therefore, PKA essentially activates fatty acid oxidation by inhibiting fatty acid biosynthesis. This increases  free fatty acids in the blood released by adipocytes. With higher free fatty acid concentration in the blood, muscle cells have an easier time grabbing them and using them for energy.  

In the liver, PKA activates glycogen breakdown to glucose and inhibits glycogen synthesis. This increases blood glucose levels allowing muscle cells to grab more glucose. The liver also releases more glucose because the breakdown of amino acids to glucose is activated by PKA.

Caffeine does not directly regulate PKA levels. There are several steps, in fact, to get from caffeine to increased levels of PKA. Caffeine inhibits cyclic nucleotide phosphodiesterase, an inhibitor of cyclic AMP. Thus, because caffeine knocks out the inhibitor of cyclic AMP, caffeine raises cyclic AMP levels via cyclic nucleotide phosphodiesterase. Cyclic AMP in turn activates PKA by phosphorylating the inactive PKA. In summary, caffeine inhibits cyclic nucleotide phosphodiesterase which in turn causes cAMP activity to rise causing PKA levels to rise.

Caffeine elicits a similar response in the liver, adipocytes and muscle cells as the hormone glucagon (activated by low-blood glucose) and the fear-response hormone adrenaline.

Caffeine boosts athletic performance because it increases the muscle's quick energy supply. If caffeine is in the body for an hour before the athletic performance, the muscle spends that hour building its energy reserves so that it is available for expenditure during competition.

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