Experimental studies also support mitochondrial transfer or mitochondrial-support signaling as a contributor to recovery [31,32,33,34,35]
This is distinct from stimulants or acetylcholinesterase inhibitors, which modulate neurotransmitter availability rather than synaptic architecture
However, since here no specific tests on testosterone release at the testicular level were performed, it cannot be definitively assumed that this phenomenon is directly related to HnB exposure on gonadal function
No human data exists
And the specific adjustments that separate mediocre results from optimal outcomes
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